Patho Flashcards
Cells of these tissues are continuously being lost and replaced by maturation from stem cells and by proliferation of mature cells. Can readily regenerate after injury as long as the pool of stem cells is preserved.
Labile tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Cells of theses tissues are quiescent and have only minimal replicative activity in their normal state. Capable of proliferating in response to injury or loss of tissue mass.
Stable tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Cells of these tissues are considered to be terminally differentiated and nonproliferative in postnatal life.
Permanent tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Labile, stable or permanent tissues:Bone marrow
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Vaginal epithelium
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Salivary glands
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Liver parenchyma
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Endothelium
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Smooth muscle cells
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
Labile, stable or permanent tissues:Neurons
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Labile, stable or permanent tissues:Cardiac muscle
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
Type of collagen found in basement membrane
Type IV collagen(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.67
This is the most abundant glycoprotein in basement membrane.
Laminin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.68
The pink, soft, granular tissue seen beneath the scab of a skin wound.
Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
Healing of a clean, uninfected surgical incision approximated by surgical sutures
Healing by first intention / Primary Union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.74
Type of healing wherein tissue is allowed to heal by itself before suturing. Used in large wounds, in the presence of abscess, or ulceration.
Healing by secondary intention / secondary union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.76
Wound strength reaches 70 - 80 % of normal in ______ months.
3 months(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Single most important cause of delay in wound healing.
Infection(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
True or false: Complete restoration can occur only in tissues composed of stable and labile cells.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Refers to the restoration of tissue architecture and function after an injury.
Repair (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
True or false:Injury to tissues composed of permanent cells does not result to scarring.
False. Injury to tissues composed of permanent cells, inevitably results to scarring.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Process of replacing damaged components of a tissue, returning to a normal state.
Regeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
Migration and proliferation of fibroblasts with deposition of ECM.
Scar formation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73
Arrange the steps in cutaneous wound healing:A. Formation of granulation tissueB. ECM remodelingC. Inflammation
C, A, B(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
It consists of a series of steps at which the cell checks for the accuracy of replication and mitosis and instructs itself to proceed to the next step.
Cell cycle(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
In the cell cycle, this is called the presynthetic growth phase.
G1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
In the cell cycle, this is also called the premitotic growth phase.
G2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
These steps in the cell cycle prevents DNA replication or mitosis of damaged cells and either transiently stop the cell cycle to allow repair, or eliminate irreversibly damaged cells by apoptosis.
Checkpoint control(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
These enzymes promote DNA replication and various aspects of mitosis. They are required for cell cycle progression. Forms complexes with cyclin.
Cyclin-dependent kinases (CDK)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
This cytokine is released from activated macrophages, and is mitogenic for keratinocytes and fibroblasts. It also stimulates keratinocyte migration and granulation tissue formation.
Epidermal Growth Factor (EGF)(TOPNOTCH)
This cytokine increases vascular permeability and is mitogenic for endothelial cells.
Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.71
Pattern of extracellular signaling wherein the target cell is itself.
Autocrine(TOPNOTCH)
Pattern of extracellular signaling wherein the target cell is adjacent to the secretory cell.
Paracrine(TOPNOTCH)
Pattern of extracellular signaling wherein the target cell is distant to the secretory cell.
Endocrine(TOPNOTCH)
Synthesized by mesenchymal cells, present in the spaces between cells in connective tissue, between epithelium and supportive vascular and smooth muscle structures.
Interstitial Matrix(TOPNOTCH)
Component of ECM which confers tensile strength and recoil.
Fibrous proteins s.a. Collagen and elastin(TOPNOTCH)
Component of ECM that permits resilience and lubrication.
Proteoglycans, hyaluronan(TOPNOTCH)
Component of ECM that connect the elements to one another and to the cells.
Adhesive glycoproteins(TOPNOTCH)
What is the hallmark of tissue repair?
Tissue granulation. (TOPNOTCH)
A 28 y/o male suffered from traumatic injury of the muscles of his left lower extremity. In this type of tissue, repair is typically dominated by? Scar formation or regeneration?
Scar formation. In permanent tissues like skeletal and cardiac muscle, repair is dominated by scar formation. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 101
Liver, kidney and pancreas. Labile, stable or permanent tissues?
Stable. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 101
A patient has a large wound on his right arm as a result of a vehicular crash. Initially his wound is filled with granulation tissue composed of fibroblast and new blood vessels. What is responsible for inducing formation of new blood vessels?
Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)
Following hepatectomy, liver undergo repair by __________.
Regeneration. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 102
Steps in scar formation
Angiogenesis, Formation of granulation tissue, Remodelling. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 102
It is characterized by proliferation of fibroblast and new thin walled, delicate capillaries in a loose ECM often admixed with inflammatory cells.
Granulation tissue. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 103
Roles of macrophage in tissue repair.
Clear offending agent and dead tissue, provide growth factor, secrete cytokines for fibroblast proliferation and connective tissue synthesis.(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 104
Granulation tissue appear after how many days after injury?
3-5 days. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 104
A 50 y/o coal worker experienced gradual onset of dyspnea and non-productive cough. He was then diagnosed with pulmonary fibrosis. What is the most important cytokine that causes the development of fibrosis following chronic inflammation?
Transforming growth factor-? (TGF-?) is the most important cytokine for synthesis and deposition of connective tissue protein. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 105
A 52 y/o diabetic female patient developed a non-healing wound on his right foot. She is currently on an anti-hyperglycemic and an antihypertensive.What factor is the most likely implicated in the abnormal wound healing?
Presence of uncontrolled blood glucose level/Diabetes. (TOPNOTCH)
Cells present within 24 hours of tissue injury.
Neutrophils (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106
Predominant cells on Day 3 after tissue injury
Macrophages.(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106
An important feature in healing by secondary intention/secondary union.
Wound contraction involving formation of myofibroblasts at the edge of the wound. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 108
True or False. Wound strength returns to normal 3 months after a carefully sutured wound.
False. Only up to 70-80% of normal and usually does not improve beyond that. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 108
Patient X had a laceration on his right arm and underwent suture and repair. Wound healing continues, however, the site was disfiguring and developed a raised nodule after 2 months. The abnormality presented is ___.
Keloid formation (TOPNOTCH)
Patient receiving glucocorticoid therapy for the autoimmune disease developed an abscess. Poor wound healing may result from glucocorticoid therapy due to:
Inhibition of TGF-B and diminished fibrosis secondary to glucocorticoid therapy. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106
One week after an exploratory laparatomy, a 30-year old obese female patient had “rupture of the wound”. This complication in tissue repair is due to inadequate formation of granulation tissue or scar formation.
Dehiscence. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 109
A 5 y/o patient had second degree burn of the palms. She is more prone to what type of abnormality in tissue repair?
Contracture. (TOPNOTCH)
Collagen deposition in cellular repair is largely a function of what cells?
Fibroblasts (TOPNOTCH)
The hallmark of tissue healing is:
Granulation tissue (TOPNOTCH)
Vitamin C retards wound healing because
Collagen synthesis is inhibited (TOPNOTCH)
Phase of cutaneous wound healing: formation of granulation tissue, proliferation and migration of connective tissue cells and re-epithelialization of wound surface
Proliferation (2nd phase) (TOPNOTCH)
Phase of cutaneous wound healing: ECM deposition, tissue remodeling and wound contraction
Maturation (3nd phase) (TOPNOTCH)
Its characteristic feature is the presence of new small blood vessels and proliferation of fibroblasts
Granulation tissue (TOPNOTCH)
True or False. Granulation tissue is more prominent in healing by secondary union.
True (TOPNOTCH)
Hypertrophic scar is due to accumulation of excessive amount of___.
Collagen (TOPNOTCH)
In wound healing, collagen is produced by:
Myofibroblasts(TOPNOTCH)
A 33 year old man sustains a stab injury on his right forearm. Two days after the incident, what can be seen in his stab wound? (A) dense collagen deposition (B) pink amorphous material devoid of cellular elements (C) accumulation of fibroblasts and macrophages (D) fibroblasts and capillaries in a loose extracellular matrix
fibroblasts and capillaries in a loose extracellular matrix (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 70-71
What is expected in the surgical scar of a 21 year old who underwent appendectomy one month ago? (A) Absence of dermal appendages (B) fibroblasts and capillaries in a loose extracellular matrix (C) intense intlammation and large amounts of granulation tissue (D) peak neovascularization
Absence of dermal appendages (Healing by First Intention) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp74-76
A 19 year old black male who got his right earlobe pierced 3 months ago developed a raised scar on that area. If examined microscopically, what should be seen? (A) dense collagen deposited in bundles (B) thickened stratum corneum of the epidermis (C) large amounts of granulation tissue (D) neutrophil aggregates with necrotic centers
dense collagen deposited in bundles (TOPNOTCH) Robbins Basic Pathology 8th ed, p 77
What is the cell responsible for wound contraction, especially in wounds that heal by second intention?
myofibroblast (TOPNOTCH) Robbins Basic Pathology 8th ed, p 76
Extravasation of fluid into interstitial spaces due to increases in vascular volume or pressure, decreases in plasma protein content or alterations in endothelial function.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
It is a severe and generalized edema with profound subcutaneous tissue swelling.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
The edema fluid occuring with volume or pressure overload or under conditions of reduced plasma protein.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
Edema secondary to increased vascular permeability and inflammation.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
The serum protein most responsible for maintaining intravascular colloid osmotic pressure.
Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
In breast cancer, infiltration and obstruction of superficial lymphatics can cause edema of the overlying skin, called _______ appearance.
Peau d’ orange(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
Microscopically, it is reflected primarily as a clearing and separation of the extracellular matrix elements with subtle cell swelling.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Diffuse edema usually more prominent in certain body areas as a result of the effects of gravity.
Dependent edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
True or false:Dependent edema is a prominent feature of left-sided heart failure.
False.Dependent edema is a feature of right-sided HF, while pulmonary congestion is a feature of left-sided HF.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Edema due to renal dysfunction which manifests disproportionately in tissues with loose connective tissue matrix, e.g. Eyelids.
Periorbital edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Finger pressure over significantly edematous subcutaneous tissue displacing the interstitial fluid, leaving a finger-shaped depression on the skin.
Pitting edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the lungs weigh 2-3x the normal, and on sectioning reveals frothy, sometimes blood-tinged mixture of air, fluid and extravasated red cells.
Pulmonary edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the brain is grossly swollen, with narrowed sulci and distended gyri showing signs of flattening against the underlying skull.
Brain edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is an active process resulting from augmented blood flow due to arteriolar dilation. Affected tissue is redder than normal, because of engorgement with oxygenated blood.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is a passive process resulting from impaired venous rturn out of a tissue.Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.
Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.
Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Hemosiderin- laden macrophages
Heart-failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated.
Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central regions of the hepatic lobules are grossly red-brown and slightly depressed and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver).
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages
CPC of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Extravasation of blood from vessels into the extravascular space.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Accumulation of blood within a tissue.
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.
Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2cm subcutaneous hematomas/bruises.
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Receptors responsible for platelet adhesion.
GpIb receptors- platelet Von Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.
Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Formation of a hemostatic plug due to platelet aggregation
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Hemostasis characterized by activation of thrombin through the coagulation cascade.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
True or false:The primary aggregation of platelets is irreversible.
False.(TOPNOTCH)
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
True or false:Activation of the coagulation cascade and subsequent thrombin formation is reversible.
False. Irreversible(TOPNOTCH)
Substance that activates the coagulation proteins.
Calcium(TOPNOTCH)
Substance that mediates further platelet aggregation and degranulation.
ADP(TOPNOTCH)
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
TXA2(TOPNOTCH)
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)
A protein found on endothelial cells involved in the breakdown of blood clots which catalyzes conversion of plasminogen to plasmin.
Tissue plasminogen activator (t-PA) and Urokinase(TOPNOTCH)
Components of Virchow’s triad?
Endothelial injuryStasisHypercoagulability(TOPNOTCH)
It is a major contributor to the development of VENOUS thrombi.
Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
Type of blood flow found in normal blood vessels, wherein platelets flow centrally in the vessel lumen, separated from the endothelium by a slow moving clear zone of plasma.
Laminar flow(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
Alteration in blood flow that contributes to arterial and cardiac thrombosis by causing endothelial injury or dysfunction as well as formation of countercurrents and local pockets of stasis.
Turbulence(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
Any alteration of the coagulation pathway that predisposes to thrombosis.
Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.
Embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.
Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Significance of Lines of Zahn?
Represents thrombosis in the setting of blood flow, seen in antemortem clots.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Thrombi occuring in heart chambers or aortic lumen
Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Gelatinous thrombi with a dark red dependent portion where red cells have settled by gravity with a yellow “chicken fat” supernatant. Usually unattached to underlying wall.
Postmortem thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Thrombi on heart valves.
Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Sterile, verrucous endocartidis occuring in patients with SLE.
Libman-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Vegetations occuring in the presence of non-infected valves in hypercoagulable states.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
Fate of a thrombus wherein the thrombus accumulates additional platelets and fibrin, eventually causing vessel obstruction.
Propagation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus wherein it may dislodge or fragment and transported elsewhere in the vasculature.
Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus as a result of of fibrinolytic activity leading to rapid shrinkage and even total lysis of recent thrombi.
Dissolution(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Fate of a thrombus wherein it may induce inflammation and fibrosis and establish some degree of blood flow.
Organization and recanalization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
True or false:Therapeutic administration of fibrinolytic agents is generally effective only within a few hours of thrombus formation.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Most common site of venous thrombosis.
Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Most common sequelae of deep venous thrombosis.
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
Tumor-associated procoagulant release largely responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers.
Migrating thrombophlebitis or Trousseau’s syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Hardening or thickening of the arteries as a result of the accumulation of fatty materials, macrophages, platelets and other inflammatory mediators.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Fates of a thrombus (4)
PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
Embolus occluding a bifurcation in the pulmonary tree.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
True or false:A patient who has had one pulmonary embolus has a decreased risk of developing another embolus.
False.The patient is at risk of developing more pulmonary emboli.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.
Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Most common symptom of pulmonary embolism.
None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Right Ventricular failure secondary to pulmonary hypertension.
Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Emboli in the arterial circulation.
Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Most common origin of systemic thrombi.
Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Major site of arteriolar embolization.
Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma.
Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?
Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.
Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
Amount of air in the circulation which produces clinical effects of air embolism.
> 100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
This occurs when individuals are exposed to sudden changes in atmospheric pressure (e.g. Deep sea divers, scuba divers).
Decompression sickness(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and around joints causing pain.
Bends(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.
Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
More chronic form of decompression sickness where persistence of gas emboli in the bones leads to multiple foci of ischemic necrosis.
Caisson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Treatment of choice for decompression sickness.
Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
Presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat and mucin.
Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Venous occlusion
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Lung infarction
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Intestinal infarct
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarct?Myocardial infarction
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarction?Splenic infact
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
White or red infarction?Wedge infarct
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
The dominant histologic characteristic of infarction.
Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Histologic characteristic of brain infarcts.
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.
Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Most common sequalae of septic infarcts.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Major determinants of the eventual outcome of an infarct. (4)
Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
Neurons undergo irreversible damage when deprived of their blood supply for _______.
3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
Myocardial cells undergo irreversible damage after ______ minutes of ischemia.
20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.
Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
End results of shock (3)
HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.
Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock results from loss blood or plasma volume.
Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi
Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
True or false:Systemic bacteremia must be present to induce septic shock.
FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102
Type of shock which occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.
Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.
Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
Septic shock caused by gram negative bacilli.
Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
Criteria for SIRS.
Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
Adrenal changes in shock.
Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Kidney changes in shock.
Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Gastrointestinal changes in shock.
Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
Lung changes in shock.
Diffuse alveolar damage if due to bacterial sepsis and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
The main mechanism of edema in inflammatory disease is:
increase vascular permeability (TOPNOTCH)
Sudden death in pulmonary embolism is due to:
Acute right heart failure (TOPNOTCH)
Accumulation of fluid within tissues
Edema (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113
Accumulation of fluid within body cavities
Effusion (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113
Patient presented with pain, swelling, and tenderness of left leg. What is the mechanism of edema in this condition?
Increased hydrostatic pressure. It is caused by impaired venous return as a result of DVT.(TOPNOTCH)
Patient presented with dyspnea, orthopnea, easy fatigability, and bipedal edema. The mechanism of edema in this condition is.
Increased hydrostatic pressure (TOPNOTCH)
Patient presented with periorbital edema and ankle edema. Lab result shows high lipid levels, and low serum albumin. What is the mechanism of edema in this condition?
Reduced plasma oncotic pressure secondary to protein/albumin loss (case of Nephrotic syndrome) (TOPNOTCH)
Mechanism of edema in severe liver disease
Reduced plasma osmotic pressure due to reduced protein synthesis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114
Mechanism of edema caused by Wuchereria bancrofti
Lymphatic obstruction(in Filariasis)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114
A chronic alcoholic male presented with easy fatigability and orthopnea. Chest radiograph showed bilateral pleural effusion, while abdominal ultrasound showed ascites and small liver. What is the mechanism of effusion in this condition?
Reduced plasma oncotic pressure (TOPNOTCH)
Patient X presented with pitting edema of the legs, jugular vein distention, and elevated transaminases. If the liver showed a nutmeg appearance, the patient most likely have:
Chronic passive congestion of the liver secondary to congestive heart failure (TOPNOTCH)
Patient with left-sided heart failure may develop pulmonary edema because of what mechanism?
Increased hydrostatic pressure (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th ed., p. 114
Assay that assesses the function of proteins in the extrinsic pathway (factors VII, X, V, II, fibrinogen)
Prothrombin time (PT) (TOPNOTCH) RobbIns Basic Pathology, 9th ed., p. 119
Assay that screens the function of proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)
Partial thromboplastin time (PTT) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119
Most important coagulation factor, its various enzymatic activities control diverse aspects of hemostasis
Thrombin (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119
Prostacyclin, nitric oxide and adenosine diphosphatase action: platelet activation or platelet inhibition?
Platelet inhibition(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 121
Patient presents with epistaxis and GI bleeding. Lab result showed low platelet count. The patient may have defect in _____. Primary or secondary hemostasis?
Primary hemostasis (TOPNOTCH)
Patient presented with knee joint and swelling after a soccer game. However, no physical evidence of injury was noted. He is most likely suffering from what defect in hemostasis?
Secondary hemostasis. Bleeding into joints following minor trauma is particularly characteristic of hemophilia. (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 122
Fatal and most feared complication of severe thrombocytopenia
Intracerebral hemorrhage (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 122
Patient was on anticoagulation therapy for the treatment of arterial thromboembolism. However, few days later she was noted to have blood in the urine and reddish spots on her legs. Platelet count was 20. What is the pathophysiologic mechanism for this condition?
Formation of antibodies against complexes of heparin and platelet factor 4 on platelet surface resulting to platelet activation, aggregration, and consumption. (HIT)(TOPNOTCH)
Syndrome presenting with recurrent thromboses, repeated miscarriages, cardiac valve vegetation, and thrombocytopenia.
Antiphospholipid antibody syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.124
Most common site of arterial thrombi
Coronary arteries (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 125
True or False. Saphenous vein thrombosis often cause embolization.
False. Superficial vein thrombosis rarely embolize. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
Lower extremity DVT are often associated with____. Turbulent blood flow, endothial injury or hypercoagulable state?
Hypercoagulable state (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
Major cause of arterial thromboses
Atherosclerosis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126
Systemic activation of thrombin leading to widespread formation of thombi in microcirculation, and consumption of platelets and coagulation factors.(TOPNOTCH)
Disseminated Intravascular Coagulation/Consumptive coagulopathy(TOPNOTCH)
Patient X fractures his right femur after falling from a height of 10 meters. After 2 days of hospitalization, he developed sudden onset of dyspnea, tachycardia, and restlessness. Diffuse petechial rashes was noted on his trunk. What is the most likely diagnosis?
Fat emboli (TOPNOTCH)
A 60 y/o female, bed-ridden, was admitted to the hospital with shortness of breath and hemoptysis. Physical examination finds the patient to be afebrile, tachycardic, calf tenderness and widely split S2. What is the most likely diagnosis?
Pulmonary embolism (TOPNOTCH)
A 30 year old female experienced dyspnea and edema after being injected with antibiotic. She later lost consciousness and BP rapidly declined, and later went into shock. The is due to:
Anaphylactic shock (TOPNOTCH))
A bedridden elderly patient experienced sudden onset of dyspnea and hemoptysis. The underlying lesion that led to this complication was most likely located in which site?
Veins lof lower extremity. It is the most common site of DVT leading to pulmonary embolism. (TOPNOTCH)
Exudate or transudate? Inflammation
Exudate(TOPNOTCH)
Exudate or transudate? Nephrotic syndrome
Transudate(TOPNOTCH)
Exudate or transudate? Chronic liver disease
Transudate(TOPNOTCH)
A stillborn baby with Turner syndrome is found to have generalized edema and a large lymphangioma around her neck at autopsy. Heart and aorta findings were unremarkable. What is the mechanism for her edema? (A) Reduced oncotic pressure (B) lymphatic obstruction (C) sodium retention (D) inflammation
Lymphatic obstruction (TOPNOTCH) Robbins Basic Pathology 8th ed. pp82-83
Which of the following will most likely produce pulmonary edema? (A) mitral valve stenosis (B) pulmonary hypertension (C) tricuspid stenosis (D) subpulmonic valve stenosis
mitral stenosis (TOPNOTCH) Robbins Basic Pathology 8th ed. P 84
In which of the following cases would cerebral edema be more generalized? (A) a meningioma on the parietal cortex (B) viral encephalitis (C) occlusion of the right cerebral artery (D) frontal abscess
viral encephalitis (TOPNOTCH) Robbins Basic Pathology 8th ed. P84
A patient with congestive heart failure dies. At autopsy, his liver appears grossly similar to nutmeg. Which describes an expected microscopic finding? (A) lymphocytic infiltrates in the portal tracts (B) hepatocyte necrosis around central veins (C) hepatocyte necrosis around hepatic arterioles (D) vacuolated hepatocytes and giant cell formation
hepatocyte necrosis around central veins (TOPNOTCH) Robbins Basic Pathology 8th ed., p. 85.
A Stage IV breast cancer patient on prolonged bed rest suddenly develops difficulty of breathing and dies. At autopsy, a blood clot in the main pulmonary artery is found. Which of the following supports a thromboembolic origin, rather than a postmortem clot? (A) pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (B) gelatinous consistency, with a dark dependent portion and a yellow supernatant (C) chicken fat appearance (D) lines of Kahn
pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (lines of Zahn) (TOPNOTCH) Robbins Basic Pathology 8th ed, p96
A pregnant patient in her third trimester is hit by a car and sustains a femoral fracture. She subsequently goes into labor and delivers a preterm baby via vaginal delivery. A few minutes later, she has sudden dyspnea, cyanosis, and dies. At autopsy, there was pulmonary edema, a ventricular septal defect, and squamous cells in the microcirculation. What is the immediate cause of death? (A) amniotic fluid embolism (B) fat embolism (C) paradoxical embolism (D) air embolism
Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
In pure hypovolemic shock, which of the following organs will manifest the least cellular changes? (A) brain (B) adrenals (C) kidneys (D) lungs
Lungs (TOPNOTCH) Robbins Basic Pathology 8th ed. P 105.
These agents cause transmissible spongiform encephalopathies.
Prions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 321
Infected cells show distinct nuclear and ill-defined cytoplasmic inclusions.
CMV infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Infected cells show glassy nuclear inclusions, frequently with a surrounding halo.
Herpesvirus infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Infected hepatocytes show diffuse granular (ground-glass) cytoplasm.
Hepatitis B viral infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
Sexually transmitted protozoan that can colonize the vagina and male urethra.
Trichomonas vaginalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
Protozoan acquired either by contact with oocyte-shedding kittens or by consumption of cyst-ridden undercooked meat.
Toxoplasma gondii(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
Size of microorganisms for them to be inhaled directly into the alveoli.
5 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
These microorganisms grow in contaminated food and releases powerful enterotoxins that cause food poisoning symptoms without any bacterial multiplication in the gut.
Staphylococcal strains(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Intestinal helminth that cause disease when present in large numbers or cause obstruction of the gut.
Ascaris lumbricoides(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 326
Helminth that causes iron deficiency anemia by chronic loss of blood.
Hookworms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Helminth that depletes vitamin B12 giving rise to an illness resembling pernicious anemia.
Diphyllobotrium latum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
Placentofetal route as a mode of transmission is also referred to as ________.
Vertical transmission(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 329
The ability of bacteria to cause disease.
Virulence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 331
Bacterial surface molecules that bind to host cells.
Adhesins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
Filamentous proteins on gram negative bacteria which allow exchange of genes between bacteria, and also involved in adherence.
Fimbriae/pili(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
Clostridium perfringens produces this toxin that disrupts plasma membranes resulting in digestion of host tissues and collagen.
Alpha toxin (lecithinase)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Bacterial toxins with the capacity to stimulate large populations of T lymphocytes, functionally resulting in a “cytokine storm”.
Superantigens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Examples of antigen presenting cells.
Dendritic cellsMacrophagesB-cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
A superantigen secreted by S. aureus which causes inflammation, fever and shock. Found in the vagina of menstruating women.
Toxic shock syndrome toxin (TSST-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
Collection of neutrophils which gives rise to localized liquefactive necrosis.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
High risk agents of bioterrorism which are easily disseminated and has high potential for mortality. An example is smallpox.
Category A(TOPNOTCH)
A distinctive form of mononuclear inflammation usually evoked by infectious agents that resist eradication, but are capable of stimulating strong T cell mediated immunity. Characterized by epitheloid cells which may fuse to form giant cells.
Granulomatous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 335
Agents that are relatively easy to disseminate and produces moderate morbidity and low mortality. An example is E.coli O157:H7 which can cause HUS.
Category B(TOPNOTCH)
Includes emerging pathogens that have the potential for mass dissemination with high morbidity and mortality. Examples are Nipah virus and Hanta virus.
Category C(TOPNOTCH)
An 8 y/o female presented with fever, sore throat, conjunctivitis, and blotchy, reddish brown rashes on the face, trunk, and extremities. In this condition, lymphoid organs have marked follicular hyperplasia, large germinal center, and randomly distributed Warthin-Finkeldey cells. The most likely cause of this disease is:
Rubeola virus. Warthin-Finkeldey cells are multinucleate giant cells with eosinophilic nuclear and cytoplasmic inclusion bodies. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355
Ulcerated mucosal lesion near the opening of Stensen duct marked by necrosis, neutrophilic exudate, and neovascularization.
Koplik spots - pathognomonic of measles (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355
What protects against reinfection with measles?
Antibody-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355
Most common extrasalivary gland complication of mumps infection
Aseptic meningitis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356
A 10 y/o male presented with fever and bilateral swelling and pain of parotid glands aggravated by intake of sour food. What is the most likely finding in the gland interstitium in this disease?
Edematous, diffusely infiltrated by macrophages, lymphocytes, and plasma cells(Mumps) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356
True of false. Poliovirus infects only humans.
True(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356
Mode of transmission of West Nile virus
Vector-borne (mosquito) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356
Viruses that most frequently establish latent infections in humans
Herpesviruses (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357
A 10 y/o child presented with vesicular around the lips and cervical lymphadenopathy. Histopathologic finding showed cells containing large, pink to purple intranuclear inclusion that consist of viral replication proteins. The etiologic agent for this condition is:
HSV-1 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357
A 28 y/o female complained of itchiness and vesicular lesions on her genitalia which later progress to ulcerations. The cause of this condition is:
HSV-2 causing genital herpes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357
Latent infection with this virus is seen in neuron and/or satellite cells around neurons in the dorsal root ganglia.
Varicella-Zoster Virus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357
A 62 y/o male presented with painful vesicular rash in a stripe-like pattern over the left side of his trunk. On microscopy, the sensory ganglia contain a dense, predominantly mononuclear infiltrate, with herpetic intranuclear inclusions within neurons. This is a case of:
Shingles/Herpes zoster (TOPNOTCH)
Syndrome caused by varicella zoster virus with involvement of geniculate nucleus causing facial paralysis
Ramsay Hunt Syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 359
A neonate was noted to have jaundice, anemia, and hepatosplenomegaly. Patient also had microcephaly, and brain showed foci of calcification. The most likely diagnosis is:
Cytomegalic inclusion disease (caused by CMV) (TOPNOTCH)
Morphology of cells in CMV
Prominent intranuclear basophilic inclusion set off from nuclear membrane by a clear halo (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 359
A 6 y/o male presented with fever, lymphadenopathy, and hepatomegaly. Lab showed abnormal liver function test and lymphocytosis. These are the most common clinical manifestion in
CMV infection in immunocompetent host. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360
Virus implicated in nasopharyngeal carcinoma and some lymphomas.
Epstein-Barr Virus. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360
A 16 y/o male presented with high fever for a week, sore throat, enlarged lymph node in the posterior cervical and axillary region, and splenomegaly. Peripheral smear showed large lymphocytes with abundant cytoplasm containing clear vacuolization, an oval, indented nucleus and scattered cytoplasmic azurophilic granules (10% atypical lymphocytes). The main target cells of this condition is/are:
B cells and epithelial ells of the oropharynx. (EBV infection) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360
Patient with EBV infecction will have a positive or negative heterophile antibody reaction (Monospot test)
Positive heterophile antibody reaction. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 362
A disorder caused by mutations in the SH2D1A gene, which encodes a signaling protein that participates in T-cell and NK-cell activation and antibody production. It is characterized by an ineffective immune response to EBV.
X-linked lymphoproliferation syndrome (Duncan Disease) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 362
Toxin responsibe for Ritter’s disease
Exfoliative A and B toxin(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 363
Other term for staphylococcal scalded-skin syndrome.
Ritter’s disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 363
A 5 y/o male was admitted due to sunburn-like rash over the entire body and evolving into fragile bullae. Presence of desquamation of the epidermis occurs at the level of the granulosa layer. What is the cause of this condition?
Staphylococcus aureus (causing Staphylococcal scalded skin syndrome) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.364
Coagulase-negative organism causing opportunistic infections in catheterized patients,patients with prosthetic valves and drug addicts.
Staphylococcus epidermidis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.364
A 30 y/o female was noted to have dyspnea and generalized erythematous rash. She developed hypotension, renal failure, coagulopathy and liver dysfunction. History revealed the use of tampons. The most likely diagnosis is:
Toxic shock syndrome caused by S. aureus (TOPNOTCH) Robbins Basic Pathogy, 9th Ed p. 363
A 50 y/o female presented with a 1-week history of progressive, productive cough, and 2 days of spiking fever. Chest examination was notable for decreased breath sounds on the right lower lung field. Chest radiograph demonstrated a right lower lobe infiltrate. A blood culture was subsequently positive for gram positive cocci in pairs. what is the likely organism causing this illness?
Streptococcus pneumoniae. (TOPNOTCH)
An 18 y/o female presented with painful swelling in her feet, knees, and wrist. The patient had been well until 10 days prior to admission when she developed a severe sore throat accompanied by fever. What is the most likely cause of his illness?
Streptococcus pyogenes/GABHS(TOPNOTCH)
Surface protein present in S. pyogenes responsible for antibodies and T cells cross-reacting with cardiac proteins.
M protein. (TOPNOTCH)
A 6 y/o male presented with tonsillopharyngitis, circumoral pallor and erythematous, sandpaper like rashes covering the trunk and extremities. What is the most likely cause of this illness?
This is a case of Scarlet fever caused by Streptococcus pyogenes (TOPNOTCH)
A 35 y/o female presented with rapidly spreading erythematous cutaneous swelling on the face with rashes that are sharp, welll-demarcated , serpiginous border forming a butterfly distribution on the face. On histologic exam, there is a diffuse, edematous, neutrophilic inflammation of the dermis and dermis extending to the subcutaneous tissue. This is caused by what microorganism?
S. pyogenes (case of erysipelas) (TOPNOTCH)
A 43 y/o male had a two-week history of fever, chills, weakness, and anorexia following a dental extraction. On physical examination, patient had high pitched murmur best heard at the apex. Echocardiogaphy done showed an irregular vegetation attached to mitral valve. The most likely cause of endocarditis in this case is:
Streptococcus viridans. (TOPNOTCH)
A 26 y/o previously healthy woman develops fever within 24 hours of delivery of an infant born at 32 weeks. Vaginal swab of the mother revealed Gram positive coci. Blood culture showed organism that are catalase negative, beta-hemolytic on blood agar. The most likely cause of bacteremia is:
Streptococcus agalactiae (Group B Streptococcus) (TOPNOTCH)
A 5 y/o old unimmunized child presented with persistent sore throat , cough and fever for 1 week. On examination, the neck was diffusely swollen with tender, bilateral cervical adenopathy. There were hemorrhagic areas on the hard palate and necrotic grayish membrane on the soft palate and tonsils. Morphologic finding of Intense neutrophilic infiltration in the tissues with marked vascular congestion, interstitial edema, and fibrin exudation were noted. This is caused by
Corynebacterium diphtheriae (TOPNOTCH)
True or false. Toxin produced by Corynebacterium diphtheriae are the ones responsible for the clinical manifestations of diphtheria.
True. (TOPNOTCH)
A 2 mo old male was admitted to the hospital with a history of fever, vomiting, and convulsions. Birth history was unremarkable. CNS finding were suggestive of meningitis. Gram staining of CSF showed mononuclear cells with moderate Gram positive bacilli with tumbling motility. The most likely etiologic agent for this condition is:
Listeria monocytogenes. (TOPNOTCH)
This organism causes a painless, pruritic papule developing into a vesicle, which ruptures with remaining ulcer becoming covered with a characteristic eschar.
Bacillus anthracis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 366
Lesion caused by this organism are typified by necrosis and exudative inflammation rich in neutrophils and macrophages and presence of large, boxcar-shaped gram-positive extracellular bacteria in chains.
Bacillus anthracis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 367
A 48 y/o male was admitted with a 4 month history of cough with purulent sputum, hremoptysis, and fever. He wa diagnosed with AIDS 2 years earlier and was on antiretivirals irregularly. On examination, HR=98bpm, RR= 26 /min. Chest auscultation revealed decreased breath sounds on the upper third of right hemithorax. CXR demonstrated consolidation in the upper lobe of the right lung. Bronchoscopy with lavage revealed presence of branching filamentous gram positive organism. The organism described is
Nocardia asteroides. (TOPNOTCH)
A 17 y/o college student presented with fever, chills, headache, joint pains and myalgia. On physical examination, she is tachycardic, febrile, with mild hypotension. There was noted petechial rashes on her trunk and legs. Gram stain revealed gram-negative coffee-bean shaped diplococci. The most likely cause of this condition is
Neisseria meningitidis. (TOPNOTCH)
A 25 y/o female complained of severe pelvic pain and fever. A greenish yellow cervical discharge was detected on physical examination. Gram negative diplococci were isolated from the endocervical swab. What is the most likely cause?
Neisseria gonorrhea (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 368
A 2-month old infant was admitted with fever, lymphocytosis, and bouts of violent coughing that often end in vomiting. Blood culture showed small gram-negative rods. The most likely diagnosis is:
Pertussis (TOPNOTCH)
Mechanism on how B. pertussis toxin impair host defenses.
Inhibits phagocytosis, inhibits neutrophils and macrophages and paralyzing cilia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 369
Bacteria causing laryngotracheobronchitis with features of bronchial mucosal erosion, hyperemia, and copious, mucopurulent exudate. It may present with hypercellularity and enlargement of mucosal lymph follicles and peribronchial lymph nodes along side a marked peripheral lymphocytosis (up to 90%)
Bordetella pertussis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369
A 67 y/o female was admitted with a 1 week history of cough and pleuritic chest pain. Physical examination revealed tachypnea, rhonchi in both upper lobes. The next day, patient’s condition deteriorated and had severe respiratory distress. Autopsy revealed extensive bilateral bronchopneumonia and necrosis in the terminal airways in a fleur-de-lis pattern, with striking pale necrotic centers and red, hemorrhagic peripheral areas. The most likely cause of this disease is:
Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369
An opportunistic aerobic gram-negative bacillus that is frequent, deadly pathogen of people with cystic fibrosis, severe burns, or neutropenia.
Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369
A 32 y/o female on chronic immunosuppressive therapy was admitted for the management of her abdominal wound infection. On hospital day 18, patient developed erythematous papulovesicules on the left upper chest and right medial leg progressing rapidly to necrotic and hemorrhagic oval ulcers. What organism most likely cause this condition?
Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370
Organism that causes lymph node enlargement (buboes) with distinct histologic features of massive proliferation of organism, early appearance of effusions with few inflammatory cells, necrosis of tissues and blood vessels with hemorrhage and thrombosis, and neutrophilic infiltrates in necrotic areas.
Yersinia pestis (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th Ed p. 370
A 25 y/o male initially presented with a tender erythematous papule on the penis which produce an irregular, painful, non-indurated ulcer over several days. The base of the ulcer is covered by shaggy, yellow-gray exudate. Microscopically, the ulcer contains a superficial zone of neutrophilic debris and fibrin, and an underlying zone of granulation tissue containing areas of necrosis and thrombosis. This infection is caused by:
Haemophilus ducreyi (causing Chancroid) (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370
A 45 y/o sexually active male presented with a 3-month history of few painless ulcerated lesions on the penis and scrotum. The painless nodules slowly evolved to red ulcerated lesions over 1 month. Physical examination revealed multiple, raised, beefy-red nontender round ulcers on the shaft of penis and scrotum. The ulcers had clean friable granulating bases. Microscopic examination with Giemsa stain revealed numerous encapsulated coccobacilli in macrophages. The most likely diagnosis is:
Granuloma inguinale/donovanosis (Klebsiella granulomatis) (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370
A 25 y/o male initially presented with a tender erythematous papule on the penis which produce an irregular, painful, non-indurated ulcer over several days. The base of the ulcer is covered by shaggy, yellow-gray exudate. Microscopically, the ulcer contains a superficial zone of neutrophilic debris and fibrin, and an underlying zone of granulation tissue containing areas of necrosis and thrombosis. This infection is caused by:
Klebsiella granulomatis (TOPNOTCH)
True or false. A positive tuberculin test differentiates active disease from infection.
False. A positive tuberculin test signifies T-cell mediated immunity to mycobacterial antigen. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 371
How many days or weeks after mycobacterium infection will it develop delayed hypersensitivity to M. tuberculosis as detected by Mantoux skin test?
2-4 weeks (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 371
The critical mediator that enables macrophages to contain M. tuberculosis infection by stimulating maturation of phagolysosome, stimulation of expression of inducible nitric oxide synthase and mobilization of defensins against bacteria.
IFN gamma(TOPNOTCH) Robbins Pathologic Basis of Disease, 9th Ed p. 372
True or False. Immunity to M. tuberculosis is primarily mediated by TH1 cells.
True. TH1 cells stimulate macrophages to kill the bacteria (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 373
Secondary pulmonary tuberculosis classically involves what part of the lungs?
Apex of the upper lobes of one or both lungs. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 373
True or false. The absence of characteristic granulomas in tissues in HIV-positive patients precludes (rule out) the diagnosis of tuberculosis.
False. Atypical features of TB in HIV-positive patients include increase frequency of false-negative sputum smears, tuberculin tests, and absence of granuloma, particularly in the late stages of HIV.(TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 374
A 1 to 1.5 cm area of gray-white inflammation with consolidation in primary tuberculosis.
Ghon focus (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 374
Most frequent presentation of extrapulmonary tuberculosis.
Lymphadenitis (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 376
A 42 y/o male nonsmoker with AIDS began to experience cough, mild hemoptysis, and progressive dyspnea. CD4 cell count was 45 cell/ul. A chest radiograph revealed hilar adenopathy and perihiral infiltrates. AFB smear was negative. Bronchoscopy was done and microscopic finding showed an abundnat acid-fast bacilli within macrophages. The organism causing the illness is:
Mycobacterium avium complex (TOPNOTCH)
Pattern of leprosy presenting with dry, scaly skin lesions that lack sensation and often have assymetric involvement of large peripheral nerves.
Tuberculoid leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377
Pattern of leprosy causing symmetric skin thickening and nodules with widespread invasion of mycobacteria into Schwann cells and into endoneural and perineural macrophages damaging the peripheral nervous system.
Lepromatous leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377
Pattern of leprosy characterized by TH1 response associated with production of IL-2 and IFN gamma
Tuberculoid leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377
Pattern of leprosy associated with weak TH1 response and in some cases increase in TH2 response resulting to weak cell-mediated immunity.
Lepromatous leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377
A 30 y/o male presented with a flat, red, anesthetic skin lesions on his left thigh extending to his knee which had been present for 2 years. These lesions enlarged and develop irregular shapes with indurated, elevated, hyperpigmented margins and depressed pale centers. On microscopic examination, all sites of involvement have granulomatous lesions. Bacilli are almost never found. This is a case of__.
Tuberculoid leprosy/Paucibillary leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377
This disease presents with macular, papular, or nodular lesion on the face, ears, wrists, elbows and knees, progressing to coalescence of nodular, anesthetic lesions. (+) leonine facies. Morphologic findings of this disease reveals skin and peripheral nerve lesions containing large aggregates of lipid laden macrophages (lepra cells) often filled with asses (globi) of acid fast bacilli.
Lepromatous/multibacillary leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 378
A 19 y/o male presents to the clinic because of a lesion on his penis. Genital exam showed a red, solitary, raised , indurated, non-tender lesion on the ventral side of his penis. Neurologic exam was within normal limits. What is the most likely diagnosis?
Primary syphilis(chancre)(TOPNOTCH)
A 34 y/o male presented with circular violaceous, papulosquamous lesions on his palms, soles, and entire body. He admitted having unprotected sex with his new partner 6 weeks before the onset of his lesions. Broad-based plaques were noted in the inner thighs and anogenital region. Silver-gray erosions were noted on the pharyngeal and genital area. What is the most likely diagnosis(and stage)?
Secondary syphilis. (TOPNOTCH)
Characteristic of all stages of syphilis
Proliferative endarteritis. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379
Serologic test/s that are sensitive for secondary syphilis
Both non-treponemal antibody tests and antitreponemal antibody tests. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379
Serologic tests that are very sensitive for tertiary and latent syphilis.
Treponemal tests (Fluorescent Treponemal antibody absorption test, T pallidum enzyme immunoassay test) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379
Most frequent involvement of tertiary syphilis
Aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 380
A 39 y/o male presented with a white-gray and rubbery mass on the forehead that had been slowly progressive over the previous 6 years. Biopsy showed that lesion have centers of coagulated, necrotic material and margins composed of plump, palisading macrophages and fibroblasts surrounded by large number of mononuclear leukocytes. What is the lesion described?
Syphilitic gumma (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381
A neonate presented with snuffles, bullous eruption of the palms and soles, saddle nose deformity, and anterior bowing of the tibia. What is the most likely cause?
T. pallidum (causing congenital syphilis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381
Late manifestations of congenital syphilis (triad)
Interstitial keratitis, Hutchinson teeth, and eighth-nerve deafness (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381
Disseminated infection from this microorganism cause secondary skin lesions, lymphadenopathy, migratory joint and muscle pain, cardiac arrythmias, and meningitis.
Borrelia burgdorferi (causing congenital syphilis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381
A 60 y/o male presented with severe pain and edema of left foot and leg, bullous vesicles, and foul-smelling wound discharge 3 days after sustaining a crushing injury. Crepitations were noted over the inflamed muscles. What is the most likely cause of this condition?
Clostridium perfringens (causing gas gangrene/clostridium myonecrosis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 383
Most common sexually transmitted bacterial disease
Chalmydia trachomatis infection(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 383
A 28 y/o male presented with painful, swollen lymph node at the inguinal area, associated with fever, and myalgia. Two weeks prior, patient recalled had a small, painless pustule on the scrotum. The most likely diagnosis is:
Lymphogranuloma venereum (TOPNOTCH)
Lymph node involvement in this condition is characterized by a granulomatous inflammatory reaction associated with irregularly shaped foci of necrosis containing neutrophils (stellate abscess).
Lymphogranuloma venereum (caused by Chlamydia trachomatis)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 384
Presents with dysphagia and retrosternal pain; endoscopic findings of white plaques and pseudomembranes resembling oral thrush on the esophageal mucosa.
Candida esophagitis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 386
Associated with intense itching and thick, curd-like discharge common in women who are diabetic, pregnant, or on OCP.
Candida vaginitis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 386
A 70 y/o male, with prior history of TB, presents with occassional cough, hemoptysis, fever, and respiratory distress. CXR showed a mass surrounded by a crescentic rim on the right upper lobe within a cavitary lesion. Biopsy done revealed no malignant cell. This is most likely a case of:
Pulmonary aspergilloma (TOPNOTCH)
A 60 y/o diabetic female presented with fever and left periorbital pain and sweling. A nasal eschar involving the enitre nose with discharge from the nasal cavity. Biopsy from the eschar showed foci of nonseptate fungal hyphae and hyphal branches at right angles. The most likely cause of her condition is:
Mycormycetes (TOPNOTCH)
The etiology of cerebral malaria, wherein brain vessels are plugged with parasitized red vessels. Around the vessels are ring hemorrhages related to local hypoxia. (TOPNOTCH)
Plasmodium falciparum (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 392
What is the major cause of sudden death in Chagas disease?
Cardiac arrythmia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 395
The causative agent of Chagas disease
Trypanosoma cruzi (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 394
Nematode that causes patchy interstitial myocarditis characterized by many eosinophils and scattered giant cells.
Trichinella spiralis (TOPNOTCH) Robbins Basic Pathology, 9th ed., 397
Pathogenesis of hepatic fibrosis in schistomiasis
Eggs carried into the parenchyma cause severe chronic inflammation; TH2 response and activated macrophages. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 398
Pipe-stem fibrosis of the liver, portal enlargement without intervening regenerative nodules, and granuloma are associated with infection caused by:
Schistosoma mansoni and S. japonicum. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 398
A chronic carrier state of typhoid fever is most likely due to persistence of the organism in the:
Gall bladder (TOPNOTCH)
A 38 y/o man with AIDS present with deteriorating mental status. Lumbar tap was done. CSF was stained with india ink and mucicarmine revealed capsulated yeasts that stain bright red. What is the most likely diagnosis?
Cryptococcosis (TOPNOTCH)
A 53 year old woman presents with 5 days of productive cough and high grade fevers. Crackles were auscultated at the left lung. Sputum cultures grew Streptococcus pneumoniae. Her lungs will show which histologic picture? (A) suppurative inflammation with sparing of alveolar septa (B) thickened alveolar septa with mononuclear infiltrates (C) lysis of alveolar walls and coalescing abscesses (D) epithelioid macrophages and giant cells
suppurative inflammation with sparing of alveolar septa (TOPNOTCH)Robbins Basic Pathology, 8th Ed p334-335
A 44 year old HIV-positive man is admitted for diarrhea of one month duration. Fecalysis did not show parasitic ova or cysts. Colonoscopy showed a diffusely erythematous mucosa. Biopsy was performed which showed sheets of macrophages filled with filamentous structures that were bright pink on acid fast staining. The likely organism is (A) Cryptosporidium parvum (B) Isospora belli (C) Mycobacterium bovis (D) Mycobacterium avim-intracellulare
Mycobacterium avium-intracellulare dx Infectious mononucleosis case (TOPNOTCH) pp326-327
This term refers to protection against infections.
Immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
It is the collection of cells and molecules that are responsible for defending against pathogenic microbes.
Immune system(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.
Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by lymphocytes and their products, and is normally silent and responds to the presence of microbes by becoming active, expanding and generating potent mechanisms for neutralizing and eliminating microbes.
Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Type of adaptive immunity mediated by T lymphocytes.
Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Mediated by antibodies and is effective against extracellular microbes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Reaction of T-lymphocytes, designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).
Cell-mediated immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Reaction of immune system against one’s own cells.
Autoimmunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.119
Results from activation of TH2 CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells.
Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies that bind to fixed tissue or cell surface antigens and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues.
Type II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies binding to antigens to form complexes that circulate and may deposit in vascular beds and stimulate inflammation, secondary to complement activation.
Type III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing cells.
Type IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:SLE
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Multiple sclerosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Transplant rejection
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Anaphylaxis
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Goodpasture syndrome
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Serum sickness
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Arthus reaction
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Allergies
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Type I DM
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Bronchial asthma
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Polyarteritis nodosa
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Rheumatoid arthritis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Inflammatory bowel disease
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculin reaction
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Reactive arthritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Graves disease
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Myasthenia gravis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Insulin resistant DM
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Pernicious anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
A special form of graft rejection occuring in the setting where preformed antidonor antibodies are present in the circulation of the host before transplant. Occurs within minutes to a few hours after transplantation.
Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which occurs within days to weeks of transplantation in a nonimmunosuppressed host. Caused by both cellular and humoral immune mechanisms.
Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection most commonly seen within the first months after transplantation, typically accompanied by signs of renal failure. Extensive CD4+ and CD8+ T-cell infiltration with edema and mild interstitial hemorrhage.
Acute cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection caused by antidonor antibodies. May take the form of necrotizing vasculitis with endothelial cell necrosis, neutrophilic infiltration, deposition of antibody, complement, and fibrin, and thrombosis.
Acute humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which present clinically months to years after transplantation with a progressive rise in serum creatinine levels. Dominated by arteriosclerosis, interstitial fibrosis and loss of renal parenchyma.
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.
Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139
SOAP BRAIN MD mnemonic for SLE stands for?
SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?
4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
Most serious and most common form of renal lesion in SLE. “Wire-loop” appearance of glomerular capillary walls.
Diffuse proliferative glomerulonephritis (Class IV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.142
Cardiac manifestation of SLE, which occurs as nonspecific mononuclear infiltrates and the presence of irregular 1-3mm warty deposits on either surface of the leaflets.
Libman-Sacks Endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.144
A systemic, chronic inflammatory disease affecting many tissues but principally attacking the joints to produce a nonsuppurative proliferative synovitis that frequently progress to destroy articular cartilage and underlying bone with resulting disabling arthritis.
Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145
Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.
Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
Cytokine which plays a central role in the pathogenesis of RA.
TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.
Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148
Characterized by progressive fibrosis involving the skin, GIT and other tissues. May be a result of activation of fibroblasts by cytokines produced by T cells.
Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149
A vascular disorder characterized by reversible vasospasm of the arteries. Typically the hands turn white due to vasospasm, then blue due to cyanosis, then red due to reactive hyperemia.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151
One of the more common forms of primary immune deficiency characterized by absent or markedly decreased numbers of B-cells in the circulation, with depressed serum levels of all classes if immunoglobulin.
X-linked agammaglobulinemia (Bruton disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.152
Most common of all the primary immune deficiencies characterized by recurrent sinopulmonary infections and diarrhea.
Isolated IgA deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
A constellation of genetically distinct syndromes with common feature of defects in both humoral and cell-mediated immune responses, making affected infants susceptible to severe recurrent infections by bacteria, viruses, fungi, protozoans, and opportunistic infections.
Severe Combined Immunodeficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
Autosomal recessive form of SCID is due to deficiency of what enzyme?
Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
An X-linked recessive disease characterized by thrombocytopenia, eczema, and marked vulnerability to recurrent infection ending in early death.
Wiskott-Aldrich Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.155
HIV viral surface proteins essential for viral entry into cells.
gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157
A form of pneumonia in HIV patients caused by a yeast-like fungus.
Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)
Main cellular target of HIV.
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158
P.carinii pneumonia occurs in AIDS patients with CD4+ T cell count of ______.
Less than 200 cells/uL(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
Most common secondary infection of the CNS in patients with AIDS.
Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
Most common neoplasm in AIDS patients, caused by HHV8. Characterized by cutaneous lesions with or without internal involvement.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.164
A disorder of protein misfolding, causing extracellular deposition of pink or red colored deposits stained with Congo red, with apple-green birefringence in polarized light.
Amyloidosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.166
Cells of immune system
T- and B-lymphocytes, dendritic cells, macrophages, natural killer cells, innate lymphoid cells. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 190
Tissues of the immune system
Bone marrow, thymus, lymph nodes, spleen, mucosal and cutaneous lymphoid tissue. (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 193
The most important antigen-presenting cells for initiating T-cell responses against protein antigens
Dendritic cells(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 191
A 48 y/o male patient underwent kidney transplant suddenly developed bloody urine few hours after the procedure. Nephrectomy was done and revealed a cyanotic, mottled, and flaccid kidney and necrotic kidney cortex. There is neutrophilic accumulation in the arterioles, glomeruli, and peritubular capillaries. Glomeruli undergo thrombotic occlusion of capillaries and fibrinoid necrosis in arterial walls. The most likely diagnosis is:
Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233
A 45 y/o female presented with signs of kidney failure 2 months after her renal transplant. Immunohistochemical staining reveals both CD4+ and CD8+ lymphocytes. Morphologic findings showed an extensive interstitial inflammation with infiltration of tubules and focal tubular injury. This is a case of:
Acute cellular (T-cell mediated) rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 234
Preformed antidonor antibodies present in the circulation of the recipient is implicated in what type of rejection pattern?
Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233
A 30 y/o male developed oliguria and subsequent renal failure 3 weeks after an uneventful kidney transplant. Renal findings showed inflammation of glomeruli and peritubular capillaries, deposition of complement breakdown and focal small vessel thrombosis. This is a case of:
Acute antibody-mediated rejection (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 234
A 24 y/o female diagnosed with renal failure underwent renal transplant. Four years later, increasing levels of creatinine was noted, and biopsy showed an interstitial fibrosis and tubular atrophy, glomerulopathy with duplication of basement membrane, and multilayering of peritubular capillary basement membranes. Interstitial mononuclear cell infiltrates, NK cells and plasma cells were also noted. This is a case of:
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.234
The result of hypoplasia or lack of thymus in DiGeorge Syndrome
Variable loss of T-cell mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.241
The hallmark of AIDS
Profound immune deficiency, primarily cell-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 245
A 32-year old female, presents to the clinic with symptoms of fatigue, joint pains, and malar rash. CBC revealed anemia and low platelet count. The most likely diagnosis is:
Systemic Lupus Erythematosus (TOPNOTCH)
The hallmark of SLE
Production of autoantibodies (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218
The fundamental defect in SLE
Failure of mechanisms that maintain self-tolerance (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 219
Most common manifestation of SLE
Hematologic manifestation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218
Most common hematologic finding in SLE
Anemia(TOPNOTCH)
Most common and most severe form of lupus nephritis
Diffuse lupus nephritis/Class IV(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 224
The most common causes of death in SLE
Renal failure and intercurrent infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 225
Cytokine most firmly implicated in the pathogenesis of Rheumatoid arthritis
TNF (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 1210
Major cytokine produced by TH1, stimulates macrophage activation and IgG antibody production. Plays a role in autoimmune and other chronic inflammatory diseases.
IFN-gamma(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198
The dominant immune reactions of these subset of helper cells are the stimulation of IgE production and activation of mast cells and eosinophils.
TH2(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198
These are the mediators of adaptive immunity and the only cells that produce specific and diverse receptors for antigens
Lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 199
Immunity mediated by antibodies and is effective against extracellular microbes in the circulation and mucosal lumens.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 9th ed p. 200
Type of immunity design to combat phagocytosed microbes and microbes in the cytoplasm of infected cells.
Cell-mediated immunity(TOPNOTCH)Robbins Basic Pathology, 9th ed p. 200
These are cells the help B cells to make antibodies, activate macrophages to destroy ingested microbes, stimulate recruitment of leukocytesand regulate all immune responses to protein antigens.
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200
These are cells that express antigens in the cytoplasm that are seen as foreign, such as virus-infected and tumor cells.
CD8+ cytotoxic T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200
The most potent vasoactive and spasmodic agents causing increasing vascular permeability and causing bronchial smooth muscle contraction.
Leukotrienes C4 and D4(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 203
A lipid mediator produced by some mast cell populations, not derived from arachidonic acid, causing platelet aggregation, increased vascular permeability, and vasodilation.
Platelet-activating factor(PAF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 203
True or False. Atopic individuals tend to have higher serum IgE levels and more IL-4 producing Th2 cells.
True. (TOPNOTCH)
This disease presents with nephritis and lung hemorrhage due to complement and Fc receptor-mediated inflammation due to antibody against noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli.
Goodpasture syndrome(TOPNOTCH)Robbbins Basic Pathology, 9th ed., p. 206
This disease causes demyelination in CNS is perivascular inflammation due to inflammation mediated by TH1 and TH17 cytokines, myelin destruction by activated macrophages.
Multiple sclerosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 209
Type of immunity primarily affected by AIDS
Cell-mediated immunity(TOPNOTCH)
Mucocutatnous ulcerations involving the mouth, esophagus, external genitalia, and perianal region in AIDS patient may be caused by
Herpes simplex virus infection(TOPNOTCH)
An 18 year old female presents with a day-old circular erythematous plaque with vesicles on her neck. She relates a history of wearing a new metallic pendant three days ago, and has had a similar history with other metallic jewelry. If the plaque is biopsied, which inflammatory cell is expected to predominate? (A) neutrophil (B) eosinophil (C) mast cell (D) lymphocyte
Lymphocyte (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp128-130
An 8 year old male with a strep throat four weeks ago develops tea-colored urine. A kidney biopsy showed hypercellular glomeruli with neutrophils. Electron microscopy showed subepithelial “humps.” These findings are caused by (A) antibodies against glomerular basement membrane (B) antibodies against endothelium (C) immune complex deposition (D) T-cell mediated recruitment of neutrophils
immune complex deposition (TOPNOTCH) Robbins Basic Pathology, 8th ed. P126
A 5 year old female with a strep throat two weeks ago develops joint pains and fever. Auscultation revealed a friction rub. What type of hypersensitivity is responsible?
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
A 33 year old female presents with morning stiffness of the PIP and MCP joints of the hands. On workup, she is positive for rheumatoid factor. Which of the following is expected in the involved joints? (A) synovial hypertrophy with dense lymphoid aggregates (B) synovial atrophy with epithelioid macrophages (C) synovial hypertrophy devoid of leukocytes (D) synovial atrophy with dense lymphoid aggregates
synovial atrophy with dense lymphoid aggregates (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp145-146
A 50 year old female with chronic red eye is diagnosed with keratoconjunctivitis sicca and is referred to by her ophthalmologist for bilateral infraauricular masses. Her oral mucosa has multiple fissures. Biopsy of the infraauricular masses will likely show (A) epithelial and myoepithelial cells admixed with chondroid stroma (B) lymphoplasmacytic infiltration with ductal hyperplasia (C) basaloid cells in cribriform structures (D) highly pleomorphic epithelial cells and numerous atypical mitoses
lymphoplasmacytic infiltration with ductal hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp148-149
Patients with diffuse scleroderma have sclerotic atrophy of the skin. Which other organ is most commonly involved? (A) kidneys (B) heart (C) lungs (D) gastrointestinal tract
gastrointestinal tract (90% of patients) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 149-150
A 22 year old male has unprotected sex and develops generalized lymphadenopathy five days later. The following month, he tests positive on HIV screening. Excision biopsy of one of his lymph nodes would likely show (A) marked follicular hyperplasia (B) epithelioid macrophages and giant cells (C) diffuse infiltration by atypical mononuclear cells (D) subcapsular necrosis
marked follicular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 165
A 68 year old female with multiple myeloma dies of acute renal failure. At autopsy, her kidneys and liver were pale gray, with waxy cut sections, while her spleen showed tapioca-like granules. On histology, these organs show deposits that (A) have empty vacuoles that uptake Sudan black (B) are infiltrated by neutrophils and histiocytes (C) will fluoresce an apple green color when stained with Congo red (D) are bluish, with concentric lamellations
will fluoresce an apple green color when stained with Congo red (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 169-170
This term literally means “new growth”.
Neoplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
An abnormal mass of tissue the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the cessation of stimuli which evoked the change.
Neoplasm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Study of tumors.
Oncology(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Localized
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Amenable to surgical removal
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Invades and destroys adjacent tissues.
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
What are the two basic components of tumors?
Parenchyma and Stroma(TOPNOTCH)
Benign or malignant?Metastasis
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors largely determines its biologic behavior.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors determines the name of the growth.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
This component of tumors is crucial to the growth of neoplasms since it carries the blood supply and provides support to the growth of cells.
Stroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
Benign or malignant?Fibroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Chondroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Adenoma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Hepatoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Papilloma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Malignant neoplasms arising in mesenchymal tissue or its derivatives.
Sarcomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Benign tumor arising in fibrous tissue is called?
Fibroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
A benign cartilagenous tumor is called?
Chondroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
This is a benign epithelial neoplasm which produces glandular patterns or neoplasms derived from glands but not necessarily exhibit glandular patterns
Adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
A mass that projects above a mucosal surface to form a macroscopically visible structure.
Polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
A cancer of fibrous tissue origin.
Fibrosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Malignant neoplasms of epithelial cell origin.
Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
Carcinoma of squamous cell origin.
Squamous cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Lymphoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
Benign or malignant?Seminoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
The extent to which neoplastic cells resemble their normal forebears morphologically and functionally.
Differentiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
This is considered a hallmark of malignancy, which literally means “to form backward”.
Anaplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
These cells display marked pleomorphism, nuclei are variable and bizzare in size and shape. Chromatin is course and clumped. Mitoses are often numerous and distinctly atypical.
Anaplastic cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
This term is defined by disorderly but non-neoplastic proliferation of cells, described as a loss in uniformity of individual cells and in their architectural orientation.
Dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
Defined as dysplastic changes which involve the entire thickness of the epithelium.
Carcinoma -in- situ(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
True or false?Dysplasia always progress to cancer.
False(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
True or false?Lack of capsule in a neoplastic growth indicates malignancy.
FalseSome benign tumors are not encapsulated.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
This term describes the development of secondary implants discontinuous with the primary tumor, in remote tissues.
Metastasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
Next to metastasis, this is the most reliable feature that distinguishes malignant from benign tumors.
Local invasiveness(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
Methods of dissemination of malignant neoplasms? (3)
SeedingLymphatic spreadHematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination of cancers of the ovary and CNS.
Spread by seeding(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination more typical of carcinomas.
Lymphatic spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
This is the mode of dissemination more typical of sarcomas.
Hematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
It is defined as the first lymph node in a regional lymphatic basin that receives lymph flow from a primary tumor.
Sentinel lymph node(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
What are the most common sites of metastasis involved in hematogenous dissemination of cancer?
Liver and lungs(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.181
This substance is a byproduct of metal smelting, a component of alloys, electrical and semiconductor devices which could cause cancer of the lungs and skin and hemangiosarcomas.
Arsenic and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance was formerly used for fire-resistant textiles and construction materials which could cause lung cancer and more prominently malignant mesothelioma
Asbestos(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is commonly used as a solvent in paint, rubber, dry cleaning, adhesives and detergents which could cause leukemias and Hodgkin lymphoma.
Benzene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is used as hardener for metal alloys used in aerospace applications and nuclear reactors which is commonly associated with cancer of the lung.
Beryllium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is used in solders, batteries and metal alloys commonly associated with cancers of the prostate.
Cadmium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
This substance is a refrigerant and used as adhesive for plastics, which causes hepatic angiosarcoma.
Vinyl chloride(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
Inherited gene : Cancer syndromeRB gene :__________
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndromep53 : ______________
Li Fraumeni Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome__________ : Familial Adenomatous Polyposis / Colon CA
APC Gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome_________ : Breast on Ovarian Tumors
BRCA 1 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome_________ : Breast Cancer only
BRCA 2 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndromeRET gene : _________
Multiple Endocrine Neoplasia 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Inherited gene : Cancer syndrome__________ : Colon cancer
kras gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.188
It is a naturally occurring carcinogenic agent produced by some strains of Aspergillus, a mold that grows on improperly stored grains and nuts.
Aflatoxin B(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
There is a strong correlation between the dietary level of Aflatoxin and what type of cancer?
Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
These substances require metabolic conversion to be carcinogenic.
Indirect - acting carcinogens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
These substances stimulate proliferation of the mutated cells.
Promoters(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
How does ionizing radiation cause cancer?
Through chromosome breakage, translocations and point mutations leading to genetic damage and carcinogenesis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
What is the mechanism of action of UV rays in the formation of neoplastic cells?
UV rays induce formation of pyrimidine dimers within DNA leading to mutations.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
This is the only retrovirus that has been demonstrated to cause cancer in humans.
Human T-cell Leukemia Virus -1 (HTLV-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.211
HPV strains which has been implicated in the genesis of cervical and anorectal cancer.
HPV 16, 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
EBV has been implicated in the pathogenesis of the following cancers except:A. Burkitt lymphomaB. Lymphoma in HIV patientsC. Nasopharyngeal carcinomaD. Hodgkin lymphomaE. None of the above
E. none of the above(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
Which hepatitis virus leads to hepatocellular carcinoma?
HBV, HCV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
This is the first bacterium to be classified as a carcinogen.
Helicobacter pylori(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
What type of cancer can be caused by H.pylori?
Gastric adenocarcinoma Gastric MALT lymphomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.214
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)
Tumor antigens are presented on the cell surface by MHC Class I molecules to which type of T lymphocytes?
CD8+ T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.215
Single most important defining characteristic of malignancy
Metastasis (TOPNOTCH)
A biopsy of the stomach reveals an area of normal appearing pancreatic tissue. This is an example of what type of lesion?
Choristoma (TOPNOTCH)
Bronchogenic carcinoma tends to metastasize where?
Adrenals and brain (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 274
The most frequent form of cancer in males
Prostate cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276
The most frequent form of cancer in females
Breast cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276
Most common cause of cancer death in both male and female
Lung cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276
Most important infectious agent associated with cervical carcinoma and head and neck cancers.
Human papilloma virus (TOPNOTCH)
Leukoplakia may give rise to what type of carcinoma?
Squamous carcinoma (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 279
Most common type of abnormality involving proto-oncogenes in human tumors
Point mutations of RAS family genes(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 286
Activation of ABL nonreceptor tyrosine kinase by chromosomal translocation and creation of BCR-ABL fusion gene is associated with what type of leukemia
CML, ALL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 290
“Guardian of the genome”, a tumor suppressor gene that regulates cell cycle progression, DNA repair, cellular senescence, and apoptosis, and the most frequently mutated gene in human cancers
TP53 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 293
“Gatekeeper of colonic neoplasia”; tumor suppressor that function by downregulating growth-promoting signaling pathways.
APC (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 296
Steps in invasion of cancer cells
Dissociation of cancer cells-Degradation of ECM-Attachment to novel ECM components-Migration and invasion of tumor cells. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 306
Autosomal dominant disorder characterized by familial carcinomas of the colon predominantly cecum and proximal colon.
Hereditary nonpolyposis colon cancer (HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314
Syndrome causing colon cancer resulting from defects in a family of genes encoding a group of proteins that work together to carry out DNA mismatch repair.
Hereditary nonpolyposis colon cancer (HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314
The increased incidence of skin cancer following UV light exposure associated with xeroderma pigmentosus is caused by:
Disorder of DNA repair/inability to repair pyrimidine dimers(HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314
Pathogenesis of this tumor involves the translocation resulting to overactivity of MYC gene
Burkitt lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 317
Philadelphia chromosome is characteristic of what type of leukemia
CML(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 317
An important cause of benign warts, cervical cancer, and oropharyngeal cancer
HPV (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 329
Implicated in gastric adenocarcinoma and MALT lymphoma
H. pylori(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 329
Cytokine implicated in cancer cachexia
TNF-alpha(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330
The most common endocrinopathy ; usually seen in small-cell lung carcinoma
Cushing syndrome(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330
The most common paraneoplastic syndrome related to cancer; seen in patients with squamous cell carcinoma
Hypercalcemia(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330
The most important humoral factor associated with paraneoplastic hypercalcemia of malignancy.
PTHRP(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330
Tumor marker:Medullary carcinoma of thyroid
Calcitonin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337
Tumor marker:Trophoblastic tumors
Human chorionic gonadotropin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337
Tumor marker: liver cell cancer and nonseminomatous germ cell tumor
Alpha fetoprotein(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337
Tumor markers: prostate cancer
PSA and prostatic acid phosphatase (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.337
Tumor marker: pheochromocytoma
Catecholamine(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337
Tumor marker: ovarian cancer
CA-125(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337
Cervical biopsy of a 35 y/o female with cervical erosion shows squamous epithelium that exhibit atypia, pleomorphism, disorderly spatial arrangement. This adaptive response is:
Dysplasia (TOPNOTCH)
RAS oncogene qualitatively changes function of proto-oncogene through which form of mutation?
Point mutations (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 286
Chemical carcinogen implicated in the causation of mesothelioma
Asbestos(TOPNOTCH)
A 56 year old woman with a breast mass has a preoperative diagnosis of invasive ductal carcinoma by core needle biopsy, with no palpable axillary lymph nodes. She undergoes surgery where her breast mass is injected with a blue dye, and the first axillary node that takes up the dye is submitted to pathology. Which method is next done on the node if the surgeon wants to know within minutes if there is metastasis? (A) fine needle aspiration (B) frozen section (C) immunohistochemistry (D) flow cytometry
frozen section (TOPNOTCH)Robbins Basic Pathology, 8th Ed, p 220
A 25 year old male with an intranasal mass undergoes a tissue biopsy that shows malignant round cells. The pathologist needs to know if it is an undifferentiated carcinoma or a lymphoma. What can be done to differentiate? (A) Frozen section (B) Immunohistochemistry (C) Flow cytometry (D) serologic tumor markers
Immunohistochemistry (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp220-221
A 12 year old female presents with pallor and gum bleeding. A complete blood count with peripheral smear shows numerous blasts. What is needed to be done on her bone marrow for a more precise diagnosis? (A) frozen section (B) papanicolau smear (C) aspiration and flow cytometry (D) serologic tumor markers
aspiration and flow cytometry (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 221
These disorders are derived from one’s parents, transmitted through gametes through the generations, and are therefore familial.
Hereditary disorders(TOPNOTCH)
This term literally means “present at birth”.
Congenital(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This term refers to permanent changes in the DNA.
Mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation results from the substitution of a single nucleotide base by a different base, resulting in the replacement of one amino acid by another.
Missense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation results in the replacement of one amino acid by a stop codon, resulting in chain termination.
Nonsense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
Missense, nonsense and silent mutations are examples of ________ mutations, wherein only one base pair is replaced.
Point mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This type of mutation occur when the insertion or deletion of one or two bse pairs alters the reading frame of the DNA strand.
Frameshift mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
These mutations are characterized by amplification of a sequence of three nucleotides.
Trinucleotide repeat mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
Disease characterized by CGG trinucleotide repeats.
Fragile X Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
This is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems.
Huntington’s disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Genetic mutation in Huntington’s disease?
CAG trinucleotide repeats(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
This disorder is a chronic, slowly progressing inherited genetic disorder characterized by muscle wasting, cataracts, heart conduction defects, endocrine changes and myotonia.
Myotonic Dystrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Genetic mutation found in myotonic dystrophy?
CTG Trinucleotide repeats(TOPNOTCH)
A point mutation wherein a single base pair is replaced but codes for the same amino acid, therefore has no effect on the functioning of the protein.
Silent mutation(TOPNOTCH)
An example of point mutation wherein a purine base is replaced by another purine base or a pyrimidine base is replaced by another pyrimidine base.
Transition(TOPNOTCH)
A point mutation wherein a purine is replaced by a pyrimidine or vice versa.
Transversion(TOPNOTCH)
Diseases caused by single gene defects are called?
Mendelian Disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A condition wherein both dominant and recessive alleles of a gene pair may be fully expressed in the heterozygote.
Codominance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
The presence of many allelic forms of a single gene is called _______.
Polymorphism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
This occurs when one gene influences or leads to multiple phenotypic traits.
Pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A phenomenon wherein a single phenotype or genetic disorder may be caused by mutations of several genetic loci or allele.
Genetic heterogeneity Note: compare with pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
A transmission pattern of inheritance which is manifested in the heterozygous state, wherein at least one parent of an index case is usually affected, both males and females are affected and both can transmit the condition.
Autosomal dominant (AD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
This pattern of inheritance occur when BOTH of the alleles at a given gene locus are mutants, wherein the parents are not affected, but offspring have 1 in 4 chance (25%) of being affected.
Autosomal recessive(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
Pattern of inheritance wherein the disorder is transmitted by heterozygous female carriers only to 50% of the sons. An affected male does not transmit the disorder to sons but all daughters are carriers.
X-linked disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
An autosomal dominant disorder of connective tissues characterized by abnormally long legs, arms and fingers, joint hyperextensibility, pectus excavatum, lens subluxation and increased risk of aortic dissection.
Marfan Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
Integral component of elastic fibers defective in Marfan Syndrome.
Fibrillin 1(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
Fibrillin 1 is encoded by what gene?
FBN1 gene (chromosome 15q21)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
A collection of disorders caused by defects in collagen synthesis or structure, characterized by hyperextensible skin and joint hypermobility, rupture of internal organs and poor wound healing.
Ehlers-Danlos SyndromesThere are 6 variants to Ehlers-Danlos (nice to know)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.231
This autosomal recessive inborn error of metabolism is characterized by inability to convert phenylalanine to tyrosine, strong mousy or musty odor of urine and sweat, decreased pigmentation of hair and skin, eczema, seizures and mental retardation.
Phenylketonuria (PKU)(TOPNOTCH)
This autosomal dominant disorder is caused by a mutation in the gene that specifies the receptor for LDL, impairing the intracellular transport and catabolism of LDL.
Familial hypercholesterolemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.232
Enzyme deficient in classic PKU.
Phenylalanine hydroxylase (PAH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
An autosomal recessive disorder of galactose metabolism characterized by jaundice, liver damage, cataracts, neural damage, vomiting and diarrhea.
Galactosemia(TOPNOTCH)
Deficiency of this enzyme can also cause symptoms of phenylketonuria due to decreased synthesis of a cofactor in the conversion of phenylalanine to tyrosine.
Dihydrobiopteridine reductase (DHPR)Enzyme responsible for the reduction of Dihydrobiopterin (BH2) to Tetrahydrobiopterin (BH4).(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
Enzyme deficient in galactosemia.
Galactose-1-phosphate uridyltransferase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.235
Lysosomal storage disease due to deficiency of glucosylceramidase.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of B-Hexosaminidase A.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of a-Galactosidase A.
Fabry disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease due to deficiency of Sphingomyelinase.
Niemann-Pick disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease common among Ashkenazi Jews characterized by motor weakness, mental retardation, blindness, neurologic dysfunction and death.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
Lysosomal storage disease characterized by accumulation of glucosylceramide in mononuclear phagocytic cells, which enlarge, forming “wrinkled tissue paper” cytoplasmic appearance.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
What do you call the pathognomonic cell characterized by “wrinkled tissue paper” cytoplasmic appearance.
Gaucher cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
These disorders result from the accumulation of mucopolysaccharides in many tissues including the liver, spleen, heart, blood vessels, brain, cornea and joints. Affected patients have coarse facial features.
Mucopolysaccharidoses(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
Mucopolysaccharidosis characterized by corneal clouding, coronary arterial and valvular depositions, which occurs due to deficiency of a-L-iduronidase, leading to accumulation of dermatan and heparan sulfate.
Hurler syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
An X-linked mucopolysaccharidosis which is due to a deficiency of L-iduronate sulfatase. Symptoms are similar to Hurler syndrome, but without corneal clouding.
Hunter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
Glycogen storage disease characterized by hepatomegaly, renomegaly, hypoglycemia, hyperlipidemia and hyperuricemia, leading to gout and skin xanthomas.
von Gierke’s disease (Type I)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
von Gierke’s disease is due to a deficiency of what enzyme?
Glucose-6-phosphatase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Glycogen storage disease characterized by accumulation of glycogen in skeletal muscles leading to painful cramps during strenuous exercise and myoglobinuria.
McArdle syndrome (type V)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Glycogen storage disease characterized by mild hepatomegaly, cardiomegaly, muscle hypotonia, and may lead to cardiorespiratory failure.
Pompe disease (type II)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
Enzyme deficient in McArdle syndrome.
Muscle phosphorylase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.241
It is a term used to describe the presence of two or more populations of cells in the same individual.
Mosaicism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.242
This refers to a lack of one chromosome of the normal complement (e.g. XO).
Monosomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
This refers to the presence of three copies of a particular chromosome, instead of two.
Trisomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
This mechanism occurs due to the failure of chromosome pairs to separate properly during meiosis stage 1 or 2.
Nondisjunction(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
This mechanism implies transfer of a part of one chromosome to another chromosome.
Translocation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
This mechanism involves loss of a portion of a chromosome.
Deletion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
Patients with this syndrome have severe mental retardation, flat facial profile, epicanthic folds, cardiac malformations, increased risk of leukemia, and premature development of Alzheimer’s disease.
Down syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
Down syndrome is also called _________
Trisomy 21(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Trisomy 18 is also called ________ syndrome.
Edwards syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Trisomy 13 is also called _________ syndrome.
Patau syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
Syndrome characterized by a prominent occiput, low set ears, micrognathia, rocker-bottom feet, renal malformation, mental retardation and heart defects.
Edwards syndrome / trisomy 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by mental retardation, microcephaly, micropthalmia, polydactyly, cleft lip and palate, cardiac and renal defects, umbillical hernia and rocker-bottom feet.
Patau syndrome/Trisomy 13(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by thymic hypoplasia with diminished T-cell immunity and parathyroid hypoplasia with hypocalcemia.
DiGeorge syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Syndrome characterized by congenital heart disease affecting outflow tracts, facial dysmorphism and developmental delay.
Velocardiofacial syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
Deletion of genes from this chromosome gives rise to DiGeorge and velocardiofacial syndromes.
22q11.2Remember mnemonic CATCH22(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
The q from 22q11.2 refers to ________.
“Long arm” of chromosome 22.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome defined as male hypogonadism that develops when there are at least two X chromosomes and one or more Y chromosomes.
Klinefelter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome manifested by a eunochoid body habitus, reduced facial, body and pubic hair, gynecomastia, testicular atrophy, decreased serum testorerone and increased urinary gonadotropin levels. It is the most common cause of hypogonadism in males.
Klinefelter syndrome (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Most common chromosomal derangement in Klinefelter syndrome.
47XXY(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
Syndrome which results from the partial or complete monosomy of the short arm of the X chromosome.
Turner syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)
Neurodegenerative disease which manifests as progressive bilateral loss of central vision that leads to blindness. This is the prototypical disorder of mutations in mitochondrial genes.
Leber hereditary optic neuropathy(TOPNOTCH)
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
An epigenetic process wherein certain genes are differentially “inactivated” during paternal and maternal gametogenesis.
Genomic imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.252
This refers to transcriptional silencing of the maternal allele.
Maternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Refers to the transcriptional silencing of the paternal allele.
Paternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Syndrome characterized by mental retardation, short stature, hypotonia, obesity, small hands and feet, and hypogonadism. Paternal imprinting.
Prader-Willi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
Syndrome manifested as mental retardation, ataxic gait, seizures and inappropriate laughter. Also called the “happy puppet syndrome”. Maternal imprinting.
Angelman syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.
Malformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
These result from secondary destruction of an organ or body region that was previously normal in development, due to an extrinsic disturbance in morphogenesis.
Disruptions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
These are due to generalized compression of the growing fetus by abnormal biomechanical forces, for example uterine constraint.
Deformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
This refers to multiple congenital anomalies that result from secondary effects of a single localized aberration in organogenesis. The initiating event may be a malformation, deformation or disruption.
Sequence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
This refers to the presence of several defects that cannot be explained on the basis of a single localizing initiating error in morphogenesis.
Malformation syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
Elements of the TORCH complex.
TOxoplasmaTreponema pallidumRubellaCytomeglovirusHerpesvirus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.256
Most common cause of neonatal mortality.
Congenital anomalies(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
Second most common cause of neonatal mortality.
Prematurity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Lungs of infants with this disease are normal size but are heavy and relatively airless. They have a mottled purple color, with poorly developed atelectatic alveoli.
Neonatal Respiratory Distress Syndrome / Hyaline Membrane Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Characteristic eosinophilic membranes line the respiratory bronchioles, alveolar ducts and random alveoli, which contain necrotic epithelial cells admixed with extravasated plasma proteins.
Hyaline Membrane Disease / Neonatal RDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
Two well known complications of high concentration ventilator administered oxygen in infants suffering from RDS.
Retrolental fibroplasia / retinopathy of prematurityBronchopulmonary dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Characteristic lesion in the retina of infants suffering from retrolental fibroplasia?
Neovascularization or retinal vessel proliferation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Main component of pulmonary surfactant.
Dipalmitoylphosphatidylcholine (DPPC) ~40%(TOPNOTCH)
Characteristic abnormality in bronchopulmonary dysplasia?
Alveolar hypoplasia or a decrease in the number of mature alveoli.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
What is the fundamental abnormality in neonatal RDS?
Insufficient pulmonary surfactant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
This condition occurs more commonly in very-low-birth-weight infants, as a result of intestinal ischemia, bacterial colonization of gut and formula milk feeding.
Necrotizing enterocolitis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
Microscopic features of NEC.
Presence of submucosal gas bubbles, transmural coagulative necrosis, ulceration and bacterial colonization.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.259
Defined as the sudden death of an infant under 1 year of age which remains unexplained after a thorough investigation.
Sudden Infant Death Syndrome / SIDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
Multiple petechiae of the thymus, visceral and parietal pleura and epicardium, congested lungs with vascular engorgement with or without pulmonary edema.
Sudden Infant Death Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
Results from antibody-induced hemolytic disease in the newborn that is caused by blood group incompatibility between mother and fetus, leading to edema fluid accumulation.
Immune Hydrops(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
Erythroid precursors with large homogenous, intranuclear inclusions and a surrounding peripheral rim of residual chromatin can be seen in the bone marrow aspirate of an infant infected with this virus. This leads to development of non-immune hydrops.
Parvovirus B19(TOPNOTCH)
Isolated postnuchal fluid accumulation in fetuses with hydrops.
Cystic hygroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
A lethal condition characterized by generalized edema of the fetus.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
Increased hematopoietic activity leading to the presence of large number of immature red cells, including reticulocytes, normoblasts and erythroblasts. Characteristic finding in fetal anemia-associated hydrops.
Erythroblastosis fetalis(TOPNOTCH)
Primary gene defect in cystic fibrosis.
Abnormal CFTR (CF transmembrane conductance regulator) Chromosome 7q31.2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
Lungs with extensive mucous plugging and dilated tracheobronchial tree. Pancreatic ducts dilated and plugged with eosinophilic mucin, atrophic parenchymal glands replaced by fibrous tissue. Hepatic steatosis, Azoospermia and infertility are some of the features of this disease.
Cystic fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
Patients with cystic fibrosis are prone to developing infections caused by these three organisms.
S. aureusH. InfluenzaeP. aeruginosa(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.266
How is cystic fibrosis diagnosed?
Persistently elevated sweat chloride concentration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Most common tumors of infancy.
Hemangioma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Microscopically normal cells or tissues that are present in abnormal locations.
Heterotopia or choristoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Port wine stains are associted with these syndromes. (2)
von Hippel-Lindau Sturge-Weber syndromes(TOPNOTCH)
This refers to an excessive but focal overgrowth of cells and tissues native to the organ in which it occurs.
Hamartoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
Large, flat to elevated, irregular, red-blue masses in the skin.
Port wine stains(Large hemangiomas)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
These represent the lymphatic counterpart of hemangiomas characterized as cystic and cavernous spaces lined by endothelial cells and surrounded by lymphoid aggregates,usually containing pale fluid.
Lymphangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
What do you call the rosettes found in neuroblastomas?
Homer-Wright pseudorosettes(TOPNOTCH)
Most common germ cell tumors of childhood,associated with meningocoele and spina bifida.
Sacrococcygeal teratomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
Tumor of the adrenal medulla composed of small, primitive-appearing cells with dark nuclei, scant cytoplasm, and poorly defined cell borders growing in solid sheets within a finely fibrillar matrix. Rosettes can be found in which tumor cells are concentrically arranged about a CENTRAL SPACE FILLED with neuropil.
Neuroblastomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.269
This is used in the screening of patients with neuroblastoma.
Urinary vanillylmandelic acid and homovanillic acid (VMA/HVA)(TOPNOTCH)
Differentiated lesions containing more large cells with vesicular nuclei and abundant eoinophilic cytoplasm, in the absence of neuroblasts, usually accompanied by mature spindle shaped Schwann cells.
Ganglioneuroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
Disseminated neuroblastoma with multiple cuteaneous metastases with deep blue discoloration to the skin.
“Blueberry muffin baby”(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
This tumor is composed of small, round cells with large hyperchromatic nuclei and scant cytoplasm, with characteristic structures consisting of clusters of cuboidal or short columnar cells arranged around a CENTRAL LUMEN. The nuclei are displaced away from the lumen, which appears to have a limiting membrane.
Retinoblastoma(Differentiate with neuroblastoma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Rosettes in retinoblastoma are called _______.
Flexner-Wintersteiner rosettes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Clinicial findings include poor vision, strabismus, whitish hue to the pupils (“cat’s eye reflex”), pain and tenderness to the eye.
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Most common primary tumor of the kidney in children.
Wilm’s tumor / Nephroblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
Components of the WAGR syndrome.
Wilm’s tumorAniridiaGenital abnormalitiesMental retardation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Presents grossly as a large, solitary, well-circumscribed mass. On cut-section, tumor is soft, homogenous, and tan to gray, with occasional foci of hemorrhage, cystic degeneration and necrosis.
Wilm’s tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Microscopically, a combination of blastemal, stromal and epithelial cell types is observed. (Triphasic combination) Blastemal components described as sheets of small blue cells with few distinctive features. Stromal cells are fibrocytic or myxoid in nature. Epithelial cells take the form of abortive tubules or glomeruli.
Wilm’s tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Associated with inactivation of the WT1 gene of chromosome 11p13.
WAGR syndrome and Denys-Drash syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
Patient presents with mental retardation, motor incoordination, and blindness. Ophthalmologic exam showeed cherry-red spots on the macula. Brain showed neurons ballooned with cytoplasmic vacuoles. What is the enzyme deficiency?
Hexosaminidase A. (Case of Tay-Sachs Disease) (TOPNOTCH)
An 18 y/o male was recently diagnosed with a genetic disorder. His parents do not manifest the disease, but one of his parent carries the gene with phenotypic expression. Some of his relatives manifest the same disease but with different presentation. What type of Mendelian disorder does the patient most likely have?
Autosomal dominant disorder. With this type, some patient do not have affected parents, has variations in penetrance and expressivity, age at onset is delayed. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 140
True or False. Male patient with hemophilia does not transmit the disorder to his sons, but all daughters are carriers.
True. Hemophilia is an X-linked disorder. (TOPNOTCH)
True or False. Female hemophilia carrier will transmit the disease to half her sons and half her daughter.
False. X-linked disorders are transmitted by heterozygous females to their sons, who manifest the disease. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 142
True or False. Female hemophilia carrier will manifest with decrease Factor VIII.
False (TOPNOTCH)
True or False. In female hemophilia carrier, only one of the X chromosome shows abnormality.
True (TOPNOTCH)
True or False. In X-linked disorders, female carriers are usually protected because of random inactivation of one X chromosome.
True (TOPNOTCH)
True or False. In X-linked disorders, heterozygous female carrier will never manifest the disease.
False (TOPNOTCH)
A 26 y/o male was referred to a cardiologist due to presence of murmur at the aortic area. On history, patient suffered from severe myopia at the age of 6. His development was normal except that he was taller than the rest of his family members and friends. Examination of abdomen showed visible pulsation above the umbilicus. The most striking feature in this syndrome is:
Skeletal abnormalities. (case of Marfan Syndrome) (TOPNOTCH)
The most life-threatening feature of Marfan syndrome
Cardiovascular lesions (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 145
The 2 most common lesions of Marfan Syndrome
Mitral valve prolapse and dilation of ascending aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 145
A 4 y/o male presented with cutaneous xanthomas on the extensor surfaces of his arms, knees, and elbow since he was 1 year old. He was found to have serum cholesterol greater than 1000 mg/dl and triglyceride level of 170 mg/dl. Both parents had high cholesterol levels. What is the cause of hypercholesterolemia in this condition?
Impared transport of LDL into the cells (Case of Familial Hypercholesterolemia) (TOPNOTCH)
A 6 mo old infant presented with failure to thrive, vomiting, fever, and hepatosplenomegaly. Progressive deterioration of the infant led to death. Autopsy finding showed lipid laden phagocytic foam cells widely distributed in the spleen, liver, lymph nodes, GIT and lungs. Tissue cells are enlarged, with innumerable vacuoles staining for fat, and lysosome contain concentric lamellated myelin figures. The patient is deficient of what enzyme?
Sphingomyelinase (case of Niemann-Pick Disease Type A) (TOPNOTCH)
A 1 y/o infant succumbed to death. Autopsy finding showed shrunken gyri and widened sulci. There is vacuolation and ballooning of neurons noted. Cells are enlarged with innumerable small vacuoles of uniform size, imparting foaminess to the cytoplasm. This is a case of:
Niemann-Pick Disease (TOPNOTCH)
Presents with fractures, bone pain and thrombocytopenia. Morphologic findings of distended phagocytic cells and have fibrillary type of cytoplasm, intensely positive for PAS staining.
Gaucher disease (TOPNOTCH)
A 21 y/o female of short stature presented with primary amenorrhea, shield-shaped chest, “thick neck”, and absence of secondary female characteristics. Estrogen level were decreased, while FSH and LH are increased. What is the most likely diagnosis?
Turner syndrome (TOPNOTCH)
The most common chromosomal disorder
Down Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 161
The most common genetic cause of mental retardation.
Down Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 161
Most common pathogenesis of Trisomy 21
Meiotic nondisjunction (TOPNOTCH)
Most common congenital heart defects in Trisomy 21
Endocardial cushion defects(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 163
Why are patients with DiGeorge syndrome has T-cell immunodeficiency?
Because of thymic hypoplasia (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 163
A 14 y/o male presented with gynecomastia and small testes. He was noted to have difficulties in school when he was 8. He was tall for his age. You would suspect:
Klinefelter syndrome (TOPNOTCH)
Classic karyotype patttern of Klinefelter syndrome
47,XXY(TOPNOTCH)
Single most important cause of primary amenorrhea
Turner syndrome (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 166
Most important cause of increased mortality in children with Turner syndrome.
Cardiovascular abnormalities (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 166
Patient presents with mental retardation, long face with large mandible, large everted ears, and large testicles. The most likely diagnosis is:
Fragile X Syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 169
Most distinctive feature of Fragile X syndrome
Macro-orchidism(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 169
The neonate was noted to have microcephaly, short palpebral fissure, maxillary hypoplasia, growth retardation, and psychomotor disturbances. The mother denies intake of drugs during pregnancy. The most likely cause
Alcohol (TOPNOTCH)
Deficiency in homogentisic oxidase results in this condition which manifests black discoloration of the urine
Alkaptonuria (TOPNOTCH)
Most common cause of respiratory distress in the newborn
Hyaline Membrane Disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 457
This teratogenic drug disrupts expression of homeobox proteins implicated in the patterning of lims, vertebrae, and craniofacial structures.
Valproic acid (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 456
Most commonly responsible for fetal growth restriction.
TORCH infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 457
Most common maternal condition associated with SGA infants
Vascular diseases (chronic hypertension, preclampsia) (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 457
A 28 week old male delivered via CS by a diabetiic mother presented with dyspnea and cyanosis. Fine rales are heard over both lung fields. CXR revealed uniform minute reticulogranular densities, producing a ground glass appearance. The fundamental defect in this condition is:
Pulmonary surfactant (Case of RDS) (TOPNOTCH)
The most common cause of mortality in children ages 1-4 years old.
Accidents (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 452
A 28 week old male dies 20 hours after birth. Autopsy findings showed a solid, airless, and reddish purple lungs with poorly developed alveoli. Necrotic cellular debris incorporated within eosinophilic hyaline membranes lines the respiratory bronchioles, alveolar ducts and alveoli. The most likely cause of death of the neonae is:
Respiratory distress syndrome/Hyaline membrane disease (TOPNOTCH)
Premature infant, bottle-fed, developed bloody stool, abdominal distention. Abdominal radiograph showed pneumotis intestinalis. Diagnosis:
Necrotizing enterocolitis(TOPNOTCH)
Morphology: intestinal segment is distended, friable and congested, with transmural coagulative necrosis, ulceration, bacterial colonization, and submucosal bubbles.
Necrotizing enterocolitis(TOPNOTCH)
Most common cause of early-onset neonatal sepsis and early-onset bacterial meningitis
Group B streptococcus(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 460
The most serious threat of fetal hydrops
CNS damage -kernicterus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 463
Most common site of neuroblastoma
Adrenal medulla (TOPNOTCH)
Presents with a large abdominal mass crossing the midline, hematuria, intestinal obstruction, and hypertension.
Wilm’s tumor (TOPNOTCH)
A 22 year old male consults an ophthalmologist for sudden blindness on the right. He is found to have lens subluxation. He is unusually tall and lean, with long limbs and fingers. These findings are due to abnormalities in fibrillin 1, which is secreted by (A) megakaryocytes (B) fibroblasts (C) histiocytes (D) fibroclasts
fibroblasts (TOPNOTCH)Robbins Basic Pathology, 8th Ed, p 230
A lysosomal storage disease with a mutation in the gene that encodes glucosylceramidase presents with an accumulation of glucosylceramide in mononuclear phagocytic cells in the liver, spleen, and marrow. These pathognomonic cells are (A) enlarged, with a “wrinkled tissue paper” cytoplasm (B) epithelioid, with “slipper-shaped” nuclei (C) multinucleated, with 8 to 20 nuclei (D) studded with reddish brown cytoplasmic granules
enlarged, with a “wrinkled tissue paper” cytoplasm (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp237-238
A baby is born with epicanthic folds, flat facial profile, simian crease, and a gap between the first and second toe. Auscultation reveals a holosystolic murmur. The clinical findings are due to an extra chromosome that is most commonly caused by (A) meiotic duplication (B) meiotic nondisjunction (C) fertilization by two spermatozoa (D) translocation
meiotic nondisjunction (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 244
A premature female neonate admitted at the PICU develops sepsis, with blood cultures showing growth of Candida sp. She is also found to be persistently hypocalcemic. She dies on her 7th day. On autopsy, she was found to have fungal endocarditis and thymic hypoplasia. She most likely has (A) an extra chromosome 22 (B) a deletion in chromosome 22 (C) a 9:22 chromosomal translocation (D) a duplication in chromosome 22
a deletion in chromosome 22 (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 245-246
A stillborn fetus is found to have polydactyly, an umbilical hernia, and cleft lip and palate. Autopsy showed a ventral septal defect, renal dysplasia, and holoprosencephaly. Karyotyping will likely show (A) Monosomy X (B) Deletion in chromosome 5 (C) Trisomy 13 (D) Trisomy 18
Trisomy 13 (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 245.
A 19 year old female consults a gynecologist for primary amenorrhea. Apart from her short stature, there are no other unusual clinical findings. Why must Turner Syndrome be ruled out? (A) mosaicism or partial monosomy may produce a mild form of the syndrome (B) 45,X abnormalities manifest in only half of females by the age of 18 (C) when combined with Fragile X, the typical features such as neck webbing and cubitus valgus are masked (D) supplementation with folate during gestation masks the typical features of neck webbing and cubitus valgus
mosaicism or partial monosomy produces a milder form (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp247-248
A stillborn male fetus delivered to a 41 year old G7P7 is found to have flattened facies and clubbed feet. Autopsy showed renal agenesis and pulmonary hypoplasia. What is the main culprit of the findings in the fetus? (A) maternal age (B) multiparity (C) renal agenesis (D) pulmonary hypoplasia
renal agenesis (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 253-254
A G3P3 mother has premature rupture of membranes at 35 weeks age of gestation, and delivers a live baby boy with poor APGAR scores. The obstetrician delivered a placenta with dull-looking membranes, which showed chorioamnionitis on histopathology. Culture of which organism from the placental tissue suggests an transcervical origin of infection? (A) Group B Streptococcus (B) Toxoplasma (C) Plasmodium (D) Rubella
Group B Streptococcus (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 256
A G1P1 preeclamptic mother delivers a live baby boy at 27 weeks age of gestation. The baby develops respiratory distress a few minutes later and is admitted at the PICU. He dies the next day, and is sent for autopsy. Which of the following supports respiratory distress syndrome of the newborn? (A) thickened alveolar septa with lymphocytic infiltrates (B) alveolar spaces filled with neutrophils (C) eosinophilic material lining the alveolar walls (D) hemosiderin laden macrophages in the alveolar spaces
eosinophilic material lining the alveolar walls (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 257-258
A premature male neonate who was delivered at 33 weeks AOG and admitted at the PICU develops abdominal distention, bloody stools, and hypotension. An abdominal radiograph shows gas within the intestinal wall. What is the expected histologic findings of the involved intestine? (A) coagulative necrosis of the mucosa and muscularis (B) arteriovenous fistulas in the submucosa (C) melanosis of the mucosa (D) crypt abscesses and noncaseating granulomas
coagulative necrosis of the mucosa and muscularis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 259
What is the most common autopsy finding in sudden infant death syndrome? (A) patent ductus arteriosus (B) multiple petechiae in the thymus and pleural surfaces (C) bilateral adrenal hemorrhage (D) flattening of gyri in the cerebral cortex
multiple petechiae on the thymus and visceral surfaces (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 260
How does parvovirus B19 infection cause fetal hydrops? (A) it causes a chronic myocarditis leading to heart failure (B) it infects the lymphatic ducts causing peripheral fluid accumulation (C) it causes placental villi atrophy, exposing the fetal circulation to maternal antibodies (D) it infects erythroid precursors, causing anemia
it infects erythroid precursors, causing anemia (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 262
A 4 month old infant with abdominal enlargement presents with multiple bluish-gray subcutaneous nodules. Workup showed a 10 cm mass in the paravertebral region. Biopsy of the nodules showed small round cells with dark nuclei scanty cytoplasm, some forming rosettes arranged in a finely fibrillar matrix. Immunohistochemical studies showed the cells to be positive for neuron specific enolase and negative for leucocyte common antigen. These tumor cells are derived from (A) antigen presenting cells in the dermis (B) neural crest (C) nephrogenic rests (D) lymphoid precursors
neural crest (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 269-270
A 2 year old male is noticed to have a whitish pupil on photographs. Workup showed a tumor in the posterior chamber. The eye is enucleated, and the tumor shows sheets of small round cells with hyperchromatic nuclei and scant cytoplasm. Occasional clustering around central lumens are seen. On further history, a cousin also had a similar tumor and died. The patient has an increased risk of developing which tumour later in life: (A) hepatoblastoma (B) pheochromocytoma (C) osteosarcoma (D) Wilms tumour
osteosarcoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 271
A 4 year old female undergoes left nephrectomy for Wilms tumor. Which of the following findings in the nephrectomy specimen is associated with an increased risk of developing the same tumor in the right kidney? (A) nephrogenic rests (B) abortive tubules or glomeruli (C) extensive fibrosis (D) adipose tissue, cartilage, and osteoid
nephrogenic rests (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 272
A gas formed by sunlight-driven reactions involving nitrogen oxides. Together with oxides and fine particulate matter, it forms “smog”.
Ozone(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
A nonirritating , colorless, tasteless, odorless gas produced bu the imperfect oxidation of carbonaceous materials. Binds to hemoglobin with high affinity causing systemic asphyxiation and CNS depression.
Carbon monoxide(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
Carbon monoxide in the blood is called _______.
Carboxyhemoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
Acute poisoning of carbon monoxide produces this characteristic color of the skin and mucous membranes.
Cherry red color(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
Microcytic, hypochromic anemia, with basophilic stippling of erythrocytes, peripheral demyelinating neuropathy which manifests as footdrop and wristdrop, colic characterized by extremely severe, poorly localized abdominal pain, and chronic renal damage are the features of poisoning with this heavy metal.
Lead(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
Main source of exposure to this heavy metal are contamintaed fish and dental amalgams, causing tremor, gingivitis and bizarre behavior.
Mercury(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Consumption of fish contaminated with methyl mercury causing cerebral palsy, deafness, blindness, and major CNS defects in children exposed in utero.
Minamata disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Antidote for mercury poisoning.
Thimerosal(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Chronic exposure with this heavy metal results in hyperpigmentation and hyperkeratosis which may develop into basal or squamous cell carcinomas.
Arsenic(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
This heavy metal is used mainly in batteries and fertilizers, which can contaminate soil. Can cause obstructive lung disease and kidney damage.
Cadmium(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Disease caused by cadmium in Japan, presenting as a combination of osteoporosis and osteomalacia, associated with renal disease.
Itai-itai disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
May be released from combustion of fossil fuels, burning of coal and gas, and also present in tar and soot. Among the most potent carcinogens, implicated in lung and bladder cancer.
Polycyclic hydrocarbons(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
Synthetic products that resist degradation and are lipophilic, typically used as pesticides, with anti-estrogenic and anti-androgenic activity, and causes neurologic toxicity.
Organochlorines (e.g. DDT)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
These can cause skin disorders such as folliculitis and chloracne, consisting of acne, cyst formation, hyperpigmentation, and hyperkeratosis, around the face and behind the ears.
Dioxins and Polychlorinatedbiphenyls (PCB)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
It is the most preventable cause of human death.
Smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
Components of cigarette smoke that are potent carcinogens in animals and are most likely involved in the causation of lung carcinomas in humans.
Polycyclic hydrocarbons and nitrosamines(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 288
Chronic alcoholics are at an increased risk of developing this type of cancer as a result of liver injury.
Hepatocellular carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 290
These refer to untoward effects of drugs that are given in conventional therapeutic settings.
Adverse drug reactions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 291
A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.
Minocycline(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293
Oral contraceptives have a protective effect against these cancers.
Endometrial and ovarian CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Oral contraceptives may increase the risk of developing this type of cancer in women.
Cervical CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Prolonged use of oral contraceptives is associated with the development of this rare benign tumor especially in older women.
Hepatic adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Toxic metabolite of paracetamol or acetaminophen causing centrilobular necrosis that may progress to liver failure.
NAPQI (N-acetyl-p-benzoquinoneimine)(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 422
Toxic dose for acetaminophen.
15-25 grams/day(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Antidote for acetaminophen poisoning.
N-acetylcysteine(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 294
Manifested by headache, dizziness, tinnitus, difficulty of hearing, mental confusion, drowsiness, nausea, vomiting, and diarrhea, with CNS changes that can progress to convulsions and coma.
Salicylism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Adult toxic dose of aspirin.
10-30 grams(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
Mixtures of aspirin and phenacetin, or its active metabolite acetaminophen, when taken over several years can cause tubulointerstitial nephritis and renal papillary necrosis called _______.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
This drug of abuse can precipitate lethal arrythmias, hyperpyrexia, seizures, amd respiratory arrest during acute overdose. Causes nasal septal perforation, decrease in lung diffusing capacity in those who inhale smoke and dilated cardiomyopathy during chronic use.
Cocaine or “crack” (cocaine derivative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 295
Addictive opiod derived from the poppy plant which can cause euphoria, hallucinations, somnolence, sedation, and increased risk of sudden death.
Heroin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 296
Drug made from the leaves of Cannabis sativa plant which can cause distortion of sensory perception and impairs motor coordination.
Marijuana(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 297
Psychoactive substance found in marijuana.
Delta 9- Tetrahydrocannabinol (THC)(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
Mechanism of action of aspirin.
Irreversibly blocks the enzyme cyclooxygenase.(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
A wound produced by scraping or rubbing resulting in removal of superficial layer of the skin.
Abrasion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound usually produced by a blunt object, characterized by damage to blood vessels and extravasation of blood into tissues.
Contusion (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A tear or disruptive stretching of tissue caused by the application of force by a blunt object, causing jagged and irregular edges to the skin.
Laceration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound inflicted by a sharp instrument, wherein bridging blood vessels are severed.
Incision(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
A wound caused by a long, narrow instrument.
Puncture wound(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Burn classification which involves total destruction of the epidermis and dermis, with loss of thermal appendages.
Full thickness burn (3rd and 4th degree)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Burn classification wherein the thermal appendages are spared but involves at least the deeper portions of the skin.
Partial thickness burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Partial thickness burn that involves both the epidermis and superficial dermis.
Second degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Partial thickness burn that involves the epidermis only.
First degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Grossly, these burns are white or charred and anesthetic due to nerve ending destruction.
Full thickness burns(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
These burns are pink or mottled with blisters and are painful.
Second degree burn (partial thickness)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Histologic change in the skin during burns.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
Leading cause of death in burn patients.
Organ system failure secondary to burn sepsis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Cramping of voluntary muscles in association with vigorous exercise as a result of electrolyte loss via sweating.
Heat cramps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Most common hyperthermic syndrome. A sudden onset of prostration and collapse, resulting from failure of the cardiovascular system to compensate for hypovolemia, secondary to water depletion.
Heat exhaustion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Associated with high ambient temperatures and high humidity. Thermoregulatory mechanisms fail, sweating ceases and core body temperature rises. Due to marked generalized peripheral vasodilation with peripheral pooling of blood and decreased effective circulating volume.
Heat stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
Two types of injuries caused by electricity.
BurnsVFib or cardiac and respiratory center failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
This may injure cells directly or indirectly by generating free radicals from water or molecular oxygen, damages DNA and rapidly dividing cells. Exposure may predispose to neoplastic transformation, vascular damage, sclerosis and tissue fibrosis.
Ionizing radiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 300
Malnutrition caused by lack of nutrients from the diet.
Primary malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
Malnutrition caused by malabsorption, impaired nutrient utilization or storage, excess losses or increased nutrient needs.
Secondary or conditioned malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
Protein energy malnutrition which occurs when protein deprivation is relatively greater than reduction in total calories. Associated with generalized edema, flaky paint appearance of the skin, alternating bands of pale and dark hair, enlarged fatty liver, apathy, listlessness and loss of appetite.
Kwashiorkor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
Protein energy malnutrition caused by a decrease in both protein and calorie intake, and weight falls below 60% of normal for sex, height and age. Serum albumin is normal or slightly reduced.
Marasmus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
Self-induced starvation, resulting in marked weight loss.
Anorexia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
A condition wherein a patient binges on food and then induces vomiting.
Bulimia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
Deficiency of this vitamin causes night blindness, xerophthalmia, keratomalacia, Bitot spots and eventually corneal ulceration.
Vitamin A(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 307
Condition in children as result of vitamin D deficiency causing the following signs and symptoms: frontal bossing of the head, rachitic rosary, pigeon breast deformity, lumbar lordosis and bow legs.
Rickets (children)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 309
Deficieny of this vitamin causes impaired collagen formation, leading to gum bleeding, easy bruisability, and impaired wound healing.
Vitamin C (Scurvy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 312
Symptoms of cheilosis, stomatitis, glossitis, dermatitis and corneal vascularization results from deficiency of this vitamin.
Vitamin B2 (Riboflavin)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
Symptoms of cheilosis, glossitis, dermatitis, and peripheral neuropathy.
Vitamin B6 (Pyridoxine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
Leading causes of death in developed countries
Ischemic heart disease and cerebrovascular disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 405
The most important catalyst of phase I reactions; detoxify xenobiotics
Cytochrome P-450 enxyme system (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 407
A 55 y/o male presented to the ER following a house fire. He was lethargic, tachycardic, tachypneic and displayed memory disturbance. Skin was noted to be cherry red. What is the most likely cause?
Carbon monoxide poisoning (TOPNOTCH)
A 5 y/o boy presented to the clinic due to hyperactivity and impulsiveness. Hearing acuity was below normal, and speech and language were slightly delayed. History reveals that the boy lives in an old house in the community. PBS showed hypochromia and microcytosis. What is the most likely diagnosis?
Lead poisoning (TOPNOTCH)
Toxic effects of this heavy metal include cerebral palsy, deafness, blindness, and kidney damage. Cause of Minamata disease.
Mercury (TOPNOTCH)
“King of poisons”
Arsenic (TOPNOTCH)
Most toxic form of arsenic
Trivalent compounds of arsenic(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 412
The most serious consequence of chronic exposure to this heavy metal is the increased risk for the development of cancers, particularly of the lungs, bladder, and skin.
Arsenic (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 412
The principal toxic effects of toxicity to this heavy metal are obstructive lung disease and renal tubular damage that may progress to ESRD.
Cadmium (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 413
Exposure to benzene increases risk of what hematologic condition
Leukemia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 413
Exposure to vinyl chloride used in the synthesis of polyvinyl resins leads to the development of what tumor?
Angiosarcoma of the liver (TOPNOTCH) Robbins Basic Pathology, 9th ed.,p.414
Main enzyme system involved in alcohol metabolism
Alcohol dehydrogenase(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 417
Enlarged and fatty liver is seen in kwashiorkor or marasmus?
Kwashiorkor(TOPNOTCH)
A major complication of anorexia nervosa and bulimia
Cardiac arrythmia and sudden death due to hypokalemia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 435
Symptos of acute toxicity to these vitamin include headache, diziness, vomiting, stupor, and blurred vission, which may be confused with those of a brain tumor (pseudotumor cerebri)
Vitamin A(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 438
Craniotabes, frontal bossing, squared appearance of the head, rachitic rosary, pigeon chest deformity, lumbr lordosis, and bowing of the legs are associated with what vitamin deficiency?
Vitamin D deficiency (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 441
Toxicity of this vitamin may cause calcification of soft tissue and bone pain.
Vitamin D(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 441
Rash around the eyes, mouth,and nose, anorexia, diarrhea, growth retardaation, depressed wound healing and impaired nigh vision are associated with ____ deficiency
Zinc(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443
Muscle weakness, neurologic defects and abnormal collagen cross-linking are associated with ___ deficiency.
Copper(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443
Disease characterized by bone disease in growing children and by hemorrhages and healing defects in both children and adults.
Scurvy(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443
Syndrome composed of respiratory abnromalities in very obese persons.
Hypoventilation syndrome/pickwickian syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 448
Hormone synthesized by fat cells which regulates food intake an energy expenditure. Its binding to its receptors in the hypothalamus increases energy consumption by stimulating POMC/CART neurons.
Leptin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 448
Aflatoxin is implicated in what type of cancer?
Hepatocellular carcinoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 449
True or False. High animal intake and low fiber has been imlicated in colon cancer.
True (TOPNOTCH)
Lead has a more damaging effect on the brains of children than in adults because of (A) a more permeable blood-brain barrier (B) immature lenticular nuclei (C) less microglia and astrocytes(D) greater proportion of fetal hemoglobin in the blood
a more permeable blood-brain barrier (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
Chronic exposure to arsenic is associated with the development of the following malignancies EXCEPT (A) squamous cell carcinoma of the skin (B) mucoepidermoid carcinoma of the salivary glands (C) lung carcinoma (D) basal cell carcinoma
mucoepidermoid carcinoma of the salivary glands (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
Exposure to vinyl chloride has been found to cause (A) multiple uterine leiomyomas (B) hepatic angiosarcoma (C) squamous cell carcinoma of the skin (D) transitional carcinoma of the bladder
hepatic angiosarcoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
Tobacco smoke, when combined with this, is known to have a multiplicative effect on the risk of developing laryngeal cancer (A) alcohol (B) diet rich in animal fat (C) dietary nitrates (D) oral sex
alcohol (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 289
Progestin is added to estrogen in hormone replacement therapy for menopausal women to reduce the risk of (A) breast cancer (B) endometrial cancer (C) thromboembolism (D) all of the above
endometrial cancer (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293
During a routine ultrasound, a 38 year old G1P0 was found to have a solitary, 4 cm diameter, hepatic mass in the right lobe, beneath the capsule. She has a history of regular oral contraceptive use since 18 years old, and stopped 1 year ago. She has never been infected by HBV or HCV. She does not drink alcohol. If the mass is excised, it would most likely show (A) benign-looking hepatocytes in cords and sheets, absent portal tracts, and prominent blood vessels (B) proliferation of endothelial cells some containing lumens with RBCs (C) portal tracts with chronic inflammation and bile duct proliferation (D) pleomorphic cells, bizarre giant cells, atypical mitoses, and necrosis
benign-looking hepatocytes in cords and sheets, absent portal tracts, and prominent vessels (hepatic adenoma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294, p664)
Liver damage in acetaminophen overdose is characterized histologically by (A) brisk neutrophilic infiltration of portal tracts (B) hepatocytes with extensively vacuolated cytoplasm (C) centrilobular necrosis (D) bile duct proliferation
centrilobular necrosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
A 65 year old man has been regularly taking aspirin and acetaminophen for 20 years. This predisposes him to developing (A) chronic interstitial nephritis (B) renal papillary necrosis (C) transitional cell carcinoma of the renal pelvis (D) all of the above
all of the above (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294, 564
An 4 year old orphan boy with a scar on his forehead was found locked in a small room under the stairs by his abusive uncle and aunt. He has been kept there and fed crackers and milk since he was 1 year old. He has a squared appearance of the head, a pigeon breast deformity, lumbar lordosis, and bowing of the legs. These physical findings are due to deficiency of (A) calcium (B) vitamin A (C) vitamin C (D) vitamin D
vitamin D (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 309-312
In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.
Large or elastic arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
In these arteries, tunica media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. Examples are the coronaries and renal arteries.
Medium-sized or muscular arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These are the principal control points for regulation of physiologic resistance to blood flow.
Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.
Capillaries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Diameter of an RBC.
7-8 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.
Lymphatics(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are small spherical dilatations, typically in the circle of Willis.
Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.
Arteriovenous fistulas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Focal, irregular thickening of the walls of medium and large muscular arteries. Segments of the vessel wall are focally thickened by combination of irregular medial and intimal hyperplasia and fibrosis, causing luminal stenosis.
Fibromuscular dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.
Arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by calcific deposits in muscular arteries, typical in persons older than 50 yrs old. The radiographically visible, palpable calcifications do not encroach on the vessel lumen, and are not clinically significant.
Mockenberg medial calcific sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Characterized by intimal lesions called atheromas that protrude into vascular lumina.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
Three principal components of an atheromatous plaque.
- Cells (SM cells, macrophages, T cells)2. Extracellular matrix (collagen, elastic fibers, proteoglycans)3. Intracellular and extracellular lipidFibrous cap, central lipid core, neovascularization(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Non-modifiable risk factors for atherosclerosis. (4)
Increasing ageMale genderFamily historyGenetic abnormalities(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
Arrange in descending order, based on which blood vessel is most extensively involved in development of atherosclerosis.Popliteal arteries, internal carotid arteries, circle of Willis, coronaries, abdominal aorta
Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 350
Fate of an atheromatous plaque wherein the luminal surface exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
Rupture, ulceration or erosion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.
Atheroembolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Fate of an atherosclerotic plaque due to increased pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, leading to weakness of the vessel wall.
Aneurysm formation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
Most common cause of hypertension.
Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355
This vascular lesion consists of a homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. A major morphologic characteristic in benign nephrosclerosis.
Hyaline arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
Characteristic of malignant hypertension, associated with “onion-skin” concentric, laminated, thickening of the walls of arterioles with luminal narrowing. These laminations consist of smooth muscle cells and thickened duplicated basement membrane.
Hyperplastic arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.
True aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.
False aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.
Arterial dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which are spherical outpouchings, involving only a portion of the vessel wall, varying in size from 5-20cm in diameter and often contain thrombi.
Saccular aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Aneurysms which involve diffuse, circumferential dilation of a long vascular segment, varies in diameter and length, and can involve extensive portions of the aortic arch, abdominal aorta,and iliacs.
Fusiform aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Two most important causes of aortic aneurysms.
AtherosclerosisCystic medial degeneration of the arterial media(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
Infection of a major artery that causes weakness to its wall.
Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
This disease can more commonly affects men >50 years old. Lesion usually positioned below the renal arteries and above the aortic bifurcation. Can be saccular or fusiform.
Abdominal aortic aneurysm (AAA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.
Inflammatory AAA(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 358
Atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a Salmonella gastroenteritis. Suppuration further destroys the media, potentiating rapid dilation and rupture.
Mycotic abdominal aortic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
Small blood vessels and vasa vasorum show luminal narrowing and obliteration (obliterative endarteritis), scarring of the vessel wall and a dense surrounding rim of lymphocytes and plasma cells that may extend into the media. Characteristic of the tertiary stage of syphilis.
Syphilitic aortitis(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 359
Most common point of origin of an aortic dissection.
Ascending aorta, 10 cms from the aortic valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 360
Most frequent pre-existing histologically detectable lesion in aortic dissection, characterized by elastic tissue fragmentation and separation of the elastic and smooth muscle cell elements of the media by cystic spaces filled with amorphous proteoglycan-rich extracellular matrix.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.
Type A dissections (proximal) Type I DeBakey - ascending aorta only Type II DeBakey - ascending and descending aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.
Type B dissection / type III DeBakey(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.
Giant cell (Temporal) arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 363
Granulomatous inflammation usually occuring in patients younger than 50 years old. Classically involves the aortic arch, with intimal hyperplasia and irregular thickening of the vessel wall. Origin of great vessels are obliterated causing weakness of peripheral pulses.
Takayasu arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.
Age of patient40 Giant cell arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
In this disease, affected blood vessels develop nodular intimal thickening, granulomatous inflammation within the inner media centered on the internal elastic membrane, and fragmentation of the internal elastic lamina. Typically involves temporal and ophthalmic arteries.
Giant - cell/Temporal arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
A systemic vasculitis causing transmural necrotizing inflammation of small to medium sized vessels, with mixed infiltvrate of neutrophils, eosinophils, and mononuclear cells, frequently accompanied by fibrinoid necrosis.Typically involves renal arteries but spares pulmonary vessels.
Polyarteritis Nodosa (PAN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
Arteritis associated with mucocutaneous lymph node syndrome, which usually occurs in children. Coronary arteries can be involved with aneurysm formation or thrombosis. Fibrinoid necrosis usually less prominent.
Kawasaki disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 366
Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including cresencteric glomerulonephritis. Associated with c-ANCA.
Wegener granulomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367
A necrotizing vasculitis that generally affects capillaries, arterioles and venules, with few or no immune deposits. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with p-ANCA.
Microscopic polyangiitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Eosinophil-rich and granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with p-ANCA.
Churg-Strauss syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Characterized by sharply segmental avute and chronic vasculitis of medium sized and small arteries, predominantly of the extremities. There is acute and chronic inflammation accompanied by luminal thrombosis, containing microabscess composed of neutrophils surrounded by granulomatous inflammation. Stromg relationship with cigarette smoking.
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
Results from an exaggerated vasoconstriction of digital arteries and arterioles, inducing paroxysmal pallor or cyanosis of the digits of the hands and feet.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects an exaggeration of central and local vasomotor responses to cold or emotion. Structural changes in the arterial walls are absent except late in course when intimal thickening can appear.
Primary Raynaud phenomenon (Raynaud disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
Reflects vascular insufficiency of the extremities in the context of arterial disease caused by other entities including SLE, Buerger disease, or atherosclerosis.
Secondary Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Abnormally dilated, tortous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. Veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis. Focal thrombosis and venous valve deformities are common.
Varicose veins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Most common blood vessels involved in development of varicose veins.
Superficial veins of the upper and lower leg(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Three sites of varices produced in the presence of portal hypertension.
GEJ (Esophageal varices)Rectum (Hemorrhoids)Periumbillical veins (Caput medusae)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
Common and serious complication of of deep vein thrombosis (DVT).
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
The acute inflammation elicited when bacterial infections spread into and through the lymphatics.
Lymphangitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
These are bright red to blue lesions, that vary from a few millimeters tomseveral centimeters in diameter. Unencapsulated aggregates of closely packed, thin-walled capillaries, usually blood-filled and lined by flattened endothelium. Vessels are separated by scant connective tissue stroma.
Capillary hemangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 372
Appears as red-blue, soft, spongy masses 1-2 cm in diameter, which can affect large subcutaneous areas of the face, extremities, and othe body regions. Mass is sharply defined but not encapsulated, composed of large, cavernous, blood-filled spaces.
Cavernous hemangioma(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 372
This form of capillar hemangioma is a rapidly growing peduncular red nodule on the skin, gingival, or oral mucosa, bleeds easily and is often ulcerated.
Pyogenic granuloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
These are round, slightly elevated, red-blue firm nodules, less than 1 cm diameter that can resemble a minute focus of hemorrhage UNDER THE NAIL. Histologically, these are aggregates, nests, and masses of tumor cells intimately associated with branching vascular channels.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
A specialized arteriovenous structure involved in thermoregulation.
Glomus body(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
This lesion is the ordinary “birthmark” and is the most common form of ectasia. Characteristically a flat lesion on the head or neck, ranging in color from light pink to deep purple.
Nevus flammeus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
This non-neoplastic vascular lesion grossly resembles a spider. There is radial, often pulsatile array of dilated subcutaneous arteries or arterioles about a central core, that blanches when pressure is applied to its center.
Spider telangiectasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
An opportunistic infection in immunocompromised persons that manifest as vascular proliferations involving skin, bone, brain and other organs. Characterized grossly by red papules and nodules, or rounded subcutaneous masses. Histologically, there is capillary proliferation with prominent epitheloid EC’s showing nuclear atypia and mitoses. Lesions contain stromal neutrophils, nuclear dust nd purplish granular material.
Bacillary angiomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
Common in patients with AIDS, caused by HHV 8, causing skin lesions ranging from patches, plaques to nodules.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
These are malignant endothelial neoplasms, with varying histology from plump, anaplastic but recognizable endothelial cells producing vascular channels to widely undifferentiated tumors having solid, spindle cell appearance and producing nondefinite blood vessels.
Angiosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 376
Form of hypertension characterized by systolic pressure more than 200 mmHg or diastolic pressure more than 120 mmHg, renal failure, and retinal hemorrhages and exudates.
Malignant Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 488
The most important independent risk factor for atherosclerosis.
Family history(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 492.
The initial event in the pathogenesis of atherosclerosis
Endothelial injury and dysfunction. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
The major lipoprotein involved in the pathogenesis of atherosclerosis.
LDL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
2 most important causes of endothelial dysfunction
Hemodynamic disturbances and hypercholesterolemia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494
The key processes in atherosclerosis
Intimal thickening and lipid accumulation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 496
The major structural component of fibrous cap in an atheromatous plaque
Collagen(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 500
Medial ischemia leading to degenerative changes of aorta, leading to scarring, loss of elastic fibers, inadequate extracellular matrix synthesis, and production of amorphous ground substance. This can be seen in Marfan syndrome and scurvy.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 502
Most common etiology associated with ascending aortic aneurysm
Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 502
A 70 y/o male, hypertensive, present with sudden severe abdominal pain. On physical examination, there is a presence of pulsatile abdominal mass. The most likely diagnosis is:
Abdominal aortic aneurysm(TOPNOTCH)
The most frequent preexisting histologically detectable lesion in aortic dissection
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 504
Presents with sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward.
Aortic dissection(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 505
Most common cause of death in aortic dissection.
Rupture of the dissection into the pericardial, pleural or peririthoneal cavities.(TOPNOTCH) Robbins Basica Pathology, 9th ed., p. 505
A 38 y/o male presents with severe headache and diplopia associated with fever and fatigue. Area along the course of the superficial temporal artery was painful to palpation. Biopsy done revealed intimal thickening of the artery, granulomatous inflmmation of the internal elastic lamina with infiltrate of T cells and macrophages. What is the most likely diagnosis?
Giant cell arteritis (TOPNOTCH)
Patient initially present with fatigue, weight loss and fever and then reduced blood pressure and weak pulses in the carotids and upper extremities, ocular disturbances and neurologic deficits. The most likely diagnosis is:
Takayasu arteritis(TOPNOTCH)
Most common involved blood vessel in Takayasu arteritis.
Aortic arch (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 509
This disease presents with rapidly accelerating hypertension, abdominal pain, bloody stool, myalgia and peripheral neuritis. The most likely diagnosi:
Polyarteritis nodosa(TOPNOTCH)
A 4 y/o female presented with fever and maculopapular rash on her trunk and extremities. This is associated with conjunctival erythema, edema of the hands and feet, and cervical lymph node enlargement. The patient is at risk for what type of blood vessel involvement?
Coronary artery aneurysm which may lead to acute MI. (Case of Kawasaki Disease) (TOPNOTCH)
Patient presents with asthma, allergic rhinitis, palpable purpura, GI bleeding, renal disease, and cardiomyopathy. Histologic findings showed vascular granulomata and hypereosinophilia. The most likely diagnosis is:
Churg-Strauss syndrome(TOPNOTCH)
It presents as a clinical triad of recurrent oral apthous ulcers, genital ulcers, and uveitis.
Behcet Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 511
This disease presents with persistent pneumonitis with bilateral nodular infiltrates, chronic sinusitis, mucosal ulceration of the nasopharynx, and renal disease. Histologic findings of upper respiratory tract lesion showed mucosal granuloma with geographic patterns of central necrosis and vasculitis. The most likely diagnosis:
Granulomatosis with polyangitis/Wegener granulomatosis(TOPNOTCH)
A 30 y/o male, smoker, presents with severe leg pain aggravated by exercise and relieved on rest. It further progressed to extremity ulcerations. What is the most likely diagnosis?
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)
Most imprortant risk factor for DVT
Prolonged immobiliztion resulting in venous stasis. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 514
A 50 y/o male, diagnosed with lung cancer, presented with edema and cyanosis of the head , neck, and arms with cyanosis. This is a case of:
Superior vena cava syndrome (TOPNOTCH)
The most common etiologic agent in lymphangitis.
Group A beta hemolyitc streptococcus. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 515
An autosomal dominant disorder caused by mutations in genes that encode components of TGF-B signaling pathway. Presents with telengiectasia that are widely distributed over the skin and mucus membranes.
Hereditary hemorrhagic telengiectasia/Osler-Weber-Rendu disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 516
Most common type of hemangioma
Capillary hemangioma(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 516
Painful tumors arising from modified smooth muscle cells of arteriovenous structure, most commonly found in the distal portion of the digits.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 517
A 13 year old male dies of a stray bullet to the head on New Year’s Eve. At autopsy, there is a flat yellowish streak seen on the intimal surface of his abdominal aorta, near the bifurcation of the renal arteries. This streak (A) causes minor disturbance in blood flow (B)is expected in his age group (C) is composed of hemosiderin-filled foam cells (D) would have certainly evolved into an atheromatous plaque if he lived to old age
expected in his age group (“fatty streak” (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 348-349)
Early atherosclerotic lesions are usually focal, patchy, and eccentric because (A) there are differences in the vascular hemodynamics at various points (B) the expression of LDL receptors along the blood vessels is varied (C) concentrations of macrophage-activating cytokines are different along blood vessels (D) certain endothelial cells are more sensitive to toxins and hyperglycemia than others
there are differences in vascular hemodynamics at various points (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
A 65 year old diabetic female with poor glycemic control and a 5 year history of intermittent chest pain develops pallor, shortness of breath and diaphoresis. She dies 16 hours later. At autopsy, the left ventricular wall is thickened, with dark mottling of the anterior portion, along with the septum and apex. Which of the following describes the likely histology of her left anterior descending artery? (A) an eccentric atheromatous plaque with a fibrous cap (B) a ruptured fibrous cap with calcifications in the lumen of the vessel (C) a ruptured fibrous cap with thrombus formation (D) complete occlusion of the original lumen by fibrous tissue, with neovascularization in the periphery
a ruptured fibrous cap with thrombus formation (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.351
What is the most common cause of aneurysms?
atherosclerosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
What is the most common site of atherosclerotic aneurysms?
abdominal aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
A 75 year old male with heart failure symptoms of 10 years dies. At autopsy, his aortic trunk is dilated, with fibrous scars and wrinkling of the intima. The aortic valve is also dilated, and the left ventricle is markedly enlarged. Microscopic examination of the aorta shows narrowed or obliterated vasa vasorum to be narrowed, with a dense rim of lymphocytes and plasma cells, some extending into the media. Which of the following can suggest the etiology of the patient’s findings? (A) family history of diabetes (B) chronic alcohol intake (C) history of sexually transmitted infection (D) occupational exposure to benzene
history of sexually transmitted infection (tertiary/cardiovascular syphilis) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.359, 703
A 30 year old female with 3 year history of fever, weight loss and fatigue presents with right eye blindness. PE showed weak pulses in the upper extremities. Which of the following suggests that she has Takayasu arteritis, rather than temporal arteritis? (A) age (B) constitutional symptoms (C) giant cells in the large blood vessels (D) giant cells in the medium blood vessels
age (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364-365
Classic polyarteritis nodosa affects small to medium sized vessels most commonly in which organ? (A) kidneys (B) heart (C) liver (D) GI tract
kidneys (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
A 2 year old boy presents with erythema of the conjunctiva, oral mucosa, palms and soles, with focal erosions. Palpation shows enlarged cervical lymph nodes. He suddenly dies a few hours after ER admission. Autopsy showed marked mononuclear infiltration of his left anterior descending artery, with fibrinoid necrosis and lumen occlusion. What could have prevented this fatal sequela? (A) low dose corticosteroids (B) Hepatitis B vaccine (C) Beta-lactam and aminoglycoside combination (D) intravenous immunoglobulin
intravenous immunoglobulin (Kawasaki disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.366
A 42 year old man with 2 weeks of epistaxis undergoes an intranasal biopsy, which showed chronic granulomatous inflammation with giant cells. Xray showed cavitary lung lesions. He is treated with anti-Koch’s for 6 months, but the epistaxis recurred. He also developed hematuria. Which of the following can help support a diagnosis of Wegener’s granulomatosis, rather than TB? (A) positive P-ANCA (B) positive C-ANCA (C) urinalysis with RBC morphology (D) biopsy of the lung lesion
positive C-ANCA (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367-368
A 27 year old Israeli expat presents with intermittent pain and pallor of the right index and middle fingers, precipitated by smoking and cold temperature. He reports symptomatic relief whenever he stops smoking. What is expected in the arteries of the involved fingers? (A) thrombus with neutrophil aggregates and necrosis (B) histiocytes and giant cells (C) ruptured fibrous cap and underlying foamy cells (D) eosinophils and lymphocytes in the media and intima
thrombus with neutrophil aggregates and necrosis (Buerger disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.368
A 21 year old G1P0, 24 weeks AOG, has a reddish 1.0 cm diameter nodule on her left lower gum. She reports that the nodule appeared at 1 month of pregnancy. A biopsy showed shows capillaries with an acute and chronic inflammatory infiltrate and stromal edema. There is no pleomorphism, necrosis, or atypical mitosis. This nodule (A) can be found in 20% of pregnant women (B) is malignant (C) may spontaneously regress or fibrose after pregnancy (D) is metastatic from an ovarian primary
may spontaneously regress or fibrose after pregnancy (granuloma gravidarum/pregnancy tumor/pyogenic granuloma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.373
A 3 year old female with a large “port wine stain” on the right side of her face has occasional seizures. Further examination showed mental developmental delay. She may also have (A) more extensive vascular malformations (B) multiple colonic polyps (C) color blindness (D) alpha thalassemia
more extensive vascular malformations (Sturge-Weber syndrome) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.374
A 38 year old HIV-positive man has multiple reddish-purple plaques and nodules on his arms and legs. He has never been on antiretroviral therapy. Biopsy of one of the nodules showed sheets of plump spindle cells encompassing small vessels and slit-like spaces, with focal hemorrhage, hemosiderin deposits, lymphocytes, and macrophages. Mitotic figures are common. This neoplasm has been shown to be infected with (A) HPV 16 (B) HHV 8 (C) Hepatitic C (D) HPV 18
HHV8 (Kaposi Sarcoma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
The morphologic and clinical effects of this condition primarily result from progressive damming of blood within the pulmonary circulation. The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-aleolar edema. Hemosiderin-laden macrophages are present.
Left sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hemosiderin laden macrophages are also called _______
Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is usually the earliest and most significant compaint of patients in Left sided HF.
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Most common cause of right sided HF.
Left sided HF(TOPNOTCH)
This is a particularly dramatic form of breathlessness, awakening patients from sleeo with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
The liver is increased in size and weight, a cut section reveals congested red centers of liver lobules surrounded bybpaler, sometimes fatty peripheral regions.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Right-sided HF produces a tense, enlarged spleen, achieving weights of 300-500 grams. Sinusoidal dilation present.
Congestive splenomegaly(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
This is a hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Most congenital heart disease arise from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These a typically smooth-walled defects near the foramen ovale, usually without associated cardiac abnormalities. Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy and dilation of the pulmonary artery.
Ostium secundum ASD(TOPNOTCH)
Reversal of blood flow through a prolonged (left-to-right shunt) due to pulmonary hypertension, yielding right-sided pressures that exceed those on the left side. This causes unoxygenated blood to go into circulation, causing cyanosis.
Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These occur at the lowest part of the atrial septum and can extend to the mitral and tricuspid valves. Abnormalities of the AV Valves are usually present, forming a cleft in the anterior leaflet of the mitral valve or septal leaflet of the tricuspid valve.
Ostium primum ASD(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
In this condition, some of the oxygenated blood flowing from the left ventricle is shunted back to the lungs. Proximal pumonary arteries, left atrium and ventricle may become dilated.
Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
The most common cause of cyanotic congenital heart disease. Heart is large and “boot shaped” as a result of right ventricular hypertrophy.
Tetralogy of Fallot(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
Components of Tetralogy of Fallot.
Pulmonary valve stenosisOverriding of aortaRight ventricular hypertrophyVentricular septal defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa. Right ventricular hypertrophy becomes prominent, while the left ventricle becomes somewhat atrophic.
Transposition of the Great Arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Characterized by tubular narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.
Preductal “infantile” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
Aorta is sharply constricted by a ridge of tissue at or just distal to the ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.
Postductal “adult” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib “notching” on xray.
Postductal coarctation of the aorta (without a PDA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
70-75% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest?
90%(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
In this disease the left ventricle may exceed 2.0cm in thickness and the heart may weigh >500 grams. Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”), and increased interstitial fibrosis.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Pathognomonic sign for rheumatic fever,consisting of of a cental zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytes, ocassional plasma cells and plump, activated macrophages.
Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
These cells have abundant cytoplasm and central nuclei with chromatin arrayed in a slender, wavy ribbon (caterpillar cells) which can be found in all three layers of the heart in rheumatic fever. A component of Aschoff bodies.
Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Characterized by organization and subsequent scarring, as a sequelae of rheumatic fever. The mitral (or tricuspid) valve is involved, with leaflet thickening, commisural fission and shortening, thickening and fusiong of the chordae tendinae. Fibrous bridging across valvular commisures create “fishmouth” or “ buttonhole” deformity.
Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Most common valve involved in RHD.
Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405
Major components Jones Criteria for RF.
CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Minor components Jones criteria for RF
FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
How many major and/or minor manifestations are needed to diagnose RF?
Remember: 20122 major 0 minor or1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis of previously normal valves, the most common causative agent is S. aureus.
Acute bacterial endocarditis(TOPNOTCH)
Serious infection characterized by microbial invasion of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues. The heart valves are friable, bulky and potentially destructive.
Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.
Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Most consistent sign of infective endocarditis.
Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Characterized by deposition of sterile, non-inflammatory, nondestructive and small (1mm) masses of fibrin, platelets and other blood components on cardiac valves, along the line of closure of leaflets or cusps.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
Sterile vegetations thatvcan develop on the valves of patients with SLE. These are small, granular, pinkish vegetations 1-4mm in diameter and can be located on the undersurface of AV valves, on the cords or endocardium.
Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
The lesions of this disease are distinctive, glistening white intimal plaquelike thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets seen in patients with carcinoid tumors. The lesions are composed of muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix.
Carcinoid heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
Cardiomyopathy which is characterized by progressive cardiac dilation and contractile dysfunction. The heart is characteristically enlarged and flabby, with dilation of all chambers,the ventricular thickness may be less than, equal to or greater than normal.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Characterized by myocardial hypertrophy, abnormal diastolic filling and ventricular outflow obstruction. The heart is thick-walled, heavy and hypercontracting. There is an assymetrical septal hypertrophy described as “banana-like”. Histologically, there is severe myocyte hypertrophy and disarray with interstitial fibrosis.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
Mechanism of heart failure in hypertrophic cardiomyopathy.
Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
A common cause of sudden death in young athlethes.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
The ventricles are of approximately normal size or slightly enlarged, the cavities not dilated, and the myocardium is firm. Biatrial dilation is common. Microscopically, there is interstitial fibrosis, varying from minimal to patchy to extensive and diffuse.
Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Mechanism of heart failure in restrictive cardiomyopathy.
Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Inflammation of the myocardium.
Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.
Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.
Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis characterized by widespread inflammatory infiltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.
Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.
Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Viruses which account for most cases of myocarditis.
Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Type of pericarditis found in patients with uremia or viral infection. The exudate imparts an irregular apperance to the pericardial surface (bread and butter pericarditis).
Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Normal amount of pericardial fluid in pericardial sac.
30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Serous pericardial effusion can be caused by _________
CHF, hypoalbuminemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Chylous pericardial fluid can be caused by _______
Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.
Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
The most common tumor of the heart.
Metastatic tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Most common primary tumor of the adult heart.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most frequent primary tumor of the heart in infants and children. These are generally small gray-white myocardial masses composed of a mixed population of cells, the most characteristic of which are large, rounded or polygonal cells containing numerous glycogen-laden vacuoles separated by strands of cytoplasm, so-called spider cells.
Rhabdomyomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
Serosanguinous pericardial effusion can be caused by ________
Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most severe pulmonary changes in congestive heart failure
Accumulation of edema fluid in the alveolar spaces (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Morphologic finding/telltale signs of previous episodes of pulmonary edema
Hemosiderin-laden macrophages (Heart failure cells) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Most common underlying etiology of diastolic failure
Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Group of congenital heart disease characterized by increase pulmonary blood flow but are not initially associated with cyanosis
Left-to-right shunts (ASD, VSD, PDA) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
Most common genetic cause of congenital heart disease
Trisomy 21 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
A 24 y/o female complained of shortness of breath and orthopnea lasting several days. The patient reported having diagnosed since childhood as having “hole in the heart.” Physical exam revealed holosystolic murmur most audible in the left parasternal area accompanied by thrill. Rales were heared in the bilateral lower lung field. The most likely cause of her condition:
VSD (TOPNOTCH)
Most common cause of myocardial ischemia
Obstructive atherosclerotic lesions in the epicardial coronary arteries (TOPNOTCH) Robbins Basic Patholgoy, 9th ed., p. 538
The cause of sudden cardiac death in myocardial infarction
Ventricular arrythmia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 539
Irreversible cell injury in MI occur in how many minutes?
20-40 minutes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Irreversible injury of ischemic myocytes in MI occurs first in what zone in the heart?
Subendocardial zone (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
What blood vessel supply the posterior third of the ventricular septum in majority of the individuals?
Right coronary artery (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Pattern of infarction caused by occlusion of an epicardial vessel
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarction caused by plaque disruption or hypotension, causing circumferential myocardial damage
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as an “ST elevation myocardial infarct”
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as a “non-ST elevation infarct”
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
The typical changes of coagulative necrosis becomes detectable in how many hours of injury?
First 6-12 hours(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 545
Microscopic findings in irreversibly injured myocytes characterized by intensely eosinophilic intracellular stripes composed of closely packed sarcomeres.
Contraction bands(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 546
A 62 y/o obese male had sudden onset of heaviness in the chest, associated with diaphoresis and dyspnea which started 3 hours prior to consult at the ER. The biomarkers that are most sensitive and specific of myocardial damage that you will request:
Troponins I and T (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 547
A 72 y/o female experienced chest pain and hypotension. A posterior transmural infarct was suspected. Most common complications in this type of infarct
Conduction blocks, right ventricular involvement, or both (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Free wall rupture, expansion, mural thrombi, and aneurysm are common in what type/location of infarct?
Anterior transmural infarct(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Most common cause of rhythm disorder
Ischemic injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 550
A 24 y/o female presents with history of recurrent fever and joint pains accompanied by ECG changes and increased ASO titer in the past 2 years. Physical examination reveals cardiac murmur. What is the clinical impression?
Rheumatic heart disease (TOPNOTCH)
Characteristic anatomic change in MVP
Interchordal ballooning of mitral leaflets (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 556
Most frequent mechanism of SCD
Lethal arrythmia (asystole, ventricular fibrillation) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Earliest microscopic change in systemic hypertensive heart disease
increase in transverse diameter of myocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Most common type of VSD
Membranous (Interventricular septum) VSD(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 535
The common feature of pulmonary thromboembolism, obstructive sleep apnea, altitude disease, and parenchymal lung disease
Pulmonary hypertension. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 530
A 5 wk old infant presents with tachypnea, diaphoresis, and difficulty feeding. A harsh, continuous, machinery-like murmur was noted upon auscultation. What is the most likely diagnosis?
Patent ductus arteriosus(TOPNOTCH)
Presents with hypertension in the upper extremities, and manifestations of arterial insufficiency such as claudication and coldness. Produce a radiographical visible erosion (notching) of the undersurfaces of the ribs.
Coarctation of the aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 537
Major cause of infective endocarditis among intravenous drug abusers
Staphylococcus aureus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Most common cause of endocarditis of native but previously damaged or otherwise abnormal valves
Streptococcus viridans (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Predominant manifestations of RF
Carditis and arthritis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Classic hallmark of Infective endocarditis
Vegetations on heart valves(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
A 72 year old hypertensive female last seen apparently well 3 days ago, is found dead in her bathroom with rigor mortis and no signs of foul play. At autopsy, her heart showed left ventricular hypertrophy and a pale tan area at the anteroseptal wall. There are no thrombi in the heart chambers. The valves are unremarkable. Microscopic examination of the pale area showed well-established granulation tissue with new blood vessels and collagen deposition. Neutrophils are rare. She died of (A) an MI that occured 1 hour prior to demise (B) an MI 12 hours prior to demise (C) an MI 2 days prior to demise (D) something else entirely
something else entirely (evolution of morphologic changes in myocardial infarction) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 393
In hypertensive heart disease, there is concentric thickening of the left ventricular wall. A concomitant left atrial dilatation may also be seen due to (A) volume overload from a ventricle with narrowed lumen (B) pressure overload from a ventricle with narrowed lumen (C) cytokines secreted by hypertrophic ventricular myocytes cause atrophy of atrial myocytes (D) cytokines secreted by hypertrophic ventricular myocytes cause metaplasia of atrial myocytes
volume overload from a ventricle with narrowed lumen (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 399
What feature in a stenotic aortic valve suggests rheumatic valvular disease, rather than calcific aortic stenosis? (A) bicuspid valve (B) masses of calcium on the outflow side of cusps (C) fibrotic cusps (D) fusion of the commmissures
fusion of the commisures (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
A 20 year old asymptomatic female is found to have a midsystolic click on her preemployment physical examination. A 2D echo showed mitral valve prolapse. The involved leaflet would show (A) numerous fibroblasts with and dense collagen deposition (B) thinning of the fibrosa layer and myxoid expansion of the spongiosa layer (C) deposition of amorphous material that shows apple-green birefringence when stained with Congo red (D) fibrous stroma with gland-like structures secreting mucin
thinning of fibrosa layer and myxoid espansion of the spongiosa layer (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
A 5 year old male who had a sore throat 3 weeks ago develops fever and joint pains. Auscultation revealed a friction rub, and ASO titers are increased. Which of the following is expected in the patient? (A) friable vegetations on the mitral valve containing fibrin, neutrophils and gram-positive cocci (B) small vegetations on the mitral valve with abundant eosinophils (C) myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (D) myocardium with poorly-circumsccribed aggregates of multinucleated giant cells
myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 403-404
A 19 year old football player dies suddenly during one training session. At autopsy, his heart showed myocardial hypertrophy with disproportionate thickening of the septum, and a narrowed left ventricular lumen. Microscopic examination showed myocyte hypertrophy, myofiber disarray, and interestitial fibrosis. These findings are due to (A) a mutation in one of his genes encoding sarcomeric proteins (B) a silent Coxsackie virus B infection (C) an undisclosed 3 year history of alcohol intake (D) anabolic steroids he has been taking for 6 months
a mutation in one of his genes encoding sarcomeric proteins (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P. 412-413
A 34 year old female on routine checkup is found to have a diastolic murmur. 2D echo showed a pedunculated 3 cm mass in her left atrium attached to the atrial septum. She has no other known masses on workup. She undergoes heart surgery where the atrial mass is resected. Which of the following is its most likely histology? (A) stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (B) sheets of large polygonal cells containing glycogen-containing vacuoles arranged around a central nucleus (C) fascicles of fibroblasts and interspersed collagen bundles (D) sheets of pleomorphic cells lining vascular spaces, some with intracytoplasmic lumens, with atypical mitoses and areas of necrosis
stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 417-418
Average volume per cell, expressed in femtoliters.
Mean cell volume (MCV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
A reduction in the oxygen-transporting capacity of blood.
Anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 422
The average content of hemoglobin per red cell, expressed in picograms.
Mean cell hemoglobin (MCH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
The average concentration of hemoglobin in a given volume of packed red cells, expressed in g/dL.
Mean cell hemoglobin concentration (MCHC)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
The coefficient of variation of red cell volume.
Red cell distribution width (RDW)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
Anemia of acute blood loss is described as ______.
Normocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
Life span of a normal red cell.
120 days(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Anemia characterized by an increased rate of cell destruction, a compensatory increase in erythropoeisis that results in reticulocytosis, and retention of products of cell destruction, including iron.
Hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
A circulating protein that binds and clears free hemoglobin.
Haptoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Hemolysis that can result from mechanical trauma, or biochemical or physical agents that damage the red cell membrane.
Intravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Hemolysis which takes place largely within phagocytic cells of the spleen and liver.
Extravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
This disorder is characterized by an intrinsic defect in the red cell membrane, that renders the cells spheroidal, less defomable and vulnerable to splenic sequestration and destruction.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
Small, dark nuclear remnants seen within red cells in PBS of hereditary spherocytosis.
Howell-Jolly bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
On PBS, red cells are spherical which lack central pallor, and they show increased osmotic fragility when placed in hypotonic salt solutions.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
Structural proteins that are defective in hereditary spherocytosis.
Spectrin and ankyrin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
This results from substitution of valine for glutamic acid at the 6th position of the B-chain, producing HbS.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 426
Bizarre, elongated, spindled or boat-shaped cells on PBS.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
Prominent cheekbones and changes in skull resembling a “crew-cut” skull x-ray.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
Patients with sickle cell disease are predisposed to infections caused by these type of bacteria.
Encapsulated bacteria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Feared complication of sickle cell disease which can be trigerred by pulmonary infections or fat emboli from necrotic marrow that secondarily involve the lung.
Acute chest syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Major complication of sickle cell disease which occurs in the setting of acute chest syndrome, causing ischemic injury to the CNS.
CNS stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
Represents a sudden but usually temporary cessation of erythropoeisis, usually trigerred by parvovirus B19 infections in patients with sickle cell disease.
Aplastic crises(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
In beta thalassemia, an individual who inherits one abnormal allele (out of 2) has this asymptomatic to mildly symptomatic condition.
B- Thalassemia minor/trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Individuals with B-thalassemia who inherit two abnormal alleles, with severe anemia requiring regular blood tranfusions.
B- Thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Red cells with a central, dark-red puddle due to collection of hemoglobin.
Target cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Target cells are often seen in this condition.
B-thalassemia minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
In the PBS of this condition, nucleated red cells (normoblasts) are seen, which reflect underlying erythropoeisis.
B-thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Anemia of beta thalassemia.
Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
Disease caused by deletion of 3 alpha globin genes.
Hemoglobin H disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of 1 alpha globin gene.
Silent carrier(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of 2 alpha globin genes.
Alpha thalassemia trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
Condition caused by deletion of all four alpha globin genes.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
Precipitates of denatured globin seen in RBC’s.
Heinz bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
Heinz bodies are seen in the blood smear of this condition.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
Bite cells are seen in ________.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
A rare disorder of unknown etiology, causes hemolytic anemia which results from an acquired membrane defect secondary to a mutation that affects myeloid stem cells. Hemolysis occurs during sleep.
Paroxysmal nocturnal hemoglobinuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
Hemolysis caused by IgG or IgA antiodies that are active at 37 degC, which results in opsonization of red cells by the autoantibodies.
Warm antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
Anemia caused by low-affinity IgM which bind to red cell membranes only at temp
Cold antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
Anemia observed in a variety of pathologic states, in which small vessels become particularly obstructed.(e.g. DIC, malignant HTN, SLE, etc.)
Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
Schistiocytes, burr cells, helmet cells, triangle cells are seen in this condition.
Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
X-linked disorder in which red cells are unusually susceptible to damage cause by oxidants.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
Red blood cells in iron deficiency anemia.
Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 436
Diagnostic criteria for iron deficiency anemia:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)
Low ferritinLow serum iron levelsLow transferrin saturationIncreased TIBC(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435
Diagnostic criteria for anemia of chronic disease:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)
Increased ferritinLow serum iron levelsLow transferrin saturationDecreased TIBCNormocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435
Principal causes of megaloblastic anemia.
Folate deficiencyVitamin B12 deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437
