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Test reviews DEDICATED > Wed Aug 5 > Flashcards

Wed Aug 5 Flashcards

1
Q

Describe the changes found in osteoporotic bone

A

Trabecular thinning, with fewer interconnections

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2
Q

Lamellar bone structure resembling a mosaic =

A

pagets disease

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3
Q

Unmineralized osteoid deposits on trabecular surfaces =

A

osteomalacia

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4
Q

Persistance of primary spongiosa in the medullary cavity =

A

osteopetrosis

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5
Q

Subperiosteal bone resorption and cystic degeneration =

A

hyperparathyroidism

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6
Q

HPV viral structure

A

DS DNA naked

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7
Q

two causes of PKU?

A
  • phenyalanine hydroxylase deficiency

- cofactor deficiency (may be from deficiency of the enzyme needed to regenerate the cofactor)

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8
Q

What is the cofactor for phenylalaline hydroxylase?

A

BH4

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9
Q

What enzyme regenerates BH4 ?

A

Dihydropterin reductase

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10
Q

Phenylalaine is converted to ____ by phenylalaine hydroxylase?

A

tyrosine

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11
Q

tyrosine is converted to…

A

DOPA

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12
Q

what enzyme converts tyrosine to DOPA?

A

tyrosine hydroxylase

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13
Q

what is the cofactor for tyrosine hydroxylase?

A

BH4

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14
Q

A deficiency of dihydropterin reductase would result in decreased activity of which TWO enzymes?

A

phenylalaine hydroxylase, tyrosine hydroxylase

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15
Q

what will cytogenic studies of fragile X syndrome usually show?

A

A small gap on the long arm of the X chromosome (the area of increased repeats does not stain)

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16
Q

pathophys of fragile X?

A

Trinucleotide repeats of CGG in the FMR1 gene on the X chromosome

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17
Q

Clinical features of fragile X syndrome?

A
  • intellectual disability
  • macrocephaly
  • long narrow face
  • prominent forehead, jaw, chin and ears
  • macroorchidism
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18
Q

inheritance of fragile X syndrome?

A

X linked

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19
Q

how does progesterone effect bile/the gallbladder?

A
  • reduces bile acid secretion

- slows gallbladder emptying

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20
Q

pathophys of chronic kidney rejection?

A

-over several months to years, antibodies are created to the graft HLA or other antigens, and lead to progressive antibody mediated inflammation. Irreversible damage leads to the kidney to reduce in size, with obliterative vasclar wall thickening, tubular atrophy and interstitial fibrosis

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21
Q

A dense, interstitial mononuclear infiltrate corresponds to which type of organ rejection?

A

Acute - t cell mediated

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22
Q

pathophys of pyruvate kinase deficiency?

A
  • the defective pyruvate kinase in RBCs means they cant convert PEP to pyruvate, which normally produces an ATP
  • RBCs rely on glycolysis for energy, and thus the decreased ATP -> dysfunction
  • > rigid RBCs, easily lysed -> extravascular hemolytic anemia
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23
Q

what will be seen on blood microscopy of someone with pyruvate kinase deficiency?

A

echinocytes (thorny projections)

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24
Q

inheritance of pyruvate kinase deficiency?

A

autosomal recessive

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25
Q

why may TCAs lead to arythmias and conduction defects?

A

they can block cardiac Na fast channels

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26
Q

why does C perfingrens present with crepitis?

A

it rapidbly metabolizes carbohydrates producing gas

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27
Q

other than gas gangrene, what illness can C perfringens cause?

A

late-onset food poisoning -> transient watery diarrhea

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28
Q

what repeats in huntingons disease?

A

CAG

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29
Q

neurotransmitter changes in huntingtons disease?

A

decreased Ach and Gaba in the caudate

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30
Q

what will be seen on neuroimaging of hungtingtons disease?

A

caudate atrophy with enlargment of the frontal horns of thewh lateral ventricles

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31
Q

which part of the brain is the first to be damaged in the setting of ischemia?

A

hippocampus (specifically the pyramidal neurons)

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32
Q

MOA of ethambutamol

A

inhibits arabinosyl transferase

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33
Q

what is streptomycin?

A

aminoglycoside

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34
Q

MOA of rifampin

A

inhibits DNA dependent RNA polymerase

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35
Q

isoniazid MOA

A

inhibits mycolic acid synthesis

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36
Q

is gonorrhea intracellular or extracellular?

A

intracellular

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37
Q

what is budosenide?

A

corticosteroid

38
Q

ibuprofen MOA

A

reversibly inhibts COX1 and COX2

39
Q

diclofenac MOA

A

reversibly inhibts COX1 and COX2

40
Q

indomethacin MOA

A

reversibly inhibts COX1 and COX2

41
Q

what occurs in the white pulp of the spleen?

A

-this is where antibody coated bacteria are filtered out and antibodies are made my B cells

42
Q

what occurs in the red pulp of the spleen?

A

this is where old and bad red blood cells are destroyed

43
Q

what are the four myeloproliferative disorders?

A
  • chronid myeloid leukemia
  • polycythemia vera
  • essential thrombocythemia
  • myelofibrosis
44
Q

What cells are increased in CML

A

mature myeloid cells, especially basophils

45
Q

what drives CML?

A

t(9:22) - BCR-ABL fusion protein

46
Q

what mutation is associated with the myeloproliferative disorders, excluding CML?

A

JAK2 kinase mutation

47
Q

what are the EPO levels in polycythemia vera?

A

decreased

48
Q

what proliferates in essential thrombocythemia?

A

mature myeloid cells, especially platellets

49
Q

what proliferates in myelofibrosis?

A

mature myeloid cells, especially megakaryocytes

50
Q

how does myelofibrosis lead to bone marrow fibrosis?

A

megakaryocytes produce excess PDGF - >fibrosis

51
Q

name 3 antioxidant enzymes that convert ROS to water?

A
  • superoxide dismustase
  • catalase
  • glutathione peroxidase
52
Q

what is bronchophony?

A

phenomenon where spoken words are heard more clearly/loudly over an area of alveolar consolidation

53
Q

explain the phys as to how estrogen is protective of bone?

A

Estrogen induces the production of OPG by osteoblast and stromal cells, which is a decoy for the RANKL, thus decreasing RANKL that can bind rank and thus prevent osteoclast differentiation and survival. It also decreased the expression of RANK on osteoclasts.

54
Q

Decreased estrogen after menopause results in what change in bone?

A

Increased RANKL and decreased OPG. Osteoclasts upregulate RANK. -> increased bone resorption

55
Q

what do MS plaques look like histologically?

A

they are characterized by perivenular inflammatory infiltrates - made of autoreactive t lymphocytes and macrophages directed against myelin

56
Q

Name 4 organisms that can cause diarhea with a small inoculum

A

Shigella
Camyplobacter jejuni
Entameba histolytica
Giardia

57
Q

NAme 4 organisms that need a relatively high inoculum to cause diarrhea?

A

Vibrio
Salmonella
Clostridium perfringins
E coli

58
Q

which cells produce CCK?

A

I cells of the duodenum

59
Q

The thalamic ventral posterior lateral nucleus receives input from…

A

dorsal columns and spinothalamic tracts

60
Q

the thalamic ventral posterior medial nucleus receives input from…

A

the trigeminal pathway

61
Q

trisomy 13 =

A

patau syndrome

62
Q

cimex lectularius =

A

bed bugs

63
Q

pediculus humanus capitis =

A

head lice

64
Q

what is teriparatide?

A

recombinant parathyroid hormone

65
Q

Serum alkaline phosphatase levels correlate with…

A

osteoblast activity (secreted by osteoblasts)

66
Q

why does H pylori lead to increased gastric acid secretion?

A

-they colonize the gastric antrum which decreases somatostatin production and increased gastrin formation leading to increased H

67
Q

sirolimus MOA

A

inhibitrs mTOR which is part of the IL2 signalling pathway in t cells

68
Q

how does the spleen appear in someone with portal hypertension?

A

It will have an apparent expansion of red pulp. This is because the blood gets backed up and can lead to congestion of teh spleen -> blood filled sinsu’s and cords

69
Q

what proteins are defected in familial chylomicronemia syndrome (type I)?

A
  • ApoCII

- LPL

70
Q

what is elevated in familial chylomicronemia syndrome (type I)?

A

chylomicrons

71
Q

what are the manifestations of familial chylomicronemia syndrome (type I)?

A
  • acute pancreatitis
  • lipemia retinitis
  • skin xanthomas
  • hepatosplenomegaly
72
Q

what proteins are defected in familial hypercholesterinemia (type II)?

A
  • LDL receptor

- ApoB 100

73
Q

what is elevated in familial hypercholesterinemia (type II)?

A

LDL

74
Q

what are the major manifestations of familial hypercholesterinemia (type II)?

A
  • premature coronary artery disease
  • corneal arcus
  • tendon xanthomas
  • xanthelasmas
75
Q

what are the major protein defects in familial dysbetalipoproteinemia (type III)?

A

ApoE

76
Q

what is elevated in familial dysbetalipoproteinemia (type III)?

A

chlyomicrons and VLDL

77
Q

major manifestations of familial dysbetalipoproteinemia (type III)?

A

premature coronary artery disease/PVD

78
Q

what is defective in familial hypertriglyceridemia (type IV)?

A

Apo A-V

79
Q

what is elevated in familial hypertriglyceridemia (type IV)?

A

VLDL

80
Q

major manifestation of familial hypertriglyceridemia (type IV)?

A

pancreatitis

81
Q

function of apoB-48?

A

mediates chylomicron secretion into lymphatics from intestine

82
Q

function of C-II?

A

binds LPL on peripheral tissue -> degrades triglycerides in chylomicron
‘cuts and cleaves’

83
Q

apoB48 is found on which molecules?

A

chylomicrons and chylomicron remnants

84
Q

CII and ApoE is provided by..

A

HDL

85
Q

function of ApoE?

A

mediates remnant uptake by the liver

86
Q

which is the only lipoprotein that does not have apoE?

A

LDL

87
Q

which molecules have B-100?

A

VLDL, IDL, LDL

88
Q

function of apo-B100?

A

binds with LDL causing endocytosis into peripheral cell

89
Q

which molecules have Apo A-I?

A

HDL

90
Q

function of ApoA-I

A

activates LCAT, which turns naiscent HDL into mature HDL

Test reviews DEDICATED (70 decks)

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