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uWorld Flashies > uWorld 34 > Flashcards

uWorld 34 Flashcards

1
Q

what is the course of fetal blood flow from highest O2 concentration to lowest

A

umbilical vein → liver → IVC → heart → pulmonary circulation or through foramen ovale

pulmonary circulation → ductus arteriosus and pass directly into the descending aorta

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2
Q

what drug that treats UTIs can precipitate THEOPHYLLINE toxicity

A

CIPROFLOXACIN b/c it is a CYP inhibitor and theophylline is a CYP substrate

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3
Q

how does theophylline work

A

adenosine receptor blocker
PDE inhibits

used of asthma and COPD b/c it causes bronchodilation by increasing cellular cAMP and it has mild-antiinflammtory effects

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4
Q

what is seen in theophylline toxicity

A 
CNS stimulation (tremor, insomnia, SEIZURES)
GI disturbances
cardiovascular abnormalities (hypotension, tachycardia, CARDIAC ARRHYTHMIAS)
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5
Q

in southwestern blotting FNA_binding proteins are recognized how

A

ability to bind SPECIFIC OLIGONUCLEOTIDE PROBES

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6
Q

the concentrations of what substances increase as fluid moves along the proximal tubule

A

PAH
creatinine
inulin
urea

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7
Q

the concentrations of what substances decrease as fluid moves along the proximal tubule

A

bicarbonate
glucose
amino acids

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8
Q

what is the rate limiting step of urea synthesis

A

barcarb, ammonia, and ATP are combined by CARBAMOYL PHOSPHATE SYNTHETASE to yield carbamoyl phosphate

happens in mitochondria

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9
Q

what serves as a regulator of the urea cycle through activation of carbamoyl phosphate synthetase I

A

N-ACETYLGLUTAMATE

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10
Q

what is the most common urea cycle disorder

A

ORNITHINE TRANSCARBAMYLASE (OTC) DEFICIENCY

results in excess carbamoyl phosphate, which stimulates pyrimidine synthesis- OROTIC ACID then accumulates and results in increased URINARY OROTIC ACID

HYPERAMMONEMIA (vomiting, confusion/coma) due to impaired ammonia excretion- a METABOLIC EMERGENCY

TACHYPNEA due to cerebral edema from ammonia buildup, resulting in central hyperventilation and respiratory alkalosis

triggered by illness, fasting or increased protein intake

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11
Q

what is seen in uridine monophosphate synthetase (UMPS) deficiency

A

part of pyrimidine synthesis pathway

deficiency leads to buildup of OROTIC ACID
MEGALOBLASTIC anemia
GROWTH DELAY

NO HYPERAMMONEMIA (differentiates this from OTC deficiency)

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12
Q

what causes tabes doralis

A

syphilis DIRECTLY damages the DORSAL SENSORY ROOTS

secondary degeneration of DORSAL COLUMNS

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13
Q

what are the clinical findings of tabes doraslis

A

sensory ataxia
lancinating pains
neurogenic urinary incontinence
associated with Argyll Roberson pupils

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14
Q

what two pathways does insulin binding to the insulin receptor activate

A

RAS/MAP kinase pathway: CELL GROWTH, DNA SYNTHESIS

PI3K pathway: lipid, protein, and GLYCOGEN (via PROTEIN PHOSPHATASE which activates GLYCOGEN SYNTHASE by dephosphorylation) synthesis

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15
Q

what is the optimal site for a femoral nerve (L2-L4) block

A

INGUINAL CREASE at the lateral border of the femoral artery

anesthetizes the skin and muscles of the anterior thigh, femur, and knee

also blocks the saphenous nerve (terminal extension of the femoral nerve) to decrease sensation to the media leg below the knee

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16
Q

what is the adductor hiatus

A

opening i nth e aponeurosis of the adductor magnus at the distal one-third of the femur that allows passage of the femoral vessels into the popliteal fossa
saphenous nerve passes near the hiatus

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17
Q

what is the femoral ring

A

upper opening of the femoral canal (which contains lymphatic vessels and a lymph node)

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18
Q

glucose is the most inprotant stimulator of glucose relate, how does this work

A

glucose enters via GLUT-2 and generates ATP via citric acid cycle

ATP binds ATP-sensitive K+ channel that then CLOSES causing MEMBRANE DEPOLARIZATION

this opens voltage-gates calcium channels that RELASE INSULIN

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19
Q

if patient has varices visible only in the gastric fundus (not esophagus or rest of stomach) what is the cause

A

SPLENIC VEIN THROMBOSIS due to chronic pancreatitis, pancreatic cancer, and abdominal tumors

GASTRIC VARICES only in the fundus form because the SHROT GASTRIC VEINS drain the fundus of the stomach into the splenic vein

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20
Q

blockage of the SMV could lead to varcieal formation where in the stomach

A

lower stomach (gastroepiploic vein)

also drains pancreas and duodenum via pancreaticoduodenal vein

21
Q

ow does a cell move from G1 to S

A

cyclin D-CDK4 hyperphosphorylates Rb (rendering it INACTIVE) causing it to RELASE EF2

22
Q

how does p27 work

A

cell cycle INHIBITOR that inhibits cyclin dependent kinases during G1

23
Q

during a cricothyrotomy is done how

A

placement of tube between CRICOID and THYROID cartilages and you must go through:

  1. skin
  2. SUPERFICIAL CERVIAL FASCIA (including subcutaneous fat and platysma muscle)
  3. investing laters of pretracheal laters of the deep cervical fascia
  4. CRICOTHYROID MEMBRANE
24
Q

meningococci are commonly isolated from where in asymptomatic carriers

A

oropharynx and nasopharynx

25
Q

antibodies that successfully impart the pili of meningococcus (important for bacterial attachment to epithelial surfaces) would inhibit pilus-meidated attachment of meningococcus to what

A

the mucosal epithelium of the NASOPHARYNX, preventing colonization and subsequent invasion

26
Q

abrupt-onset GROSS HEMATURIA of an otherwise healthy patient with a family history of SICKLE CELL disease suggests what

A

RENAL PAPILLARY NECROSIS (RPN)

27
Q

what conditions are associated with renal papillary necrosis (RPN)

A

SICKLE CELL disease or trait (sickled cells cause obstruction of small kidney vessels, predisposing to ischemia)

ANALGESIC nephropathy: NSAIDs inhibit renal blood flow by decreasing PG synthesis and vasoconstriction the affect arterioles

DIABETES mellitus: nonenzymatic glycosylation causes changes in vascular walls, leading to renal vasculopathy and hypo perfusion

PYELONEPHRITIS and urinary tract obstruction: compression of medullary vasculature, leading to ischemia

28
Q

what is seen in fanconi syndrome

A

polyuria
acidosis
hypophosphatemia

29
Q

patients receiving PARENTERAL NUTRITION (through a central venous CATHETER) are at high risk for what kind of infection

A

CANDIDEMIA (candida in the blood stream)

see BRANCHING PSEUDOHYPHAE with BLASTOCONIDIA

TX: echinocandins (caspofungin and relatives) for all species and C albicans fluconazole pretty much always works

30
Q

what medications are associated with osteoporotic fracutres

A

anticonvulsants that induce CYP450 (phenobarbital, phenytoin, carbamazepine)- ↑ Vit D catabolism

aromatase inhibitors: ↓ estrogen

medroxyprogesterone: ↓ estrogen

GnRH agonists: ↓ testosterone and estrogen

PROTON PUMP INHIBITORS: ↓ CALICUM ABSORPTION

Glucocorticoids: ↓ bone formation

Unfractioned Hep: ↓ bone formation

Thiazolidinediones (pioglitazone, rosiglitazone): ↓ bone formation

31
Q

what is the most common benign tumor of the breast and what characterizes it

A

FIBROADENOMA
young women 15-35
nodules that are well-demarcated, painless, mobile, and spherical

usually discovered by palpable inspection

often increase in size during pregnancy, lactation, or with estrogen therapy

usually regress after menopause

benign-appearing cellular or MYXOID STROMA that encircles epithelium-lined glandular cystic spaces

well-defined border but may compress and distort the surrounding glandular epithelium

32
Q

why is seen in mamarry duct ectasia

A

ductal dilation
inspissated breast secretions
chronic granulomatous inflammation in the preductal and interstitial areas

33
Q

what characterizes sclerosing adenomas (seen in fibrocystic change)

A

central acinar proliferation and compression with surrounding fibrotic tissue and peripheral ductal dilation

34
Q

what are plexiform lesions

A

interlacing tufts of small vascular channels

seen in pulmonary hypertension due to underlying lung, vascular, or cardiac disease and in idiopathic or familial pulmonary arterial hypertension (PAH)

35
Q

what is seen in PAH (pulmonary arterial hypertension)

A

dyspnea and exercise intolerance in women 2-40

usually do to inactivating mutations in pro-apoptotic BMPR2 gene → endothelial and smooth muscle cell proliferation leading to vascular remodeling, elevated pulmonary vascular resistance, and progressive pulmonary hypertension

36
Q

what is BOSETAN

A

ENOTHELIN-RECEPTOR ANTAGONIST that blocks the effects of endothelia (a potent vasoconstrictor that also stimulates endothelial proliferation)

decreases pulmonary arterial pressure
lessens progression of vascular and rich ventricular hypertrophy

used to treat IDIOPATHIC PULMONARY ARTERIAL HYPERTENSION (PAH)

37
Q

what accounts for most deaths in Cystic Fibrosis in the united states

A

pneumonia
bronchiectasis
cor pulmonale

38
Q

what is the “squirt sign” and when is it seen

A

forceful expulsion of stool after rectal examination

seen in Hirschsprung disease (but not in CF and both have meconium so can use this to differentiate)

39
Q

what is the most common cause of mortality in Hirschsprung

A

ENTEROCLOLITIS (diarrhea, abdominal pain/distension, and fever

40
Q

what increases the expression of phenylethanolamine-N-methyltransferase (conversion of norepi to epi)

A

CORTISOL

41
Q

what is Werdnig-Hoffman syndrome

A

anterior horn cell damage
lower motor neuron lesion signs are present: flaccid weakness, areflexia, muscle atrophy, fasciculation (“floppy child” syndrome)

42
Q

what kind of rash is seen in ROSEOLA INFANTUM

A

3-5 days of high fever followed by blanching maculopapular rash

starts on the TRUNK and spread to the face and extremities

infection is typically benign and self limited

seen in children less than 2

43
Q

where are endorphins synthesized and released rom

A

corticotrophin cells in anterior pituitary

44
Q

what are the action of TGF-beta

A

arrest of the cell cycle (tumor suppressing agent)

promotion of angiogenesis (allows tumor mets to survive after resistance to TGF)

stimulation of fibroblasts to lay down extracellular matrix proteins (implication in atherosclerosis and fibrotic diseases)

45
Q

what causes septic shock

A

ENDOTOXIN release into the BLOODSTREAM

endotoxins are found on the outer membrane of GRAM-NEGATIVE bacterial, which is composed of LIPOPOLYSACCHARIDE )LPS)

LPS is realized during destruction of bacterial cell wall

long, heat-stable molecular with 3 regions:
O antigen
core polysaccharide
LIPID A- responsible for TOXIC PROPERTIES of LPS that lead to GRAM-NEGATIVE SEPSIS and ENDOTOXIC SEPTIC SHOCK

46
Q

how does LIPID A of the LPS induce shock

A

activation of MACROPHAGES and GRANULOCYTES resulting in synthesis of endogenies PYROGENS (like IL-1), prostaglandins, and inflammatory mediators (like TNF-alpha and interferon)

FEVER (IL-1), hypotension, diarrhea, oliguria, vascular compromise, and DIC

47
Q

what is flagellar (H) antigen seen on E. Coli

A

heat-labile protein which is one component of the serologic classification of the enterobacteriaceae

48
Q

what is verapamils action in the pacemaker cells and cardiomyocytes

A

pacemaker cells: slows the depolarization that occurs in phase 0 (diastolic depolarization)
-decreases SA node drying and slows AV node conduction

cardiac myocytes: decrease the amount of intracellular calcium available for excitation- contraction coupling within cardiomyocytes
-this can reduce contractility (which may be harmful in pts with impaired ventricular function)

uWorld Flashies (62 decks)

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