uworld assessment block #3 4.15 Flashcards

1
Q

genetic pulmonary hypertension? demographic?

A

inactivating mutation in BMPR2. normally inhibits smooth muscle proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

uterine leoimyomas presentation? demographic?

A

some asymptomatic. others: pelvic pressure, pain, menorrhagia, reproductive difficulties.

more common in women in thirties and forties. black women esp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ischemic colitis

A

mucosal hemorrhage, patchy areas of necrosis.

eventually becomes edematous and bowel wall thickens. then transmural infarction –> bowel perforation.

crampy abdominal pain, tenderness to palpation, bloody stool.

caused by (1) hypoperfusion 2nd to diministed cardiac output (2) occulusion of bowel vascular supply (atheroma, thrombosis, embolism)

common cause of GI hemorrhage in elderly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

presentation of whipple’s disease

A

PAS+ foamy macrophages in lamina propria

CANN:
cardiac symptoms (valves), arthalgia (synovial), mesenteric Nodes, and Neurologic symptoms (CNS). 

–> fat malabsorption // steatorrhea bc of occlusion of lymphatics

nfxn w/ tropheryma whipplei (gram positive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

type 1 collagen important in

A

bone, fibrous tissue, tendon, ligament, skin, sclerae.

body is 30% collagen by weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

mutations in osteogenesis imperfecta

A

COL1A1 and COL1A2. both combine to form type 1 collagen –> results in qualitative and quantitative type I collagen defects

brittle bone, short stature, scoliosis, blue sclerae (translucent CT over choroidal veins), hearing loss (abnormal ossicles), skin and ligament laxity, easy bruising.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

blue sclerae seen in..

A

osteogenesis imperfecta, progeria, menkes syndrome, cutis laxa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

general beta oxidation & ketone production

A

sequential removal of two-carbon units (acetyl-CoA) from fatty acids

first step. Acyl CoA dehydrogenase. when a lot of acetyl-CoA is made via beta oxidation, shunt to ketone body production (acetoacetate, 3-hydroxybutyate, acetone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 forms of acyl CoA dehydrogenase

A

short, medium, long-chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most common genetic defect in beta oxidation

A

medium chain acyl CoA dehydrogenase deficiency. symptoms first few years of life w/ prolonged fasting.

see increased dicarboxylic acids [from omega oxidation]. low glucose & ketones. acetyl-CoA low, cannot stimulate pyruvate carboxylase in gluconeogenesis. low acetyl-CoA, low glucose.

[energy from beta oxidation needed for gluconeogenesis!]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

glycogen phosphorylase

A

cleave alpha-1,4-glycosidic link between glycogen, liberates glucose-1-phosphate.

results in McArdles, when missing from muscle.

results in Hers disease, when missing from liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ras

A

oncoprotein component of MAP-kinase. inactive-GDP bound. active-GTP bound.

brings signal from receptor of cell surface into nucleus – promote mitogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

c-myc

A

nuclear phosphoprotein. fxns as a transcription activator controlling cell proliferation, differentiation, and apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rb

A

nuclear phosphoprotein, regulates G1-S checkpoint.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

velocity of a chemical reaction depends on.. (3)

A

concentration of enzyme, substrate, and product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

increasing enzyme concentration

A

increases Vmax.
Km unchanged.

lower Y intercept on lineweaver-burke plot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

increased Km on lineweaver burke plot

A

right on x-intercept (-1/Km)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what do chlamydia have INSTEAD of cell wall

A

cysteine-rick out membrane w/ S-S bridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hyphae are..

A

multicellular branching filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

fungi genome

A

diploid (eukaryotes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

four rRNA in eukaryotic cells

A

28S, 18S, 5.8S, 5S.

first: 45S transcript made by rRNA (pre-RNA) and cleaved in nucleolus by ribonucleases to make 28S, 18S, 5.8S rRNA molecules.

(ensures equal amounts are made)

5S rRNA made separately by RNA pol III

note additive, based on molecule size and how they move during centrifugation in a viscous medium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do thiazolidinediones increase insulin sensitivity

A

PPar gamma.

increase GLUT4 expression, increases number of insulin-responsible adipocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

glyburide

A

second generation sulfonyurea. closes K+ channel of pancreatic B cell, induces depolarization and L-type Ca2+ opening; stimulating insulin release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

repaglinide

A

meglitinide dervative: short-acting insulinotropic agent. adjunct to diet & exercise in DM-2. mechanism similar to sulfonyureas.

unlike sulfonyureas, repaglinide does NOT stimulate insulin release when extracellular glucose levels are lw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

first generation sulfonyureas

A

tolbutamide, chlorpropamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

second generation sulfonyureas

A

glyburide, glimepiride, glipizide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

amylin analogs

A

pramlintide; reduce gastrin emptying, reduce glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

GLP-1 analogs

A

exenatide, liraglutide.

increase insulin release, reduce glucagon release

like DDP-4 inhibitors

(side effect: pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

DDP-4 inhibitors

A

linagliptin, saxagliptin, sitagliptin

increase insulin, reduce glucagon (like GLP-1 analogs).

side effect: urinary or upper respiratory infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

metformin (biguanide)

A

can be used in absence of B cell function. decrease gluconeogenesis and increases glycolysis in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Crohn’s disease extrainstestinal signs

A

perineal abscess, kidney stones, sacroilitis, strictures/fistula

(ankylosing spondylitis, uveitis, apthous ulcers, pyoderma gangrenosum, erythema nodosum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ulcerative colitis extraintestinal signs

A

primary sclerosing cholangitis

pyoderma gangrenosum, erythema nodosum, ankylosing spondylitis, apthous ulcers uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

crohn’s disease vs ulcerative colitis on barium swallow

A

crohn’s = string sign (bowel wall thickening)

ulcerative colitis = loss of haustra (lead pipe sign)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

common area involved in crohn’s disease? second?

A

1st: terminal ileum
2nd: colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

common area involved in ulcerative colitis

A

always rectal involvement. only colon (no small bowel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

normal half life of warfarin

A

40 hours (steady state 4 hours later – 6.7 days)

therefore, P450 inducers/inhibitors take a few days to alter levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

warfarin in pregnancy

A

crosses placenta! teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why does warfarin cause skin / tissue necrosis

A

early –> prothrombotic bc kills off protein C before factors 2, 7, 9, 10 (due to protein C half life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

rx for hepatic encephalopathy

A

remove ammonia, acidify intestinal contents (i.e. lactulose –> lactic acid), to increase NH4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

lactulose rx for hepatic encephalopathy

A

nonabsorbable dissacharide, degraded by colonic bacteria –> lactic & acetic acid. acidify GI content – convert NH3 -> NH4+ –> osmotic effect, results in luminal distention, promote peristalsis –> levels of ammonia in circulation gradually declines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does B2 agonist cause bronchodilation

A

increase cAMP INHIBITS myosin light chain kinase

vasodilation, bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

bony callus

A

after trauma: firm but flexible hyaline cartilage, gradually strengthened by Ca2+ deposition and a surrounding meshwork of woven bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

physical signs of peripheral artery disease (i.e. DM)

A

thinning of skin, calf claudication (w/ rest pain), prolonged venous filling time, shiny coloured skin, hair loss, nail changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

signs & symptoms of DVT

A

leg pain, tenderness, edema, fever, Homan’s sign, venous distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

diabetic patient w/ foot infxn

A

think peripheral artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

RET in MEN2

A

single allele ACTIVATING mutation, predisposes to malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

DDx for hoarseness

A

laryngitis (most common), vocal cord paralysis, vocal cord nodules, laryngeal cancer, GERD, thyroid masses, overuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

path of right and left recurrent laryngeal n

A

RIGHT: loops below right SUBCLAVIAN (junction between brachiocephalic artery)

LEFT: loops below AORTIC ARCH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

fxn of recurrent laryngeal

A

intrinsic muscles of larynx except CRICOTHYROID (external laryngeal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

most DNA virus replicate where? except one DNA to replicate in cytosol completely? partially?

A

most in nucleus

completely cytosol: pox virus (largest DNA virus, carries own DNA-dependent RNA polymerase)

partially: hepadnavirus

51
Q

membrane of Herpesvirus?

A

from nuclear membrane

52
Q

circular DNA viruses (3)

A

polyoma, papilloma, hepadna

53
Q

RNA viruses mostly replicate in? except?

A

mostly: cytosol.
except: retrovirus and influenza virus

54
Q

naked DNA viruses

A

PAPP:

parvovirus, adenovirus, polyoma virus, papilloma virus

55
Q

naked RNA virus

A

CPR-Hepe

calicivirus, picornavirus, reovirus, hepevirus

56
Q

capsid of all DNA viruses

A

icosahedral (except pox, complex)

57
Q

all arboviruses cause.. name classes (3)

A

encephalitis & fever.

flaviviridae, togaviridae, bunyviridae

58
Q

papoviridae include

A

papillomavirus and polyomavirus

59
Q

infection w/ coccidiodes immitis

A

spherules w/ endospores that propogate. usually mild pneumonia w/ pleural effusion, can have thin-walled cavities (fever, hemoptysis)

also skin

SOUTHWEST.

60
Q

currant jelly hemopytsis

A

klebsiella! lobar, alcoholic

61
Q

PCP

A

less than 200ml. weakness and dyspnea, ground glass on x-ray

62
Q

mycoplasma

A

walking pneumonia. fever, malaise, nonproductive cough

63
Q

which cells are affected in hashimoto thyroiditis?

A

auto-immune mediated apoptosis of epithelial cells in thyroid gland.

see intense, diffuse (B & T) cell lymphocytic infiltration, germinal center formation.

high levels of serum thyroid autoantibodies (anti-TG & TPO)

64
Q

histology of graves disease

A

thyroid gland follicular epithelium TALL & crowded, forming pseudopapillae into follicular lumen

65
Q

colloid goiter

A

diffuse, nontoxic goiter. can occur sporadically. flattening of crowded columnar epithlium in follicles. gland becomes enlarged and colloid rich.

66
Q

follicular adenoma presentation

A

presents as unilateral neck mass. intact capsule separate normal thyroid tissue from numerous large, well-differentiated, colloid-containing follicles

67
Q

follicular carcinoma

A

single nodule in older woman. relatively uniform cells forming small follicles, nests, or sheets. colloid may be in follicles. capsular invasion with areas of hemorrhage or vascular invasion are common,

68
Q

VSD murmur

A

holosystolic murmur over left sternal border

69
Q

PDA on oxygenation of blood

A

allows oxygenated blood to flow from AORTA to pulmonary artery (spike in PO2)

70
Q

by when does Duchenne’s present?

A

age 3-5 progressive weakness, gower’s.

by age 12: loose ability to walk

71
Q

supression vs. repression

A

suppression: mature, conscious, TEMPORARY withhold unpleasant information from one’s awareness to postpone dealing with it.
repression: immature, unpleasant feelings pushed away, not to be dealt with.

72
Q

two key features of achalasia

A

hypertensive LES. absence of esophageal peristalsis in distal esophagus

due to less inhibitory ganglion cells in esophageal wall (imbalance favoring activity of excitatory ganglion cells)

73
Q

Glanzmann thrombasthenia

A

reduced GpIIb/IIIa. labs: no platelet clumping on smear (less platelet-platelet interaction)

like ITP / abciximab

74
Q

Bernard Soulier syndrome

A

reduced GpIb (less platelet-vWF interaction)

75
Q

what motor abnormality often accompanies broca’s aphasia?

A

located inferior frontal gyrus.

head and upper limb (near primary motor cortex

76
Q

damage to frontal eye field (frontal lobe)

A

IPSILATERAL eye deviation

normally points eye in opposite direction

77
Q

astereognosis

A

inability to identify objects based on touch

78
Q

agraphesthesia

A

inability to identify characters drawn on skin by touch alone

79
Q

hemihypesthesia

A

loss of sensation on one side of body

80
Q

on axial MRI, prostate is located

A

posterior to the pubic symphysis

81
Q

RBF =

A

RPF/ (1-Hct)

82
Q

RPF =

A

can be related to MAP and total vascular resistance in afferent and efferent arterioles

RPF = MAP / TVR

TVR = resistant in afferent + efferent

83
Q

postganglionic autonomic nervous system axons are..

A

UNMYELINATED

84
Q

important unmyelinated axons

A

(1) postganglionic autonomic axons
(2) afferent neurons that conduct heat sensation & from slow-onset dull, burning or visceral pain.
(3) first order bipolar sensory neurons of OLFACTION

unmyelinated referred to: group C fibers

85
Q

preganglionic autonomic nervous system fibers are..

A

MYELINATED.

both sympathetic and parasympathetic.

86
Q

grey vs. white rami communicans

A

white: preganglionic (myelinated) fibers from spinal cord to sympathetic chain.
grey: post-ganglonic (unmyelinated) fibers from sympathetic chain to spinal nerve.

87
Q

shared psychotic disorder

A

development of delusion in a person who is in a close relationship w/ a delusional person

(when not better explained by another psychotic disorder, medication, drug of abuse)

88
Q

magical thinking in schizotypial

A

odd beliefs (telepathy, superstitions, bizarre fantasies, preoccupations)

eccentric behavior, odd thinking, & ideas of reference

often lack close relationship

89
Q

delusional disorder

A

non-bizarre delusions present for at least one month.

non-bizzare: situations that, while unlikely, are possible. being followed, cheated, poisoned.

also: preserved occupational/social functioning, failure to meet diagnostic criteria for schizophrenia.

90
Q

formula for standard error

A

standard deviation / square root of n (same size)

SE decreases when sample size is increased

larger sample size, smaller standard error

91
Q

aseptic meningitis often caused by

A

picornaviridae

(usu enteroviruses: poliovirus, coxsackie A & B, echorvirus)

enterovirus that doesn’t cause asceptic meningitis: hepatitis A)

picornavirus that is not an enterovirus: rhinovirus

92
Q

two important arenaviruses

A
  • ssRNA:
  • LCV (lymphocytic choriomeningitis virus): aseptic meningitis
  • lassa virus: hemorrhagic fever virus, passed to humans when dirt / dust contaminated by rodent urine inhaled.
93
Q
  • ss RNA
A

always bring polymerase or fail replication

must bring own RNA-dependent RNA polymerase

arenavirus, bunyviridae, paramyxovirus, orthomyxovirus, filovirus, rhabdovirus

note: FILO (not flavi) and RHABDO (not reo or retro)

filo - ebola, marbug, crazy.
rhabdo - rabies, crazy

94
Q

what’s included in paramyxoviridae

A

mumps, measles, RSV, parainfuenza

mumps & measles can cause encephalitis

95
Q

most common cause of infant pneumonia? croup?

A

infant pneumonia & bronchiolitis: RSV

croup: parainfuenza

96
Q

MHC II coded by

A

HLA-DR, DP, DQ

97
Q

MHC I coded by..

A

HLA-A, B, C

98
Q

composition of MHC class I? class II

A

MHC I: alpha chain & b2 macroglobulin

(proteosomal fragments load peptides (via TAPs) into ER, assemble w/ b2 macroglobulin and alpha chain)

TAP = transporter associated w/ antigen processing

MHCII: alpha & beta chain

(invariant chain in ER) – invariant chain degraded in endosome

99
Q

possible presentation of iron deficiency anemia

A

(typical anemia: weakness, fatigue, headache, irritability)

& glossal pain, dry mouth, atrophy of tongue papillae, alopecia, pagophagia (eating ice)

100
Q

pagophagia

A

craving for ice, specific for iron deficiency

101
Q

presentation of folate deficiency

A

megaloblastic anemia w/..

sore tongue, pain on swallowing, angular stomatitis, GI upset, hyperpigmentation

102
Q

inheritance of sideroblastic anemia

A

associated w/ MDS

x-linked recessive defect in d-ala synthase

(can’t turn glycine + succinyl CoA —> d-ALA)

103
Q

acquired sideroblastic anemia causes

A

most common: alcohol. also, lead, B6 deficiency, Cu deficiency, isoniazid

104
Q

histology of sideroblastic anemia

A

ringed sideroblasts w/ iron-laden mitochondria.

105
Q

presentation of pernicious anemia

A

usu older women of northern european descent.

  1. lemon-yellow colouring
  2. smooth shiny tongue (atrophic glossitis)
  3. shuffling broad-based gait
106
Q

high baseline plasma insulin w/ normoglycemia?

A

EARLY insulin resistance

(even when glucose levels are normal, and respond to oral glucose just fine)

eventually, amyloid deposition in pancreas w all this glucose secretion will make it fail

107
Q

early insulin resistance vs. insulinoma

A

both have chronically elevated insulin levels.

normal serum glucose w/ EARLY insulin resistance.

insulinoma: fasting HYPOGLYCEMIA (i.e. after exercising)

108
Q

marfan syndrome (fibrillin gene mutation) and homocystinuria (cystathione beta-synthase deficiency) both result in..

A

genetic heterogeneity. mutations of diff genes –> same phenotype.

marfanoid body habitus, tall, thin stature, elongated extremities, arachnodacty, ectopia lentis.

109
Q

how many ATP made in glycoylsis? anerobic. (aka RBC; no mitochondria, no oxidative phosphorylation)

A

2 ATP per glucose (+ 2 NADH, which are used to convert pyruvate to lactate)

110
Q

how many ATP made with aerobic metabolism of 1 glucose

A

38 per glucose

111
Q

1 cycle of TCA (w/ 1 acetyl-CoA) makes

A

consume acetyl-CoA –> 3 NADH, 1 FADH2, 1 GTP

112
Q

how many ATP per NADH? FADH? GTP

A

NADH = 3 ATP
FADH2 = 2 ATP
1 GTP = 1 ATP

113
Q

net aerobic metabolism of glucose via malate/aspartate shuttle (heart and liver)? via glycerol-3-phosphate shuttle (muscle)

A

net glucose via malate/aspartate: 32

net glucose via glycerol-3-phosphate: 30

114
Q

enzyme inhibited by -azoles

A

prevent ergosterol synthesis.

block 14-alpha-sterol-demethylase

build up lanosterol

115
Q

flutacytosine fxn

A

antifungal, disrupts nucleic acid synthesis, inhibits thymidylate synthetase

116
Q

V max depends on…

A

concentration of enzyme.

117
Q

Km depends on..

A

affinity of drug for enzyme, inverse

118
Q

enzyme inhibited by -binafine’s

A

prevent formation of lanosterol.

block squalene epoxide

build up squalene

119
Q

lichen sclerosus et atrophocis

A

inflammatory condition. thought to have underlying autoimmune pathophysiology. autoantibodies against ECM1 protein.

both genders, any part of body. females –> genital and perineal region usu.

pruitis, dysuria, pain w/ defecation and dyspareunia.

lesions: white, atrophic macules w/ a “cigarette paper” quality. coalesce into plaques as condition progresses.

long term sequelae: squamous cell carcinoma, genital disfigurement.

rx: ultra high potency topical corticosteroids

120
Q

leukoplakia

A

mucosal surfaces of mouth / genital (labia majora not considered mucosal).

white thickening of mucosal surface.

many diff causes. often EBV w/ immunosuppression

121
Q

vaginal candidiasis presentation? cutaneous?

A

vaginal: white, curd-like malodorus discharge.
cutaneous: skin folds. erythema and satellite pustules.

122
Q

lichen planus

A

6 P’s: pruitic, purple, polygonal, planar papules & plaques.

mucosal presentation: wickham striae (reticular white lines)

histology: sawtooth infiltrate of lymphocytes at dermal-epidermal junction

123
Q

extrinsic causes of ATN?

intrinsic causes?

A

aminoglycosides, amphotericin B, radiographic contrast dye, heavy metals.

myoglobinuria, hyperuricemia, bence-jones protein in multiple myeloma