2/25 UWORLD test # 24 Flashcards

1
Q

Q 1. biceps reflex is mediated by what nerve root?

A

C5, C6

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2
Q

Q 1. Musculocutaneous nerve is derived from which nerve root? What functions are lost with musculocutaneous n. injury?

A
  • C5, C6

- bicep reflex, forearm flexion, lateral forearm sensation, and supination

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3
Q

Pancreas embryology: Each structure gives rise to what?

  • ventral pancreatic bud
  • dorsal pancreatic bud
A
  • ventral: head and uncinate process of pancreas, main pancreatic duct
  • dorsal: body and tail of pancreas, accessory pancreatic duct
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4
Q

Q2. Annular pancreas

  • Which embryological defect?
  • symptoms
  • clinical finding
A
  • abnormal migration of ventral pancreatic bud
  • abdominal pain, non-villious vomiting, pancreatitis (obstruction of pancreatic duct). Mostly asymptomatic
  • narrowed duodenum
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5
Q

Pancreas divisum

  • Which embryological defect?
  • symptoms
A
  • failure of fusion of ventral pancreatic bud with dorsal pancreatic bud
  • abdominal pain, pancreatitis, mostly asymptomatic
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6
Q

Q 4. polyuria, polydipsia, fruity odor to breath or urine. Diagnosis?

A

DKA

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7
Q

Q 5. Compare: cross-sectional vs. Ecological study

A

They both randomly select samples and evaluate exposure & outcome.

Cross-sectional: individual
Ecological: population

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8
Q

Q 6. T cell development: explain brief picture of what is happening in each structure

  • bone marrow
  • thymus
  • secondary lymphoid tissues (lymph node- paracortex / spleen- PALS)
A
  • bone marrow: T cell production
  • thymus: T cell maturation- CD4+ T cell and CD8+ T cell
  • Secondary lymphoid tissues: T cell activation ( Th becomes Th1, Th2, Th3 & CD8 cell becomes killer T cell)
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9
Q

Q 6. T cell maturation: describe what is happening in thymus

A
  • before thymus: bone marrow - CD4-/CD8- double negative
  • cortex: positive selection, CD4+/CD8+ double positive
    => majority of T cell get killed during positive selection
  • medulla: negative selection, single positive (either CD4+ or CD8+)
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10
Q

Q 7. Inheritance pattern of G6PD deficiency?

A

X-linked recessive

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11
Q

Q 7. Two reactions (oxidative & non-oxidative) of HMP shunt

  • which rxn is reversible? which is irreversible?
  • key enzymes
  • what are reactant and product?
A
  • oxidative: irreversible, first couple of rxns
    non-oxidative: reversible, final couple of rxns
  • oxidative: G6PD
    non-oxidative: transketolase (B1 dependent)
  • oxidative: G6P ->->->5P-ribosulase+ NADPH
  • no-oxidative: 5P- ribosulase Ribose 5-P, F6P, Glyceraldehyde-3P
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12
Q

Q 8. What are three symptoms of Hodgkin lymphoma? How these symptoms are collectively called? (there is fancy word for it) Another medical condition that results in these symptoms?

A

B signs

  1. fever
  2. night sweat
  3. weight loss

These B signs may also be seen in TB

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13
Q

Q 9. Which cells undergo clonal expansion by TSS toxin from S.aureus?

A

T cell

TSST works as supraantigen that leads to polyclonal T cell exapansion

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14
Q

Q 9. Which toxin is made by C.perfringens? What does it do?

A

alpha toxin

disruption of phospholipid membrane

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15
Q

Q 10. Define intellectualization

A

using fact and logic to put emotional distance from situation
- focusing only on survival rate after cancer diagnosis

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16
Q

Q 10. Define passive aggression

A

indirect expression of emotion

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17
Q

Q 10. Define projection

A

attributing unacceptable internal impulse to another person

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18
Q

Q 10 . Define regression

A

INVOLUNTARILY going back to premature state UNDER STRESSFUL SITUATION, commonly seen in kids

  • kids urinating in bed when they are stressed
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19
Q

Q 11. In a non-emergency situation, where should physician contact to report impaired colleagues? What if such a body does not exist?

A

physician health program

state licensing board if physician health program does not exist

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20
Q

Q 13. After period of starving, patient develops hypoketotic hypoglycemia: what is going on? what enzyme is most likely missing?

A

inability to undergo beta-oxidation for ketogenesis

Either cartine acyltransferase or acyl-coA dehydrogenase may be deficient

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21
Q

Q 13. What is role of carnitine in beta- oxidation? what are phenotypes for carnitine deficiency?

A

to shuttle long chain (over 14 carbons) fatty acyl-coA into mitochondria, where further steps in beta oxidation occurs

with carnitine deficiency, hypoketotic hypoglycemia after fasting

22
Q

Q 14. How are PaO2 and PaCO2 during exercise in healthy people?

A

generally well maintained due to adjusted ventilation, V/Q

23
Q

Q 15. Define nature of mutation in factorV laiden.

coagulability state? inheritance pattern?

A

resistance against protein C -> hypercoagulable state

gain of function so autosomal dominant

24
Q

Q 16. How diet should be modified in celiac disease?

A

no grains (wheat, barly, rye)

25
Q 16. How diet should be modified in lactose intolerancE?
no dairy
26
Q 16. Describe histologic finding of duodenal biopsy in celiac
loss of villi crypt hyperplasia * check image FA 358
27
Q 16. Which parts of GI (2) are most susceptible to damage by gliadin mediated inflammation in celiac?
distal duodenum and proximal jejunum
28
Q 20. Non-depolarizing neuromuscular blocking drug - mechanism of action - examples - explain physiology of train of four (TOF) stimulation
- Ach receptor antagonist, compete with Ach - tubocurarine, atracurium (-cur-) - gradual decrease with each stimulation as further decrease in Ach release (it also acts on presynaptic Ach receptor)
29
Q 20. Depolarizing neuromuscular blocking drug - mechanism of action - example (1) - explain physiology of train of four (TOF) stimulation
- Ach receptor agonist, generates weaker response with sustained contraction - succinylcholine deposustained constant but much weaker response followed by gradual decrease due to desensitization
30
Q 21. Mechanism of action of alcohol as antiseptic agent? Can it also kill bacterial spore?
disruption of cell membrane -> leakage alcohols can NOT kill bacterial spore
31
Q 22. What is Tzanck test? What does it look for? What infections are indicated?
smear of scrap of ulcered skin multinuclear giant cells will be seen with infected HSV-1 &2, VZV
32
Q 22. Difference: primary HSV infection vs. reactivation of HSV
primary HSV infection shows some systemetic symptoms including fever, malaise, while reactivation of HSV results in vesicles around lips/eyes
33
Q 23. What additional contact precautions (2) are required for enteric bacteria (C. Diff)?
- NONSTERILE gloves (sterile gloves are only required during surgery) - gown
34
Q 24. Major sites (2) for iron absorption?
duodenum and proximal jejunum
35
Q 24. What is common complication of gastrojejunostomy?
iron deficiency anemia
36
Q 25. Pathophysiology of ataxia in Ataxia-Telangiectasia?
cerebellar atrophy
37
Q 26. Describe pathophysiology of low body weight induced secondary amenorrhea
low body weight - > decreased leptin (leptin is released from adipose tissue) - > decreased GnRH -> decreased FSH/LH -> amenorrhea
38
Q 27. What is major difference between testosterone vs. DHT in male genitalia development?
testosterone: internal genitalia DHT: external genitalia
39
Q 29. Dantrolene - mechanism of action - indications
- block ryanodine receptor in SR | - neuroleptic malignant syndrome, malignant hyperthermia
40
Q 30. List 4 clinical symptoms/ findings in NMS (neuroleptic malignant syndrome)
- DIFFUSE muscle rigidity - hyperthermia - autonomic instability (tachycardia) - rhabdomyolysis (elevated CK, myoglobinuria)
41
Q 30. serotonin syndrome vs. NMS: What is major difference in terms of clinical symptom
serotonin syndrome is more like clonus movement of ankle, while NMS is diffuse muscle rigidity
42
Q 30. Why ACEI (or ARB) is used for diabetic nephropathy?
ACEI (or ARB if patient is not compliant with massive cough from ACEI) is used to slow progression of chronic renal failure by reducing GFR : GFR reduction diminishes hyperfiltration induced glomerular injury
43
Q 30. What is mechanism of cough production by ACEI?
ACE breaks down bradykinin and substance P Elevated bradykinin and substance P by ACEI produces cough. Patients non-compatible with cough can use ARB instead
44
Q 31. Explain physiology of GI stress induced vomiting
GI stress -> SEROTONIN release -> stimulation of afferent vagus -> vomiting center in medulla
45
Q 32. Jaw deviation to left side - what CN is injured? - This CN passes exits through what skull structure?
- CN 5-III ( mandibular branch) | - foramen ovale
46
Q 35. What is serum calcium level in patient with calcium kidney stone? why?
normocalcemic vitamin D and PTH are intact to regulate Ca2+
47
Which step in collagen synthesis is impaired with vitamin C deficiency?
hydroxylation
48
Which step in collagen synthesis is impaired with Ethlers-Danlos syndrome?
cross linking
49
Q 37. Craniopharyngioma - adult or kid? - origin of tumor - gross appearance/ MRI finding - symptoms
- kid - remnant cells f Rathke's pouch - cystic, calcified tumor - visual field defects, headache
50
Q 38. Axonal reaction - what is it? - microscopic changes (2)? - what is fancy word for this?
- axon's response to damage to increase protein synthesis 1. dispersed Nissl substance (rough ER) within cytoplasm 2. peripheral displacement of nucleus within cytoplasm - chromatolysis make sure to check figure in FA220
51
Q 39. What are clinical presentations (3) of superior vena cava syndrome?
- puffy, red face - dilated veins in upper chest - headache/ confusion due to increased ICP
52
Q 40. What is role of choline acetyltransferase?
synthesis of acetylcholine in presynaptic neuron