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basic pathology Flashcards

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1
Q

what is pyknosis?

A

nuclear shrinkage in apoptosis

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2
Q

what is karyorrhexis

A

nuclear fragmentation

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3
Q

what are two pathways of extrinsic apoptosi?

A
  1. ligand recpetor ineractions (Fas ligand binds to Fas = CD95)
  2. immune cell (cytotoxic release of performin and granzyme B)
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4
Q

name 6 types of necrosis

A

coagulative

liquefactive

caseous

fatty

fibrinoid

gangrenous

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5
Q

3 organs coag necrosis

A

heart

liver

kidney

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6
Q

3 examples of liquefactive necrosis

A

brain

bacterial abscess

pleural effusion

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7
Q

2 examples of caseous necrosis

A

TB

systemic fungi

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8
Q

fatty necrosis

A

perinpancreatic fat (saponification via lipase)

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9
Q

fibrinoid necrosis

A

blood vessels

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10
Q

gangrenous necrosis example

A

dry (ischemic coagulative) or wet (with bacteria); common in limbs and GI tract

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11
Q

what types of cell injury are reverisble with O2 (6)

A

decreased ATP synthesis

cellular swelling (no ATP –> impaired Na+/K+ ATPase)

nuclear chromatin clumping

decreased glycogen

fatty change

ribosomal detachment

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12
Q

what 5 changes are seen in irreversible cell injury?

think: membran damage

A
  1. nuclear pyknosis, karyolysis, karyorrhexis
  2. ca2+ influx–>caspase activation
  3. plasma membrane damage
  4. lysosomal rupture
  5. mitochondrial permeability
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13
Q

what areas are susceptible to hypoxia in:

brain -

heart -

kidney (2)

liver -1

colon -

A

brain - watershed areas of ACA/MCA/PCA/boundary - pyramidal cells of hippocampus and purkinje cells

heart - subendocardium (LV)

kidney: straight segment of proximal tubule(medulla) + thick ascending limb (medulla)

liver = area around central vein

colon - splenic flexure and rectum

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14
Q

where do red infarcts occur(3)?

damage of reperfusion

A

hemorhagic infarcts occur in **loose tissue ** with collaterals : liver, lung, intestine following **reperfusion **

reperfusion –>damage by free radicals

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15
Q

pale infarcts - 3 organs w/one blood supply

A

heart

kidney

spleen

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16
Q

hypovolemic/cardiogenic shock

type of output

tpr?

cardiac output

skin

A

Low-output failure

increased TPR

low cardiac output

cold, clammy pt (vasoconstriction)

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17
Q

septic shock

type of output

tpr?

cardiac output

skin

A

high-output failure

decreased TPR

dilated arterioles, high venous return

hot patient (vasodilation)

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18
Q

what are 6 causes of atrophy?

A

decreased hormones

decreased: innervation (motor neuron damage), blood flow, nutrients

increased pressure: nephrolithiasis

occlusion of secretory ducts: ie cystic fibrosis.

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19
Q

5 cardinal signs of inflammation

A

rubor -redness

dolor -pain

calor -heat

tumor -swelling

function laesa-loss of function

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20
Q

3 vascular components of acute inflammation

A

increased vascular permeability

vasodilation

endothelial injury

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21
Q

what are vascular components of inflammation

A
  1. increased vascular permeability (post cap venules)
  2. vasodilation of arterolies
  3. endothelial injury
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22
Q

3 things that mediate acute inflammation

A

neutrophil

eosinophil

antibody

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23
Q

what type of inflammation if a granuloma

A

chronic = nodular collections of epitheliod macrophages and giant cells

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24
Q

what are two outcomes of chronic inflammation?

A

scarring and amyloidosis

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25
mononuclear cell mediated: charaterized by destruction and repair associated with blood vessel proliferation, fibrosis
chronic inflammation
26
what are the four steps of leukocyte extravasation note location: post capillary venules
1. rolling (leukocyte: siall-lewis X; endothelial cell: e-selectin(induced by TNF-1 and IL-2), P-selectin(from weibel paladie bodies and mediated by histamine) 2. tight binding: leukocyte: ICAM-1 (upregulated by TNF and IL-1) neutrophil - has **LFA-1 = integrin upregulated by C5a, LTB4** **3. diapedesis - PECAM-1** **4. migration - guided by chemotactic singals: C5a IL-8, LTB4, Kallikrein (CILK) **
27
what type of drug metabolism --\> free radical injury?
phase I
28
which 3 enzymes can neutralize free radicals which vitamins?
enzymes: H2O2: catalase +glutathione, peroxidase superoxide: superoxide dismutase, vitamins: ACE
29
1. retinopathy of prematurity 2. bronchopulmonary dysplasia 3. CCL4 ---\> liver necrosis(fatty change) 4. acetaminophen OD 5. iron overload (hemochromatosis) 5. reperfusion after anoxia(superoxide) are all examples of:
free radical injury
30
how do free radicals damage cells: 3 ways here
membrane lipid peroxidation protein modification DNA breakage
31
what from macrophages induces and maintains granuloma formation?
TNF alpha
32
transudate cellularity protein specific graviy 3 causes
hypocellular protein poor specific gravity \<1.012 due to: increased hydrostatic pressure, decreased oncotic pressure, Na+ retention
33
exudate ## Footnote cellularity protein specific graviy 3 causes
cellular protein rich specific gravity \>1.020 due to: lymphatic obstruction and inflammation
34
2 caseating granulomas
TB and fungal infections
35
when fibrinogen coats RBCs, what does it cause?
fibrinogen = product of inflammation that coats RBCs and causes aggregation. when aggregated, RBCs fall at a faster rate within test tube (ESR)
36
4 causes of increased ESR PIICS
infections inflammations cancer pregnancy SLE
37
3 causes of decreased ESR? CPS
sickle cell (altered shape) polycythemia (too many) CHF
38
what is deposited in dialiysis realted beta-amyloid? how does it present?
b2-microglobulin in pts w/ESRD + long-term dialysis presents as carpal tunnel and other joint tissue
39
8 hall marks of cancer
evasion of apoptosis self-sufficiency in growth signals insensitvity to anti-growth signals sustained angiogenesis limitless replicative potential tissue invation metastasis.
40
which two enzymes used to invade basement membrane?
collagenases and hydrolaes
41
what is a fibrous tissue formation in resonse to neoplasm
desmoplasia
42
stage vs grade
grade - degree of cellular proliferation based on histologic appearance of individual tumor stage - degree of localiztion/spread based on site and primary lesion, spread to regional lymph node, presence of mets, TNM
43
what is TNM staging system?
T- tumor size N - node involvement M - metastases
44
which 3 cytokines mediate cachexia?
TNF-alpha IFN-gamma IL-6
45
down syndroma associated cancers
AML ALL
46
xerodermal pigmentosa and albinism associated cancers?
melanoma basal cell carcinooma squamous cell of skin
47
tuberous sclerosis (facial angiofibroma + seizures + metnal retardation)
giant cell astrocytoma renal angiomyolipoma cardiac rhabdomyoma
48
actinic keratosis
squamous cell carcinoma
49
plummer vinsion syndrome
squamous cell of esophagus
50
acanthosis nigricans (hyperpigmenation and epidermal thickening)
visceral malignancy (stomach, lung, uterus)
51
dysplastic nevus
malingant melanoma
52
radiation exposure
leukemia sarcoma papillary thyroid cancer breast cancer
53
name 9 oncogenes note: all gain of function ---\> increased cancer risk, need only to damage 1 allele
1. abl- CML - tyrosine kinase 2. c-myc - burkitt lymphoma -transcirption factor 3. bcl-2 - follicular lymphoma - antiapoptotic gene 4. HER2/neu breast-ovariang gastric - tyrosine kinase 5. ras - colonic carcinoma - GTPase 6. L-myc - lung tumor - transcription 7. N-myc - adrenal medulla neuroblatoma - transcription factor 8. ret - MEN2A, 2B, tyrosine kinase 9. c-kit - Gastrointestial stromal tumor - cytokine receptor
54
what are the symptoms of acute iron poisoning? chronic?
acute - gastric bleeding chronic = metabolic acidosis, scarring --\> GI obstruction
55
heritable type of amyloid? age-related?
heritable = mutated transthyretin age related - normal transthyretin TRR
56
at risk for which cancer: AIDs patientw
Kaposi sacrocma and aggressive malignant lymphoma
57
autoimmune diseases associated with which cancer (hashimoot's thyroiditis, myasthenia gravis?
lymphoma myasthenia gravis = thymoma
58
abl oncogene
abl oncogene CML - tyrosine kinase
59
c-myc oncogene
c-myc oncogene Burkitt lymphoma - transcription factor
60
ras oncogene
ras oncogene colonic carcinoma - GTPase
61
c-kit oncogene for which cancer?
c-kit gastrointestinal tumor - cytokine receptor - oncogene
62
what are the tumor suppressor genes? 10
tumor suppressor genes Rb, p53, BRCA1+BRCA2, p16, BRAF, APC, WT1, NF1 + NF2, DPC4, DCC
63
Rb tumor suppressor gene - which cancer?
Rb retinoblastoma, osteosarcoma, inhibits E2F; blocks G1-S phase
64
p53 which cancer?
p53 most human cancers; Li-Fraumeni syndrome; transcription factor for p21, blocks G1---\>S phase
65
p16 tumor suppressor gene - which cancer?
p16 melanoma
66
which cancer for BRAF?
BRAF melanoma
67
NF-1 and NF-2 which cancers?
NF1 neurofibromatosis type 1 on chromosome 17 - RAS GTPase activating proten (RAS-GAP) NF2 Neurofibromatosis type 2 ch. 22 = merlin (schwannomin protein)
68
marker for which tumors? bombesin
bombesin neuroblastoma + lugn and gastric cacioma
69
S-100 marks which tumors?
S-100 melanoma, schwannoma, neural tumor
70
aflatoxins - whch cancer?
aflatoxins liver -hepatocellular carcinoma
71
vinyl chloride which cancer?
vinyl chloride angiosarcoma
72
carbon tetrachloride which cancer?
Carbon tetrachlordie liver - centrilobular necrosis + fatty change
73
nitrosamines - which cancer?
nitrosamines (smoked food) stomach - gastric caner
74
cigarette smoke, which cancers?
cigarrete smoke larynx (squamous), lung (squamous and small cell), kidney (renal cell carcinoma), bladder (transitional cell), pancrease(adenocarcinoma), cervical carcnoma
75
arsenic which cancers?
arsenic skin - squamous cell; liver- angiosarcoma
76
which four cancers produce EPO?
EPO polycythemia - renal cell carcinoma, hemagioblastoma, hepatocellular carnioma, pheochromocytoma
77
which four cancers associated with psammoma bodies?
psammoma bodies PSaMMoma: papillary(thyroid), serous(ovary), meningioma, mesothelioma

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