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STEP 1 > 01a: Pathology > Flashcards

01a: Pathology Flashcards

1
Q

Mutations in Fas, leading to impaired (intrinsic/extrinsic) apoptosis pathway, results in:

A

Extrinsic;

Increased number of self-reacting lymphocytes (Fas-FasL interaction necessary in thymic medullary negative selection)

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2
Q

Which proteins are pro-apoptotic in intrinsic pathway? And which are anti-apoptotic?

A

Pro: BAX, BAK
Anti: Bcl-2, Bcl-x

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3
Q

Immune cells can play role in extrinsic pathway apoptosis by which actions?

A

T-Lymphocyte release of perforin and granzyme B (one extrinsic pathway for apoptosis)

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4
Q

Key difference between necrosis and apoptosis is presence/absence of:

A

Inflammation (present in necrosis; intracellular components leak)

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5
Q

In (X) necrosis, cell outlines are preserved, but nuclei disappear and there is high cytoplasmic binding of (Y) dyes.

A 
X = coagulative
Y = eosin
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6
Q

Acute pancreatitis: what type of necrosis?

A

Fat (enzymatic; saponification aka damaged cells release lipase and liberated FAs bind Ca)

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7
Q

Breast tissue trauma: what type of necrosis?

A

Fat (non-enzymatic/traumatic)

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8
Q

Fibrinoid necrosis: mechanism of action

A

Fibrin combines with immune complexes (Type III HS) and damage vessel walls

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9
Q

Cell injury: ribosomes detach from ER, indicating a (reversible/irreversible) injury.

A

Reversible

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10
Q

Cell injury: lysosomes rupture, indicating a (reversible/irreversible) injury.

A

Irreversible (autolysis)

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11
Q

Cell injury: mitochondrial vacuolization, a (reversible/irreversible) injury.

A

Irreversible (increased permeability)

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12
Q

Mechanism behind cell and mitochondrial swelling in (reversible/irreversible) cell injury.

A

Reversible; low ATP means low activity of Na/K and Ca pumps

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13
Q

Which signs in nucleus would lead you to believe cell injury is reversible?

A

Chromatin clumping; overall intact nucleus

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14
Q

Which signs in nucleus would lead you to believe cell injury is irreversible?

A

Pyknosis (condensation), karyorrhexis (fragmentation), karyolysis (fading) of chromatin

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15
Q

Brain regions most vulnerable to hypoxia/ischemia:

A

Watershed areas (ACA/MCA/PCA boundaries)

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16
Q

Brain cells most vulnerable to hypoxia/ischemia:

A
  1. Purkinje cells of cerebellum

2. Pyramidal cells of hippocampus and neocortex

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17
Q

Kidney regions most vulnerable to hypoxia/ischemia:

A

Medulla:

  1. Proximal tubule (straight segment)
  2. Thick ascending limb
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18
Q

Zone (1/2/3) of liver is most vulnerable to hypoxia/ischemia.

A

3 (area around central v)

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19
Q

Colon regions most vulnerable to hypoxia/ischemia:

A

Splenic flexure and rectum (watershed areas/border zones)

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20
Q

Red, aka (X), infarct occurs in which tissues?

A

X = hemorrhagic

Those with multiple blood supplies (liver, lung intestine, testes)

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21
Q

Reperfusion injury is an example of (X) infarct. What’s the mechanism behind this?

A

X = Red/hemorrhagic (REperfusion, REd)

Free radical damage (LIPID PEROXIDATION; irreversible mito injury, inflammation, complement activation)

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22
Q

Pale, aka (X), infarct occurs in which tissues?

A

X = anemic

Solid organs with single (end-arterial) blood supply (heart, kidney, spleen)

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23
Q

Key immune cell participants in acute inflammation:

A
  1. PMNs
  2. Eosinophils
  3. Mast cells
  4. Basophils

Also (pre-existing) Abs

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24
Q

Key immune cell participants in chronic inflammation:

A
  1. Mononuclear cells (monocytes/macrophages, lymphocytes, plasma cells)
  2. Fibroblasts (blood vessel proliferation, fibrosis)
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25
Q

Aortic stenosis is an example of (dystrophic/metastatic) (X) deposition, which tends to occur in (normal/abnormal) tissues and is secondary to (Y).

A

Dystrophic
X = Ca
Abnormal
Y = injury/necrosis

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26
Q

Metastatic calcification tends to occur in (normal/abnormal) tissues, predominantly in (X). Why?

A

Normal
X = kidney interstitium, lung and gastric mucosa
These tissues lose acid quickly (high pH favors Ca deposition)

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27
Q

Patient with metastatic calcification of collecting ducts may develop:

A

Nephrogenic DI and renal failure

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28
Q

Metastatic calcification of tissues usually occurs secondary to:

A
  1. Hypercalcemia (hyper-PTH, sarcoid)

2. High Ca-PO4 product levels (long-term dialysis, multiple myeloma, calciphylaxis)

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29
Q

Extravasation of leukocytes occurs predominantly at which part of vessel?

A

Post-cap venules

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30
Q

Deficiency of Sialyl-Lewis-X epitope results in defective:

A

Leukocyte margination/rolling (aka leukocyte adhesion deficiency type 2)

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31
Q

E and P selectins play important role in (margination/tight adhesion) of leukocytes. What is responsible for releasing/upregulating these selectins?

A

Margination/rolling
E: upregulated by TNF and IL1
P: released from weibel-palade bodies

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32
Q

ICAM and VCAM play important role in (margination/tight adhesion) of leukocytes. They interact with (X).

A

Tight adhesion;

X = integrins (CD11/18; VLA-4)

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33
Q

Leukocyte adhesion deficiency type 1 is a result of decreased:

A

CD18 integrin subunit (interacts with ICAM)

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34
Q

(X) molecule responsible for diapedesis of WBCs.

A

X = PECAM-1

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35
Q

Key chemotactic products released to help guide leukocytes through interstitium.

A

C5a, IL-8, LTB4, Kallikrein, platelet-activating factor

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36
Q

Which vitamins serve as antioxidants?

A

ACE

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37
Q

Neonate with respiratory distress syndrome improves on treatment but then develops symptoms of rapid/labored breathing, wheezing, and perioral cyanosis. What likely happened?

A

Bronchopulmonary dysplasia (free radical injury due to prolonged mechanical ventilation)

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38
Q

Scar formation: (X)% of tensile strength regained at 3 months. Which ECM component required to increase this strength?

A

X = 70-80

Collagen

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39
Q

T/F: Keloids are painful and pruritic.

A

True

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40
Q

Radiation for cancer treatment uses (UV/gamma) rays and works by which mechanisms?

A

Gamma and X-rays (ionizing radiation)

  1. DNA double-strand breakage
  2. Free radical formation (ionization of H2O and DNA/cell damage)
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41
Q

List the tissue mediators that stimulate angiogenesis in wound healing. What other functions do they have?

A
  1. FGF and VEGF (“fruits and veggies”); no other roles

2. TGFb; fibrosis

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42
Q

PDGF is secreted by which cells?

A

Macrophages and platelets

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43
Q

PDGF roles in wound healing:

A
  1. Vascular remodeling
  2. Smooth muscle cell migration
  3. Fibroblast growth (for collagen synthesis)
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44
Q

List the 3 phases of wound healing and the primary cells involved in each.

A
  1. Inflammatory (platelets, PMNs, macros)
  2. Proliferative (fibroblast, myofibroblast, endothelial cells, keratinocytes, macros)
  3. Remodeling (fibroblasts)
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45
Q

Which stage of wound healing is delayed in both vit C and (X) deficiency?

A

X = Cu

Proliferative (deposition of type III collagen)

46
Q

Remodeling stage of wound healing is delayed in (X) deficiency. What key event takes place in this stage?

A

X = Zn

Replacement of Type III Collagen by Type I (increasing tensile strength)

47
Q

Pt with hx of severe burns on bilateral hands presents with inability to extend wrists due to significant scarring. This phenomenon is referred to as (X) and occurs in which stage of wound healing?

A

X = contracture (mediated by myofibroblasts)

Proliferative stage

48
Q

List some auto-inflammatory vasculitides associated with granuloma formation

A
  1. Granulomatosis with polyangiitis (Wegener’s)
  2. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  3. Giant cell (temporal) arteritis
  4. Takayasu arteritis
49
Q

How does the body handle retained foreign bodies (ex: sutures) or other foreign material (berylliosis, talcosis)?

A

Granuloma formation

50
Q

Granuloma cell layers, from inside to outside.

A
  1. Epithelioid macrophages

2. Lymphocytes and Multinucleated giant cells

51
Q

Granuloma: (X) lymphocytes play key role by secreting (Y).

A 
X = TH1
Y = IFN-gamma (activates macrophages)
52
Q

Reason behind testing for (X) before anti-TNF drug is administered.

A

X = TB

TNFa (secreted by macros) induces/maintains granuloma formation so anti-TNF drugs can break down granuloma (disseminated disease)

53
Q

AA female with dyspnea, cough, lymphadenopathy has hypercalcemia due to:

A

Sarcoidosis (granulomas have overactive 1-alpha hydroxylase, so high calcitriol production)

54
Q

(Transudate/exudate) is high in protein and (high/low) in LDH.

A

Exudate (cellular fluid; cloudy)

High

55
Q

Fluid buildup in HF is (transudate/exudate). In lymphatic obstruction is (transudate/exudate). In nephrotic syndrome is (transudate/exudate).

A

Transudate (high hydrostatic P)
Exudate
Transudate (low oncotic P)

56
Q

Fluid buildup in malignancy is (transudate/exudate) and in inflammation/infection is (transudate/exudate).

A

Exudate for both

57
Q

Why does polycythemia vera present with (high/low) ESR?

A

Low;

High number of RBCs “dilute” the inflammation products (fibrinogen) which serve as aggregation factors

58
Q

T/F: Amyloidosis is the abnormal aggregation of proteins into disorganized, clumpy deposits in various tissues.

A

False - aggregate into linear beta-pleated sheets (insoluble fibrils)

59
Q

AL amyloidosis involves deposition of (X). AA involves deposition of (Y).

A 
X = Ig light chains (primary; multiple myeloma)
Y = Amyloid A (secondary; chronic inflammatory conditions like RA, IBD)
60
Q

Heritable form of amyloidosis due to (X) mutation

A

X = transthyretin

61
Q

Senile amyloidosis is due to (X) deposition, primarily in which tissue(s)?

A 
X = normal transthyretin
Cardiac ventricles (restrictive cardiomyopathy)
62
Q

List some examples of organ-specific amyloid deposition

A
  1. AD (most important; beta amyloid)
  2. Pancreatic islets (DM II; amylin)
  3. Thyroid medullary carcinoma
  4. Atrial amyloidosis (increased risk of Afib; ANP)
63
Q

Lipofuscin is seen in (X) condition and is formed from:

A 
X = normal aging
Lipid oxidization (yellow/brown, wear and tear pigment)
64
Q

T/F: Normal aging involves increase in heart chamber sizes.

A

False - decrease LV chamber (septum acquires sigmoid shape) and myocardial atrophy

65
Q

Define “anaplasia” and “neoplasia”

A

A: Complete lack of differentiation of cells in malignant neoplasm
N: Uncontrolled, clonal proliferation (benign or malignant)

66
Q

Multi-nucleated giant cells in tumor are marker for (metaplasia/dysplasia/anaplasia/neoplasia).

A

Anaplasia

67
Q

T/F: Invasive carcinoma involves over-expression of E-cadherin to allow neoplastic cell adhesion and invasion of BM.

A

False - increase expression of laminin for this purpose; inactivate E-cadherin to decrease cell-cell contact

68
Q

In most cases, tumor (stage/grade) holds more prognostic value.

A

Grade (degree of differentiation/mitotic activity);

TNM staging more important for some cancers (ex: colon)

69
Q

T/F: Lymphoma is benign, leukemia is malignant.

A

False - both malignant

70
Q

Malignant version of hemangioma:

A

Angiosarcoma

71
Q

Three most common cancers in children, in order of incidence

A
  1. Leukemia
  2. Brain/CNS
  3. Neuroblastoma

Same order for cancer mortality

72
Q

Sign of Leser-Trelat:

A

Sudden outbreak of multiple seborrheic keratoses (indication of GI/visceral malignancy)

73
Q

(X) carcinomas present with hypo-PTH hypercalcemia via which mechanism?

A 
X = squamous cell (lung, H/N, and others)
PTHrP secretion (increase bone resorption and decrease renal excretion of Ca)
74
Q

Endocrine-related paraneoplastic syndromes associated with small cell lung cancer:

A
  1. SIADH

2. Cushing’s (high ACTH)

75
Q

Pure red cell aplasia is neoplastic syndrome associated with (X). What are the Sx and what’s the mechanism?

A

X = thymoma
Anemia with low retic count but normal WBC, platelets (absence only of erythroid precursors in bone marrow)

MOA: inhibition of precursors by IgG auto-Ab or cytotoxic T-cells

76
Q

Presence/simultaneous onset of anterior mediastinal mass and recurrent sinopulmonary infections in an adult is likely due to:

A

Thymoma with Good (paraneoplastic) Syndrome (hypogammaglobulinemia and immunodeficiency)

77
Q

(X) syndrome: migratory superficial thrombophlebitis, an early sign of (Y) cancer.

A 
X = Trousseau
Y = Adenocarcinoma (esp pancreatic) that produce thromboplastin-like substance
78
Q

Myasthenia gravis can be a paraneoplastic syndrome in which cancer(s)?

A

Thymoma

79
Q

“Dancing eyes, dancing feet” in child indicates which underlying malignancy? And in adults?

A

Paraneoplastic syndrome (opsoclonus-myoclonus ataxia)

C: neuroblastoma
A: small cell lung cancer

80
Q

65 yo patient with lung cancer develops dizziness, limb/trunk ataxia, visual disturbances. Which paraneoplastic syndrome? And which lung cancer?

A

Paraneoplastic cerebellar degeneration (Ab against purkinje cells)

Small cell

81
Q

65 yo lifetime smoker with SOB/cough, weight loss. Difficulty rising from chair, dysphagia, and dry mouth.

A

Small cell lung cancer with Lambert Eaton myasthenic syndrome (Ab against pre-synaptic Ca channel, decrease ACh release)

82
Q

JAK2 is (oncogene/tumor suppressor) with (X) gene product. Implicated in which cancers?

A

Oncogene
X = non-R (cytoplasmic) tyrosine kinase
Chronic myeloproliferative disorders (ET, PCV, 1o myelofibrosis)

83
Q

APC is (oncogene/tumor suppressor) with (X) gene product. Implicated in which cancers?

A

Tumor suppressor
X = negative regulator of beta-catenin/WNT path

Colorectal (associated with FAP)

84
Q

BRCA1/2 are (oncogenes/tumor suppressors) with (X) gene product. Implicated in which cancers?

A

Tumor suppressors
X = DNA ds break repair proteins

Breast, ovarian, pancreatic

85
Q

MEN1, associated with (X) gene mutation:

A

X = MEN1 (tumor suppressor)

  1. Pancreatic endocrine tumors (ZES, insulinoma, VIPomas, glucagonoma)
  2. Pituitary adenoma (prolactin, GH)
  3. Parathyroid adenoma
86
Q

NF1 on chromosome (X) and NF2 on chromosome (Y).

A 
X = 17
Y = 22
87
Q

Rb is (oncogene/tumor suppressor) that inhibits (X), unless modified via (Y).

A

Tumor suppressor
X = E2F (thus inhibits G1 to S transition)
Y = phosphorylation

88
Q

Multiple malignancies at early age associated with (X) syndrome, (Y) mutation, and thus impaired (Z).

A 
X = Li Fraumeni (SBLA cancer: Sarcoma, Breast, Leukemia, Adrenal)
Y = TP53 (p53)
Z = apoptosis
89
Q

MEN2A, associated with (X) gene mutation:

A

X = RET (oncogene)

  1. Pheochromocytoma
  2. Parathyroid hyperplasia
  3. Medullary thyroid cancer
90
Q

MEN2B, associated with (X) gene mutation:

A

X = RET (oncogene)

  1. Pheochromocytoma
  2. Medullary thyroid cancer
  3. Mucosal neuromas
91
Q

HTLV-1 microbe associated with which cancer?

A

Adult T cell leukemia/lymphoma

92
Q

Clonorchis sinensis (liver fluke) associated with which cancer?

A

Cholangiocarcinoma

93
Q

Schistosomiasis associated with which cancer?

A

Squamous cell bladder

94
Q

How does one’s genetic profile determine his/her susceptibility to chemical carcinogens?

A

Most enter body as pro-carcinogens and are activated by CYP450 (microsomal monooxygenase), and activity of these enzymes is genetically determined

95
Q

Aromatic amines are carcinogens that predispose to which type of cancer? And nitrosamines?

A

Aromatic: Transitional cell carcinoma (bladder)

Nitros (smoked food): gastric

96
Q

Asbestos associated with (X) cancer.

A

X = bronchogenic carcinoma (way more than, but as well as, mesothelioma)

97
Q

Cigarette smoke increases risk for which cancers?

A
  1. Larynx (squamous)
  2. Esophagus (squamous, adeno)
  3. Lung (squamous, SCLC)
  4. Kidney (RCC)
  5. Pancreas (adeno)
  6. Bladder (transitional cell)
  7. Cervix (carcinoma)
98
Q

Ethanol increases risk for which cancers?

A
  1. Esophagus (squamous)

2. Liver

99
Q

Ionizing radiation increases risk for which cancers?

A

Thyroid (papillary thyroid carcinoma)

100
Q

Second leading cause of lung cancer after cigarette smoke.

A

Radon exposure

101
Q

Both arsenic and vinyl chloride exposure increase risk for which cancer?

A

Angiosarcoma of liver

102
Q

Psammoma bodies are seen in which cancers?

A

PSaMMoma

  1. Papillary thyroid carcinoma
  2. Serous papillary cystadenoma of ovary
  3. Mesothelioma
  4. Meningioma
103
Q

MDR1 (multidrug resistance protein 1), aka (X), is seen in (Y) cells and functions to:

A 
X = P-glycoprotein
Y = cancer (classically in adrenocortical carcinoma)

ATP-dependent efflux pump (pumps out chemo agents; mechanism of resistance to drugs over time)

104
Q

Mechanism of cachexia in chronic disease:

A

TNFa (cachectin; acts on hypothalamus to suppress appetite and increase BMR)

Also IFN-gamma, IL1, IL6

105
Q

Most carcinomas spread via (blood/lymph) and most sarcomas spread via (blood/lymph). List the four key exceptions.

A

Lymph; blood

FCRH (Four Carcinomas Route Hematogenously):

  1. Follicular thyroid
  2. Choriocarcinoma
  3. RCC
  4. Hepatocellular
106
Q

If you were to bet on the origin of a liver met, what would you bet on?

A

Colon

107
Q

CA 15-3/CA27-29 tumor markers for:

A

Breast cancer

108
Q

CA 19-9 tumor marker for:

A

Pancreatic adenocarcinoma

109
Q

CA 125 tumor marker for:

A

Ovarian cancer

110
Q

CEA tumor marker for:

A

Colorectal and pancreatic cancers mainly (nonspecific); in colorectal, indicates worse prognosis or recurrence

111
Q

Chromogranin tumor marker for:

A

Neuroendocrine tumors

STEP 1 (21 decks)

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