uWorld 34

Question 1

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

Answer 1

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

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

Question 2

what drug that treats UTIs can precipitate THEOPHYLLINE toxicity

Answer 2

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

Question 3

how does theophylline work

Answer 3

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

Question 4

what is seen in theophylline toxicity

Answer 4

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

Question 5

in southwestern blotting FNA_binding proteins are recognized how

Answer 5

ability to bind SPECIFIC OLIGONUCLEOTIDE PROBES

Question 6

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

Answer 6

PAH
creatinine
inulin
urea

Question 7

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

Answer 7

bicarbonate
glucose
amino acids

Question 8

what is the rate limiting step of urea synthesis

Answer 8

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

happens in mitochondria

Question 9

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

Answer 9

N-ACETYLGLUTAMATE

Question 10

what is the most common urea cycle disorder

Answer 10

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

Question 11

what is seen in uridine monophosphate synthetase (UMPS) deficiency

Answer 11

part of pyrimidine synthesis pathway

deficiency leads to buildup of OROTIC ACID
MEGALOBLASTIC anemia
GROWTH DELAY

NO HYPERAMMONEMIA (differentiates this from OTC deficiency)

Question 12

what causes tabes doralis

Answer 12

syphilis DIRECTLY damages the DORSAL SENSORY ROOTS

secondary degeneration of DORSAL COLUMNS

Question 13

what are the clinical findings of tabes doraslis

Answer 13

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

Question 14

what two pathways does insulin binding to the insulin receptor activate

Answer 14

RAS/MAP kinase pathway: CELL GROWTH, DNA SYNTHESIS

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

Question 15

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

Answer 15

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

Question 16

what is the adductor hiatus

Answer 16

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

Question 17

what is the femoral ring

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

lower stomach (gastroepiploic vein)

also drains pancreas and duodenum via pancreaticoduodenal vein

Question 21

ow does a cell move from G1 to S

Answer 21

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

Question 22

how does p27 work

Answer 22

cell cycle INHIBITOR that inhibits cyclin dependent kinases during G1

Question 23

during a cricothyrotomy is done how

Answer 23

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

Question 24

meningococci are commonly isolated from where in asymptomatic carriers

Answer 24

oropharynx and nasopharynx

Question 25

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

Answer 25

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

Question 26

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

Answer 26

RENAL PAPILLARY NECROSIS (RPN)

Question 27

what conditions are associated with renal papillary necrosis (RPN)

Answer 27

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

Question 28

what is seen in fanconi syndrome

Answer 28

polyuria acidosis hypophosphatemia

Question 29

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

Answer 29

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

Question 30

what medications are associated with osteoporotic fracutres

Answer 30

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

Question 31

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

Answer 31

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

Question 32

why is seen in mamarry duct ectasia

Answer 32

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

Question 33

what characterizes sclerosing adenomas (seen in fibrocystic change)

Answer 33

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

Question 34

what are plexiform lesions

Answer 34

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)

Question 35

what is seen in PAH (pulmonary arterial hypertension)

Answer 35

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

Question 36

what is BOSETAN

Answer 36

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)

Question 37

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

Answer 37

pneumonia bronchiectasis cor pulmonale

Question 38

what is the "squirt sign" and when is it seen

Answer 38

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)

Question 39

what is the most common cause of mortality in Hirschsprung

Answer 39

ENTEROCLOLITIS (diarrhea, abdominal pain/distension, and fever

Question 40

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

Answer 40

CORTISOL

Question 41

what is Werdnig-Hoffman syndrome

Answer 41

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

Question 42

what kind of rash is seen in ROSEOLA INFANTUM

Answer 42

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

Question 43

where are endorphins synthesized and released rom

Answer 43

corticotrophin cells in anterior pituitary

Question 44

what are the action of TGF-beta

Answer 44

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)

Question 45

what causes septic shock

Answer 45

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

Question 46

how does LIPID A of the LPS induce shock

Answer 46

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

Question 47

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

Answer 47

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

Question 48

what is verapamils action in the pacemaker cells and cardiomyocytes

Answer 48

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)