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Pathology Flashcards

1
Q

Cell adaptation

  • hypertrophy
  • hyperplasia
  • atrophy
  • metaplasia
  • dysplasia
A
  • increase in structural proteins and organelle which increases size of cell
  • controlled proliferation of stem cells -> increase in amnt of cells
  • decrease in tissue mass because decrease in size or number of cells
  • reprogramming of stem cells causing replacement of one cell type to another because it is better at adapting to certain stressor
  • disordered precancerous epi cell growth characterized by loss of uniformity of cell size and shape
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2
Q

Injury

  • reversible: ATP, ribosomes, membrane, nuclear, function
  • irreversible: membrane, mito, lysosome, nuclear
A
  • decrease in ATP -> decrease Ca activity and Na/K pmp -> cellular swelling; ribosomal detachment -> decrease protein synthesis; plasma membrane changes; nuclear changes; rapid loss of function
  • breakdown of plasma membrane -> Ca into cell -> activates proteases; mito damage dysfunction -> loss of ETC -> low ATP; rupture of lysosomes -> autolysis; nuclear degradation
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3
Q

Apoptosis

  • intrinsic: what is it, regulated by, Function of apoptotic, Function of anti-apoptotic
  • extrinsic: 2 pathways
A
  • regulating factor is withdrawn from proliferating cell causing apoptosis; BCL2 family, BAX and BAK: form pores into mito membrane -> release of cyto C from inner mito membrane to cytoplasm -> activation of capases; BCL2: keep mito membrane impermeable
  • ligand binding receptor (Fas-FasL or TNF-alpha) or immune cell mediated (CD8+ or NK)
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4
Q

Types of Necrosis

  • coagulative: seen in, due to, histo
  • liquefactive
  • caseous
  • fat
  • fibrinoid
  • gangrenous
A
  • ischemia / infarct; injury that denatures proteins; preserved cell architecture but nuclei disappear
  • bacterial abcesses or brain infarcts; PMN release lysosomal enzymes that digest tissue; cellular debris and macro -> cystic spaces and cavitations
  • TB, systemic fungi; macro wall off infecting organism -> granular debris; fragmented cells and debris surrounded by lymphocytes
  • enzymatic: acute pancreatitis, non-enzymatic: trauma; damaged pancreatic cells release lipase which breaks down trigly and FFA binds to CA -> causing chalk white appearance of fat; outline of dead fat cell w/o peripheral nuclei
  • immune vascular reaction; immune complex deposition and or plasma protein leakage from damaged vessel; vessel walls are thick and pink
  • distal extremity and GI tract after chronic ischemia; Dry: ischemia, wet: super-infection; coagulative or liquefactive on top of coagulative
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5
Q

Ischemia

  • what is it
  • mechanism
A
  • inadequate blood supply to meet demand

- decrease arterial perfusion, decreased venous drainage, shock

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6
Q

Type of infarct

  • red
  • white
A
  • occurs in venous occlusions and tissues w/ multiple blood supplies and with re-perfusion
  • occurs in solid organ with single blood supply
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7
Q

Free radical injury

  • function
  • caused by
A
  • damage cell membrane by lipid peroxidation
  • radiation, meds, redox reactions, NO
  • scavenging enzymes, spontaneous decay, anti-oxidant
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8
Q

Type of calcification

  • dystrophic: cell type, extent, etiology, serum Ca levels, associated conditions
  • metastatic: cell type, extent, etiology, serum Ca levels, associated conditions
A
  • in diseased tissue; localized; secondary to injury or necrosis; normal; TB, chronic abcess, fat necrosis, infarct
  • in normal tissue; widespread; secondary to hyper Ca; abnormal; in interstitum of kidney, lung, GI mucosa,
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9
Q

Lipofuscin

  • what is it
  • cause
  • found in
A
  • yellow-brown wear and tear pigment associated w/ normal aging
  • oxidation and polymerization og autophagocytosed organellar membranes
  • heart, colon, liver, kidney, eye of elederly on autopsy
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10
Q

Amyloidosis

  • what is it/ pathogenesis
  • visualized w/
  • location
A
  • abnormal aggregation of proteins into beta pleated linear sheets -> insoluble fibrils -> cell damage and apoptosis
  • congo-red stain
  • glomerular mesangial areas
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11
Q

Systemic amyloidosis

  • primary: fibril protein, seen in
  • secondary
  • dialysis
A
  • AL protein, seen in plasma cell disorders
  • serum amyloid A, seen in chronic inflamm conditions
  • B2 microglobulin, seen in pts with ESRD
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12
Q

Localized amyloidosis

  • Alzheimers: protein, from
  • Type II DM: protein, cause
  • Medullary thyroid CA: protein
  • Isolated atrial amyloidosis: protein, pathogenesis, risk
  • systemic senile amyloidosis: protein, location
A
  • Beta amyloid protein; cleaved from amyloid precursor protein
  • Islet amyloid polypeptide; caused by deposition of amylin in pancreatic islet cells
  • calcitonin
  • ANP, common in normal aging but puts at risk for a fib
  • transthyretin, seen predominantly in cardiac ventricles
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13
Q

Hereditary amyloidosis

  • familial amyloid cardiomyopathy: protein, location, causes
  • familial amyloid polyneuropathy: protein
A
  • mutated transthyretin, ventricular endocardium -> restrictive cardiomyopathy
  • mutated transthyretin -> caused by tranthyretin gene mutation
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14
Q

Inflammation

  • what is it
  • signs
  • acute phase
  • fever
A
  • response to eliminate cause of cell injury, remove necrotic cells and initiate tissue repair
  • erythema / heat (histamine/ prostaglandin/ bradykinin causing increase in vasodilation), tumor / swelling (leukotrienes, hitamine, serotonin causeeing endothelial disruption allowing for leakage of proteins and increasing interstial oncotic pressure), pain (bradykinin, PGE2, histamine causing sensitization of nerve endings), loss of function
  • fever, leukocytosis, increase in plasma acute phase protein produced by liver
  • pyrogens cause macro to release IL-1 and TNF -> increase COX -> in pervacsular cells in hypothal -> increase PGE2 -> increase set point
  • elevation of WBC count and type of cell depends on inciting agent
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15
Q

Acute phase reactants

  • ferritin
  • fibrinogen
  • serum amyloid A
  • hepcidin
  • CRP
  • albumin
  • transferrin
A
  • upreg, binds and sequesters iron to inhibit microbial iron scavenging
  • upreg, coag factor, promotes endo repain, correlates with ESR
  • upreg, prolonged leads to amyloidosis
  • upreg, decrease iron absorption and release
  • upreg, opsonin
  • down reg, conserves AA
  • down reg, internalized by macrophages to sequester iron
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16
Q

Erythrocyte sedimentation rate

- what is it

A
  • RBC normally able to remain separated by neg charge but with inflammation fibrinogen will coat RBC and decrese negative charge -> increase in RBC aggregation
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17
Q

Exudate vs Transudate

  • exudate: cell, protein, caused by
  • transudate
  • light criteria
A
  • cellular (cloudy), high protein, lymph obstruction/ inflammation/ infection/ malignancy
  • hypocellular (clear), low protein, increase in hydrostatic pressure or decrease in oncotic pressure
  • pleural fluid is exudative if more than 1 of following criteria is met: has fluid/serum protein ration > 0.5, fluid/serum LDH ration > .6, pleural fluid LDH > 2/3 of upper limit of normal serum LDH
18
Q

Acute inflammation

  • what is it
  • characterized by
  • stimuli
  • mediators
  • vascular component
  • cellular component
  • outcomes
A
  • transient and early response to injury or infection
  • PMNs in tissue and edema
  • infection, trauma, necrosis, foreign bodies
  • TLR, arachadonic acid metabolites, PMN, eosinophil
  • vasodilation and increase in endothelial permeability
  • extravasion of leukocytes from post-cap venules and accumulation in location of injury
  • resolution and healing, abcess, scarring
19
Q

Leukocyte extravasion

  • margination and rolling: endo cells express, leukocytes express
  • tight binding: endo cells express, leukocytes express
  • diapedesis: what is it, endo cells express, leukocytes express
  • migration: what is it, endo cells express, leukocytes express
A
  • endo: E-selectin, P-selecting, GlyCAM1; Leuko: Sialyl lewis and L-selectin; leukocyte adhesion deficiency type 2 bs of decrease in sialyl lewis
  • endo: ICAM and VCAM; Leukocyte: CD11/12 and VLA4; defective in leukoocyte adhesion deificiency type 1
  • WBC travel between endo cell and exits blood vessel; PECAM-1 (both endo and leuko)
  • WBC travels in interstitium to site of injury or infection guided by chemotactic signal; endo: C5a, IL8
20
Q

Wound healing tissue mediators

  • FGF
  • TGF beta
  • VEGF
  • PDGF
  • Metalloproteinases
  • EGF
A
  • stimulates angiogenesis
  • angiogenesis and fibrosis
  • stimulate angiogenesis
  • secreted by platelets, induces vascular remodeling and smooth muscle cell migration, stimulates fibroblast growth for collagen synthesis
  • tissue remodeling
  • stimulates cell growth via tyrosine kinase
21
Q

Phase of wound healing

  • inflammatory
  • proliferative
  • remodeling
A
  • immediate to 3 days after wound; pleatelets, PMN, macro; clot formation, increase vessel permeability and PMN migration into tissue, macro clear debris 2 days later
  • 3 days to weeks after wound; fibroblasts, myofibrblasts, endothelial cells, keratinocytes, macro; deposition of granulation tissue and type III collagen, angiogenesis, epi cell proliferation, dissolution of clot and wound contraction
  • 1 week to 6 month; fibroblasts; type III colagen replaced by type I collagen to increase tensile strength of tissue, collagenases, zinc deficiency
22
Q

Phase of wound healing

  • inflammatory: time frame, cells involved, characteristics
  • proliferative: time frame, cells involved, characteristics
  • remodeling: time frame, cells involved, characteristics
A
  • immediate to 3 days after wound; pleatelets, PMN, macro; clot formation, increase vessel permeability and PMN migration into tissue, macro clear debris 2 days later
  • 3 days to weeks after wound; fibroblasts, myofibrblasts, endothelial cells, keratinocytes, macro; deposition of granulation tissue and type III collagen, angiogenesis, epi cell proliferation, dissolution of clot and wound contraction
  • 1 week to 6 month; fibroblasts; type III colagen replaced by type I collagen to increase tensile strength of tissue, collagenases, zinc deficiency
23
Q

Granulomatous inflammation

  • what is it
  • caused by
  • used for
  • histo
  • types
  • mechanism
  • anti TNF
A
  • pattern of chronic inflammation
  • by persistent T-cell response to certain infections
  • wall off a resistant stimulus w/o completely eradicating or degrading it
  • activated macrophage w/ abundant pink cytoplasm surrounded by lymphocytes lymphocytes and giant cells
  • caseating w/ central necrosis or non caseating w/o necrosis
  • APC present antigens to CD4 helper T cells and secrete IL-2 -> differentiate into Th1 cells -> secrete INF gamma -> macrophages activated -> macrophage increase cytokine secretion -> formation of giant cells
  • cause sequestering granulomas to break down -> disseminated disease
24
Q

Scar formation

  • what?
  • hypertrophic
  • keloid
A
  • occurs when repair cannot be accomplished by cell regeneration, non-regenerated cells replaced by CT
  • increased type III collagen, collagen is parallel, scar confined to to borders of original wound, infrequent recurrence and no predispostion
  • very high type I and III collagen, disorganized collagen organization, extends beyond border of original would with claw like projections typically on earlobes, face, UE, frequently recur, increase incidence in ethnic groups w/ darker skin
25
Q

Neoplasia

  • what is it
  • components
  • dysplasia
  • carcinoma in situ
  • invasive carcinoma
  • mets
A
  • uncontrolled, monoclonal proliferation of cells, can be malignant or benign
  • parenchyma (neoplastic cells) and supporting stroma (blood vessels, CT)
  • loss of uniformity in cell size and shape, loss of tissue orientation, nuclear changes
  • irreversible severe dysplasia that involves the entire thickness of epi but the basement membrane is intact
  • cells have invaded the basement membrane using collagenases and hydrolases, cell-cell contacts lost bu inactivation of E-cadherin
  • spread to distant organs via lymphatics or blood
26
Q

Tumor nomenclature

  • carcinoma
  • sarcoma
  • benign
  • malignant
  • hamartoma
  • choriostoma
A
  • epthelial origin
  • mesenchymal origin
  • well differentiated and wll demarcated, low mitotic activity, no mets, no necrosis
  • poor diferentiation, erratic growth, local invasion, mets, decreased apoptosis
  • disorganized growth of tissue in native location
  • normal tissue in foreign location
27
Q

Cell type and types of CA

  • Epi: benign, malignant
  • blood cells: malignant
  • blood vessels: benign, malignant
  • SM: benign, malignant
  • Striated muscle: benign, malignant
  • CT: benign, malignant
  • Bone: benign, malignant
  • Fat: benign, malignant
  • Melanocyte: benign, malignant
A
  • adenoma, papilloma; adenocarcinoma, papillary carcinoma
  • leukemia, lymphoma
  • hemangioma; angiosarcoma
  • leiomyoma; leiomyosarcoma
  • rhabdomyoma; rhabdomyosarcoma
  • fibroma; fibrosarcoma
  • osteoma; osteosarcoma
  • lipoma; liposarcoma
  • nevus; melanoma
28
Q

Tumor grade vs Stage

  • grade
  • stage
A
  • degree of cellular differentiation (how much it looks like tissue of origin) on histo
  • degree of localization/ spread based on site and size of primary location, spread to regional LN, presence of mets; determines survival
29
Q

Immune evasion in CA

  • what happens
  • escape mechanisms
A
  • immune cells can recognize and attack tumor cells
  • decreased MHC class I expression -> cytotoxic T cells unable to recognize tumor cells, secrete immunosuppressive factors, up-reg immune chekpoint mutations
30
Q

Common Mets

  • sarcoma
  • carcinoma
  • four carcinoma route hemato
A
  • hematogenously
  • lymph
  • follicular thyroid, choriocarcinoma, renal cell, and heptaocellular
31
Q

Oncogenic Microbes

  • EBV
  • HBV, HCV
  • HHV-8
  • HPV
  • H pylori
  • HTLV-1
  • Liver fluke
  • Schistosoma
A
  • Burkitt lymphoma
  • Heptaocellular carcinoma
  • Kaposi sarcoma
  • Cervical and penile/anal carcinoma, head and neck CA
  • gastric adenocarcinoma and MALT lymphoma
  • adult t-cell leukemia
  • cholangiocarcinoma
  • squamous cell bladder CA
32
Q

Serum tumor marker

  • alk phos
  • alpha fetoprotein
  • hCG
  • CA-15/ CA 27-29
  • CA 19-9
  • CA 125
  • Calcitonin
  • CEA
  • chromogranin
  • LDH
  • Neuron specific enolase
  • PSA
A
  • mets to bone or liver, pagets dx, seminoma
  • hepatocellular carcinoma, mixed germ cell tumor, neural tube defects
  • hydatidiform mole and choriocarcinoma
  • breast CA
  • pancreatic adenocarcinoma
  • ovarian carcinoma
  • medullary thyroid carcinoma
  • colorectal and pancreatic carcinoma
  • neuroendocrine tumor
  • testicular germ cell tumors, ovarian dysgerminoma
  • neuroendocrine tumor
  • prostate CA
33
Q

IHC stains

  • chromogranin
  • cytokeratin
  • desmin
  • GFAP
  • neurofilament
  • s-100
  • TRAP
A
  • neuroendocrine cells -> small cell carcinoma of lung
  • epithelial cells
  • muscle
  • neuroglia -> astrocytoma, glioblastoma
  • neurons
  • neural crest cells
  • hair cell leukemia
34
Q

P- glycoprotein

  • in
  • for
A
  • in adrenocortical carcinoma

- used to pump out toxins including chemo agents

35
Q

Psammoma bodies

  • histo
  • which cancers
A
  • laminated, concentric spherules w/ dystrophic calcification
  • papillary carcinoma of thyroid, somatostatinoma, meningioma, mesothelioma, ovarian serous papillary cystadenocarcinoma, prolactinma
36
Q

Cachexia

  • what is it
  • caused by
A
  • weight loss, muscle atrophy, and fatigue that occurs w/ chronic dx
  • TNF alpha, IFN gamma, IL-1 and 6
37
Q

Paraneoplastic Syndrome MS and cutaneous

  • dermatomyositis: description/ mechanism; most common tumor
  • acanthosis nigricans
  • sign of leser-trelat
  • hypertrophic osteoathropathy
A
  • progressive proximal muscle waekness, gottron papules, heliotrope rash
  • hyperpigmented velvety plaques in axilla and neck
  • sudden onset of mult seborrheic keratoses
  • abnrml proliferation of skin and bone at distal extremities
38
Q

Paraneoplastic Syndrome endocrine

  • hypercalcemia: description/ mechanism; most common tumor
  • cushing syndrome
  • hyponatremia
A
  • PTHrP; suamous cell carcinoma of lung, head, and neck
  • high ACTH, small cell lung CA
  • High ADH, small cell lung CA
39
Q

Paraneoplastic Syndrome hematologic

  • polycythemia: description/ mechanism; most common tumor
  • pure red cell plasia
  • good syndrome
  • trosseau syndrome
  • nonbacterial throbmotic endocarditis
A
  • increased erythropoietin; pheochromocytoma, renal cell carcinoma
  • anemia w/ low reticulocytes; thymoma
  • hypogammaglobulinemia; thymoma
  • migratory superficial thrombophlebitis; adenocarcinoma
  • deposition of sterile platelet thrombi on heart valves; adenocarcinoma
40
Q

Paraneoplastic Syndrome Neuromuscular

  • anti NMDA receptor encephalitis: description/ mechanism; most common tumor
  • opsoclonus-myoclonus ataxia syndrome
  • paraneoplastic cerebellar degeneration
  • paraneoplastic encephalomyelitis
  • lamber-eatn myasthenic syndrome
  • myasthenia gravis
A
  • psych disturbances, memory deficits, seizures; ovarian teratoma
  • dancing eyes and feet; neuroblastoma and small cell lung
  • antibodies against purkinje cells; small cell, gycenologic and breast CA
  • antibodies against Hu antigen in neuron; small cell lung CA
  • antibodies against pre-synaptic channels at NMJ; small cell lung CA
  • antibodies against postsynaptic Ach receptors at NMJ; thymoma

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