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UWorld mixed > test #44 5.4 > Flashcards

test #44 5.4 Flashcards

1
Q

kidney is entirely derived from..

A

metanephros

metanephric diverticulum (ureteric bud – collecting duct system)

metanephric mesenchyme (glomeruli & tubules)

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2
Q

when does the metanephros develop

A

5-6th week of gestation

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3
Q

most common cause of unilateral fetal (antenatal) hydronephrosis

A

ureteric bud = initially solid cord, then canalizes (done by 10th wk)

metanephros can produce urine before ureteric bud canalizes –> hydronephrosis

last segment to canalize: ureteropelvic junction (between kidney and ureter)

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4
Q

cause of antenatal hydronephrosis obstruction

A

most common:
-ureteropelvic junction (last to recanalize)

other:

  • vesicoureteral junction
  • posterior urethral valve (membrane in posterior urethra)
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5
Q

when is a fetus able to make urine

A

8-10th wk

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6
Q

pilocytic astrocytoma on imaging

A

usu in cerebellum, but can’t be in cerebral hemisphere

cystic component w/ a tumor nodule.

nodule: active part of tumor

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7
Q

most common malignant brain tumor in children

A

medulloblastoma

exclusively cerebellum

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8
Q

histology of medulloblastoma

A

small, blue cells. hyperchromatic nuclei, scant cytoplasm

can see homer-right rosettes

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9
Q

histology of ependymoma

A

perivascular rosettes w/ rod-shaped blepharoplasts (basal ciliary bodies) near nucleus

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10
Q

odds ratio vs relative risk

A

odds ratio: ad/bc

relative risk: [a/(a+b) / c/(c+d) ]

given chart:
a b
c d

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11
Q

expressing support in interview

A

express concern independent of understanding.

express concern & interest for patient by acknowledging what the patient says. does NOT claim to know how the patient feels

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12
Q

facilitation in interview

A

interviewer encourages patient to talk more about experience. asking “and then what happened”

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13
Q

empathy in interview

A

expression of understanding of experience.

try to “walk in the shoes” to vicariously experience feelings, thoughts, actions.

differs from support, bc tries to project into the experience.

“i can imagine how that experience affected your perspective on life”

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14
Q

reflection in interview

A

when physicial repeats what patient tells him, i.e. by summarizing

“so, you’re telling me you were molested as a kid”

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15
Q

confrontation in interview

A

interviewer draws attention to discrepancy in response

“although you say you were disturbed, you sound unaffected as you describe it”

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16
Q

mitral valve problems in rheumatic fever

A

early: mitral valve regurgitation
late: mitral valve stenosis

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17
Q

death with rheumatic fever

A

early: myocarditis
late: valvular heart disease –> valvular issues!

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18
Q

diffuse fibrous thickening & distortion of mitral valve leaflets.

commissural fusion at leaflet edges

stenotic orifice w/ diastolic murmur

all suggest

A

rheumatic fever mitral valvular disease

mitral stenosis –> atrial dilation –> atrial mural thrombus –> stroke

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19
Q

most common cardiac manifestation of rheumatoid arthritis

A

fibrinous pericarditis

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20
Q

almost all causes of mitral valve STENOSIS are caused by…

A

chronic rheumatic heart disease

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21
Q

infective endocarditis of mitral valve tends to be..

A

destructive and regurgitant

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22
Q

mitral valvular calcinosis

A

usually does not impair valve function

usu in women > 60w/o w/ myxomatous floppy mitral valve or elevated left ventricular pressure

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23
Q

ASD on ausculation

A

wide fixed S2 splitting.

does not change w/ respiration

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24
Q

split S1?

A

suggests delayed closure of tricuspid valve, due to right bundle branch block

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25
Q

mid-systolic crescendo-decrescendo

A

aortic stenosis

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26
Q

early diastolic decrescendo murmur

A

aortic regurgitation

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27
Q

late systolic crescendo murmur w/ mid-systolic click

A

mitral valve prolapse

click: sudden tensing of chordae tendinae

most frequent valvular lesion

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28
Q

holosystolic high pitched blowing murmur

A

mitral regurgitation

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29
Q

holosystolic harsh murmur, loudest in tricuspid area, accentuated w/

A

VSD

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30
Q

presystolic accentuation

A

intensity of diastolic murmur before louder just before S1

or when diastolic murmur appears just prior to S1

can result from mitral/tricuspid valve stenosis OR physiological increased flow through valves

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31
Q

systolic ejection murmur accentuated by standing

A

decrease preload

hypertrophic obstructive cardiomyopathy

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32
Q

early diastolic decrescendo murmur decreased by amyl nitrate

A

vasodilate –> decrease afterload

aortic regurgitation

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33
Q

late diastolic murmur eliminated by atrial fibrillation

A

mitral and/or tricuspid stenosis

related to atrial contraction

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34
Q

drug induced lupus

A

ANA, anti-histone antibody = specific

Q CHIMPPS

quinidine
chlorpromazine
hydralazine
isoniazid
methyl-dopa
procainimide
phenytoin
sulfa drugs

also etanercept & minocycline

high risk: hydralazine & procainamide

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35
Q

immediate side effects of adenosine

A

chest burning, flushing transient hypotension

but has very short half life

vasodilator in chemical cardiac stress tests & stops acute supraventricular tachycardias

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36
Q

where are ureas nitrogen dervived from

A
  1. NH3

2. aspartate (sweet pee)

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37
Q

biochemical pathways involving aspartate (3)

A

-urea cycle (contributes one N)
-pyrimidine synthesis
combines w/ carbamoyl phosphate to make orotic acid (temporary base)

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38
Q

orotic acid + PRPP makes

A

UMP

this path is blocked in orotic acidura

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39
Q

leflunomide

A

blocks combination of carbamoyl phosphate + aspartate –> orotic acid

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40
Q

urea cycle

A

ordinarily, careless crappers are also frivulous about uriantion

ornithine + carbamoyl phosphate –> citrulline + aspartate –> arginninosuscinate –> fumarate (released) + arginine –> urea + ornithine

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41
Q

rate limiting step in urea cycle

A

carbamoyl phosphate synthase I

remember: I pee

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42
Q

what forms asparagine. relevance?

A

non essential amino acid.

produced from oxaloacetate in transamination reaction.

oxaloacetate -> aspartate
using glutamate amino group

aspartate -> asparagine
using glutamine amino group
via asparagine synthase

only comes up as site of N-linked modification in golgi

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43
Q

alanine formed by

A

transfer of an amino group onto pyruvate

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44
Q

parasympathetic agents on blood vessels

A

do not have cholinergic innervation, but do have muscarinic receptors on ENDOTHELIAL surface

  1. promote release of NO (endothelium-derivived relaxing factor),
  2. activates guanylate cyclase,
  3. increase cGMP
  4. activates Ca2+ pump &
  5. causes Ca2+ efflux.

decrease in Ca2+ in vascular smooth wall –> RELAXATION

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45
Q

muscarinics on GI system

A

increase tone of smooth muscle in viscera; increase motility & secretion, opens sphincters

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46
Q

tibial n. sensation & motor

A

can’t TIP toe w/ damage

inversion & plantar flex & toe flex
plantar region of foot

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47
Q

common peroneal n. sensation & innervation

A

foot dropPED w/ damage

eversion & dorsiflex
dorsum of foot

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48
Q

cutaneous medial leg?

A

cutaneous branch of saphenous n (branch of femoral)

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49
Q

accentuated second heart sound over upper left sternal border suggests..

A

pulmonary HTN

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50
Q

common cardiac features that can be seen in CREST

A

pulmonary HTN –> leading to cor pulmonale (right heart failure)

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51
Q

pathogenesis of CREST and systemic sclerosis

A

increased proliferation & accumulation of monoclonal T cells in affected tissue

secrete cytokine, esp TGF-b, increase production of collagen & ECM by fibroblasts

any tissue affected

SMALL ARTERIOLES & capillaries FIRST

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52
Q

presentation of lichen planus

A

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

mucosal involvement
Wickham striae: reticular white lines

sawtooth infiltrate of lymphocytes at dermal-epidermal junction

associated w/ hep C

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53
Q

most common cause of death in scleroderma

A

pulmonary!

interstitial fibrosis or
pulmonary HTN –> COR PULMONALE

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54
Q

neisseria meningitidis vaccine

A

capsular polysaccharide vaccine

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55
Q

meningitis in young college student w/ purpuric rash

A

neiseria meningitidis

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56
Q

virulence factors in neisseria meningitidis

A
  1. polysacharide capsule
  2. IgA protease
  3. LPS endotoxin
  4. pili (attach on respiratory mucosa)
    5.
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57
Q

heat-killed bacteria vaccine

A

bordetella pertusis, vibrio cholera, yersenia pestis vaccine

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58
Q

borrelia burgdorferi vaccine

A

recombinant bacterial outer surface protein

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59
Q

corynebacterium diptherium & clostridium tetani vaccine

A

inactivated toxin (toxoid)

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60
Q

BCG vaccine

A

TB: live attenuated organisms of a different mycobacterium species

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61
Q

salmonella typhi & francisella tularensis vaccine

A

live attenuated

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62
Q

protein A

A

staph aureus

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63
Q

IgA protease

A

SHiN

strep pneumo
haemphilus influenza
neisseria meningitidis

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64
Q

where is proinsulin cleaved to insulin + c-peptide?

A

endoplasmic reticulum of beta-pancreatic cells

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65
Q

what is a good marker of total rate of B-cell endogenous insulin secretion

A

C-peptide

unlike insulin: C-peptide is not significantly extracted on first pass through the liver!

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66
Q

what drug stimulates insulin release from pancreas

A

sulfonyureas

also GLP-analogues

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67
Q

GLUT-2 transporter

A

liver and pancreas

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68
Q

how do GLP-1 analogs increase insulin secretion

A

increase cAMP, which increases insulin secretion

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69
Q

99mTc-pertechnetate detects..

A

gastric mucosa

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70
Q

diagnosis of meckel diverticulum

A

pertechnetate radionucleotide study

accumulates in gastric mucosa &zenker diverticulum often forms gastric / pancreatic tissue

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71
Q

how does meckel diverticulum form

A

failure of complete obliteration of omphalomesenteric duct / vitelline duct

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72
Q

most common manifestation of meckel diverticulum?

A

lower GI bleed & RLQ pain (due to acid secretion by ectopic gastric mucosa)

could also cause intusseception – colicky abdominal pain, currant jelly stool

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73
Q

inflammed meckel diverticulum difficult to differentiate from..

A

acute appendicitis

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74
Q

failure of proper descent of hindgut

A

different degrees of anal agenesis or imperforate anus

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75
Q

abnormal midgut rotation around SMA can lead too..

A

fibrous adhesive bands that can lead to intestinal obstruction

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76
Q

genetics of tuner’s

A

genetically heterogeneous

in cases of monosomy 45 XO: loss of parental X chromosome during mitosis (after fertilization

  • 50% complete monosomy (45, XO)
  • 30% mosaicism (46 XX / 45 XO)
  • remainder have structural abnormalities of X (such that X fragments or isochromosomes) or partial monosomy deletions of X.
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77
Q

weight loss despite normal to increased food intake, polyuria, polydypsia, and fatigue in young adult

A

type 1 DM

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78
Q

diagnosis of type 1 DM

A

fasting blood sugar > 126 mg/dL on 2 occasions

only need 1 if symptomatic

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79
Q

when is oral glucose tolerance test used?

A

usually reserve for pregnant women for gestational diabetes. rarely used. fasting glucose is key.

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80
Q

helicotrema

A

far part of cochlea w/o basilar membrane, allows for communication of scala vestibuli (top) and scala tympani (bottom)

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81
Q

high frequency sounds on which part of basilar membrane? low frequency?

A

high frequency: stiff part (base) closer to oval/round window

low frequency: floppy part (apex) near helicotrema

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82
Q

what’s in the inner ear

A

fluid filled site encased in bone that houses cochlea, semicircular canals & vestibule

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83
Q

fluid in scala vestibuli, scala media, scala tympani

A

VMT

vestibuli & tympani have perilymph (high Na+ like extracellular fluid)

media (high K+ like intracellular)

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84
Q

what separates scala media from scala tympani

A

basilar membrane

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85
Q

what is housed in scala media

A

tectorial membrane & organ of corti

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86
Q

sources of alkaline phosphate. how can it be differentiated (3)?

A

bone

also: placenta, liver, intestine

can differentiate between liver & bone via..

  1. electrophoresis &
  2. specific monoclonal antibodies
  3. denaturation (bone denatures easy: bone=boil)
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87
Q

tartare resistant acid phosphatase

A

specific to osteoclasts, but not commonly measured bc not stable protein

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88
Q

calcitonin

A

inhibit osteoclasts

doesn’t affect osteoblasts much.

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89
Q

urinary deoxypyridinoline and hydroxyproline

A

measures of osteoclast activity

breakdown of collagen material

note: hydroxyproline not good measure, common in meat products.

90
Q

most reliable measure of osteoclast activity

A

urinary deoxypyridinoline

91
Q

side effects of thiazides

A 
HYPER GLUC
increase in..
1. glucose
2. lipids & cholesterol
3. uric acid: gouty arthritis
4. calcium: useful rx for calcium nephrolithiasis

HYPO:
decrease in
1. potassium
2. BP : decreased blood volume and peripheral vascular resistance

92
Q

which diuretic is helpful rx for renal nephrolithiasis

A

thiazides, reabsorb calcium, less in tubules

93
Q

which drugs increase HDL

A

niacin and fibrates (via ppar-a)

94
Q

high HbA2 suggests

A

thalasemia trait
a2d2 globin

(due to decrease production of a2b2 = HbA1)

95
Q

Hb types in sickle cell

A

HbS high
HbA1 low

no affect on HbA2

96
Q

most common pediatric malignancy

A

acute lymphoblastic leukemia

97
Q

distinguishing between pre-B and pre-T cell ALL clinically?

A

T-ALL present w/ mediastinal mass

can compress..

  • great vessels: SVC syndrome
  • esophagus: dysphagia
  • trachea: stridor, dyspnea
bcell = 80% of cases
tcell = 15%

B cell: fever, malaise, bleeding, bone pain, hepatosplenomegaly

98
Q

black pigment stones

A

calcium billirubinate
increased unconjugated bilirubin
associated w/ chronic extravascular hemolysis

small, spiculated, crumbly.

radioopaque– appear on X-ray

99
Q

glucagon’s major effect

A

liver: increased production of glucose
pancreas: insulin secretion

unlike epinephrine, insignificant affects on skeletal muscle & adipocytes

100
Q

epinephrine glucose related effects?

A
  1. liver: increased glycogenolysis / gluconeogenesis
  2. skeletal muscle: decrease glucose uptake & increase alanine release (for liver gluconeogenesis)
  3. adipose tissue: increased breakdown of triglycerides, increasing free fatty acids & glycerol in circulation
101
Q

kidney’s role in hypoglycemia

A

first 24 hrs of fasting: liver makes glucose

sustained hypoglycemia: gluconeogenesis in kidney can kick in

102
Q

major risk of clozapine

A

agranulocytosis, look at complete blood count

also seizures

103
Q

clozapine receptor target

A

D4

unlikely to cause dopaminergic side effects of pseudoparkinsonism, tardive dyskinesia, hyperprolactinemia

(unlike other antipsychotics: D2)

104
Q

ziprasidone side effect

A

long QT

105
Q

leading cause of end stage renal disease in US

A

diabetic nephropathy

106
Q

earliest detection of diabetic nephropathy?

A

microalbuminemia

30-300mg/day in 24hr collection

30-300microgram/mg of creatinine in spot collection

107
Q

patient w/ dry cough & swollen face & dilated vessels?

A

superior vena cava syndrome, consider mediastinal mass

108
Q

SVC syndrome

A
  • facial edema / plethora
  • venous distension distal to obstruction

due to mass compressing SVC like lung tumor

impaired venuos return from upper body

109
Q

where does SVC form

A

union of right & left brachiocephalic veins behind 1st costal cartilage

110
Q

most common causes of SVC syndrome

A

(1) lung mass

2) non-hodgkin’s lymphoma (of perihilar, paratracheal lymph nodes

111
Q

what hormones does small cell lung cancer secrete

A

ACTH and ADH

112
Q

what hormone does squamous cell carcinoma in lung secrete

A

PTHrP

113
Q

superior sulcus tumor

A

i.e. pancost tumor
at lung apex: cause shoulder pain due to compression of bachial plexus & superior cervical ganglion = horner’s

can sometimes cause SVC, but less common than mediastinal mass

114
Q

inactivation of hep A

A

water chlorination, bleach (1:100), formalin, UV irradiation, boiling to 85 C for 1 min

will not die w/ frying, 20%diethy ether (bc naked), acid (recall - survives in stomach)

115
Q

autoclaving

A

120 degrees for 20 min

116
Q

boiling in celcius

A

100

117
Q

cholesterol med w/ unbearable pruritus & flushing

A

niacin

118
Q

mechanism of niacin

A

decrease synthesis of hepatic TG and VLDL (due to its suppression of free fatty acid release from peripheral tissue)

also increases HDL

119
Q

how do bile acid resins reduce cholesterol

A

cholesterol is used in synthesis of bile acids

cholesterol 7a-hydroxylase

120
Q

side effects of bile acid resins

A

GI upset

increased TG!

121
Q

ezetimibe mechanism

A

reduces reabsorption of cholesterol and bile acids too

122
Q

what is effective against chlamydia

A

doxycycline

macrolides

123
Q

risperidone side effect

A

hyperprolactinemnia (due to dopamine antagonist effect):

prolactin inhibits release of GnRH from hypothalamus

can lead to amenorrhea, galactorrhea, breast soreness

124
Q

anytime see amenorrhea

A

must rule out pregnancy (b-hCG)

125
Q

“lake-like” cavitary brain lesion

A

lacunar stroke! HTN arteriolar sclerosis

126
Q

brain injury that does not show up in acute CT, but later does as cystic space in basal ganglia / deep white matter

A

think lacunar stroke, occlusion of distal penetrating arteriole

most commonly: due to hypertensive changes in arterioles (lipohyalinosis and microatheromas)

127
Q

cause of lacunar infarcts

A

often chronic HTN –> lipohyalinosis, microatheroma –> ARTERIOLAR SCLEROSIS

diabetes & smoking also risk factors

will not present in acute CT, bc small, later show up as lake-like lesion

128
Q

pure motor hemiparesis

A

infarct to posterior limb of internal capsule

129
Q

pure sensory stroke

A

infarct to VPL or VPM of thalamus

130
Q

ataxia-hemiplegia syndrome

A

infarct to base of pons

131
Q

dysarthria-clumsy hand syndrome

A

infarct to base of pons or genu of internal capsule

132
Q

types of infarcts caused by cardiac thrombosis & carotid atherosclerosis

A

usu strokes often involve large territories, due to involvement of large / medium sized vessels

CAN cause lacunar strokes if no other pathological cause can be identified, but these are most often by arteriolar sclerosis due to HTN

133
Q

hypoxic encephalopathy defined as

A

abrupt cessation to CBF, as from cardiac arrest or shock.
more global

pyramidal cells of hippocampus & purkinjee cells & watershed most often affected

134
Q

hypertensive encephalopathy

A

leads to cerebral edema due to breakthrough hyperperfusion that is not compensated for by cerebral autoregulation.

headache, nausea and vomiting, other non-localizing neuro symptoms

135
Q

sequelae of cerebral amyloid angiopathy

A

results in hemorrhage within cortex & subcortical white matter. not usu ischemic stroke

136
Q

Charcot-Bouchard aneursyms

A

microaneursyms < 1mm in diameter. occur in small penetrating arterioles that perfuse basal ganglia, pons, subcortical white matter

due to long standing HTN and prone to rupture

–> hemmorhagic stroke w/ intraparenchyma hyperdensity

137
Q

what goes into calculating reid index

A

thickness of gland / thickness of wall between epithelium & cartilage

NOT including cartilage

138
Q

severity of bronchitis depends on.

A

extent to which the luminal diameter of bronchi / bronchioles is decreased = reid index

major contributor to increase : thickness of mucous gland layer

139
Q

normal reid index

A

40%

in chronic bronchitis > 50%

140
Q

what rxn does sphingomyelinase normally do

A

absent in nieman pick

sphingomyelin -> ceramide & phosphorylcholine

141
Q

enzyme deficiency in metachromatic leukodystrophy & accumulated substance

A

arylsulfatase A

accumulate: sulfatides

142
Q

enzyme deficiency in tay sachs & accumulated substance

A

hexosaminidase A

accumulate GM2 ganglioside

143
Q

Fabry disease enzyme deficiency & accumulated substances

A

X-linked recessive
alpha-galactosidase A

accumulate ceramide trihexoside

144
Q

Farber disease

A

ceramidase deficiency

autosomal recessive

ceramide accumulation in neurons & within skin granulomas

145
Q

IV anesthetics (5)

A

barbituates, benzodiazepines, arylcyclohexylamines (ketamine), opiods, propofol

146
Q

pharmacokinetics of thiopental (bartibituate)

A

high potency, high lipid solubility (brain fast), but rapidly redistributed to tissue –> skeletal muscle & fat

induction

decreases CBF

antidote: charcoal / bicarb

IV

147
Q

benzodiazepine for anesthetic

A

IV

midazolam, for endoscopy

can combine w/ gas & narcotics.

associated w/ anterograde amnesia and respiratory depression

antidote: flumazenil

IV

148
Q

arylcyclohexylamine (ketamine) for anesthetic

A

PCP analogue, dissociated anesthetic. NMDA receptor antagonist.

cardiovascular stimulant, causes disorientation, hallucination, and bad dreams,

increases CBF

IV

149
Q

opiods for anesthetic

A

morphine, fentanyl.

used w/ other CNS depressants during anesthesia

IV

150
Q

propofol for anesthesia

A

IV

sedation in ICU
rapid induction, short procedure

less postop nausea than thiopental

potentiates GABAa

151
Q

local anesthetic classes

A

esters: cocaine, procaine, tetracaine
amides: lidocaine, bupivacaine, mepivacaine

152
Q

mechanism of action for local anesthetics (esters & amides)

A

enter cell, bind to voltage gated Na+ channels, prevent AP.

[like class I antiarrhythmics]

enter cell uncharged, bind charged

often given w/ vasconstrictors to increase local concentration

note: if acidic tissue, need increased dose, bc charged species cannot enter cell to work.

153
Q

order of nerve blockade w/ local anesthetics

A

size is most important

  1. small myelinated
  2. small unmeylinated
  3. large myelinated
  4. large unmyelinated
154
Q

order of loss of sensation w/ local anesthetic

A
  1. pain
  2. temperature
  3. touch
  4. pressure
155
Q

succinylcholine mechanism of action

A

nAch strong agonist (insensitive to AchE)
depolarizing muscle relaxant

phase 1: sustained depolarization & inactivation.
- POTENTIATED w/ AchE inhibitors

phase 2: desensitized to succinylcholine, but continued block of nAchR (nondepolarizing phase)
- ANTIDOTE w/ AchE inhibitors

side effects: hyperkalemia, hypercalcemia, malignant hyperthermia

156
Q

important side effects of succinylcholine

A

increased:

  • potassium
  • calcium

malignant hyperthermia

157
Q

nondepolarizing muscle relaxants

A

nAch antagonists
nondepolarizing muscle relaxants

tubocurarine, atracurium, mivacurium, pancurionium, vecuronium,

reversal: AchE inhibitors (+ atropine, to prevent muscarinic effects)

158
Q

AchE inhibitor during phase I of succinylcholine? phase II?

A

phase I: depolarizing / inactivating. potentiate

phase II: nondepolarizing block: antidote

159
Q

AchE inhibitor w/ nondepolarizing muscle relaxant (tubocurarine, etc)

A

antidote! give atrophine to block muscarcinic effects

160
Q

dantrolene

A

prevent release of Ca2+ from sarcoplasmic reticulum

used as rx: for malignant hyperthermia & neuroleptic malignant syndrome

161
Q

time frame of succinylcholine vs. nondepolarizing NMJ blockers

A

succinylcholine more rapid (60 seconds)

162
Q

train-of-four stimulation response

A

used during anesthesia to assess degree of muscle relaxation

stimulate presynaptic neuron & increase Ach in cleft. like an AchE inhibitor

163
Q

train-of-four response to phase I succinylcholine

A

no response initially

then quickly will gave gradually increased equivalent response in subsequent sets of stimulations

(bc normally quickly metabolized by plasma cholinesterases)

164
Q

train-of-four response to phase II succinylcholine

A

mirrors nondepolarizing NMJ blockers
nAchR insensitive to depolarization by succinylcholine, but will still block the receptor.

fading pattern w/ progressive reduction in each of the 4 responses

fading, bc of blockade of presynaptic nAchR preventing preparation of vesicle fusion.

165
Q

train-of-four response to nondepolarizing NMJ blockers

A

nAchR antagonists

fading pattern w/ progressive reduction in each of the 4 responses.

occurs bc nAchR antagonists prevent presynaptic neuron from preparing additional vesicles for release

mirror phase II succinylcholine

166
Q

duration of action of succinylcholine? variation?

A

determined by
1. diffusion out of NMJ &
2. metabolism by plasma cholinesterase
(insensitive to AChE)

usu < 10min

but! 1/3000 pt homozygous for atypical plasma cholinesterase, which breaks succinylcholine SLOWLY over 1-3 hrs.

neostigmine early: potentiate
neostigmine late: antidote

167
Q

explain normal train-of-four response

A

stimulate presynaptic neuron & measure depolarization in muscle

in sequential twitches, presynaptic nAchR play an important role in preparing additional vessicles for release

*impt when using NMJ blockers that are depolarizing agonists / nondepolarizing antagonists

168
Q

train-of-four response to succinylcholine in phase I

A

sustained and equal reduction of all 4 twitches

can overcome w/ additional train-of-four bc drug is metabolized by plasma cholinesterase

169
Q

succinylcholine transition from phase I to phase II

A

occurs w/ continued infusion

  1. depolarized & inactivated
  2. eventually desensitize to succinylcholine; acts as a nondepolarizing nAchR blocker

will also block / inactivate presynaptic nAchR needed to prepare vesicles for fusion in phase II

normally succinylcholine rapidly degraded via plasma cholinesterase: phase I then gone.

170
Q

how many Ach molecules must bind to nAchR?

A

2 molecules!

171
Q

whenever have a drug that is dependent on -esterase, worry about? (i.e. drugs metabolized by AchE)

A

slow and fast metabolizers!

172
Q

atracurium special considerations

A
  1. safe w/ renal & hepatic impairment
  2. spontaneous breakdown to: laudonisine, which can cause SEIZURES
  3. activates histamine -> BP fall, flushing, bronchoconstriction
173
Q

mivacurium special considerations

A
  1. very short acting

2. metabolized by AchE (therefore: consider slow / fast metabolizers)

174
Q

special considerations with NMJ blockers

A

paralytics! patient can still sense things! must give anesthetic & analgesics too.

175
Q

impt feature of nAchR

A

desensitizes quickly! generally, too much Ach –> depolarization –> cholinergic crisis, which can happen w/ overmedicating for myasthenia gravis.

176
Q

why does succinylcholine trigger malignant hyperthermia?

A

initially depolarizes muscle, lots of Ca2+ release and ATP generation

177
Q

dilated esophagus, microbial cause? congenital?

A

microbial: esp from central / south america: trypanosomi cruzi
congenital: achalasia

178
Q

neurotoxin in trypanosoma cruzi?

A

destroys myenteric plexus in esogagus. similar in colon & ureter

–> megaesophagus, megaureter, megacolon

(also dilated cardiomyopathy)

179
Q

babesia divergens infxn

A

endemic in northeast US.
transmitted by ticks

malaria-like illness w/ predilection for asplenic patients

fever & hemolytic anemia

see blood smear w/ maltese cross or ring

rx: atovaquone & azithromycin

180
Q

brucella melitensis

A

drinking infected milk / contact w/ infected sheep & goats

fever, malaise, lymphadenopathy, hepatosplenomegaly

“undulating fever”

181
Q

camplyobacter fetus / intestinalis

A

opportunistic pathogen
infects immunocompromised

septicemia in newborns, women in 3rd trimester of pregnancy, debilitated elderly

182
Q

intial steps of ketogenesis

A

start from: leucine / lysine
or

acetyl-CoA –> HMG CoA
via HMG CoA synthase

HMG CoA –> acetoacetate
via HMG CoA lyase

acetoacetate –> B-hydroxybutyrate
via NADH -> NAD+

183
Q

where does ketogenesis occur

A

mitochondria of hepatocytes

184
Q

metabolism of ketones

A

in mitochondria of: skeletal muscle, cardiac muscle, renal cortex, brain. (not RBC)

b-hydroxybutyrate -> acetoacetate

acetoacetate –> acetoacetate CoA
via thiophorase
(convert succinyl CoA –> succinate)

acetoacetate –> 2 acetyl CoA

185
Q

what is the major stimulus for ketogenesis

A

increase in acetyl-CoA

due to..
depletion of oxaloacetate.

  1. starving: oxaloacetate used in gluconeogenesis
  2. alcoholic: NAD+ depletion converts oxaloacetate -> malate (to generate more NAD+)
186
Q

which 2 cells cannot use ketones

A
  1. RBC; no mitochondria
  2. hepatocytes (liver): no thiophorase / succinyl-CoA-acetoacetate CoA transferase

can’t convert acetoacetate –> acetoacetyl CoA

187
Q

2 mechanisms for removal of cholesterol

A
  1. excretion of free cholesterol in bile

2. conversion to bile salts (cholesterol 7-a-hydroxylase)

188
Q

bile acid synthesis steps

A

cholesterol -> cholic & chenodeoxycholic acid
via: cholesterol 7-a-hydroxylase
(rate limiting step)

conjugated w/ taurine / glycine
–> bile salt

189
Q

what solubilizes cholesterol in bile?

A

bile salt & phosphatidylcholine

190
Q

abnormal keratinization of mucus-secreting columnar epithlelium suggests

A

vitamin A deficiency
epithelial cell metaplasia

can occur w/ cystic fibrosis
fat-soluble vitamin deficiency & damage to glands w/ inspissated mucous

191
Q

most likely outcome of hepatitis B infection

A

acute hepatitis w/ complete resolution

192
Q

possible outcomes w/ hepatitis B infection

A

most common: 1. acute hepatitis w/ complete resolution >95%

  1. chronic hepatitis
    w/ or w/o cirrhosis & increased risk of hepatocellular carcinoma (4-5% chronic hepatitis; of those 20-50% develop cirrhosis; those 10% get HCC)
  2. fulminant hepatitis w/ massive liver necrosis (<1%)
193
Q

fate of patients w/ chronic hepatitis B infection

A

only occurs w/ 4-5% of hep B infxn

20-50% develop cirhhosis
10% HCC

(hep B–> usu acute hepatitis w/ complete resolution)

194
Q

ras

A

proto-oncogene

cancer of bladder, lung, colon, pancreas, kidney

195
Q

n-myc

A

proto-oncogene

neuroblastoma
small cell lung cancer

196
Q

erb-b1

A

proto-oncogene

squamous cell carcinoma of lung

197
Q

TGF-a

A

proto-oncogene

astrocytoma, hepatocellular carcinoma

198
Q

sis

A

proto-oncogene

astrocytoma, osteosarcoma

199
Q

abl

A

proto-oncogene

CML
ALL

200
Q

BRCA-1, BRCA-2

A

tumor suppressor

DNA repair gene

breast & ovarian cancer

201
Q

NF-1

A

tumor supressor

neuroblastoma
neurofibromatosis 1
sarcoma

202
Q

APC/B-catenin

A

tumor supressor

gastric
colonic
pancreatic cancer

FAP

203
Q

DCC

A

tumor supressor

colon cancer

204
Q

P53

A

tumor supressor

majority of cancer
Li-fraumeni

205
Q

Rb

A

tumor supressor

retinoblastoma
osteosarcoma

G1-S

206
Q

WT-1

A

tumor supressor

wilms tumor
pediatric kidney, primitive glomeruli

207
Q

etiology of ARDs

A

widespread injury to pulmonary microvasculature endothelium and/or alveolar epithelium

–> causes alveolocapillary membrane to be leaky

208
Q

where do atherosclerotic plaques normally form

A

in large elastic arteries
(aorta, carotid artery, iliac artery)

& larger medium caliber muscular artery
(coronary, popliteal)

usu not pulmonary artery

209
Q

hyperosmotic volume contraction cause (2)

A
  1. diabetes insipidus

2. profuse sweating

210
Q

GI hemorrhage alters what fluid volume

A

isotonic fluid loss from ECV only

bc loose both fluid & osmoles, no pull on fluid from intracellular component

211
Q

most common cause of death in diabetic?

A

coronary heart disease!
MI (40%)

(even though have ESRD, still die from coronary heart disease)

stroke also happen, but only 10%

212
Q

HIGHEST risk factors for coronary heart disease

A
  1. noncoronary atherosclerotic disease
  2. diabetes mellitus
  3. chronic kidney disease

these basically = coronary heart disease equivalents

also: HTN, hyperlipidemia, cigarette smoking, advanced age, obesity, physical inactivity

213
Q

leading causes of ESRD

A
  1. diabetes

2. HTN

214
Q

lung: nodular apical densities w/ calcified nodes filled w/ birefringent particles surrounded by fibrous tissue

A

silicosis

215
Q

silicosis is defined by

A

upper lobe nodular densities on x-ray

  1. eggshell calcifications of hilar nodes
  2. birefringent silica particles surrounded by fibrous tissue
216
Q

x-ray of asbestosis

A

interstitial pattern, more prominent in lower lobes.

calcified pleural plaques

histology: ferruginous bodies, best w/ prussian blue stain

217
Q

berylliosis x-ray & histology

A

ill-defined nodular or irregular opacity on x-ray

hilar adenopathy 40%

histology: noncaseating granulomas like sarcoidosis

218
Q

inhalation of organic dust on x-ray, histology

A

hypersensitivity pneumonitis

diffuse nodular interstitial infiltrates

histology: noncaseating granuloma (foreign body response)

219
Q

which 3 lung diseases can have noncaseating granulomas

A
  1. sarcoidosis
  2. hypersensitivity pneumonitis w/ organic dust inhalation
  3. berylliosis
220
Q

coal worker pneumoconiosis

A

x-ray: interstitial opacity

nodal / perilymphatic lung tissue coal dust-laden macrophages

221
Q

most common cause of SCD

A

death within 1 hr of cardiac symptom

usu cardiac arrhythmia –> ventricular fibrillation

222
Q

Caplan syndrome

A

rheumatoid arthritis & pneumoconioses w/ intrapulmonary nodules

UWorld mixed (60 decks)

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