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Kaplan Path > Path Ch 2 > Flashcards

Path Ch 2 Flashcards

1
Q

increase in lactic acid –>

A

decrease pH –> denaturation of proteins (may precipitate) = decreased activity of many enzymes

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2
Q

fatty change seen in

A

liver, kidney, heart (organs involved in/dependent on fat metabolism)

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3
Q

CCl4

A
  • carbon tetrachloride
  • dry cleaning
  • causes liver cell necrosis
  • first converted to free radicals (CCl3) in SER
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4
Q

tylenol toxicity

A
  • main cause of drug-induced hepatic necrosis
  • converted by hepatocyte p450 into free radical
  • FR neutralized by glutathione GSH (part of pentose phosphate pathway)
  • reduction in GSH –> damage to hepatocyte by FR
  • pathogenesis: FR acts on sulfhydryl groups in hepatocyte cell membrane
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5
Q

Vit A def

A
  • night blindness, squamous metaplasia (renal squamous cell stones (keratin pearls), immune deficiency (increased # of bacterial infections)
  • Vit A –> cell proliferation and maturation, therefore give Vit A to AML patients
  • bumps on skin where hair follicles are = squamous metaplasia of hair follicles
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6
Q

vitamin C def

A
  • scurvy (poor wound healing from lack of collagen I and III; petechiae, poor bones)
  • if petechiae + purpura –> scurvy
  • remember, Vit C hydroxylates collagen, without it have weak collagen –> bowing of long bones in kids or lots of bleeding when brush teeth
  • 1st affects collagen w/ highest hydroxyproline content (i.e. blood vessels–> early symptom = bleeding gums)
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7
Q

vit D def

A

rickets (bowing of long bones in kids) and osteomalacia

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8
Q

vitamin K def

A
  • bleeding diathesis
  • kids with CF will often have Vit K deficiency from malabsorption
  • adults with vitamin K def = warfarin patients or someone who lost a colon (bc lost the bacteria)
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9
Q

Vit B12 def

A
  • megaloblastic anemia, neuropathy, spinal cord degeneration

- megaloblastic anemia with neurologic deficits –> B12 deficiency

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10
Q

folate def

A

megaloblastic anemia and neural tube defects

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11
Q

niacin (Vit B3) def

A

pellagra, rough skin (diarrhea, dermatitis and dementia, death if don’t treat)

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12
Q

kwashiorkor

A
  • decrease in total protein intake –> decreased oncotic pressure –> edema in eyes, belly, hands
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13
Q

Thiamine (Vit B1) def

A

wernicke-korsakoff, dilated cardiomyopathy (beri beri)

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14
Q

Excess Vit A

A
  • stored in Ito cells (liver) –> liver disease, jaundice
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15
Q

excess Vit D

A
  • excess Vit D –> increased calcium –> irritability, fatigue, muscle weakness, bone resorption and metastatic calcifications
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16
Q

superoxide dismutase

A

superoxide O2- –> H202

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17
Q

glutathione peroxidase

A

hydroxyl ions or H2O2 –> H2O

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18
Q

catalase

A

H2O2 –> H20 + O2

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19
Q

decrease in Na/K+ pump

A
  • influx of Na+ and efflux of K+ –> cell swelling, ER swelling, loss of microvilli, membrane blebs
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20
Q

apoptosis on H and E

A
  • deeply eosinophilic cytoplasm and basophilic nucleus
  • pyknosis (nuclear shrinkage)
  • karyorrhexis (gragmentatino caused by endonuclease-mediated cleavage)
  • cell membrane typical remains intact without significant inflammation (unlike necrosis)
  • both intrinsic and extrinsic pathways (both activate caspases aka cytosolic proteases) –> cellular breakdown including cell shrinkage, chromatin condensation, membrane blabbing and formation of apoptotic bodies (which are then phagocytosed)
  • DNA laddering: fragments in multiples of 180bp is a sensitive indicator of apoptosis
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21
Q

intrinsic pathway for apoptosis

A
  • mitochondrial pathway
  • involved in tissue remodeling in embryogenesis
  • occurs when regulating factor is withdrawn from a proliferating cell population (i.e. decrease in IL-2 after a completed immunologic reaction –> apoptosis of proliferating effector cells)
  • also occurs after exposure to injurious stimuli (i.e. radiation, toxins, hypoxia) –> p53 activation –> BAX/BAK –> cytochrome c released from mitochondria –> initiator caspases –> apoptosis
  • regulated by Bcl-2 family of proteins. BAX and BAK are proapoptotic, while Bcl-2 and Bcl-x are antiapoptotic
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22
Q

extrinsic pathway for apoptosis

A

2 pathways:

  • 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
  • Fas-FasL interaction is necessary in thymic medullary negative selection. Mutations in Fas –> increased numbers of circulating self-reacting lymphocytes due to failure of clonal deletion
  • defective Fas-FasL interactions –> autoimmune lymphoproliferative syndrome
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23
Q

fibrinoid necrosis

A
  • immune reactions in vessels (ie PAN, preeclampsia, malignant HTN)
  • immune complexes combine with fibrin –> vessel wall damage (Type 3 hypersensitivity reaction)
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24
Q

antiapoptotic proteins

A
  • Bcl-2 and Bcl-x are antiapoptotic
  • Bcl-2 keeps the mitochondrial outer membrane impermeable and therefore prevents cytochrome c release from the inner mitochondrial matrix
  • Bcl-2 overexpression (ex follicular lymphoma t[14,18] –> decreased caspase activation –> tumorigenesis
25
Q

wet gangrene

A
  • liquefactive necrosis (resulting from superinfection) superimposed on coagulative necrosis
  • in coagulative necrosis proteins denature then enzymes degrade. In liquefactive necrosis neutrophils release lysosomal enzymes that digest the tissues. Enzymes degrade first and proteins denature 2nd.
26
Q

pro-apoptotic proteins

A

Bcl-2 family of proteins. BAX and BAK are proapoptotic

27
Q

Regions of brain most vulnerable to hypoxia/ischemia and subsequent infarction

A
  • ACA/MCA/PCA boundary areas.
  • ACA/MCA = anterior watershed area
  • MCA/PCA = posterior watershed area
  • watershed area = border zone that receives blood 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 parking cells of cerebellum and pyramidal cells of hippocampus and neocortex (zones 3, 5, 6)
28
Q

Regions of kidney most vulnerable to hypoxia/ischemia and subsequent infarction

A
  • straight segment of proximal tubule (medulla)

- thick ascending limb (medulla)

29
Q

Regions of liver most vulnerable to hypoxia/ischemia and subsequent infarction

A

area around central vein (zone III)

30
Q

Regions of colon most vulnerable to hypoxia/ischemia and subsequent infarction

A

splenic flexure, colon

31
Q

increased alkaline phosphatase in the blood signifies

A

biliary tract obstruction –> cell damage –> leaking enzymes into blood

32
Q

heterolysis

A
  • release of proteolytic enzymes from inflammatory cells

- seen in liquefactive necrosis

33
Q

liquefactive necrosis occurs in

A

brain infarcts, abscesses and pancreatic necrosis

34
Q

genetic control of apoptosis

A
  • bcl-2 (which inhibits apoptosis) prevents release of cytochrome c from mito and binds pro-apoptotic protease activating factor (Apaf-1)
  • p53 (which stimulates apoptosis) is elevated by DNA injury and arrests cell cycle. If DNA repair is impossible, p53 stimulates apoptosis
  • oncogenic viruses can inactivate p53 (i.e. Hep B, HIV, EBV, HPV)
  • in viral hepatits see councilman body (pathologic examples of apoptosis will have inflammation; physiologic apoptosis have NO inflammation)
35
Q

execution of apoptosis

A

mediated by cascade of caspases that digest nuclear and cytoskeletal proteins and activate endonucleases

36
Q

graft vs host disease

A
  • example of pathogenic apoptosis (will see inflammation)
  • occurs in allogenic bone marrow transplant recipients
  • the transplanted marrow has cytotoxic T cells that recognize the new host proteins (usually HLA) as foreign
  • signals cell to undergo apoptosis while releasing their TNF-α and interferon-γ
  • organs typically involved = skin, mucosa, liver, GI
  • path: see single-cell apoptosis occurring in affected organs and adjacent T cells
37
Q

cells unable to undergo hyperplasia

A
  • hyperplasia = increase in # of cells

- nerve, cardiac, skeletal muscle cells

38
Q

secondary polycythemia

A
  • living at high altitudes (where O2 content of air is relatively low) –> compensatory hyperplasia of RBC precursors in BM –> increase in # of circulating RBC
39
Q

HPV

  • high risk strains
  • E6 does
  • E7 does
A
  • high risk: 16, 18, 31, 33
  • E6 knocks out p53
  • E7 knocks out RB
  • low risk: 6, 11: genital wart. condolyoma lata “go to heaven”
  • 1-4: get from floor = plantar wart
40
Q

black liver

A
  • durbin-johnson
  • melanin binds bilirubin
  • asymptomatic
41
Q

lysozymes containing peroxided free-radical injured lipid

A

lipofuscin

42
Q

melanin is derived from

A
  • tyrosine
  • found in melanocytes (neural crest cell derivatives) and substantial nigra
  • S100+
43
Q

dystrophic calcification

A

ppt of calcium phosphate in dying or necrotic tissues. dying tissues expose phosphates –> calcium is attracted.
- Ex: fat necrosis (saponification) psammoma bodies (laminated calcifications that occur in meningiomas) papillary carcinomas of thyroid and ovary

44
Q

when the substantial nigra is pale think

A

parkinsons

45
Q

mullerian duct derivatives

A
  • fallopian tube, uterus, cervix, upper portion of vagina
46
Q

wolffian duct derivatives

A

epididymis, vas deferens, seminal vesicles, ejaculatory ducts

47
Q

AR inheritance

  • onset
  • penetrance
  • mutation
  • requires
A

AR inheritance

  • onset: early uniform onset (infancy/childhood)
  • penetrance: complete penetrance
  • mutation: usually an enzyme protein
  • requires: mutation of both alleles
48
Q

AD inheritance

  • onset
  • penetrance
  • mutation
  • requires
A

AD inheritance

  • onset: variable; may be delayed into adulthood
  • penetrance: incomplete with variable expression
  • mutation: usually a structural protein or receptor
  • requires: mutation of one allele
49
Q

what causes fat accumulation in kwashiorker

A

decreased synthesis of apolipoproteins, can’t get VLDL out of liver, lipoproteins make VLDL soluble in fluid

50
Q

Russell body

A

pink; accumulation of Ig in RER of plasma cells

51
Q

mallory body

A
  • masses of keratin intermediate filaments (alcohol hyaline) within hepatocytes
  • seen in pts with alcoholic liver disease
52
Q

alkaptonuria

A
  • enzyme def: homogentisate oxidase
  • ochronosis: accumulation of black homogentisate pigments in joints, cartilage, urine (turns black on exposure to sunlight)
53
Q

melanosis coli (black bowel syndrome)

A
  • refers to deposition of black anthracene pigments in macrophages within lamina propria of large intestine
  • associated w/ laxative abuse from which pigment is derived
54
Q

causes of melanin excess

A
  • increases in ACTH (ie pit adenoma, ectopic ACTH, addison’s dz, adrenogenital syndrome)
55
Q

albinism

A
  • lack of tyrosinase

- melanocytes present, but don’t contain melanin in melanosomes

56
Q

PKU

A
  • missing enzyme: phenylalanine hydrolyzes (normally converts phenylalanine into tyrosine)
  • deficiency of Tyr –> blonde hair
57
Q

Things that cause an increase in unconjugated bilirubin

A
  • bilirubin is derived from the breakdown of Hb by macrophages in the spleen and BM, released from Macrophages as lipid soluble, UCB
  • hemolytic anemia (hereditary spherocytosis - spectrin)
  • problem w uptake and conjugation of bilirubin (physiologic jaundice of newborn)
  • newborns w Rh disease of newborns (may develop kernicterus due to entry of dissolution of UCB in brain tissue)
58
Q

things that cause an increase in conjugated bilirubin

A
  • bilirubin is derived from the breakdown of Hb by macrophages in the spleen and BM, released from Macrophages as lipid soluble, UCB, bound to plasma in albumin
  • bound to albumin in plasma, delivered to hepatocytes for conjugation into CB
  • hepatitis
  • obstructive jaundice (gallstones in CBD)

Kaplan Path (8 decks)

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