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UWorld mixed > test #34 4.22 > Flashcards

test #34 4.22 Flashcards

1
Q

3 determinants of malignant potential of an adenomatous polyp

A
  1. size (> 4cm have 40% risk of malignancy
  2. histology: villous more prone to be malignant than tubular
  3. degree of dysplasia
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2
Q

bell curve: what %age of population falls in 1 standard deviation? 2? 3?

A

1 standard deviation = 68%

2: 95% (2.5 below, 2.5 above)
3: 99.7

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3
Q

where is CCK made

A

I cells of duodenum and jejuneum.

increase pancreatic enzyme secretion and gallbladder contraction

decrease gastric emptying

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4
Q

where is vasoactive intestinal peptide made?

A

pancreas & parasympathetic ganglia

stimulates intestinal water secretion, counteracts gastrin, promotes bicarb secretion for pancreas

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5
Q

classic galactosemia is inherited as..

A

autosomal recessive

lack galactose-1-phosphate uridyltransferase

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6
Q

3 steps of deglutition (swallowing)

A
  1. oral: voluntary
    food bolus collected at back of mouth, lifted upwards to posterior wall of pharynx
  2. pharyngeal, involuntary
    pharyngeal muscle contractions propel food bolus to esophagus
  3. esophageal phase
    - enters & stretches walls. peristalsis begins above site of distention and moves food down.
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7
Q

difficulty swallowing “felt at the throat”

A

cricopharyngeal muscle dysfunction. diminished relaxation of pharyngeal muscles during swallowing.

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8
Q

how does cricopharyngeal muscle dysfunction lead to zenker diverticulum?

A

diminshed relaxation of pharyngeal muscles during swallowing demands more force to move food bolus down.

more intense contraction of pharyngeal muscles –> increase oropharyngeal intraluminal pressure.

eventually, pharyngeal mucosa herniate through muscle fibers in zone of weakness (posterior hypopharynx).

only mucosa –> FALSE / pulsion (as opposed to all walls of organ –> true / traction)\

can lead to aspiration of food – bc food stuck in diverticulum high up

can be palpated as lateral neck mass

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9
Q

mediastinal lymphadenitis (TB, fungal) can lead to what esophagus problem

A

scarring & traction –> true diverticula, mid portion of esophagus

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10
Q

hemoglobin synthesis in fetus (4)

A

yolk sac, liver, spleen, bone marrow.

liver begins HbF 10-12 wks of gestation –> spleen –> bone marrow.

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11
Q

when does HbF transition to HgA?

A

HbF (a2y2) –> HbA (a2b2) during first 6 months.

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12
Q

a2d2 (HbA2)

A

normal variant of human hemoglobin. 2-5% of adult hemoglobin

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13
Q

hemoglobin gower (z2e2)

A

earliest hemoglobin in fetus.

synthesized in yolk sac, replaced by hemoglobin portland –> hemoglobin gower 2 –> hemoglobin F (10-12 wks)

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14
Q

hemoglobin bart

A

gamma4.
no alpha made.
alpha thalaseemia.

high affinity for oxygen, never gives it up, get hydrops fetalis

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15
Q

muscles that attach to clavicle

A
  • pec major (inferomedial)
  • deltoid (inferolateral)
  • subclavius (inferolateral)
  • trapezius (superolateral)
  • sternocleidomastoid (superior medial aspect)
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16
Q

where does sternocleidomastoid articulate

A

3 points:

manubrium, medial clavicle, and mastoid

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17
Q

rhomboid muscle articulation

A

vertebral bodies to medial border of scapula

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18
Q

pec minor articultation

A

3-4th rib, insert on coracoid process

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19
Q

serratus anterior

A

1-8th rib, insert on medial border of scapula

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20
Q

subclavius muscle

A

originates on 1st rib, inserts on inferolateral aspect of clavicle

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21
Q

floor of anatomical snuff box

A

scaphoid and trapezium

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22
Q

dupuytren’s contracture

A

benign, slowly progressive fibroproliferative disease of palmar fascia.

as scarring progresses, nodules form on palmar fascia, fingers gradually loose flexibility, eventually resulting in CONTRACTURE that draws fingers in FLEXION

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23
Q

celiac comes out at what vertebral level? SMA & renal artery? IMA?

A

celiac: T12
SMA & renal: L1
IMA: L3

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24
Q

transverse duodenum lies at what vertebral level?

A

L3, between aorta and SMA (can be compressed)

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25
Q

ligament of treitz

A

suspensory ligament of duodenum (connect right crus of diaphragm to duodenal jejunal flexure)

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26
Q

what can be compressed when mesenteric fat is lost between SMA and aorta?

A

left renal vein & transverse duodenum

also occurs w/ pronounced lordosis, or surgical correction of scoliosis

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27
Q

filtration fraction =

A

GFR/RPF

usu = .2 (1/5th of RPF is filtered)

how much of renal plasma flow is filtered

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28
Q

how does RPF, GFR, and FF change in SEVERE dehydration

A

RPF falls a lot
GFR falls less (efferent arteriole constricts to maintain some GFR)
FF goes UP

end up compensating to filter a larger amount of the little incoming renal plasma

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29
Q

what forms erythema migrans of ixodes bite? how does it look

A

erythematous macule that enlarges w/ advancing erythematous borders as BACTERIA MIGRATE slowly through skin outward from inoculation site

classically has central clearing, but NOT ALWAYS!

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30
Q

scrofula

A

caused by mycobacterium scrofulaceum.

found in and around environmental water sources.

characterized by lymphadenitis (usu cervical) in kids

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31
Q

leptospirosis & weil’s disease

A

lepto:
exposure to animal urine.
no cutaneous manifestation
usu asymptomatic, self limited

progression to weil’s:
jaundice, renal dysfunction, thrombocytopenia, bleeding

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32
Q

sucrose is..

A

fructose and glucose

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33
Q

lactose is..

A

galactose and glucose

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34
Q

maltose is..

A

glucose and glucose

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35
Q

which two dissacharides are in breast milk

A

maltose and galactose

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36
Q

what is starch made of..

A

major carbohydrate in plants

only glucose molecules:

  • unbranched: amylose
  • branched: amylopectin
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37
Q

what is cellulose made of..

A

linear polysach of glucose, mainly present in cell wall of plants.

not digested by GI enzymes.

composes one form of non-soluble dietary fiber –> bulk of fecal matter.

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38
Q

aldolase B deficiency

A

hypoglycemia after fructose ingestion due to phosphate trapping by fructose-6-phosphate.

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39
Q

essential fructosuria & galactokinase deficiency are..

A

MILD

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40
Q

fructose intolerance & classic galactosemia are..

A

more severe

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41
Q

violaceous discoloration of upper eyelids & raised violaceous scaling eruption on kuckles

A

heliotrope rash & grotton’s sign.
(w/ proximal muscle weakness)

dermatomyositis.

usu elevated cpk

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42
Q

2 main diff between pemphigus vulgaris & bullous pemphigoid

A

pemphigus vulgaris 1. affects oral mucosa 2. ruptures easily

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43
Q

mutation in ALS?

A

copper zinc superoxide dismutase (SOD1)

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44
Q

rx for ALS

A

riluzole, decreases glutamate release

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45
Q

macroscopic changes in ALS

A

thin anterior roots, atrophy of precentral gyrus

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46
Q

PKU that does not alleviate w. phenylalanine restriction / tyrosine supplementation

A

dihydrobiopterin reductase deficiency.

needed for both

  1. phenylalanine -> tyrosine
    (via phenylalanine hydroxylase)
  2. tyrosine -> DOPA
    (via tyrosine hydroxylase)

“atypical” or “malignant” phenylketonuria

47
Q

problems w/ dihydropterin reductase deficiency

A

inability to convert phenylalanine -> tyrosine, tyrosine -> dopa.

tetrahydrobiopterin is impt for tyrosine, DOPA, 5-HT and NO synthesis.

present w/ high prolactin bc can’t make dopamine in tuberoinfundibular system

48
Q

alkaptonuria

A

autosomal recessive
deficiency in homogentisic acid

(break down homogentistic acid, which is a toxic tyrosine byproduct, harmful to bone & cartilage)

49
Q

PMNT

A

phenylethanolamine N-methyltranserase

convert NE -> E

need SAM (s-adenosyl-methionine) as cofactor –> s-adenosylhomocysteine

50
Q

how does WPW present (2)

A

accessory pathway bypassing bundle of kent

(1) pre-excitation: first impulse through accessory path, then shortly thereafter via AV node.
(2) allows for recurrent, temporary tachyarrhythmias due to atrioventricular re-entry circuit involving AV node & accessory path

51
Q

WPW pre-excitation on EKG

A

shortened PR interval ( makes for wider QRS

delta wave goes away in re-entrant tachyarrhythmia bc no longer pre-excitation

52
Q

what can trigger malignant hyperthermia?

A

inhaled anesthetics (esp halothane)

& succinylcholine

53
Q

why does malignant hyperthermia happen?

rx?

A

autosomal dominant

skeletal muscles hypersensitive to inhalation anesthetics (esp halothane) & succinylcholine.

defect on ryanodine receptors of sarcoplasmic reticulum. release too much Ca2+, stimulating ATP-dependent reuptake of Ca2+ into SR. excessive ATP consumption –> generate lots of heat

loss of ATP + heat –> muscle damage –> rhabdomyolysis –> release K+, myoglobin, creatinine kinase

dantrolene: prevent Ca2+ release from ryanodine receptors

54
Q

phentolamine & phenoxybenzamine

A

alpha-adrengeric blockers

55
Q

which drug causes increased triglyceride levels as side effect

A

cholestyramine (bile acid resins)

bile acid production increases, but so does hepatic production of TG and VLDL.

56
Q

cholestyramine side effects (3)

A

bile acid resin:

  • GI upset
  • impaired nutrient absorption & drugs
  • elevated triglycerides
  • also increase cholesterol content of bile –> stones
57
Q

niacin on triglycerides

A

reduces serum TGs

also decreases VLDL conversion to LDL (less LDL)

58
Q

B6-deficiency related anemia

A

needed for hemoglobin synthesis. can cause hypochromic microcytic pyridoxine responsive sideroblastic anemia

59
Q

segmental granulomatous large vessel arteritis

A

takayasu arteritis

60
Q

when can hepatitis D virus cause infection?

A

when encapsulated with HBsAg.

hepatitis D is replication defective RNA.

  • acute coinfection w/ hep B (hep B established to provide HBsAg) or superinfection of a chronic HBV carrier
61
Q

common extrahepatic disease in chronic hep C infection (2)

A

(1) membranous glomerulonephropathy

(2) mixed cryoglobulinemia

62
Q

2 forms of chronic gastritis?

acute gastritis?

A

chronic:
type A: autoimmune (fundus/body)
type B: h. pylori bacteria (antrum)

acute:
disruption of mucosal barrier
(stress, NSAID, alcohol, uremia, burns (curling ulcer), brain injury (cushing ulcer), chemo, shock..

63
Q

autoimmune type A chronic gastritis

A

autoantibodies to parietal cells / intrinsic factor, results in

  1. achlorhydia
  2. anemia (no b12)

also increased risk of gastric adenocarcinoma

64
Q

type B gastritis is associated w/ increased risk of

A

Maltoma & gastric adenocarcinoma

65
Q

what’s one way acute gastritis can be differentiated from chronic gastritis?

A

acute: neutrophil predominant
chronic: lymphocyte & plasma cell

66
Q

what kind of reaction does a foreign body cause? how does this happen.

A

granuloma!

takes several days/wks. antigen that cannot be eradicated by usu mechanism

activated Th1 CD4+ cells secrete IFN-gamma, activates macrophages. macrophage secrete THF-alpha, which forms granuloma.

67
Q

Marjolin’s ulcer

A

aggressive, ulcerating squamous cell carcinoma.

presents in an area of previously traumatized, chronically inflammed, or scarred skin.

malignant transformation occurs long after initial trauma, usu > 10yrs later.

68
Q

time frame of wound healing

A
  1. inflammatory (immediate):
    - clot & clean
  2. proliferative (2-3 d later):
    - granulation & contrature
  3. remodeling (1wk later):
    - type III -> type I
69
Q

which class III antiarrhythmics is not associated w/ Tdp

A

amiodarone (silver lining!)

70
Q

which class I antiarrhythmics predispose to Tdp?

A

class IA (have class III properties too)

71
Q

adenosine on EKG

A

expect it to prolong PR, but cleared so quickly (t1/2: <10seconds)

72
Q

digoxin 2 fxn

A
  1. increase vagal tone of AV: antiarrhythmic

2. increase contractility

73
Q

characterestics of glioblastoma multiforme

A

necrosis and vascular proliferation

pseudopalisading

74
Q

prognosis of glioblastoma

A

highly malignant. will die within 1-2 years

75
Q

cyst formation & rare mitosis in brain suggests?

A

colloid cyst – pathologically benign tumor, usu in 3rd ventricle. can cause lethal obstructive hydrocephalus

76
Q

reticulin deposits and chronic inflammatory infiltrate in brain suggests?

A

pleomorphic xanthoastrocytoma.

variant of astrocytoma, can progress to GBM

77
Q

what causes congenital pyloric stenosis? acquired?

A

congenital: smooth muscle hypertrophy of pyloric muscularis mucosae
acquired: associated w/ gastritis, peptic ulcer in pylorus, neoplasm

78
Q

psoas articulation

A

transverse processes & lateral aspect of T12 through L5 vertebrae –> down across pelvic brim anterior to hip joint capsule & deep to inguinal ligament to insert into the lesser trochanter (shared tendon w/ iliacus)

79
Q

psoas abscess forms from..

A

direct spread of infection from adjacent structure (vertebral bodies, appendix, hip joint)

or hematogenous / lymphatic seeding from distant site

80
Q

psoas sign

A

movement that causes psoas muscle to be stretched/extended.

associated w/ appendicitis

81
Q

quadratus lumborum

A

coarses posterior to psoas muscle. connects 12th rib & upper lumbar vertebra to iliac crest –> extension & lateral flexion of vertebral column

82
Q

rx for warfarin reversal

A

fresh frozen plasma

vit K would help, but takes time bc need to resynthesize clotting factors

83
Q

aminocaproic acid

A

antifibrinolytic agent – inhibit plasminogen activators

84
Q

protamine

A

heparin reversal, binds/inactivates heparin

85
Q

what’s contained in cryoprecipitate vs. fresh frozen plasma

A

fresh frozen plasma: all coagulation factors

cryoprecipitate: only cold soluble proteins: factor VIII, fibrinogen, vWF, and vitronectin

86
Q

serum vs plasma

A

serum = plasma w/o clotting factor

87
Q

desmopressin in heme

A

increases factor VIII activity (in pts w/ hemophilia A & vWD)

88
Q

most common cause of overdose related deaths?

A

prescription opiod pain relievers

(exceeds heroin + cocaine combined)

due to increase in prescribing w/o adequate drug monitoring.

89
Q

potency of inhaled anesthetic depends on..

A

inversely related to minimal alveolar concentration

when inhaled anesthetic administered at constant rate over prolonged period, its partial pressure in brain = partial pressure in other compartments.

since concentration in brain directly proportion to partial pressure, it is a measure of potency

intrinsic property of anesthetic, does not depend on surgery, duration, sex/height/weight.

90
Q

anesthetics arteriovenous concentration gradient is a measure of

A

measure of solubility in tissue.

high = increased time for blood to be saturated = slow time of onset

91
Q

blood/gas partition coefficient is a measure of

A

solubility in blood –

high blood/gas partition = very soluble in blood = slower onset of action

92
Q

steepness of arterial tension curve of inhaled anesthetic measures..

A

depends on solubility of anesthetic in blood.

partial pressure rises steeply when less soluble

93
Q

2 fxn of von willebrand factor

A
  1. protect factor VIII from degradation

2. connects collagen to platelets (via GpIb)

94
Q

what activates protein C

A

thrombin-thrombomodulin complex

95
Q

von Gierke disease

A

type 1 glycogen storage disease
autosomal recessive

deficiency glycogen phosphorylase

cannot do: glycogen -> glucose 1-phosphate
via glycogen phosphorylase, breaks alpha (1,4) glucosidase link

severe fasting hypoglycemia, increased glycogen in liver, increased blood lactate.

NOTE: in muscle
[glycogen-> glucose 1-phosphate]
via myophosphorylase]

btw: glucose 1-phosphate –> glucose 6-phosphate (via phosphoglucomutase) and then…

in LIVER:
glucose 6-phosphate -> glucose
via glucose phosphorylase

96
Q

synthesis of glycogen

A

glucose 6-phosphate –> glucose 1-phosphate
via phosphoglucomutase

glucose 1-phosphate –> UDP glucose
via: UDP-glucose pyrophosphorylase

UDP-glucose -> glycogen
via: glycogen synthase
(stimulated by insulin, inhibited by PKA)

branches made via branching enzyme

97
Q

pompe disease

A

type 2 glycogen storage disease

deficient in lysosomal alpha 1,4-glucosidase (aka acid maltase)
[limited amount in lysosomes]

trashes the pump –> cardiomyopathy, liver, and muscle problems

early death

98
Q

cori disease

A

type 3 glycogen storage disease

alpha 1,6 glucosidase
[debranching enzyme]

milder than type 1, normal blood lactate

99
Q

mcArdle disease

A

type 5 glycogen storage disease

myophosphorylase

can’t use glycogen in muscle

cannot do: glycogen -> glucose 1-phosphate

[note, in muscle glucose 1-phosphate -> glucose 6-phosphate via phosphoglucomutase]

glucose 6-phosphate is used as is! no glucose phosphorylase, bc don’t want to release glucose into circulation

symptoms: decreased exercise tolerance, myoglobinuria, muscle pain w/ activity

relieved w/ exogenous glucose

100
Q

breakdown of glycogen requires 4 enzymes (in liver).. [3 in muscle]

A
  1. glycogen phosphorylase
    glycogen -> glucose 1-phosphate
  2. debranching enzyme
    glycogen -> glucose 6-phosphate
  3. phosphoglucomutase
    glucose 1-phosphate -> glucose 6-phosphate

MUSCLE just uses glucose 6-phosphate

  1. glucose 6-phosphatase (only in liver)
    glucose 6-phosphate -> glucose
101
Q

limit dextran

A

when there are 4 residues on a glycogen branch (glycogen phosphorylase already did its thing)

first: 4-alpha-D-glucanotransferase takes off 3 glucose 1-phosphates
second: alpha 1,6-glucosidase takes off 1 glucose 1-phosphate

102
Q

how does HBV allow hepatitis D virus?

A

hep D = 35nm double-shelled particle.

HDAg + short ssRNA

needs to be COATED w/ HBsAg.

acute coinfection or superinfection of chronic HBV carrier.

only w/ HBsAg can it: penetrate hepatocyte, survive in cell, replicate viral RNA, and translate genome

103
Q

constitutional symptoms, mid-diastolic rumbling murmur at apex, positional dyspnea, large pedunculated mass in left atrium suggests..

A

atrial myxoma

make lots of IL-6, constitutional symptoms

most common primary cardiac neoplasm.
approx 80% arise in left atrium

104
Q

histology of atrial myxoma

A

scattered cells within a mucopolysaccharide stroma, abnormal blood vessels (lots of VEGF), and hemorrhaging (hemosiderin depositions)

al

105
Q

drug-induced acute interstitial nephritis characterized by..

A

eosinophilia [serum & urine]

drug acts as hapten, hypersensitivity

106
Q

down syndrome, ataxia-teleangiectasia, and NF-1 associated w. increased risk of..

A

ALL

107
Q

twinning:

cleavage during 0-4 days (from zygote to morula)

A

dichorionic diamniotic

108
Q

twinning:

cleavage during 4-8 days (from morula to blastocoele)

A

monochorionic diamniotic

109
Q

twinning:
cleavage during 8-12 days
(from blastocoele to embryonic disc)

A

monochorionic monoamniotic

110
Q

twinning

cleavage from 13+ days

A

fused babies

111
Q

dizygotic twins

A

dichorionic diamniotic

112
Q

dichorionic monoamniotic

A

does NOT EXIST

chorion = outer cover

113
Q

how long does busipirone take to work

A

several weeks

5-HT1a receptor agonist, safe and effective. delayed response for 2 wks.

long-term rx. 1st line for generalized anxiety disorder. not as dependent.

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