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Step1 > Pathology > Flashcards

Pathology Flashcards

1
Q

Increase in size of cells

A

hypertrophy

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2
Q

Increase in number of cells

A

hyperplasia

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3
Q

decrease in tissue mass due to decrease in size

A

atrophy

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4
Q

reprogramming of stem cells which results in replacement of one cell type by another that can adapt to a new stress

A

Metaplasia

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5
Q

Disordered precancerous epithelial growth

A

Dysplasia

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6
Q

Apoptosis

A

ATP dependent programmed cell death with intrinsic and extrinsic pathways which activate caspases (cytosolic proteases) that cause cellular breakdown –> phagocytosed

deeply eosinophilic cytoplasm and basophilic nucleus. pyknosis or nuclear shrinkage, and karyorrhexis or fragmentation caused by endonuclease mediated cleavage

cell membrane intact without significant inflammation unlike necrosis

DNA laddering is a sensitive indicator of apoptosis

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7
Q

Intrinsic pathway of apoptosis

A

mitochondrial pathway

involved in tissue remodeling in embryogenesis and after exposure to injurious stimuli. occurs when a regulating factor is withdrawn from a proliferating cell population.

The intrinsic pathway is regulated by the Bcl-2 family of proteins. BAX and BAK (proapoptotic) form pores in the mitochondrial membrane which cause release of cytochrome C from inner mitochondrial membrane into the cytoplasm which activates caspases. Bcl-2 keeps the mitochondrial membrane impermeable and thereby preventing cytochrome C release

Bcl-2 ( antiapoptotic) can decrease caspase activation and cause tumorigenesis

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8
Q

Extrinsic pathway

A

Death receptor pathway

two pathways:

1) ligand receptor interactions
- Fas-FasL interaction (important for thymic medullary negative selection) or TNF alpha binding its receptor
- defect in Fas-FasL will incrase numbers of circulating self-reacting lymphocytes due to failure of clonal deletion and thus autoimmune lymphoproliferative syndrome

2) immune cell (cytotoxic T cell release of perforin and granzymes B)

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9
Q

Coagulative necrosis

A
  • due to ischemia or infarction; injury denatures enzymes and proteolysis blocked
    histology: preserved cellular architecure (cell outlines seen), but nuclei disappear. Increased cytoplasmic binding of eosin stain. The increase in eosinophilia gives it a red/pink color
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10
Q

liquefactive necrosis

A

-due to neutrophils release lysosomal enzymes that digest the tissue

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11
Q

caseous necrosis

A

-In TB or fungi. Due to lymphocytes and macrophages walling off the infecting microorganism –> cellular debris. Forming a granuloma

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12
Q

fat necrosis

A

-In acute pancreatitis or trauma. Damaged cells release lipase which breaks down TGs. Liberated FA bind calcium and saponify (appears blue on H&E stain)

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13
Q

Fibrinoid necrosis

A

Due to immune complexes that combine with fibrin –> vessel wall damage (type 3 hypersensitivity rxn).

on histology the vessel walls appear thick and pink

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14
Q

gangrenous necrosis

A

Dry: ischemia. Coagulative on histology
Wet: superinfection. liquefacive superimposed on coagulative (histology)

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15
Q

Watershed areas

A

i.e. splenic flexure

Watershed areas are borderzones that receive blood supply from most distal branched of 2 arteries with limited collateral vascualrity. These areas are susceptible to ischemia fromhypoperfusion

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16
Q

Red infarct

A

Hemorrhagic

occurs in venous occlusions and tissues with multiple blood supplies

reperfusion injury that is due to damage by free radicals

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17
Q

Pale infarct

A

Anemic

occurs in solid organs with a single (end-arterial) blood supply

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18
Q

Inflammation

A

Response to eliminate initial cause of cell injury, to remove necrotic cells resulting from original insult, and to initiate tissue repair

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19
Q

Cardinal signs of inflammation

A
  • Rubor/Redness and Calor/Warmth due to histamine, prostaglandins, and bradykinin
  • Tumor/swelling due to endothelial contraction/disruption (leukotrienes C4,D4, E4 and histamine and serotonin). Increase in vascular permeability causes leakage of protein-rich from postcapillary venules into interstitital space (exudate) which increases oncotic pressure
  • Dalor (pain) due to bradykinin and PGF2
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20
Q

Systemic/acute phase rxn of inflammation

A

Fever (pyrogens induce macrophages to release IL1 and TNF which increases COX activity in perivascular cells of hypothalamus which in turn increase PGE3 –> increases temperature set point)

Leukocytosis - elevation of WBC count.
Leukemoid reaction is a severe elevation in WBC (>40,000 cells)

Increase in plasma acute phase proteins. They are produced by the liver and notably induced by IL-6

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21
Q

Positive/upregulated Acute phase reactants

A

Ferritin - binds and sequesters iron
Fibrinogen - coagulation, ESR
Serum amyloid A- elevation leads to amyloidosis
Hepcidin - decreases iron absorption and iron release. Anemia of chronic disease
C-reactive protein(CRP)-opsonin; fixes complement and facilitates phagocytosis. Nonspecific sign of ongoing inflammation

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22
Q

Negative/downregulated acute phase reactants

A

Albumin -reduction conserves AA for positive reactants

Transferrin- internalized by macrophages to sequester iron

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23
Q

Erythrocyte sedimentation rate (ESR)

A

Products of inflammation (eg fibrinogen) coat RBCs and cause aggregation. The denser RBC aggregates fall at a faster rate within a pipette tube and thus higher ESR

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24
Q

Acute inflammation

A
  • neutrophils in tissue and edema
  • involves the innate immune system (first line of defense, i.e. skin etc)
  • Inflammasome- cytoplasmic protein complex which recognizes cell products of dead cells, microbial products, and crystals –> activates Il-1 and inflmmatory response
  • extravasation of leukocytes (mainly neutrophils) from postcapillary venules and accumulation in the focus of injury followed by leukocyte activation
  • macrophages dominate in the later stages
  • outcomes:
    1) resolution and healing due to Il-10 and TNF beta which attenuate immune response
    2) IL-8 can cause persisten acute inflammation
    3) chronic inflammation due to APCs activaing CD4+ Th cells
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25
Q

Leukocyte extravasation

A

Postcapillary venules

1) margination and rolling:
- E selectin is upregulated by TNF and IL-1 on the endothelium and binds sialyl-Lewisx
- P selectin is released from weibel-palade bodies
- GLYCAM-1,CD 34 which bind L-selectin

2) Tight binding and adhesion
- ICAM-1(CD54) on endothelium binds leukocytes CD11/18 integrins (LFA-1. Mac-1)
- VCAM-1 (CD106) binds VLA-4 integrin

3) Diapedesis (Transmigration)
- PECAM-1(CD31) binds PECAM-1(CD31)

4) Migration
- due to C5a,IL-8, LTB4,Kallikrein, plately activating factor

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26
Q

Leukoyte adhesion deficiency type 2

A

due to decrease in Sialyl Lewis x which normally binds E selectin or P selectin on endothelial cells of vasculature

blocks leukocyte extravasation step of margination and rolling

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27
Q

Leukoyte adhesion deficiency type 1

A

Due to drop in CD18 integrin subunit on the leukocyte which normally binds ICAM-1(CD54) and is important for the tight binding/adhesion step of extravasation

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28
Q

Chronic inflammation

A

infiltration of tissue by mononuclear cells (dominant is macrophages which interact with T lymphocytes)

Type 4 hypersensitivity rxn, autoimmune dz, prolong exposure to toxic agents or foreign material

Th1 cells secrete IFN gamma –> macrophage classical activation

Th2 cells secrete IL-4,IL-13 –> macrophage alternative activation (repair and anti inflammatory)

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29
Q

Granulomatous diseases

A

Granulomas are part of chronic inflammation

composed of epithelioid cells with surrounding multinucleated giant cells and lymphocytes

Associated with hypercalcemia due to calcitriol (1,25-OH2) or vit D3 production

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30
Q

Metastatic calcification

A

Calcification in degenerated or necrotic tissue

localized and secondary to injury or necrosis

blood serum is normocalcemic

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31
Q

Dystrophic calcification

A

Deposition of calcium salts in otherwise normal tissue because of elevated serum levels of calcium

widespread and secondary to hypercalcemia or high calcium-phosphate levels

predominately in tissues of kidney,lung, and gastric mucosa because these lose acid quickly and high h favors calcium deposition

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32
Q

Lipofuscin

A

yellow-brown wear and tear pigment associated with normal aging

formed by oxidation and polymerization of autophagocytosed organellar membranes

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33
Q

_____ is NONCASEATING granuloma

A

Sarcoidosis

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34
Q

Pathway for granuloma formation

A

Th1 secretes IFN gamma which activated macrophages

macrophages then release TNF alpha which induces and maintains granuloma formation

It is important to always test for latent TB before starting anti TNF regimen because they cause granuloma breakdown –> disseminated disease

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35
Q

Free radical injury

A

free radicals damage cells via membrane lipid peroxidation, protein modification,and DNA breakage

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36
Q

Process of having nonregenerated cells replaced by CT

A

scar formation

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37
Q

Hypertrophic scar formation

A

increase in type 3 colalgen, parallel, confined to borders of original wound

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38
Q

Keloid scar

A

Great increase in disorganized types I and III collagen

extends beyond borders of original wound

earlobes, face, and UE mostly

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39
Q

Tissue mediators that stimulate angiogenesis

A

FGF, VEGF, TGF beta (also fibrosis)

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40
Q

Tissue mediators that induce vascular remodeling and smooth mm cell migration, fibroblast growth for collagen synthesis

A

PDGF

secreted by activated platelets and macrophages

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41
Q

Tissue mediator for tissue remodeling

A

Metalloproteinases

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42
Q

Tissue mediator that stimulates cell growth via tyrosine kinases

A

EGF

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43
Q

Phases of wound healing

A

1) inflammatory - platelets, neutrophils, macrophages cause clot formation, increased vessel permeability and neutrophil migration to tissue
2) Proliferative- fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages cause deposition of granulation tissue and type II colalgen, angiogenesis, epithelial cell prolif, dissolution of clot, wound contration. This is delayed in Vit C or copper deficiency
3) REmodeling- fibroblasts cause type 3 collagen replacement with type 1 to increase tensile strength, type 3 is broken down by collagenase. This is delayed in zinc deficiency

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44
Q

Exudate vs transudate

A

exudate is cloudy while transudate is clear/hypocellular

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45
Q

Light criteria

A

Exudative if >or= 1 of the following criteria is met:

1) pleural effusion protein/ serum protein ratio >0.5
2) pleural effusion LDH/serum LDH ratio is >0.6
3) pleural effusion LDH > 2/3 of the upper limit of normal for serum LDH

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46
Q

Abnormal aggregation of proteins or their gragments into beta pleated linear sheets that form insoluble fibrils that result in cellular damage and apoptosis

A

Amyloidosis

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47
Q

Accumulation of AL fibril protein from Ig light chain

A

primary amyloidosis

plasma cell disorders and multiple myeloma

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48
Q

Accumulation of serum amyloid A (AA)

A

secondary amyloidosis

chronic inflammatory conditions

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49
Q

Accumulation of beta2-microglobulin

A

Dialysis-related amyloidosis

end stage renal dz and or long term dialysis

50
Q

Accumulation of beta amyloid protein

A

Alzheimer disease

cleaved from amyloid precursor protein (APP)

51
Q

Accumulation of islet amyloid polypeptide (IAPP)

A

Type II DM

caused by deposition of amylin in pancreatic islet cells

52
Q

Accumulation of Calcitionin (A cal)

A

medullary thyroid cancer

53
Q

Accumulation of ANP

A

Isolated atrial amyloidosis

normal aging increases risk of atrial fibrillation

54
Q

Accumulation of normal (wild-type) transthyretin (TTR)

A

Systemic senile (age related) amyloidosis

cardiac venricles mostly. cardiac dysfunction more insidious than in AL amyloidosis

55
Q

Accumulation of mutated transthyretin (ATTR)

A

Familial amyloid cardiomyopathy

ventricular endomyocardium deposition which causes restrictive cardiomyopathy and arrhythmias

56
Q

Accumulation of mutated transthyretin (ATTR) due to transthyretin gene mutation

A

Familial amyloid polyneuropathies

57
Q

_______ is a shift of glucose metabolism away from mitochondria towards glycolysis

A

Warburg effect

58
Q

Invasive carcinoma

A

cells have invaded basement membrane using collagenases and hydrolases (metalloproteinases).

cell-cell contacts lost by inactivation of E cadherin

59
Q

Metastasis seed? soil?

A

Seed is thumor embolus

soil is the target organ that is often first encountered capillary bed

60
Q

Origin of a carcinoma

A

Epithelial

61
Q

Origin of sarcoma

A

mesenchymal origin

62
Q

Disorganized overgrowth of tissues in native location

A

hamartoma

63
Q

normal tissue in a foreign location

A

choristoma

64
Q

Blood vessel benign and malignant tumors?

A

benign is hemangioma

malignant is angiosarcoma

65
Q

Smooth mm benign tumor and malignant

A

leiomyoma is benign

leiomyosarcoma is malignant

66
Q

Tumor grade vs stage

A

Stage determines SURVIVAL (more important than grade)

67
Q

Tumor grade

A

degree of cellular differentiation and mitotic activity on histology

68
Q

Tumor stage

A

degree of localization/spread

TNM staging system:
T-tumor size/invasiveness
N-Node involvement
M-Metastases

*N and M are most important

69
Q

Paraneoplastic syndromes

A

Triggered by altered immune system response to a neoplasm

70
Q

Progressive proximal mm weakness, gottron papules, heliotrop rash

A

paraneoplastic syndrome

Dermatomyositis related to adenocarcinomas (esp ovarian)

71
Q

Hyperpigmented velvety plaques in axilla and neck

A

paraneoplastic syndrome

acanthosis nigricans related to gastric adenocarcinoma and other malignancies

72
Q

Sudden onset of seborrheic keratoses

A

paraneoplastic syndrome

sign of leser-trelat related to GI malignancy

73
Q

Abnormal proliferation of skin and bone at distal extremities causing clubbing, arthalgias, joint effusions, periostosis of tubular bones

A

paraneoplastic syndrome

hypertrophic osteoarthropathy related to adenocarcinoma of the lung

74
Q

PTHrP secretion by a tumor that causes hypercalcemia

A

paraneoplastic syndrome

SCC

75
Q

Vitamin D3 secretion by a tumor that causes hypercalcemia

A

paraneoplastic syndrome

lymphoma

76
Q

Increased ATCH causing cushing syndrome related to

A

paraneoplastic syndrome

sMALL CELL LUNG CANCER

77
Q

Increased ADH related to hyponatremia (SIADH) caused by a tumor

A

paraneoplastic syndrome

small cell lung cancer

78
Q

Increased erythropoietin

A

paraneoplastic syndrome

polycythemia caused by pheochromocytoma, renal cell carcinoma, HCC, hemangioblastoma, leiomyoma

79
Q

Anemia with low reticulocytes causing ____ due to ____ tumor

A

paraneoplastic syndrome

Pure red cell aplasia due to thymoma

80
Q

Hypogammaglobulinemia due to ____Syndrome and ____ tumor

A

paraneoplastic syndrome

due to good syndrome and caused by a thymoma

81
Q

Migratory superficial thrombophebitis

A

paraneoplastic syndrome

trousseau syndrome due to adenocarcinomas (Esp pancreatic)

82
Q

Deposition of sterile platelet thrombi on heart valves

A

paraneoplastic syndrome

nonbacterial thrombotic endocarditis due to most adenocarcinomas of pancreas

83
Q

Psychiatric disturbances, memory deficits, seizures, diskinesias, autonomic instability, language dysfunction

A

paraneoplastic syndrome

anti-NMDA receptor encephalitis due to ovarian teratoma

84
Q

Dancing eyes and ancing feet

A

paraneoplastic syndrome

opsoclonus-myclonus ataxia syndrome due to neuroblastoma in childrena nd small cell lung cancer in adults

85
Q

Antibodies against antigens in purkinje cells

A

paraneoplastic syndrome

paraneoplastic cerebellar degeneration due to small cell lung cancer (anti hu), gyn and breast cancers (anti yo), hodgkins lymphoma (anti tr)

86
Q

Antibodies against Hu antigens in neurons

A

paraneoplastic syndrome

small cell lung cancer causing paraneoplastic encephalomyelitis

87
Q

Antibodies against presynaptic Ca channels at NMJ

A

paraneoplastic syndrome

Lambert-eaton myasthenic syndrome due to small cell lung cancer

88
Q

Antibodies against postsynaptic Ach receptors at NMJ

A

paraneoplastic syndrome

myasthenia gravis due to thymoma

89
Q

Oncogenes

A

GOF mutation

coverts proto-oncogene (normal) to onvogene

needs damage to only one allele of a proto-oncogene

90
Q

tumor suppressor genes

A

LOF increases cancer risk

need both alleles of tumor suppressor gene to be lsot for expression of dz

91
Q

What are psammoma bodies seen in

A
  • papillary carcinoma of thyroid
  • serious papillary cystadenocarcinoma of ovary
  • meningioma
  • malignant mesothelioma
92
Q

Serum tumor markers: Alkaline phosphatase

A

metastases to bone or liver

paget disease of bone

seminoma

93
Q

Serum tumor markers: alpha feto protein

A 
hepatocellular carcinoma
endodermal sinus (yolk sac) tumor
Mixed germ cell tumor
Ataxia telangiectasia
neural tube defects
94
Q

Serum tumor markers: beta Hcg

A

produced by syncytiotrophoblasts of the placenta

hydatidiform moles and choriocarcinomas
testicular cancer
mixed germ cell tumor

95
Q

Serum tumor markers: CA 15-3/ CA 27-29

A

breast cancer

96
Q

Serum tumor markers: CA 19-9

A

pancreatic adeocarcinoma

97
Q

Serum tumor markers: CA 125

A

ovarian cancer

98
Q

Serum tumor markers: calcitonin

A

medullary thyroid carcinoma

99
Q

Serum tumor markers: CEA

A

colorectal and pancreatic cancers

100
Q

Serum tumor markers: chromogranin

A

neuroendocrine tumors

101
Q

Serum tumor markers: LDH

A

testicular germ cell tumors

ovarian dysgerminoma

102
Q

Serum tumor markers: PSA

A

prostate cancer

103
Q

Immunohistochemical stain

A

used to identify origin of metastatic tumor

104
Q

Immunohistochemical stain: vimentin

A

Mesenchymal tissues

105
Q

Immunohistochemical stain: S-100

A

neural crest cells

106
Q

Immunohistochemical stain: Desmin

A

Muscle

107
Q

Immunohistochemical stain: cytokeratin

A

epithelial cells

108
Q

Immunohistochemical stain: GRAP

A

neuroglia

109
Q

Immunohistochemical stain:neurofilament

A

neurons

110
Q

Immunohistochemical stain: PSA

A

prostatic epithelium

111
Q

Immunohistochemical stain: TRAP

A

tartrate resistant acid phosphatase

112
Q

Immunohistochemical stain: chromogranin and synaptophysin

A

neuroendocrine cells

113
Q

P-glycoprotein

A

multidrug resistance protein 1 (MDR1) classically seen in adrenocortical carcinoma

used to pup out toxins (decreases chemotherapy effectiveness)

114
Q

Cachexia

A

weight loss, muscle atrophy, fatigue due to chronic dz

TNF, IFN gamma, IL1 and IL6

115
Q

Most common cause of cancer related mortality in men? women? children?

A

Men: lung >prostate> colon/rectum
Women: lung>breast>colon/rectum
children: leukemia>CNS>neurblastoma

116
Q

Most sarcomas spread via

A

hematogenously

117
Q

Most carcinomas spread via lymphatics EXCEPT these 4 which are hematogenously

A

follicular thyroid carcinoma
choriocarcinoma
renal cell carcinoma
hepatocellular carcinoma

118
Q

Primary tumors that commonly met. to brain?

A

lung>breast>melanoma,colon, kidney

119
Q

primary tumors that commonly met. liver

A

colon&raquo_space; stomach> pancreas

120
Q

primary tumors that commonly met. bone

A

prostate,breast>kidney,thyroid, lung

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