Flashcards in 3/5 UWORLD test #33 Deck (57):
Q 1. How does inflammatory acne form?
overproduction of keratin & sebum
-> blocks follicles (forming comedones)
-> propionibacterium acnes infection
-> bacteria produces lipase that breaks down TG in sebum
Q 1. Definition and example of each
- aporcine: vesicle mediated release
ex) mammary gland (remember apocrine metaplasia that does not progress to cancer?)
- merocrine: exocytosis mediated release
ex) eccrine/apocrine sweat gland, salivary gland
- holocrine: lysis and release of cytoplasmic contents
ex) sebaccus gland (thus acne is example of holocrine)
* all of these are exocrine system: release via duct
Q 2. common infection source of osteomyleitis
- sickle cell (2)
- pott disease
- children: S. aureus
- sickle cell: S.aureus, Salmonella
- pott disease: Mycobacteria
Q 2. Moraxella catarrhalis: associated disease? (3)
* This bug is not covered in sketchy/FA
exacerbation of COPD
Q 3. How to calculate median?
sum two middle values/2
data set should be in even number
-> median: (3+4)/2=3.5
Q 4. Which viral encoded protein is the major determinant for viral tropism on specific host tissue?
viral surface glycoprotein attaches to corresponding receptors on host cell membrane: the very initial step.
This makes sense as orthomyxovirus major antigenic variation is on hemagluttin (surface gylcoprotein)- shift/drift
Q 6. epigenetics: histone acetylation vs. histone deacetylation? What each does for txn?
- acetylation: txn activation
- deacetylation: txn deactivation
Q 6. Huntington disease
- which gene is mutated? what chromosome? how?
- nature of mutation: gain of function or loss of function?
- huntingtin protein, chromosome 4, multiple CAG repeats
- gain of function, mutated hungtingtin protein promotes histone deacetylation, causing transcriptional repression of many other genes
Q 7. histologic finding in glioblastoma multiforme? what about macroscopic finding?
- mcroscopic finding: butterfly lesion that crosses corpus callosum
- histologic finding: pseudopallisading necrosis ( cells lining up around necrosis) & angiogensis
Q 7. glioblastoma multiforme is tumor of what neuronal cell origin? what is kid's brain tumor that has equivalent cell origin? What stain can be used for this cell origin?
- kids: pilocytic astrocytoma
- both are GFAP positive
Q 7. What is prognosis for glioblastoma multiforme?
very bad. it progresses rapidly. Pt usually die within 2 years after diagnosis
Q 8. Tetanus vaccine
- what is it?
- what immune response is triggered?
- tetanus toxoid: formaldehyde inactivated tetanus toxin
- humoral response: antibody
Q 9. Lactase degrades lactose to what two sugars?
Q 9. galactose metabolism disorder: galactose kinase deficiency vs. classic galactosemia
- compare phenotypes
Galactose kinase deficiency
- failure to track objects/ social smile
- intellectual instability
- also cataracts
*LIVER manifestations are only for CLASSIC GALATOSEMIA
Q 10. Ethics: What are four exceptions for protecting patient's confidentiality?
- harming oneself/ another that may happen in the future again
- child or elder abuse
- knife or gunshot wounds
- reportable communicable disease ( transmittable infectious disease such as ebola)
Q 12. Describe the location of AV node. Radiofrequency ablation of AV node is indicated in what heart condition?
- endocardial surface near atrial septum & coronary sinus
- Atrial fib
Q 12. Describe the location of SA node.
- upper anterior atrium near opening of SVC
Q 12. Radiofrequency ablation of which part of heart is indicated for atrial flutter?
- isthmus between IVC & tricuspid annulus
Q 13. What is the most effective approach to enhance adherence to medication for adolescent patient?
Finding support and role models within PEER group
Q 14. What determines coronary dominance? What is the most common dominance type?
- Blood that supplies PDA (posterior descending artery)
- Right dominance is about 85%
Q 14. SA node and AV node are supplied by what coronary artery?
Dominant artery. Either by RCA (for right dominance) or LCA (for left dominance)
Q 15. Nitroprusside
- side effect
- increase cGMP by direct release of NO => balanced vasodilation of BOTH artery and vein. Very SHORT acting
- hypertensive crisis
- cyanide toxicity (also releases cyanide)
Q 17. pancreatic head is derived from what pancreatic bud?
- inferior/posterior head: ventral pancreatic bud
- rest of head: dorsal pancreatic bud
* Remember: ventral pancreatic bud does give rise to uncinate process, but NOT all parts of head
Q 17. main pancreatic duct vs. accessory pancreatic duct each is derived from what pancreatic bud?
- main pancreatic duct: ventral pancreadic bud
- accessory pancreatic duct: dorsal pancreatic bud
Q 19. What urine pH condition will precipitate kidney stones
- Ca oxalate
- Ca phosphate
- MAP (what is this?)
- Uric acid
- Ca oxalate: - (neutral)
- Ca phosphate: basic
- MAP (magnesium ammonium phosphate): basic
- uric acid: acidic
- cystine: acidic
Q 19. Pathophysiology of cystine kidney stone? What other amino acids will be accumulated
- mutation on transporter-> impaired reabsorption in kidney and reabsorption at gut as well
These all share same transporter
Q 20. What mutation on what gene is implicated in melanoma? What does this mutation do?
increase signaling pathway in melanocyte proliferation/metastasis/survival
Q 22. What is co-infection mechanism of HDV? (Why HepD virus needs HepB virus to infect hepatocyte? )
HepD virus (delta virus) must be COATED by HepB surface antigen to infect hepatocytes
Q 21. Diazepam
- What class of drug is this?
- indications (6)
- side effects (3)
- should be avoided with what drugs?
- increase frequency (vs. phenobabitol- duration) of GABA-A
- status epilepticus (1st line), alcohol withdrawal, insomnia, anxiety, analgesia, muscle relaxant ( to stop spasticity in stroke)
- sedation, mental status change-confusion/disorientation (elderly), dependence/tolerance
- Any drugs that cause same side effects
ex: Anti-histamines (first generation, sedation is less significant in second gen.)
Q 21. Chlorpheniramine: what class of drug is this? What other drugs (2) are in this class?
first generation anti-histamine
- Diphenhydramine, dimenhydrinate
Q 21. Loratadine: what class of drug is this? What other drugs (3) are in this class?
second generation anti-histamine
- fexofenadine, cetirizine, desloratadine
Q 22. Ranitidine
- side effect (1)
- H2 receptor blocker -> less gastric acid secretion
- peptic ulcer disease, GERD, gastritis
- decrease renal excretion of creatinine
- side effects (3)
- H2 receptor blocker -> less gastric acid secretion
- peptic ulcer disease, GERD, gastiritis
- side effects
1. potent CYP450 inhibitor (DDI)
2. decrease renal excretion of creatinine (so does ranitidine)
3. anti-androgen effects (gynecomastia, impotence, decreased libido, prolactinemia)
Q 23. Cheyne- stroke breathing
- Describe breathing pattern?
- explain physiology
- under what medical conditions? explain physiology
- apnea followed by gradual increase then decrease tidal volume
- apnea induced hypercapnea -> hyperventilation to compensate and then hypoventilation to reduce hypocapnea
-CHF, brain trauma, stroke
w/ CHF: lack of effective ventilation (due to pulmonary conjestion) -> unbalanced hyper/hypo ventilation
w/ brain trauma/stroke: delayed pCO2 sensation in central chemoreceptor-> unbalanced hyper/hypo ventilation
Q 24. What are diagnostic criteria for diabetes
- fasting glucose level
- 2hr glucose tolerance
- Hb1AC >6.5
- fasting glucose >126
- 2hr glucose tolerance >200
Q 24. elevated free serum fatty acid vs. elevated C-peptide: which one contributes to progress of T2DM?
elevated free serum acid
Elevated free serum acid -> less need of insulin dependent glucose uptake -> insulin resistance
- elevated C-peptide is also seen in T2DM, but it is byproduct of insulin resistance (increased insulin synthesis in insulin resistance), not causation of insulin resistance
Q 25. What is eplerenone?
just like spironolactone
Q 27. What ECG finding is seen after beta-blocker?
Q 28. Varicose vein
- What is gross appearance ?
- etiologies (4)?
- what is complication?
- dilated & tourtuous vein
- long standing, >50 age, multiple pregnancy, obesity
- ischemic necrosis and skin ulceration
Q 30. What agent decreased radioactive I uptake treatment for Graves disease? why?
Pertechneate or Perchlorate
These two agents also undergo uptake by Na+/I- cotransporter. Thus, it will reduce radioactive Iodine uptake
Q 30. What is additional function of propylthiouracil that methimazole doesn't have? What is the function that these two commonly have?
Both propylthiouracil and methimazole can block TPO (thyroid peroxidase- iodine oxidation/ organification/ coupling)
Q 31. What is the best therapy for febrile seizure?
supportive care only
Q 31. Is active cooling recommended for febrile seizure? what about antipyretics?
- active cooling is not recommended. It can precipitate seizure by inducing shivering
- antipyretics do not show efficacy in reuding seizure
Q 32. What do leukotrines (LTC4, LTD4, LTE4) do? Which medications target leukotrines for asthma?
- Monteleukast/ Zafirleukast: leukotrine receptor inhibitor
- Ziluton: Direct LOX inhibitor
Q 33. hemoptysis, elevated DLCO, proteinuria, hematuria. what is diagnosis?
Elevated DLCO is due to accumulation of blood within alveoli. Blood will uptake CO (hemoglobin has great affinity to it)
Q 34. Which vitamin is precursor for NAD?
Q 35. peripheral chemoreceptor vs. central chemoreceptor
- senses what?
: carotid body
=> senses pO2
: ventral surface of medulla
=> senses pCO2, pH
Carotid body vs. Carotid sinus
- difference: body is chemoreceptor, sinus is pressure receptor
- similarity: they both fires glossopharyngeal nerve to solitary nucleus of medulla
Q 37. Blue toes, livedo reticularis after surgery. What is happening?
After surgery, cholesterol gets dislodged from big size arteries, and lodged to small size arteries.
Q 37. Histologic finding of hyperplastic arteriolor changes in kidney. What is diagnosis?
Q 38. Screening marker in urinalysis for early stage diabetic nephropathy? explain pathophysiology
In diabetes, upregulation of heparanse will result in loss of negative charge barrier in GBM
Q 38. What is earliest morphological change in diabetic nephropathy?
GBM thickening & mesangial matrix expansion due to non-enzymatic glycosylation
Q 38. Which molecule in GBM is responsible for barrier for protein filtration?
: it is negatively charge. so it creates charge barrier (most protein is negatively charged)
Q 38. What medication slows progression of diabetic nephropathy? explain mechanism
dilation of efferent arteriole to reduce hyperfiltration damage of glomeruli
Q 39. lepromatous leprosy vs. tuberculoid leprosy
- immune response
- severe presentation- diffuse/leonine face (lion face)
- mediated by Th2
- less severe presentation- limited, skin plaques
- mediated by Th1
* think like this: lepromatous is more nasty one. so you need to stimulate Th2 -> antibody to handle this nasty shit
Q 39. What is lepromin skin test? which form of leprosy is more sensitive? why?
- injection of M leprae antigen (like PPD): positive result will show indurated nodule
- lepromin skin test is more sensitive to tuberculoid as it has stronger Th1 response.