2/6 UWORLD test #8 Flashcards

1
Q

Q 2. What phospholipid in amniotic fluid can be used for what abnormal fetal condition?

A

dipalmitoyl phosphotidylcholine

ARDS

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2
Q

Q 2. What can be measured in amniotic fluid to screen neural tube defect?

A

Alpha-fetoprotein

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3
Q

Q 6. low leukocyte with infection symptoms. What is it?

A

non bacterial infection (viral)

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4
Q

Q 6. Histologic finding of CMV infection?

A

eosinophilic intranuclear inclusion (owl eye)

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5
Q

Congenital Toxoplasma gondii vs. Congenital CMV?

A

Both of them are ToRCHeS infection
They have similar, but different clinical manifestations

- Toxoplasma gondii
\: ring shaped contrast on MRI
  intracranial calcification
  retinitis
  Hydrocephalus
  \+/- Blueberry muffin rash
- CMV
\: periventricular calcification
  seizure
  hearing loss
  Blueberry muffin rash
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6
Q

What are two possible ways to get CMV infection?

A
  • organ transplant

- sexual

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7
Q

Q 7. Explain how squatting helps alleviating cyanosis in tetralogy of Fellot

A

increased blood flow into pulmonary circulation due to increased pre-load and after-load (less deoxygenated blood will go to aorta)

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8
Q

Q 9. Key phenotype difference between fructokinase deficiency (essential fructosuria) vs. Adolase B deficiency (Fructose intolerance) ?

A
  • essential fructosuria: benign, excess fructose will pee out
  • Fructose intolerance: accumulation of toxic metabolite (1P-Fructose)
  1. Hypoglycemia (less phosphate available for gluconeogenesis)
  2. liver toxicity (cirrhosis), jaundice
    Cataract will NOT be seen (this is only for galactose and sorbitol)
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9
Q

Q 10. What drugs can cause serum sickness?

A
  • non protein drugs: penicillin

- chimeric monoclonal antibodies: rituximab

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10
Q

Q 10. What are symptoms (3) of serum sickness?

A
  • fever
  • pruritic skin rash
  • arthralgia
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11
Q

Q 10. What will be seen in terms of complement level in serum sickness?

A

decreased C3 due to complement fixing by antibody (IgG/IgM)- drug complex

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12
Q

Q 11. What is the requirement for referring a patient for hospice care?

A

prognosis <6 months

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13
Q

Q 12. What is key difference between factitious disorder and malingering?

A

factitious disorder: goal is to meet psychological (internal) need- absence of obvious reward

malingering: goal is to achieve external reward

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14
Q

Q 13. What is conversion disorder?

A

unexplained neurologic complain, often acute onset with stress

Think like this: stress is CONVERTED to neurologic symptoms

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15
Q

Q 13. What is somatic symptom disorder?

A

unexplained generalized somatic symptoms (fatigue, pain) + excessive anxiety due to those symptoms

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16
Q

Q 15. What is argatroban?

What is its indication?

A

direct factor 2a (thrombin) inhibitor

Indicated for HIT (Heparin Induced Thrombocytopenia)

17
Q

Q 19. What is area postrema? Where is it located? What is special for this structure?

A

chemoreceptor trigger zone- vomiting center, located in dorsal medulla
no BBB so that plasma material can freely move into area postrema -> chemoreceptor trigger for toxic material -> vomiting

18
Q

Q 20. What is transmission pathways (3) for congenital toxoplasmosis gondii

A
  • Congenital: vertical transmission
  • Cat feces
  • meat
19
Q

Q 20. What is intrapartum infection?

A

Infection during delivery

20
Q

Q 21 Which cells express MHC1? What about MHC2?

A

MHC1: most nucleated cells except erythrocyte - this makes sense that CD8 basically kills any virally infected cells. Needs nucleus that can express viral genome

MHC2: APCs (macrophage, B cells, Langerhan cells)

21
Q

Q 21. What kind of antigen is presented in MHC1? What about MHC2?

A

MHC1: endogenously synthesized antigen, viral

MHC2: exogenous antigen, bacterial

22
Q

Q 21. MHC1 vs MHC2: structural difference?

A

MHC1: heavy chain + beta 2- microglobulin

MHC2: alpha and beta chains

23
Q

Q 22. Therapeutic measurement efficiency: Formula for absolute risk reduction?

A

% disease without medication - % disease with medication

24
Q

Q 22. Therapeutic measurement efficiency: Formula for number needed to treat? What is its definition?

A

1/ARR

number of people to treat with medication to reduce one person from getting disease

25
Q

Q 24. Severity of myopathy in statin can be exacerbated when statin is combined with that?

A

gemfibrozil

sketchy: statin captain holding chicken is on gemfirozil jelly fish

26
Q

Q 25. Along with respiratory tract, what is major specific histologic features of following

  • bronchi
  • bronchiole
  • Respiratory bronchiole
  • alevoli
A

Bronchi- pseudostratified ciliated columnar cell, goblet cell, cartilage

Bronchiole- club cell, simple ciliated columnar

Respiratory bronchiole- club cell, ciliated columnar cells become squamous cell as it reaches closer to alveoli

Alveoli- pneumocyte type 1 and 2, alveolar macrophage

27
Q

Q 26. DKA is prevalent in what type of diabetes?

A

Type 1

In type 2, insulin is still present, inhibiting lipolysis

28
Q

Q 26. What is the most common etiology of type 1 diabetes?

A

autoimmune beta cell desturction

29
Q

Q 26. Genetic defects in insulin secretion accounts for what % of total cases of type 1 diabetes?

A

less than 5% (super rare)

30
Q

Q 30. What is pathophysiology of increased risk of gallstone in Crohn’s disease?

A

impaired bile acid reabsorption at terminal ileum

-> decreased cholesterol solubility

31
Q

Q 30. What are side effects of statin? (3)

A
  • myopathy (increased CK)
  • teratogen
  • hepatotoxicity (elevated LFT)
32
Q

Q 30. What dyslipidemia drugs have side-effects of increased risk of gallstone?

A
  • Cholestyramine: decreased bile acid resorption

- fibrates

33
Q

Q 31. What are 4 symptoms of typhoid fever?

A
  • fever
  • rose spots (erythematous rash) on abdomen
  • abdominal pain
  • hepatosplenomegaly
34
Q

Q 36. What is neutrophil elastase? How is it regulated?

A

protease of extracellular elastin degradation.

It is released by neutrophil & macrophages, and inhibited by AAT1 (alpha-antitripsin 1)

35
Q

Q 37. What is chest-X ray finding in sarcoidosis? Is this finding specific to sarcoidosis?

A

bilateral hilar adenopathy (patchy medial side of middle lobe)

36
Q

Q 38. When does glial scar form after ischemic stroke? Which brain cells are responsible for glial scar formation?

A

1 week-2 weeks post ischemic stroke

astrocyte

37
Q

Q 39. What is fatal condition in Crigler-Najjar syndrome? Explain pathophysiology (why not in other bilirubin diseases?

A

Kernicterus: indirect bilirubin deposition in brain
-> CNS defect

Indirect bilirubin is not water soluble, thus not excreted via urine, rather it is deposited in brain
vs. direct bilirubin (Rotor syndrome) can be excreted via urine, deposition is less likely- jaundiced but normal life expectancy

38
Q

Q 40. What is the best way to prevent idwelling catheter associated UTI?

A

Removal of catheter quickly as it is no longer indicated

39
Q

Q 40. Is frequent change of catheter helpful to reduce indwelling catheter associated UTI?

A

Nope