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USMLE Step 1 > Pathology - First Aid > Flashcards

Pathology - First Aid Flashcards

1
Q

_____ are reversible changes that can be physiologic (eg. uterine enlargement during pregnancy) or pathologic (eg. myocardial hypertrophy 2° to systemic HTN to prevent injury). If stress is excessive or persistent, adaptations can progress to cell injury (eg. significant LV hypertrophy → injury to myofibrils → HF).

A

Cellular Adaptations

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2
Q

Cellular Adaptations

A
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3
Q

Cellular Adaptations:

↑ structural proteins and organelles → ↑ in size of cells.

A

Hypertrophy

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4
Q

Cellular Adaptations:

  • controlled proliferation of stem cells and differentiated cells → ↑ in number of cells.
  • excessive stimulation → pathologic _____, which may progress to dysplasia and cancer
A

Hyperplasia

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5
Q

Cellular Adaptations:

  • ↓ in tissue mass due to ↓ in size (↑ cytoskeleton degradation via ubiquitin-proteasome pathway and autophagy; ↓ protein synthesis) and/or number of cells (apoptosis)
  • causes include disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition
A

Atrophy

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6
Q

Cellular Adaptations:

  • reprogramming of stem cells → replacement of one cell type by another that can adapt to a new stress
  • usually due to exposure to an irritant, such as gastric acid (Barrett esophagus) or cigarette smoke (respiratory ciliated columnar epithelium replaced by stratified squamous epithelium)
  • may progress to dysplasia → malignant transformation with persistent insult (eg. Barrett esophagus → esophageal adenocarcinoma)
  • connective tissue can also be affected (eg. myositis ossificans, the formation of bone within muscle after trauma)
A

Metaplasia

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7
Q

Cellular Adaptations:

  • disordered, precancerous epithelial cell growth
  • characterized by loss of uniformity of cell size and shape (pleomorphism); loss of tissue orientation; nuclear changes (eg. ↑ nuclear:cytoplasmic ratio and clumped chromatin)
  • mild and moderate dysplasias (ie. do not involve entire thickness of epithelium) may regress with alleviation of inciting cause
  • severe dysplasia usually becomes irreversible and progresses to carcinoma in situ
  • usually preceded by persistent metaplasia or pathologic hyperplasia
A

Dysplasia

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8
Q

Cell Injury

A
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9
Q

Cell Injury:

  • ATP-dependent programmed cell death
  • intrinsic and extrinsic pathways; both pathways activate caspases (cytosolic proteases) → cellular breakdown including cell shrinkage, chromatin condensation, membrane blebbing, and formation of apoptotic bodies, which are then phagocytosed
  • characterized by deeply eosinophilic cytoplasm and basophilic nucleus, pyknosis (nuclear shrinkage), and karyorrhexis (fragmentation caused by endonuclease- mediated cleavage
  • cell membrane typically remains intact without significant inflammation (unlike necrosis)
  • DNA laddering (fragments in multiples of 180 bp) is a sensitive indicator
A

Apoptosis

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10
Q

Apoptosis:

  • involved in tissue remodeling in embryogenesis
  • occurs when a regulating factor is withdrawn from a proliferating cell population (eg, ↓ IL-2 after a completed immunologic reaction → apoptosis of proliferating effector cells)
  • also occurs after exposure to injurious stimuli (eg. radiation, toxins, hypoxia)
  • regulated by Bcl-2 family of proteins
  • BAX and BAK are proapoptotic, while Bcl-2 and Bcl-xL are antiapoptotic
  • BAX and BAK form pores in the mitochondrial membrane → release of cytochrome C from inner mitochondrial membrane into the cytoplasm → activation of caspases
  • Bcl-2 keeps the mitochondrial membrane impermeable, thereby preventing cytochrome C release
  • Bcl-2 overexpression (eg. follicular lymphoma t[14;18]) → ↓ caspase activation → tumorigenesis
A

Intrinsic (Mitochondrial) Pathway

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11
Q

Apoptosis:

  • Fas-FasL interaction is necessary in thymic medullary negative selection
  • mutations in Fas ↑ numbers of circulating self-reacting lymphocytes due to failure of clonal deletion
  • defective Fas-FasL interactions cause autoimmune lymphoproliferative syndrome
A

Extrinsic (Death Receptor) Pathway

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12
Q

Extrinsic (Death Receptor) Pathways

A
  • Ligand Receptor Interactions
    • FasL binding to Fas [CD95] or TNF-α binding to its receptor
  • Immune Cell
    • cytotoxic T-cell release of perforin and granzyme B
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13
Q

Cell Injury:

  • enzymatic degradation and protein denaturation of cell due to exogenous injury → intracellular components leak
  • inflammatory process (unlike apoptosis)
A

Necrosis

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14
Q

Necrosis:

  • seen in ischemia/infarcts in most tissues (except brain)
  • injury denatures enzymes → proteolysis blocked
  • preserved cellular architecture (cell outlines seen), but nuclei disappear
  • ↑ cytoplasmic binding of eosin stain (↑ eosinophilia; red/pink color)
A

Coagulative

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15
Q

Necrosis:

  • seen in bacterial abscesses and brain infarcts
  • neutrophils release lysosomal enzymes that digest the tissue
  • Early: cellular debris and macrophages
  • Late: cystic spaces and cavitation (brain)
  • neutrophils and cell debris seen with bacterial infection
A

Liquefactive

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16
Q

Necrosis:

  • seen in TB, systemic fungi (eg. Histoplasma capsulatum), and Nocardia
  • macrophages wall off the infecting microorganism → granular debris
  • fragmented cells and debris surrounded by lymphocytes and macrophages (granuloma)
A

Caseous

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17
Q

Necrosis:

  • Enzymatic: acute pancreatitis (saponification)
  • Nonenzymatic: traumatic (eg. injury to breast tissue)
  • damaged cells release lipase, which breaks down triglycerides liberated fatty acids bind calcium → saponification
  • outlines of dead cells without peripheral nuclei
  • saponification (combined with Ca2+) appears dark blue on H&E stain
A

Fat

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18
Q

Necrosis:

  • immune reactions in vessels (eg. polyarteritis nodosa), preeclampsia, hypertensive emergency
  • immune complexes combine with fibrin → vessel wall damage (type III hypersensitivity reaction)
  • vessel walls are thick and pink
A

Fibrinoid

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19
Q

Necrosis:

  • distal extremity and GI tract after chronic ischemia
  • Dry: ischemia, coagulative
  • Wet: superinfection, liquefactive superimposed on coagulative
A

Gangrenous

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20
Q

Cell Injury:

  • inadequate blood supply to meet demand
  • mechanisms include ↓ arterial perfusion (eg. atherosclerosis), ↓ venous drainage (eg. testicular torsion, Budd-Chiari syndrome), and shock
A

Ischemia

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21
Q

Ischemia:

Brain

A

ACA/MCA/PCA boundary areas

  • Watershed areas (border zones) receive blood supply from most distal branches of 2 arteries with limited collateral vascularity. These areas are susceptible to ischemia from hypoperfusion.
  • Neurons most vulnerable to hypoxic-ischemic insults include Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex (zones 3, 5, 6).
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22
Q

Ischemia:

Heart

A

Subendocardium (LV)

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23
Q

Ischemia:

Kidney

A
  • straight segment of proximal tubule (medulla)
  • thick ascending limb (medulla)
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24
Q

Ischemia:

Liver

A

area around central vein (zone III)

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25
Q

Ischemia:

Colon

A
  • Splenic flexure
  • Rectum

Watershed areas (border zones) receive blood supply from most distal branches of 2 arteries with limited collateral vascularity. These areas are susceptible to ischemia from hypoperfusion.

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26
Q

Infarcts:

  • occur in venous occlusion and tissues with multiple blood supplies, such as liver, lung, intestine, testes; reperfusion (eg. after angioplasty)
  • reperfusion injury is due to damage by free radicals
A

Red (Hemorrhagic) Infarct

Red = reperfusion

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27
Q

Infarcts:

occur in solid organs with a single (end-arterial) blood supply, such as heart, kidney, and spleen

A

Pale Infarct

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28
Q

Cell Injury:

  • response to eliminate initial cause of cell injury, to remove necrotic cells resulting from the original insult, and to initiate tissue repair
  • divided into acute and chronic
  • can be harmful to the host if the reaction is excessive (eg. septic shock), prolonged (eg. persistent infections such as TB), or inappropriate (eg. autoimmune diseases such as SLE)
A

Inflammation

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29
Q

Cardinal Signs of Inflammation

A
  • Rubor (redness)
  • Calor (warmth)
  • Vasodilation (relaxation of arteriolar smooth muscle)
  • Tumor (swelling)
  • Dolor (pain)
  • Functio Laesa (loss of function)
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30
Q

Cardinal Signs of Inflammation:

  • vasodilation (relaxation of arteriolar smooth muscle) → ↑ blood flow
  • Mediators:
    • Histamine
    • Prostaglandins
    • Bradykinin
A
  • Rubor (redness)
  • Calor (warmth)
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31
Q

Cardinal Signs of Inflammation:

  • endothelial contraction/disruption (eg. from tissue damage) → ↑ vascular permeability → leakage of protein-rich fluid from postcapillary venules into interstitial space (exudate) → ↑ oncotic pressure
  • Endothelial Contraction:
    • Leukotrienes (C4, D4, E4)
    • Histamine
    • Serotonin
A

Tumor (swelling)

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32
Q

Cardinal Signs of Inflammation:

  • sensitization of sensory nerve endings
  • Mechanism:
    • Bradykinin, PGE2
A

Dolor (pain)

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33
Q

Cardinal Signs of Inflammation:

other cardinal signs impair function (eg. inability to make fist with hand that has cellulitis)

A

Functio Laesa (loss of function)

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34
Q

Systemic Manifestations (Acute-Phase Reaction) of Inflammation

A
  • Fever
  • Leukocytosis
  • ↑ Plasma Acute-Phase Proteins
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35
Q

Systemic Manifestations (Acute-Phase Reaction) of Inflammation:

pyrogens (eg. LPS) induce macrophages to release IL-1 and TNF → ↑ COX activity in perivascular cells of hypothalamus → ↑ PGE2 → ↑ temperature set point

A

Fever

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36
Q

Systemic Manifestations (Acute-Phase Reaction) of Inflammation:

  • elevation of WBC count
  • type of cell that is predominantly elevated depends on the inciting agent or injury (eg. bacteria → ↑ neutrophils)
A

Leukocytosis

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37
Q

_____ is the severe elevation in WBC (> 40,000 cells/mm³) caused by some stressors or infections (eg. Clostridium difficile).

A

Leukemoid Reaction

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38
Q

Systemic Manifestations (Acute-Phase Reaction) of Inflammation:

  • factors whose serum concentrations change significantly in response to inflammation
  • produced by the liver in both acute and chronic inflammatory states
  • induced by IL-6
A

↑ Plasma Acute-Phase Proteins

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39
Q

⊕ Acute Phase Reactants of Inflammation

A

More FFiSH in the C (sea).

  • Ferritin
  • Fibrinogen
  • Serum Amyloid A
  • Hepcidin
  • C-Reactive protein
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40
Q

⊕ Acute Phase Reactants of Inflammation:

binds and sequesters iron to inhibit microbial iron scavenging

A

Ferritin

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41
Q

⊕ Acute Phase Reactants of Inflammation:

  • coagulation factor
  • promotes endothelial repair
  • correlates with ESR
A

Fibrinogen

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42
Q

⊕ Acute Phase Reactants of Inflammation:

prolonged elevation can lead to amyloidosis

A

Serum Amyloid A

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43
Q

⊕ Acute Phase Reactants of Inflammation:

↓ iron absorption (by degrading ferroportin) and ↓ iron release (from macrophages) → anemia of chronic disease

A

Hepcidin

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44
Q

⊕ Acute Phase Reactants of Inflammation:

  • opsonin
  • fixes complement and facilitates phagocytosis
  • measured clinically as a nonspecific sign of ongoing inflammation
A

C-Reactive Protein

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45
Q

⊝ Acute Phase Reactants of Inflammation

A
  • Albumin
  • Transferrin
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46
Q

⊝ Acute Phase Reactants of Inflammation:

reduction conserves amino acids for positive reactants

A

Albumin

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47
Q

⊝ Acute Phase Reactants of Inflammation:

internalized by macrophages to sequester iron

A

Transferrin

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48
Q

Products of inflammation (eg, fibrinogen) coat RBCs and cause aggregation. The denser RBC aggregates fall at a faster rate within a pipette tube → ↑ _____. Often co-tested with CRP levels.

A

Erythrocyte Sedimentation Rate (ESR)

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49
Q

↑ Erythrocyte Sedimentation Rate (ESR)

A
  • Anemia
  • Infection
  • Inflammation (eg. giant cell [temporal] arteritis, polymyalgia rheumatica)
  • Cancer (eg. metastases, multiple myeloma)
  • Renal Disease (end-stage or nephrotic syndrome)
  • Pregnancy
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50
Q

↓ Erythrocyte Sedimentation Rate (ESR)

A
  • Sickle Cell Anemia (altered shape)
  • Polycythemia (↑ RBCs “dilute” aggregation factors)
  • HF
  • Microcytosis
  • Hypofibrinogenemia
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51
Q

_____ is the transient and early response to injury or infection. Characterized by neutrophils in tissue,
often with associated edema. Rapid onset (seconds to minutes) and short duration (minutes to days). Represents a reaction of the innate immune system (ie. less specific response than chronic inflammation).

A

Acute Inflammation

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52
Q

Acute Inflammation Stimuli

A
  • Infections
  • Trauma
  • Necrosis
  • Foreign Bodies
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53
Q

Acute Inflammation Mediators

A
  • Toll-Like Receptors
  • Arachidonic Acid Metabolites
  • Neutrophils
  • Eosinophils
  • Antibodies (pre-existing)
  • Mast Cells
  • Basophils
  • Complement
  • Hageman Factor (Factor XII)
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54
Q

_____ is a cytoplasmic protein complex that recognizes products of dead cells, microbial products, and crystals (eg. uric acid crystals) → activation of IL-1 and inflammatory response.

A

Inflammasome

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55
Q

Acute Inflammation Components:

  • vasodilation (→ ↑ blood flow and stasis)
  • ↑ endothelial permeability
  • brings cells and proteins to site of injury or infection
A

Vascular

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56
Q

Acute Inflammation Components:

  • extravasation of leukocytes (mainly neutrophils) from postcapillary venules
  • accumulation in the focus of injury followed by leukocyte activation
A

Cellular

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57
Q

Acute Inflammation Outcomes

A
  • resolution and healing (IL-10, TGF-β)
  • persistent acute inflammation (IL-8)
  • abscess (acute inflammation walled off by fibrosis)
  • chronic inflammation (antigen presentation by macrophages and other APCs → activation of CD4+ Th cells)
  • scarring

*Macrophages predominate in the late stages of acute inflammation (peak 2–3 days after onset) and influence the outcome of acute inflammation by secreting cytokines.

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58
Q

_____ predominantly occurs at postcapillary venules. WBCs exit from blood vessels at sites of tissue injury and inflammation in 4 steps.

A

Leukocyte Extravasation

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59
Q

Leukocyte Extravasation

A
  1. Margination and Rolling
  2. Tight Binding (Adhesion)
  3. Diapedesis (Transmigration)
  4. Migration (Chemoattraction)
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60
Q

Leukocyte Extravasation:

defective in leukocyte adhesion deficiency type 2 (↓ Sialyl-LewisX)

A

Margination and Rolling

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61
Q

Leukocyte Extravasation:

Margination and Rolling

Vasculature/Stroma—Leukocyte

A
  • E-selectin (upregulated by TNF and IL-1)—Sialyl-LewisX
  • P-selectin (released from Weibel-Palade bodies)—Sialyl-LewisX
  • GlyCAM-1, CD34—L-selectin
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62
Q

Leukocyte Extravasation:

defective in leukocyte adhesion deficiency type 1 (↓ CD18 integrin subunit)

A

Tight Binding (Adhesion)

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63
Q

Leukocyte Extravasation:

Tight Binding (Adhesion)

Vasculature/Stroma—Leukocyte

A
  • ICAM-1 (CD54)—CD11/18 Integrins (LFA-1, Mac-1)
  • VCAM-1 (CD106)—VLA-4 Integrin
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64
Q

Leukocyte Extravasation:

WBC travels between endothelial cells and exits blood vessel

A

Diapedesis (Transmigration)

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65
Q

Leukocyte Extravasation:

Diapedesis (Transmigration)

Vasculature/Stroma—Leukocyte

A

PECAM-1 (CD31)—PECAM-1 (CD31)

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66
Q

Leukocyte Extravasation:

WBC travels through interstitium to site of injury or infection guided by chemotactic signals

A

Migration

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67
Q

Leukocyte Extravasation:

Migration

Vasculature/Stroma—Leukocyte

A

Chemotactic Products Released in Response to Bacteria:

  • C5a
  • IL‑8
  • LTB4
  • Kallikrein
  • Platelet-Activating Factor

*various leukocytes

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68
Q

_____ is inflammation of prolonged duration characterized by infiltration of tissue by mononuclear cells (macrophages, lymphocytes, and plasma cells). Tissue destruction and repair (including angiogenesis and fibrosis) occur simultaneously. May or may not be preceded by acute inflammation.

A

Chronic Inflammation

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69
Q

Chronic Inflammation Stimuli

A
  • Persistent Infections (eg, TB, T pallidum, certain fungi and viruses) → Type IV Hypersensitivity
  • Autoimmune Diseases
  • Toxic Agents (eg. silica)
  • Foreign Material
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70
Q

Chronic Inflammation Mediators

A
  • Macrophages
    • dominant cells
    • chronic inflammation is the result of their interaction with T lymphocytes
      • Th1 cells secrete INF-γ → macrophage classical activation (proinflammatory)
      • Th2 cells secrete IL-4 and IL-13 → macrophage alternative activation (repair and antiinflammatory)
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71
Q

Chronic Inflammation Outcomes

A
  • Scarring
  • Amyloidosis
  • Neoplastic Transformation
    • chronic HCV infection → chronic inflammation → hepatocellular carcinoma
    • Helicobacter pylori infection → chronic gastritis → gastric adenocarcinoma
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72
Q

Granulomatous Diseases

A
  • Bacterial:
    • Mycobacteria (tuberculosis, leprosy)
    • Bartonella henselae (cat scratch disease)
    • Listeria monocytogenes (granulomatosis infantiseptica)
    • Treponema pallidum (3° syphilis)
  • Fungal: endemic mycoses (eg. histoplasmosis)
  • Parasitic: schistosomiasis
  • Chronic Granulomatous Disease
  • Autoinflammatory:
    • Sarcoidosis
    • Crohn disease
    • Primary Biliary Cholangitis
    • Subacute (de Quervain/granulomatous) Thyroiditis
    • Granulomatosis with Polyangiitis (Wegener)
    • Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss)
    • Giant Cell (temporal) Arteritis
    • Takayasu Arteritis
  • Foreign Material: berylliosis, talcosis, hypersensitivity pneumonitis
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73
Q

_____, a pattern of chronic inflammation, are composed of epithelioid cells (macrophages with abundant pink cytoplasm) with surrounding multinucleated giant cells and lymphocytes.

A

Granulomas

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74
Q

Th1 cells secrete _____, activating macrophages.

A

IFN-γ

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75
Q

_____ from macrophages induces and maintains granuloma formation.

A

TNF-α

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76
Q

_____ drugs can cause sequestering granulomas to break down → disseminated disease. Always test for latent TB before starting _____ therapy.

A

Anti-TNF

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77
Q

Granulomas are associated with hypercalcemia due to _____ production.

A

Calcitriol (1,25-[OH]2 vitamin D3)

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78
Q

_____ necrosis is more common with an infectious etiology (eg. TB).

A

Caseating

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79
Q

Diagnosis of Sarcoidosis requires _____ on biopsy.

A

Noncaseating Ggranulomas

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80
Q

Types of Calcification

A
  • Dystrophic Calcification
  • Metastatic Calcification
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81
Q

Calcification:

  • Ca2+ deposition in abnormal tissues
  • tends to be localized (eg. calcific aortic stenosis)
  • 2° to injury or necrosis
  • patients are usually normocalcemic
A

Dystrophic Calcification

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82
Q

Calcification:

  • TB (lung and pericardium) and other granulomatous infections
  • liquefactive necrosis of chronic abscesses
  • fat necrosis
  • infarcts
  • thrombi
  • Schistosomiasis
  • Congenital CMV
  • Toxoplasmosis
  • Rubella
  • Psammoma Bodies
  • CREST Syndrome
  • atherosclerotic plaques
A

Dystrophic Calcification

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83
Q

Calcification:

  • Ca2+ deposition In normal tissues
  • widespread (ie. diffuse, metastatic)
  • metastatic calcifications of alveolar walls in acute pneumonitis (arrows)
  • patients usually have abnormal serum Ca2+ levels
A

Metastatic Calcification

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84
Q

Calcification:

  • predominantly in interstitial tissues of kidney, lung, and gastric mucosa (these tissues lose acid quickly; ↑ pH favors Ca2+ deposition)
  • nephrocalcinosis of collecting ducts may lead to nephrogenic diabetes insipidus and renal failure
A

Metastatic Calcification

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85
Q

Calcification:

  • Hypercalcemia
    • 1° hyperparathyroidism
    • sarcoidosis
    • hypervitaminosis D
  • High Calcium-Phosphate Product Levels
    • chronic renal failure with 2° hyperparathyroidism
    • long-term dialysis
    • calciphylaxis
    • multiple myeloma
A

Metastatic Calcification

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86
Q

_____ is a yellow-brown “wear and tear” pigment associated with normal aging. Formed by oxidation and polymerization of autophagocytosed organellar membranes. Autopsy of elderly person will reveal deposits in heart, colon, liver, kidney, eye, and other organs.

A

Lipofuscin

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87
Q

Free radicals damage cells via _____.

A
  • Membrane Lipid Peroxidation
  • Protein Modification
  • DNA Breakage
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88
Q

Free radical injury is initiated via _____.

A
  • Radiation (eg. cancer therapy)
  • Metabolism of Drugs (phase I)
  • Redox Reactions
  • Nitric Oxide (eg. inflammation)
  • Transition Metals
  • WBC (eg. neutrophils, macrophages) Oxidative Burst
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89
Q

Free radicals can be eliminated by _____.

A
  • Scavenging Enzymes (eg. catalase, superoxide dismutase, glutathione peroxidase)
  • Spontaneous Decay
  • Antioxidants (eg. vitamins A, C, E)
  • Certain Metal Carrier Proteins (eg. transferrin, ceruloplasmin)
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90
Q

Free Radical Injuries

A
  • Oxygen Toxicity
    • retinopathy of prematurity (abnormal vascularization)
    • bronchopulmonary dysplasia
    • reperfusion injury after thrombolytic therapy
  • Drug/Chemical Toxicity
    • acetaminophen overdose (hepatotoxicity)
    • carbon tetrachloride (converted by cytochrome P-450 into CCl3 free radical → fatty liver [cell injury → ↓ apolipoprotein synthesis → fatty change], centrilobular necrosis)
  • Metal Storage Diseases
    • hemochromatosis (iron)
    • Wilson disease (copper)
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91
Q

_____ occurs when repair cannot be accomplished by cell regeneration alone. Nonregenerated cells (2° to severe acute or chronic injury) are replaced by connective tissue. 70–80% of tensile strength regained at 3 months; little tensile strength regained thereafter.

A

Scar Formation

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92
Q

Scar Formation:

  • ↑ collagen formation—type III collagen
  • parallel collagen organization
  • confined to borders of original wound
  • infrequent recurrence
  • no predisposition
A

Hypertrophic

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93
Q

Scar Formation:

  • ↑↑↑ collagen formation—disorganized types I and III collagen
  • disorganized collagen
  • extends beyond borders of original wound with “claw-like” projections typically on earlobes, face, upper extremities
  • frequent recurrence
  • ↑ incidence in ethnic groups with darker skin
A

Keloid

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94
Q

Tissue Mediators:

stimulates angiogenesis

A
  • FGF
  • VEGF
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95
Q

Tissue Mediators:

  • angiogenesis
  • fibrosis
A

TGF-β

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96
Q

Tissue Mediators:

  • secreted by activated platelets and macrophages
  • induces vascular remodeling and smooth muscle cell migration
  • stimulates fibroblast growth for collagen synthesis
A

PDGF

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97
Q

Tissue Mediators:

tissue remodeling

A

Metalloproteinases

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98
Q

Tissue Mediators:

stimulates cell growth via tyrosine kinases (eg. EGFR/ErbB1)

A

EGF

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99
Q

Phases of Wound Healing

A
  • Inflammatory—up to 3 days after wound
  • Proliferative—day 3–weeks after wound
  • Remodeling—1 week–6+ months after wound
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100
Q

Phases of Wound Healing:

  • up to 3 days after wound
  • Effector Cells:
    • platelets
    • neutrophils
    • macrophages
  • clot formation
  • ↑ vessel permeability and neutrophil
  • migration into tissue
  • macrophages clear debris 2 days later
A

Inflammatory

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101
Q

Phases of Wound Healing:

  • day 3–weeks after wound
  • Effector Cells:
    • fibroblasts
    • myofibroblasts
    • endothelial cells
    • keratinocytes
    • macrophages
  • deposition of granulation tissue and type III collagen
  • angiogenesis
  • epithelial cell
  • proliferation
  • dissolution of clot
  • wound contraction (mediated by myofibroblasts)
  • delayed wound healing in vitamin C deficiency and copper deficiency
A

Proliferative

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102
Q

Phases of Wound Healing:

  • 1 week–6+ months after wound
  • Effector Cells: fibroblasts
  • type III collagen replaced by type I collagen
  • ↑ tensile strength of tissue
  • collagenases (require zinc to function) break down type III collagen
  • zinc deficiency → delayed wound healing
A

Remodeling

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103
Q

Effusion:

  • cellular (cloudy)
  • ↑ protein (> 2.9 g/dL)
  • due to:
    • lymphatic obstruction (chylous)
    • inflammation/infection
    • malignancy
A

Exudate

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104
Q

Effusion:

  • Hypocellular (clear)
  • ↓ protein (< 2.5 g/dL)
  • due to:
    • ↑ hydrostatic pressure (eg. HF, Na+ retention)
    • ↓ oncotic pressure (eg. cirrhosis, nephrotic syndrome)
A

Transudate

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105
Q

Light Criteria

A

Fluid is exudative if ≥ 1 of the following criteria is met:

  • pleural effusion/serum protein ratio > 0.5
  • pleural effusion/serum LDH ratio > 0.6
  • pleural effusion LDH > 2⁄3 of the upper limit of normal for serum LDH
106
Q

_____ is the abnormal aggregation of proteins (or their fragments) into β-pleated linear sheets → insoluble fibrils → cellular damage and apoptosis.

A

Amyloidosis

107
Q

Amyloid deposits are visualized by _____.

A
  • Congo Red sStain
  • Polarized Light (apple green birefringence)
  • H&E Stain
108
Q

Amyloidosis:

  • Cardiac (eg. restrictive cardiomyopathy, arrhythmia)
  • GI (eg. macroglossia, hepatomegaly)
  • Renal (eg. nephrotic syndrome)
  • Hematologic (eg. easy bruising, splenomegaly)
  • Neurologic (neuropathy)
  • Musculoskeletal (carpal tunnel syndrome)
A

Systemic Amyloidosis

109
Q

Systemic Amyloidosis

A
  • Primary Amyloidosis
  • Secondary Amyloidosis
  • Dialysis-Related Amyloidosis
110
Q

Systemic Amyloidosis:

  • Fibril Protein: AL (from Ig light chains)
  • seen in plasma cell disorders and multiple myeloma
A

Primary Amyloidosis

111
Q

Systemic Amyloidosis:

  • Fibril Protein: Serum Amyloid A (AA)
  • seen in chronic inflammatory conditions
    • rheumatoid arthritis
    • IBD,
    • familial Mediterranean fever
    • protracted infection
A

Secondary Amyloidosis

112
Q

Systemic Amyloidosis:

  • Fibril Protein: β2-Microglobulin
  • seen in patients with ESRD and/or on long-term dialysis
A

Dialysis-Related Amyloidosis

113
Q

Localized Amyloidosis

A
  • Alzheimer Disease
  • Type 2 Diabetes Mellitus
  • Medullary Thyroid Cancer
  • Isolated Atrial Amyloidosis
  • Systemic Senile (Age-Related) Amyloidosis
114
Q

Localized Amyloidosis:

  • Fibril Protein: β-Amyloid Protein
  • cleaved from amyloid precursor protein (APP)
A

Alzheimer Disease

115
Q

Localized Amyloidosis:

  • Fibril Protein: Islet Amyloid Polypeptide (IAPP)
  • caused by deposition of amylin in pancreatic islets
A

Type 2 Diabetes Mellitus

116
Q

Localized Amyloidosis:

Fibril Protein: Calcitonin (A Cal)

A

Medullary Thyroid Cancer

117
Q

Localized Amyloidosis:

  • Fibril Protein: ANP
  • common in normal aging ↑ risk of atrial fibrillation
A

Isolated Atrial Amyloidosis

118
Q

Localized Amyloidosis:

  • Fibril Protein: Normal (wild-type) Transthyretin (TTR)
  • seen predominantly in cardiac ventricles
  • cardiac dysfunction is more insidious than in AL amyloidosis
A

Systemic Senile (Age-Related) Amyloidosis

119
Q

Hereditary Amyloidosis

A
  • Familial Amyloid Cardiomyopathy
  • Familial Amyloid Polyneuropathies
120
Q

Hereditary Amyloidosis:

  • Fibril Protein: Mutated Transthyretin (ATTR)
  • ventricular endomyocardium deposition → restrictive cardiomyopathy, arrhythmias
  • 5% of African Americans are carriers of mutant allele
A

Familial Amyloid Cardiomyopathy

121
Q

Hereditary Amyloidosis:

  • Fibril Protein: Mutated Transthyretin (ATTR)
  • due to transthyretin gene mutation
A

Familial Amyloid Polyneuropathies

122
Q

____ is the uncontrolled, clonal proliferation of cells. Can be benign or malignant.

A

Neoplastic Progression

123
Q

Hallmarks of Cancer

A
  • evasion of apoptosis
  • growth signal self-sufficiency
  • anti-growth signal insensitivity
  • Warburg effect—shift of glucose metabolism away from mitochondria toward glycolysis
  • sustained angiogenesis
  • limitless replicative potential
  • tissue invasion
  • metastasis
124
Q

Neoplastic Progression

A
  1. Normal Cells
    • normal cells with basal → apical polarity
  2. Dysplasia
    • _​​l_oss of uniformity of cell size and shape (pleomorphism)
    • loss of tissue orientation
    • nuclear changes (eg. ↑ nuclear:cytoplasmic ratio)
  3. Carcinoma In Situ/Preinvasive
    • irreversible severe dysplasia that involves the entire thickness of epithelium but does not penetrate the intact basement membrane
  4. Invasive Carcinoma
    • _​_cells have invaded basement membrane using collagenases and hydrolases (metalloproteinases)
    • cell-cell contacts lost by inactivation of E-cadherin
  5. Metastasis
    • spread to distant organ(s) via lymphatics or blood
    • “Seed and Soil” theory of metastasis:
      • Seed = tumor embolus
      • Soil = target organ is often the first-encountered capillary bed (eg. liver, lungs, bone, brain, etc)
125
Q

Tumor Nomenclature:

  • epithelial origin
  • malignant
126
Q

Tumor Nomenclature:

  • mesenchymal origin
  • malignant
127
Q

Tumor Nomenclature:

  • well differentiated
  • well demarcated
  • low mitotic activity
  • no metastasis
  • no necrosis
A

Benign Tumors

128
Q

Tumor Nomenclature:

  • poor differentiation
  • erratic growth
  • local invasion
  • metastasis
  • ↓ apoptosis
  • upregulation of telomerase prevents chromosome shortening and cell death
A

Malignant Tumors

129
Q

Tumor Nomenclature:

  • disorganized overgrowth of tissues in their native location
  • Peutz-Jeghers polyps
130
Q

Tumor Nomenclature:

  • normal tissue in a foreign location
  • gastric tissue located in distal ileum in Meckel diverticulum
A

Choristoma

131
Q

Benign Epithelial Tumors

A
  • Adenoma
  • Papilloma
132
Q

Malignant Epithelial Tumors

A
  • Adenocarcinoma
  • Papillary Carcinoma
133
Q

Benign Mesenchymal Tumors:

blood vessels

A

Hemangioma

134
Q

Benign Mesenchymal Tumors:

smooth muscle

135
Q

Benign Mesenchymal Tumors:

striated muscle

A

Rhabdomyoma

136
Q

Benign Mesenchymal Tumors:

connective tissue

137
Q

Benign Mesenchymal Tumors:

bone

138
Q

Benign Mesenchymal Tumors:

fat

139
Q

Benign Mesenchymal Tumors:

melanocyte

A

Nevus/Mole

140
Q

Malignant Mesenchymal Tumors:

blood cells

A
  • Leukemia
  • Lymphoma
141
Q

Malignant Mesenchymal Tumors:

blood vessels

A

Angiosarcoma

142
Q

Malignant Mesenchymal Tumors:

smooth muscle

A

Leiomyosarcoma

143
Q

Malignant Mesenchymal Tumors:

striated muscle

A

Rhabdomyosarcoma

144
Q

Malignant Mesenchymal Tumors:

connective tissue

A

Fibrosarcoma

145
Q

Malignant Mesenchymal Tumors:

bone

A

Osteosarcoma

146
Q

Malignant Mesenchymal Tumors:

fat

A

Liposarcoma

147
Q

Malignant Mesenchymal Tumors:

melanocyte

148
Q

_____ is the degree to which a tumor resembles its tissue of origin.

A

Differentiation

  • well-differentiated tumors (often less aggressive) closely resemble their tissue of origin
  • poorly differentiated tumors (often more aggressive) look almost nothing like their tissue of origin
149
Q

_____ is the complete lack of differentiation of cells in a malignant neoplasm.

150
Q

_____ is the degree of cellular differentiation and mitotic activity on histology.

151
Q

_____ is the degree of localization/spread based on site and size of 1° lesion, spread to regional lymph nodes, presence of metastases. Based on clinical (c) or pathology (p) findings. Generally has more prognostic value.

A

Stage

Stage determines Survival.

152
Q

TNM Staging System

A
  • *T** = Tumor size/invasiveness
  • *N** = Node involvement
  • *M** = Metastases

(Stage = Spread)

*Each TNM factor has independent prognostic value; N and M are often most important.

153
Q

Paraneoplastic Syndromes:

Musculoskeletal and Cutaneous

A
  • Dermatomyositis
  • Acanthosis Nigricans
  • Sign of Leser-Trélat
  • Hypertrophic Osteoarthropathy
154
Q

Paraneoplastic Syndromes:

  • progressive proximal muscle weakness
  • Gottron papules
  • heliotrope rash
  • adenocarcinomas—especially ovarian
A

Dermatomyositis

155
Q

Paraneoplastic Syndromes:

  • hyperpigmented velvety plaques in axilla and neck
  • gastric adenocarcinoma
  • visceral malignancies—associated with obesity and insulin resistance
A

Acanthosis Nigricans

156
Q

Paraneoplastic Syndromes:

  • sudden onset of multiple seborrheic keratoses
  • GI adenocarcinomas
  • visceral malignancies
A

Sign of Leser-Trélat

157
Q

Paraneoplastic Syndromes:

  • abnormal proliferation of skin and bone at distal extremities → clubbing, arthralgia, joint effusions, periostosis of tubular bones
  • adenocarcinoma of the lung
A

Hypertrophic Osteoarthropathy

158
Q

Paraneoplastic Syndromes:

Endocrine

A
  • Hypercalcemia
  • Cushing Syndrome
  • Hyponatremia (SIADH)
159
Q

Paraneoplastic Syndromes:

  • PTHrP—squamous cell carcinomas of lung, head, and neck; renal, bladder, breast, and ovarian carcinomas
  • ↑ 1,25-(OH)2 vitamin D3 (calcitriol)—lymphoma
A

Hypercalcemia

160
Q

Paraneoplastic Syndromes:

  • ↑ ACTH
  • small cell lung cancer
A

Cushing Syndrome

161
Q

Paraneoplastic Syndromes:

  • ↑ ADH
  • small cell lung cancer
A

Hyponatremia (SIADH)

162
Q

Paraneoplastic Syndromes:

Hematologic

A
  • Polycythemia
  • Pure Red Cell Aplasia
  • Good Syndrome
  • Trousseau Syndrome
  • Nonbacterial Thrombotic (Marantic) Endocarditis
163
Q

Paraneoplastic Syndromes:

  • ↑ Erythropoietin
  • pheochromocytoma
  • renal cell carcinoma
  • HCC
  • hemangioblastoma
  • leiomyoma
A

Polycythemia

Paraneoplastic Rise to High Hematocrit Levels:

  • Pheochromocytoma
  • Renal Cell Carcinoma
  • HCC
  • Hemangioblastoma
  • Leiomyoma
164
Q

Paraneoplastic Syndromes:

  • anemia with low reticulocytes
  • thymoma
A

Pure Red Cell Aplasia

165
Q

Paraneoplastic Syndromes:

  • hypogammaglobulinemia
  • thymoma
A

Good Syndrome

166
Q

Paraneoplastic Syndromes:

  • migratory superficial thrombophlebitis
  • adenocarcinomas—especially pancreatic
A

Trousseau Syndrome

167
Q

Paraneoplastic Syndromes:

  • deposition of sterile platelet thrombi on heart valves
  • adenocarcinomas—especially pancreatic
A

Nonbacterial Thrombotic (Marantic) Endocarditis

168
Q

Paraneoplastic Syndromes:

Neuromuscular

A
  • Anti-NMDA Receptor Encephalitis
  • Opsoclonus Myoclonus Ataxia Syndrome
  • Paraneoplastic Cerebellar Degeneration
  • Paraneoplastic Encephalomyelitis
  • Lambert-Eaton Myasthenic Syndrome
  • Myasthenia Gravis
169
Q

Paraneoplastic Syndromes:

  • psychiatric disturbance
  • memory deficits
  • seizures
  • dyskinesias
  • autonomic instability
  • language dysfunction
  • ovarian teratoma
A

Anti-NMDA Receptor Encephalitis

170
Q

Paraneoplastic Syndromes:

  • “dancing eyes, dancing feet”
  • neuroblastoma (children)
  • small cell lung cancer (adults)
A

Opsoclonus Myoclonus Ataxia Syndrome

171
Q

Paraneoplastic Syndromes:

  • antibodies against antigens in Purkinje cells
  • small cell lung cancer (anti-Hu)
  • gynecologic and breast cancers (anti-Yo)
  • Hodgkin lymphoma (anti-Tr)
A

Paraneoplastic Cerebellar Degeneration

172
Q

Paraneoplastic Syndromes:

  • antibodies against Hu antigens in neurons
  • small cell lung cancer
A

Paraneoplastic Encephalomyelitis

173
Q

Paraneoplastic Syndromes:

  • antibodies against presynaptic (P/Q-type) Ca2+ channels at NMJ
  • small cell lung cancer
A

Lambert-Eaton Myasthenic Syndrome

174
Q

Paraneoplastic Syndromes:

  • antibodies against postsynaptic ACh receptors at NMJ
  • thymoma
A

Myasthenia Gravis

175
Q

Gain of function mutation converts proto-oncogene (normal gene) to _____ → ↑ cancer risk. Need damage to only one allele of a proto-oncogene.

176
Q

Oncogenes:

  • receptor tyrosine kinase
  • lung adenocarcinoma
A

ALK

(Adenocarcinoma of the Lung Kinase)

177
Q

Oncogenes:

  • tyrosine kinase
  • CML
  • ALL
178
Q

Oncogenes:

  • antiapoptotic molecule (inhibits apoptosis)
  • follicular and diffuse large B cell lymphomas
179
Q

Oncogenes:

  • serine/threonine kinase
  • melanoma
  • non-Hodgkin lymphoma
  • papillary thyroid carcinoma
180
Q

Oncogenes:

  • cytokine receptor
  • gastrointestinal stromal tumor (GIST)
181
Q

Oncogenes:

  • transcription factor
  • Burkitt lymphoma
182
Q

Oncogenes:

  • receptor tyrosine kinase
  • breast and gastric carcinomas
A

HER2/neu (c-erbB2)

183
Q

Oncogenes:

  • tyrosine kinase
  • chronic myeloproliferative disorders
184
Q

Oncogenes:

  • GTPase
  • colon cancer
  • lung cancer
  • pancreatic cancer
185
Q

Oncogenes:

  • transcription factor
  • lung tumor
186
Q

Oncogenes:

  • transcription factor
  • neuroblastoma
A

N-myc (MYCN)

187
Q

Oncogenes:

  • receptor tyrosine kinase
  • MEN 2A and 2B
  • papillary thyroid carcinoma
188
Q

Loss of function of _____ → ↑ cancer risk; both (two) alleles must be lost for expression of disease.

A

Tumor Suppressor Genes

189
Q

Tumor Suppressor Genes:

  • negative regulator of β-catenin/WNT pathway
  • colorectal cancer (associated with FAP)
190
Q

Tumor Suppressor Genes:

  • DNA repair protein
  • breast, ovarian, and pancreatic cancer
A

BRCA1/BRCA2

191
Q

Tumor Suppressor Genes:

  • p16, blocks G1 → S phase
  • melanoma
  • pancreatic cancer
192
Q

Tumor Suppressor Genes:

colon cancer

A

DCC

Deleted in Colon Cancer

193
Q

Tumor Suppressor Genes:

pancreatic cancer

A

SMAD4 (DPC4)

Deleted in Pancreatic Cancer

194
Q

Tumor Suppressor Genes:

  • menin
  • Multiple Endocrine Neoplasia 1
195
Q

Tumor Suppressor Genes:

  • neurofibromin (Ras GTPase activating protein)
  • Neurofibromatosis type 1
196
Q

Tumor Suppressor Genes:

  • merlin (schwannomin) protein
  • Neurofibromatosis type 2
197
Q

Tumor Suppressor Genes:

  • negatively regulates PI3k/AKT pathway
  • breast, prostate, and endometrial cancer
198
Q

Tumor Suppressor Genes:

  • inhibits E2F
  • blocks G1 → S phase
  • retinoblastoma
  • osteosarcoma
199
Q

Tumor Suppressor Genes:

  • p53, activates p21, blocks G1 → S phase
  • most human cancers
  • Li-Fraumeni syndrome—multiple malignancies at early age, aka, SBLA cancer syndrome: Sarcoma, Breast, Leukemia, Adrenal gland
200
Q

Tumor Suppressor Genes:

  • hamartin protein
  • tuberous sclerosis
201
Q

Tumor Suppressor Genes:

  • tuberin protein
  • tuberous sclerosis
202
Q

Tumor Suppressor Genes:

  • inhibits hypoxia inducible factor 1a
  • von Hippel-Lindau disease
203
Q

Tumor Suppressor Genes:

  • transcription factor that regulates urogenital development
  • Wilms tumor (nephroblastoma)
204
Q

Oncogenic Microbes:

  • Burkitt lymphoma
  • Hodgkin lymphoma
  • nasopharyngeal carcinoma
  • 1° CNS lymphoma (in immunocompromised patients)
205
Q

Oncogenic Microbes:

hepatocellular carcinoma

206
Q

Oncogenic Microbes:

Kaposi sarcoma

207
Q

Oncogenic Microbes:

  • cervical and penile/anal carcinoma (types 16, 18)
  • head and neck cancer
208
Q

Oncogenic Microbes:

  • gastric adenocarcinoma
  • MALT lymphoma
209
Q

Oncogenic Microbes:

adult T-cell leukemia/lymphoma

210
Q

Oncogenic Microbes:

cholangiocarcinoma

A

Liver Fluke (Clonorchis sinensis)

211
Q

Oncogenic Microbes:

bladder cancer (squamous cell)

A

Schistosoma haematobium

212
Q

Carcinogens:

  • stored grains and nuts
  • hepatocellular carcinoma
A

Aflatoxins (Aspergillus)

213
Q

Carcinogens:

  • oncologic chemotherapy
  • leukemia
  • lymphoma
A

Alkylating Agents

214
Q

Carcinogens:

  • textile industry (dyes)
  • cigarette smoke (2-naphthylamine)
  • bladder—transitional cell carcinoma
A

Aromatic Amines

  • Benzidine
  • 2-Naphthylamine
215
Q

Carcinogens:

  • herbicides (vineyard workers)
  • metal smelting
  • liver—angiosarcoma
  • lung—lung cancer
  • skin—squamous cell carcinoma
216
Q

Carcinogens:

  • old roofing material
  • shipyard workers
  • lung—bronchogenic carcinoma > mesothelioma
217
Q

Carcinogens:

  • bladder—transitional cell carcinoma
  • cervix—squamous cell carcinoma
  • esophagus—squamous cell carcinoma/adenocarcinoma
  • kidney—renal cell carcinoma
  • larynx—squamous cell carcinoma
  • lung—squamous cell and small cellcarcinoma
  • pancreas—pancreatic adenocarcinoma
A

Cigarette Smoke

218
Q

Carcinogens:

  • esophagus—squamous cell carcinoma
  • liver—hepatocellular carcinoma
219
Q

Carcinogens:

papillary thyroid carcinoma

A

Ionizing Radiation

220
Q

Carcinogens:

  • smoked foods
  • gastric cancer
A

Nitrosamines

221
Q

Carcinogens:

  • by-product of uranium decay
  • accumulates in basements
  • lung cancer (2nd leading cause after cigarette smoke)
222
Q

Carcinogens:

  • used to make PVC pipes (plumbers)
  • liver—angiosarcoma
A

Vinyl Chloride

223
Q

_____ are laminated, concentric spherules with dystrophic calcification.

A

Psammoma Bodies

224
Q

Psammoma Bodies are seen in _____.

A

PSaMMoma Bodies:

  • Papillary Carcinoma of the Thyroid
  • Serous Papillary Cystadenocarcinoma of the Ovary
  • Meningioma
  • Malignant Mesothelioma
225
Q

Serum Tumor Markers:

  • metastases to bone or liver
  • Paget disease of bone
  • seminoma (placental)
  • exclude hepatic origin by checking LFTs and GGT levels
A

Alkaline Phosphatase

226
Q

Serum Tumor Markers:

  • hepatocellular carcinoma
  • endodermal sinus (yolk sac) tumor
  • mixed germ cell tumor
  • ataxia-telangiectasia
  • neural tube defects
  • normally made by fetus
  • transiently elevated in pregnancy
  • high levels associated with neural tube and abdominal wall defects
  • low levels associated with Down syndrome
A

α-Ftoprotein

HE-MAN is the alpha male!

  • Hepatocellular Carcinoma
  • Endodermal Sinus (Yolk Sac) Tumor
  • Mixed Germ Cell Tumor
  • Ataxia-Telangiectasia
  • Neural Tube Defects
227
Q

Serum Tumor Markers:

  • hydatidiform moles
  • choriocarcinomas
  • gestational trophoblastic disease
  • testicular cancer
  • mixed germ cell tumor
  • produced by syncytiotrophoblasts of the placenta
A

β-hCG

HCG:

  • Hydatidiform Moles
  • Choriocarcinomas
  • Gestational Trophoblastic Disease
228
Q

Serum Tumor Markers:

breast cancer

A

CA 15-3/CA 27-29

229
Q

Serum Tumor Markers:

pancreatic adenocarcinoma

230
Q

Serum Tumor Markers:

ovarian cancer

231
Q

Serum Tumor Markers:

  • medullary thyroid carcinoma
  • MEN2A
  • MEN2B
A

Calcitonin

232
Q

Serum Tumor Markers:

  • Major Associations:
    • colorectal cancer
    • pancreatic cancer
  • Minor Associations:
    • gastric carcinoma
    • breast carcinoma
    • medullary thyroid carcinoma
  • carcinoembryonic antigen
  • very nonspecific
A

CEA

CarcinoEmbryonic Antigen

233
Q

Serum Tumor Markers:

neuroendocrine tumors

A

Chromogranin

234
Q

Serum Tumor Markers:

  • testicular germ cell tumors
  • ovarian dysgerminoma
  • can be used as an indicator of tumor burden
235
Q

Serum Tumor Markers:

  • prostate cancer.
  • can also be elevated in BPH and prostatitis
  • questionable risk/benefit for screening
  • surveillance marker for recurrent disease after prostatectomy
A

PSA

Prostate-Specific antigen

236
Q

_____ determine primary site of origin for metastatic tumors and characterize tumors that are difficult to classify. Can have prognostic and predictive value

A

Immunohistochemical Stains

237
Q

Immunohistochemical Stains:

  • mesenchymal tissue (eg. fibroblasts, endothelial cells, macrophages)
  • Mesenchymal tumors (eg. sarcoma)
  • many other tumors (eg. endometrial carcinoma, renal cell carcinoma, meningioma)
238
Q

Immunohistochemical Stains:

  • neural crest cells
  • melanoma
  • schwannoma
  • Langerhans cell histiocytosis
239
Q

Immunohistochemical Stains:

muscle tumors (eg. rhabdomyosarcoma)

240
Q

Immunohistochemical Stains:

epithelial tumors (eg. squamous cell carcinoma)

A

Cytokeratin

241
Q

Immunohistochemical Stains:

  • neuroglia (eg. astrocytes, Schwann cells, oligodendrocytes)
  • astrocytoma
  • glioblastoma
242
Q

Immunohistochemical Stains:

neuronal tumors (eg. neuroblastoma)

A

Neurofilament

243
Q

Immunohistochemical Stains:

  • prostatic epithelium
  • prostate cancer
244
Q

Immunohistochemical Stains:

hairy cell leukemia

A

TRAP

Tartrate-Resistant Acid Phosphatase

245
Q

Immunohistochemical Stains:

  • neuroendocrine cells
  • small cell carcinoma of the lung
  • carcinoid tumor
A
  • Chromogranin
  • Synaptophysin
246
Q

_____ is also known as multidrug resistance protein 1 (MDR1). Classically seen in adrenocortical carcinoma but also expressed by other cancer cells (eg. colon, liver). Used to pump out toxins, including chemotherapeutic agents (one mechanism of ↓ responsiveness or resistance to chemotherapy over time).

A

P-glycoprotein

247
Q

_____ is weight loss, muscle atrophy, and fatigue that occur in chronic disease (eg. cancer, AIDS, heart failure, COPD). Mediated by TNF, IFN-γ, IL-1, and IL-6.

248
Q

_____ is the most common cancer.

A

Skin Cancer

basal > squamous >> melanoma

249
Q

Cancer Incidence in Men

A
  1. Prostate
  2. Lung
  3. Colon/Rectum
250
Q

Cancer Incidence in Women

A
  1. Breast
  2. Lung
  3. Colon/Rectum
251
Q

Cancer Incidence in Children (0-14 yrs.)

A
  1. Leukemia
  2. CNS
  3. Neuroblastoma
252
Q

Cancer Mortality in Men

A
  1. Lung
  2. Prostate
  3. Colon/Rectum
253
Q

Cancer Mortality in Women

A
  1. Lung
  2. Breast
  3. Colon/Rectum
254
Q

Cancer Mortality in Children (0-14 yrs.)

A
  1. Leukemia
  2. CNS
  3. Neuroblastoma
255
Q

_____ is the 2nd leading cause of death in the United States (heart disease is 1st).

256
Q

Most sarcomas spread _____.

A

hematogenously

257
Q

Most carcinomas spread via _____.

A

lymphatics

258
Q

Hematogenously Spreading Carcinomas

A

Four Carcinomas Route Hematogenously:

  • Follicular Thyroid Carcinoma
  • Choriocarcinoma
  • Renal Cell Carcinoma
  • Hepatocellular Carcinoma
259
Q

Common Metastases:

  • lung > breast > melanoma, colon, kidney
  • 50% of _____ tumors are from metastases
  • commonly seen as multiple well-circumscribed tumors at gray/white matter junction
260
Q

Common Metastases:

  • colon >> stomach > pancreas
  • _____ and lung are the most common sites of metastasis after the regional lymph nodes
261
Q

Common Metastases:

  • prostate, breast > kidney, thyroid, lung
  • _____ metastasis >> 1° _____ tumors (eg. multiple myeloma, lytic)
  • Common Mets:
    • breast (mixed)
    • lung (lytic)
    • thyroid (lytic)
    • kidney (lytic)
    • prostate (blastic)
  • predilection for axial skeleton
A

Bone

Lead (PB) KeTtLe

Prostate, Breast > Kidney, Thyroid, Lung

USMLE Step 1 (18 decks)

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