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UWorld mixed > facts from sim test 4.30 > Flashcards

facts from sim test 4.30 Flashcards

1
Q

venous drainage to anal canal above/below the pectinate line

A

above: superior rectal vein -> inferior mesenteric -> portal circulation
below: middle & inferior rectal vein -> internal pudendal -> inferior mesenteric -> internal iliac -> IVC

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2
Q

most likely site for external hemorrhoids

A

posterior canal – poor perfusion

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3
Q

coarctation murmur

A

systolic, best auscultated in interscapular region

due to turbulent flow through narrow lumen

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4
Q

braf v600e mutation in? rx?

A

melanoma!. mutation in BRAF kinase.

rx: vemurafenib: BRAF kinase inhibitor

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5
Q

origin of gut tube lining from esophagus to above pectinate line

A

endoderm

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6
Q

VACTERL syndrome

A

mesodermal origins

vertebral defects
anal atresia
cardiovascular defects
tracheoesophageal fistula
renal defects
limb defects (bone & muscle)
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7
Q

luminal epithelial derivatives: endoderm

A

lung, liver, gallbladder, pancreas, eustachian tube, thymus, parathyroid, thyroid follicular

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8
Q

toxic shock syndrome toxin (TSST-1) vs. toxic shock-like toxin

A

both toxin shock syndrome

TSST-1: staph aureus

Toxic shock-like toxin: S. pyogenes

both superantigens

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9
Q

arthus reaction

A

local subacute antibody mediated HSR Type III reaction.

intradermal injection of antigen induces antibodies, form antigen-antibody complexes in skin.

edema, necrosis, complement activation

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10
Q

Streptococcus mitis

A

alpha-hemolytic strep in mouth

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11
Q

modifications made in golgi (3)

A
  1. add N-olgosaccharides in asparagine
  2. adds O-oligosacch on serine/threonine
  3. mannose-6-phosphate to traffic to lysosomes
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12
Q

endosomes

A

sorting center for material from outside cell or from golgi – send to lysosome for destruction or back to membrane/golgi

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13
Q

I cell disease: defect & presentation

A

inherited.

defective in mannose-6-phosphotransferase –> lysosomal proteins secreted extracellular

presentation:
1. coarse facial features
2. clouded cornea
3. restricted joint movement.

high plasma levels of lysosomal enzymes.

often fatal

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14
Q

COPI vesicle trafficking protein

A

golgi -> golgi (retrograde)

gogi -> ER

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15
Q

COPII vesicle trafficking protein

A

golgi -> golgi anterograde

ER to golgi

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16
Q

clathrin

A

trans-golgi -> lysosomes; plasma membrane -> endosomes

–> receptor mediated endocytosis

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17
Q

peroxisome

A

membrane-enclosed organelle involved in catabolism of

  1. very long chain fatty acids,
  2. branched chain fatty acids, &
  3. amino acids
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18
Q

recurrent fungal and myobacterial infection?

A

IL-12 receptor deficiency
autosomal recessive

reduced Th1 response

reduced IFN-gamma

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19
Q

mnemonic for branchial arches

A 
chew (1), 
then smile (2), 
then swallow stylishly (3), 
or simply swallow (4), & 
then speak (4)
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20
Q

1st branchial arch

A

M

cartilage: meckel cartilage: Mandible, Malleus & incus, spheno-Mandibular ligament
muscles: muscles of Mastication (temporalis, Masseter, lateral & Medial pterygoid), mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini

CN: V2 and V3

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21
Q

treacher-collins

A

1st arch neural crest fails to migrate -> mandibular hypoplasia and facial abnormalities

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22
Q

2nd branchial arch

A

S
Reichert cartilage:
Stapes, Styloid process, lesser horn of hyoid, Stylohoid ligament

mucles of facial expression, stapedius, stylohyoid, plastysma, belloy of digastric

CN: VII

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23
Q

congenital pharyngocutaneous fistula

A

persistence of cleft & pouch –> fistula between tonsilar area and lateral neck

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24
Q

3rd branchial arch

A

cartilage: greater arch of the hyoid
muscle: stylopharyngeus

CN IX: glossopharyngeal

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25
Q

4th branchial arch

A

(w/ 6th for cartilage): thyroid, cricoid, arytenoid, cornuculate, cuneiform

muscle: most PHARYNGEAL constrictors; laryngeal: CRICOTHYROID, levator veli palatini

CN X: superior laryngeal branch (swallow)

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26
Q

6th branchial arch

A

(w/ 4th for cartilage): thyroid, cricoid, arytenoid, cornuculate, cuneiform

muscle: all intrinsic muscle of LARYNX, EXCEPT CRICOTHYROID.

CN X: recurrent laryngeal branch (speak)

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27
Q

which branchial arches make up the posterior 1/3 of tongue

A

arches 3 & 4

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28
Q

mnemonic for branchial pouches

A

ears, tonsils bottom to top
1. ear (endoderm-lined structures: middle ear cavity, eustachian tube, mastoid air cells)

  1. tonsil: epithelial lining of palatine
  2. dorsal wings: inferior parathyoid
    ventral: wings: thymus

4: dorsal wings: superior parathyroids

4th & 5th pouch – parafollicular cells of medullary thyroid

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29
Q

cleft lip follows failed fusion of..

A

maxillary & medial nasal processes (primary palate)

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30
Q

cleft palate follows failed fusion of..

A

two lateral palatine processes

or lateral palatine process w/ nasal septum / medial palatine fossa

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31
Q

kinase vs. phosphorylase

A

kinase: adds phosphate using ATP
phosphorylase: adds inorganic phosphate w/o consuming ATP

32
Q

how do epi & glucagon increase glycogenolysis

A

both increase adenylate cyclase -> cAMP -> PKA -> glycogen phosphorylase kinase -> glycogen phosphorylase -> glucose from glycogen

33
Q

what stimulates glycogen phosphorylase kinase (3)

A
  1. PKA (from glucagon/epi stim)
  2. Ca2+/calmodulin complex
  3. Ca2+ directly
34
Q

anti-Ro, anti-La
or
anti-SSA, anti-SSB

A

Sjorgen syndrome

35
Q

anti-Jo, anti SRP, anti-Mi-2

A

polymyositis, dermatomyositic

36
Q

anti-Scl-70
or
anti-DNA topo I

A

Scleroderma (diffuse)

37
Q

anti-smooth muscle

A

autoimmune hepatitis

38
Q

1st generation sulfonylurea (2)

A

tolbutamide

chlorpropamide

39
Q

2nd generation sulfonylurea (3)

A

glyburide
glimepride
glipizide

40
Q

what stimulates Th17 formation

A

TGF-beta & IL-6

41
Q

what stimulates Treg formation

A

TGF-beta

42
Q

TGF-beta (3)

A
  1. anti-inflammatory
  2. TH17 formation (w/ IL-6)
  3. Treg formation
43
Q

regulation of nf-kB

A

normally inhibited by IkB, released when ikB is phoshparylated.

nfKb then goes to nucleus –> transcription factor

44
Q

carbon dioxide transport in RBC

A
  1. HCO3- (90%)
  2. carbaminohemoglobin: co2 bound to hb at n-terminus of globin (not heme) –> favors O2 unloading by stabilizing taut form (5%)
  3. dissolved CO2 (5%)
45
Q

carboxyhemoglobin, methemoglobin, carbaminohemoglobin

A

carboxyhemoglobin: CO in place of O2
methemoglobin: Fe3+, does not bind O2 as readily (high affinity for cyanide)
carbaminohemoglobin: CO2 bound to Hb at N-terminus of globin (NOT HEME). CO2 binding favors taught form (oxygen unloading)

46
Q

haldane effect

A

lungs: oxygenation of Gb promotes dissociation of H+ from Hb (shifts equilibrium towards CO2 formation –> release)

47
Q

Bohr effect:

A

peripheral tissue, H+ from tissue shifts curve to right, unloading O2

48
Q

majority of CO2 carried as

A

HCO3-

49
Q

SLE presentation

A

usu: rash, joint pain, fever

RASH OR PAIN

rash: malar or discoid
arthritis
soft tissue/serositis
hematologic disorder (cytopenia

oral-nasopharyngeal ulcer
renal disease, raynaud

photosensitivity, positive VDRL
antinuclear antibodies
immunosuppressants
neurologic disorder (seizure, psychosis)

50
Q

renal disease in lupus

A

nephrotic: membranous nephropathy
nephritic: diffuse proliferative glomerulunephropathy

51
Q

cause of death in lupus (3)

A
  1. cardiovascular disease
  2. immunosuppresion
  3. renal disease
52
Q

gingival hyperplasia side effect (4)

A

phenytoin, verapamil, cyclosporine, nifedipine

53
Q

metoclopramide

A

D2 receptor antagonist

INCREASE resting tone, contractility, LES tone, motility

does not influence colon transport time.

use: diabetic / postsurgery gastroparesis, antiemetic
toxicity: antiparkinson. interact w/ digoxin and diabetic meds.

54
Q

irradiated blood? washed?

A

irradiate: destroys DNA (WBC) prevents graft vs. host
washed: remove all plasma, less often done

55
Q

autosomal dominant polycystic kidney disease vs. hydronephrosis

A

hydronephrosis: smooth surface

ADPKD: rough and bumpy surface

56
Q

tanner stages

A

1: childhood (prepubertal)
2: pubic hair (pubarche) and breast bud (thelarche)
3: pubic hair darkens & curly, penis size/length increase, breast enlarge (adrenarche)
4: penis width increasese, darken scrotal skin, development of glans, raised areolae
5: adult: areola are no longer raised

57
Q

HTN, bradycardia, and respiratory depression

A

cushing reaction

  1. increased cranial pressure constricts arterioles –> cerebral ischemia –> reflex sympathetic increase in perfusion pressure – HTN
  2. HTN increases stretch –> reflex baroreceptor induced bradycardia
58
Q

baroreceptor innervation (aortic arch & carotid)

A

carotid sinus: glossopharyngeal (both high & low)

aortic arch: just high

both go to solitary nucleus

59
Q

describe hypotension detection at carotid sinus

A

hypotension -> less stretch -> decreased glossopharyngeal firing in solitary nucleus of medulla

  1. relieves tonic inhibition on sympathetic
  2. decreases firing of parasympathetic

–> vasoconstriction, increase HR, contracility, BP

60
Q

describe hypertension detection at carotid sinus:

A

hypertension -> increased stretch -> increased afferent glossopharyngeal firing in solitary nucleus

  1. tonic inhibition of sympathetic
  2. stimulation of parasympathetic

decrease HR (increased AV node refractory)

(aortic arch & vagus will also respond)

61
Q

what stimulates carotid & aortic chemoreceptor (peripheral)

A
  1. PO2 < 60mmHg
  2. increased PCO2
  3. low blood pH
62
Q

what stimulates central chemoreceptors?

A
  1. pH
  2. PCO2

(not directly to O2

63
Q

CREST

A

calcinosis, raynaud phenomenon, esophageal dysmotility, scerlodactylyl, telangiectasia

anti-centromere

64
Q

side effects of niacin (3)

A
  1. hyperuricemia
  2. hyperglycemia
  3. facial flushing
65
Q

sorbitol dehydrogenase in tissues. lens? schwann cells, retina, & kidney?

A

usu glucose -> sorbitol (w/ aldolase reductase &NADPH)

sorbitol -> fructose
w/ sorbitol dehydrogenase & NAD+

most tissues have sufficient sorbitol dehydrogenase

lens: less active, can be overwhelmed

schwann cells, retina, kidney: much less active, but exists!

66
Q

arteries coming off of celiac trunk

A
  1. common hepatic
  2. splenic
  3. left gastric (near lesser curvature). anastomose w/ right gastric (from common hepatic) & gives off esophageal branch
67
Q

common hepatic splits into (3)

A
  1. gastroduodenal -> anterior superior & posterior superior pancreaticoduodenal artery & right gastricepiploic (around greater curvature)
  2. hepatic artery proper
  3. right gastric artery -> less curvature, anastomose w/ left gastric
68
Q

inferior epigastric artery comes off of

A

external iliac artery

69
Q

ulcer on posterior wall of duodenum can cause bleeding from..

A

gastroduodenal artery (from common hepatic, from celiac trunk

70
Q

ruptured ulcer on lesser curvature of stomach results in bleeding from

A

left gastric (from celiac)

71
Q

what does the ventral pancreatic bud contribute? dorsal bud?

A

main pancreatic duct & pancreatic head (uncinate process specf)

everything else: body, tail, isthmus, accessory pancreatic duct –> dorsal bud

72
Q

special embryology of spleen

A

supplied by foregut (celiac artery) but arises from mesentary of stomach –> MESODERM

(pancreas, liver, gallbladder, etc –> endoderm

73
Q

histology of abetalipoproteinemia

A

decrease synthesis of apolipoprotein B-48, can’t make chylomicrons. decreased secretion of cholesterol, VLDL into blood stream –> fat accumulation in enterocytes

failure to thrive, acanthocytosis, ataxia, night blindness

74
Q

Wernicke’s area specifically located

A

posterior section of superior temporal gyrus

75
Q

diabetic neuropathic pain is often..

A

BURNING

UWorld mixed (60 decks)

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