Uworld 5 Flashcards

1
Q

what are the regenerative source for ciliated cells in the bronchioles?

A

Club (clara) cells

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2
Q

what is enterobiasis?

A

pinworm! (the scotch tape test one)

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3
Q

what is the treatment for enterobiasis (pinworm)?

A

Albendazole

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4
Q

what is the treatment for Chagas (trypansomoma cruzi)

A

Nirurtimox

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5
Q

what is praziquantel used for?

A

schistosoma, (and clonorchiasis, and paragonimusis) infections…

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6
Q

which levels of the transverse spinal cord have increasing amounts of white matter and more ovoid sections?

A

more proximal levels.

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7
Q

which levels of the transverse spinal cord have large ventral horn

A

lower cervical and lumbosacral regoins

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8
Q

which levels of the transverse spinal cord have lateral gray matter horns?

A

T1-L2

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9
Q

antimichondrial antibodies are found in what?

A

Primary biliary cirrhosis!!!!!

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10
Q

CTG repeat.

A

codes for a myotonia protein kinase.

causes myotonic dystrophy. auto. dom.

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11
Q

abnormally slow relaxation of muscles. cataracts, frontal balding, gonadal atrophy

A

myotonic dystrophy. type 1 fibers affected

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12
Q

how does N-acetylcysteine help CF pts?

A

cleaves disulfide bonds in mucus glycoproteins. loosening thick sputum

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13
Q

abnormal Rinne test and Weber localizes to affected ear

A

conductive hearing loss (bone >air)

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14
Q

normal rinne test and weber localizes to unaffected ear

A

sensorinueural hearing loss (air>bone)

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15
Q

what parts of the ear does sensorineural loss deal with?

A

inner ear, cochlea auditory nerve

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16
Q

how do you get a conductive hearing loss?

A

obstruction of external soudn vibrations to the inner ear

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17
Q

what type of virus is Parvovirus?

A

small!!! SS DNA, non-enveloped

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18
Q

where are promoter regions of a gene?

A

25-70 base pairs upstream

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19
Q

most common causes of infectious esophagitis in HIV + pts.

A

CANDIDA!! (and also CMV and HSV-1 often the cause)

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20
Q

patches of adherent, grey/white pseudomembranes on erythematous mucosa on endoscopy

A

candida!

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21
Q

small vesicles that evolve into typical “punch out” ulcers on endoscopy

A

HSV-1 (herpes)

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22
Q

linear ulceration on endoscopy. both intranuclear and cytoplasmic inclusion on micro

A

CMV!

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23
Q

asplenic patient. from NE US. flu-like symptoms, hepatosplenomegaly, anemia. from a tick bite

A

babesia diergens (babesiosis)

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24
Q

HIV + ring enhancing brain lesions. and chorioretinitis

A

toxoplasma!

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25
Q

does Herpes zoster cause esophagitis in HIV patients?

A

NO!! ONLY HERPES SIMPLEX!

26
Q

chronic dz –> cardiomyopathy, achalasia, megacolon, megaureter

A

Chagas! (trypanosome cruzi)

27
Q

cryptococcosis causes what in HIV + patients?

A

meningitis!

28
Q

common mets to the brain (3)

A

lung CA, renal CA, and melanoma

29
Q

side effects of HIV meds–> protease inhibitors.

A

hyperglycemia, lipodystrophy (buffalo hump), inhibition of P-450

30
Q

4 situations where you can disclose patient info without consent of the patient

A
  1. suspected child or elder abuse
  2. gunshot or stabbing injuries
  3. diagnosing a reportable communicable disease
  4. pt threatens to harm themselves or others AND has reasonable ability to carry out threat in near future.
31
Q

colon adenoma to carcinoma sequence of gene mutations

A

APC–> KRAS –> (now has adenoma) –> loss of tumor surpressor (eg. p53 or DCC) converts it to CA

32
Q

How would ARDS affect lung compliance?

A

interstitial and intra alveolar edema, inflammation, and hyaline membrane formation will cause lung compliance to decrease

33
Q

How would ARDS affect oxygen diffusion capacity

A

it would decrease due to the edema, inflammation, and hyaline membrane formations

34
Q

How would ARDS affect V/Q matching?

A

atelectasis may foorm, and cause decreased ventilation with maintained perfusion

35
Q

increased pulmonary capillary wedge pressure would lead you to what cause of pulmonary edema?

A

cardiogenic cause…

36
Q

what is the most common cause of acute infective endocarditis?

A

staph aureus

37
Q

how is staph aureus unlike other endocarditis causing pathogens?

A

it can invade intact valvular endothelium due to expression of multiple surace adhesins

38
Q

what happens after the bacteria invades the endothelium in endocarditis

A

expresses tissue factor –> platelet and fibrin deposition and the formation of valvular vgetations. then the bacteria can embolize into the systemic circulation causing sepsis…

39
Q

dude has gonorrhoeae. you give him intramuscular ceftriaxone…but he doesn’t get better….what do you give him now?

A

a macrolide like azithromycin! because he has a coinfection with chlamydia!!

40
Q

what is metronidazole used for?

A

anaerobic bacteria or protozoa

41
Q

what is fluconazone used for?

A

candidiasis, crypto, histo, blasto, coccidio

42
Q

how do -azoles work? (antifungals)

A

inhibit the synthesis of ergosterol by the fungal cyt P450. erg. is essential in the fungal cell wall. they may also surpress the human cyt P450

43
Q

common viral causes of meningitis

A

enterovirus
arbovirus
HSV 2

44
Q

how is the Sabin and Salk vaccines for polio different?

A

Sabin is live attenuated oral
Salk is inactivated poliovirus.
Sabin produces a stronger mucosal secretory IgA response

45
Q

for how long will viable sperm remain after a vasectomy?

A

3 months!

46
Q

what amino acid is responsible for transferring nitrogen to the liver for disposal (into the urea cycle)

A

Alanine. during catabolism, amino groups are transferred to a-ketoglut. to make glutamine. the glutamate is then processed in the liver to make urea.

free ammonia goes to the urine via the kidney (to regulate acid-base)

47
Q

how is acid excreted in the urine? (conjugated to what?)

A

NH4+, and H2PO4-

48
Q

what happens to urine pH, free H+, NH4+,H2PO4- in DKA?

A

pH decreases
free H+, NH4+,H2PO4- all decrease in tthe serum, as they are excreted.l
bicarb is completely reabsorbed in the tubules in acidotic states

49
Q

metabolic acidosis compensation: incr or decr pCO2?

A

Decr!! –> trying to get rid of acid, so blow more CO2 off. so decr in pCO2. (kussmal respirations)

50
Q

what are acute vit A toxicity symptoms?

A

nausea, vomiting, vertigo, blurred vision

51
Q

what are chronic Vit A tox symptoms?

A

alopecia, dry skin, hyperlipidema, hepatotox, hepatosplenomegaly, vision problems, papilledema (suggestive of cerebral edema…pseudotumor cerebri)

52
Q

what are teratogenic effects of vit A tos?

A

microcephaly, cardiac anomalies, and fetal death (esp. in first trimester)

53
Q

niacin deficiency…what happens?

A

3 D’s of pellara: dementia, dermatitis, diarrhea

54
Q

what can large doses of vitamin E cause?

A

hemorrhagic stroke in adults, and necrotizing enterocolitis in infants

55
Q

where does C1 bind?

A

to the Fc portion of the heavy chain near the hinge point

56
Q

what is thiopental used for?

A

short acting barbiturate used for the induction of anesthesia.

57
Q

retroperitoneal hematoma in a stable patient is probably coming from where?

A

pancreatic injury!

58
Q

what sequence at the 3’ end of tRNA is the recognition sequence for proteins to bind?

A

CCA

59
Q

what anomalies are associated with polyhydramnios

A

decreased fetal swallowing
like GI obstruction (duodenal, esophageal or intestinal atresia) or anencephaly
OR increased fetal urination (high cardiac output due to anemia, twin to twin transfusion syndrome)

milder polyhydramnios can be due to maternal DM or multiple gestations

60
Q

what is in the deeper aspect of the gastric glands?

A

small basophilic, granular chief cells that synthesize and secrete pepsinogen