USMLE STEP 1 Pathology Flashcards

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1
Q

Acute phase reactants

A

Increase in response to inflammation:

C-reactive protein (opsonin, facilitated phagocytosis)
Ferritin (sequesters iron)
Fibrinogen (coagulation factor, promotes endothelial repair)
Haptoglobin (binds extracell Hb, protects oxidative stress)
Hepcidin (decreases iron absorption and release **anemia of chronic disease)
Procalcitonin (only increases in bacterial infections)
Serum amyloid A
Negative (down regulated):
Albumin (conserve GAs for positive reactants)
Transferrin (internalized by macrophages to sequester Fe)
Transthyretin (pre-albumin)

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2
Q

Acute radiation syndrome

A

develops after sudden whole-body exposure to high doses of ionizing radiation; nausea, vomiting, diarrhea, hair loss, erythema, cytopenias (decrease in blood cells), headache, altered mental status

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3
Q

Acute vs chronic inflammatory mediators

A

Acute: early response neutrophils, macrophages predominate late stages of acute (2-3 days) and secrete cytokines

Chronic: mononuclear infiltration (macrophages, lymphocytes, plasma cells) —> tissue destruction and repair

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4
Q

Amyloidosis

A

abnormal aggregation of proteins into B-pleated linear sheets —> insoluble fibrils —> cellular damage and apoptosis

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5
Q

Atrophy

A

Decrease in tissue mass due to decrease in size and/or number of cells

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6
Q

Cancer incidence and mortality

A

MALES (I;M)
1. Prostate; Lung
2. Lung; prostate
3. Colon/rectum;colon/rectum

FEMALES (I;M)
1. Breast; lung
2. Lung; breast
3. Colon/rectum;colon/rectum

CHILDREN
1. Leukemia; leukemia
2. CNS;CNS
3. Neuroblastoma/ neuroblastoma

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7
Q

Carcinoma vs sarcoma

A

Carcinoma: implies endothelial origin

Sarcoma: mesenchymal origin (connective tissue, blood vessels, lymphatic tissues)

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8
Q

Common types of amyloidosis

A

Primary: AL (IgG light chains); seen in plasma cell disorders (ex. Multiple myeloma)

Secondary: serum amyloid A (AA); seen in chronic inflammatory conditions

Dialysis-related amyloidosis: B2-microglobulin; seen in end stage renal failure (ESRF) or on long term dialysis

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9
Q

Dysplasia

A

Disordered, precancerous epithelial cell growth; loss of uniformity of cell size and shape (pleomorphism), loss of tissue orientation, nuclear changes

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10
Q

ESR

A

Erythrocyte sedimentation rate: inflammation products coat RBCs —> decrease (-) charge —> increase RBC aggregation —> increase ESR

Increased ESR:
- Most anemias
- Infections
- Inflammation
- Cancer
- Renal disease
- Pregnancy

Decreased ESR:
- Sickle cell anemia
- Polycythemia (more RBCs dilute aggregation factors)
- HF
- Microcytosis
- Hypofibrinogenemia

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11
Q

Free radical injury

A

Damage cells via membrane lipid peroxidation, protein modification, DNA breakage

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12
Q

Granulomatous inflammation

A

A pattern of chronic inflammation; wall off a resistant stimulus without completely eradicating/degrading it —> persistent inflammation —> fibrosis, organ damage

Bacterial :Thanks buddy., leprosy, cat scratch disease
Fungus: endemic plasmosis
Parasitic: schistosomiasis
Immune: sarcoidosis, Crohn’s
Vasculitis

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13
Q

Hamartoma vs Chortistoma

A

Terms for non-neoplastic malformaions

Hamartoma: disorganized overgrowth of tissues in native location
Choristoma: normal tissue in a foreign location

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14
Q

Hypertrophy vs Hyperplasia

A

Hypertrophy: increase in cell size due to increase in structural proteins and organelles

Hyperplasia: increase in number of cells due to controlled proliferation of stem cells and differentiated cells; excessive stimulation leads to pathologic hyperplasia

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15
Q

Immune evasion of cancer

A
  • Decreased MHC I expression on tumor cells –> cytotoxic Ts unable to recognize
  • Secrete immunosuppressive factors (TGF-B) and recruit regulatory T cells to down regulate immune response
  • Up regulate immune checkpoint molecules to inhibit immune response
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16
Q

Metaplasia

A

reprogramming of stem cells leading to the replacement of one cell type by another that can adapt to a new stress

Usually due to an irritant (gastric acid —> Barrett esophagus, tobacco smoke —> ciliated columnar ep cells to stratified squamous epithelium)

17
Q

Necrosis

A

Exogenous injury –> plasma membrane damage —> cell undergoes enzymatic degradation and protein denaturation, intracellular components leak —> local inflammatory reaction

18
Q

Neoplasia

A

uncontrolled, monoclonal proliferation of cells; can be benign or malignant.
Two components: parenchyma (neoplastic cells) and supporting storm (blood vessels, connective tissue)

19
Q

Neoplastic progression

A
  1. Dysplasia: loss of uniformity in cell size and shape (pleomorphism), loss of orientation, nuclear changes
  2. Carcinoma in situ/preinvasive: irreversible dysplasia of entire thickness of epithelium
  3. Invasive carcinoma: invade basement membrane using collagenases and hydrolyses, cell-cell contacts lost by inactivation of E-cadhirin
  4. Metastasis: spread to distant organ(s) via lymphatics or blood
20
Q

Reversible vs irreversible cell damage

A

Reversible: decrease in ATP and activity —> cell swelling —> decreased protein synthesis

Irreversible: breakdown of plasma membrane —> enzymes leak —>activation of degradative enzymes —> nuclear degradation

21
Q

Scar formation

A

Excess TGF-B associated with aberrant scarring, such as hypertrophic and keloid scars

Hypertrophic scar: increased type III collagen in parallel; confined to borders of original wound

Keloid scar: types I and III collagen disorganized; extends beyond borders of original wound with “claw-like” projections (increased incidents in people with darker skin)

22
Q

Tumor grade vs stage

A

GRADE
Degree of cell differentiation (tissue of origin resemblance) and mitotic activity on histology; higher grade often correlates with higher aggressiveness

STAGE
Degree of invasion and spread from initial site
TMN —> M > N > T —> primary Tutor size/invasion, regional lymph Node metastasis, distant Metastasis
Stage usually more prognostic value than grade (Stage determines Survival)

23
Q

Warburg Effect

A

Shift of glucose metabolism away from mitochondrial oxidative phosphorylation toward glycolysis

24
Q

Which cells are most susceptible to radiation therapy

A

Stem cells of rapidly regenerating tissues:
Skin, bone marrow, GI tract, gonads
are the most susceptible to radiation injury