Uworld 4 Flashcards

1
Q

clasp kinife spasticity –> initial resistance to passive extension followed by a sudden release. ….upper motor neuron lesion = lose inhibition on spinal stretch reflex.
purely motor affecting contralateral arm, leg, and lower face
where is the lesion?

A

Internal capsule

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2
Q

lesion in caudate nucleus… caused by?

A

Huntington’s

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3
Q

chorea and athetosis…where is the lesion?

A

caudate nucleus

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4
Q

contralateral tremor, bradykinesia, and rigidity…where is the lesion?

A

putamen of basal ganglia (involved in initiation of movement)

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5
Q

difference between damaging the internal and external segments of the globus pallidus

A

lesion internal = excessive motion/ movements

lesion external= decreased motion

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6
Q

what dz is an arrest in the migration of neural crest cells

A

Hirschsprung

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7
Q

what region of the GI tract is always involved with Hirschsprung? and why?

A

Rectum (and anus)! cause it’s last to be innervated by the ganglion cells. nerve cells migrate caudally

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8
Q

what things are Down syndrome pts more at risk for?

A

alzheimers (early)
brushfield spots (speckled iris)
Simian crease (single transverse palmar crease)
Endocardial cushion defects (AV septal defects), ASD, VSD, PDA, ToF
duodenal atresia or stenosis, annular pancreas, TE fistula, Hirschsprung’s dz, omphalocele, imperforate anus
AML
ALL
hypo/hyperthyroidism, Type 1 DM, infertility in males

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9
Q

how does a bug get resistant to vancomycin?

A

changing the binding site from DalaDala to Dala D lactate

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10
Q

how does a bug get resistant to penicillin?

A
  1. makes beta lactamase. which destroys the beta lactam ring to render them ineffective. cephalosporins, carbapenems, and penicillinase resistance penicillins like nafcillin and methicillin are not susceptible.
  2. modify penicillin binding protein….like MRSA

but vanco is not a beta lactam drug! (has a different binding site)

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11
Q

how does a bug get resistant to tetracycline?

A

it binds to 30S subunit and inhibits binding of aminoacyl-tRNAs

resistance is through increased efflux of drug or the production of a protein that allows translation to take place anyways.

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12
Q

how is a bug get resistant to aminoglycosides?

A

it inhibits the 30S subunit.

resistance is by inactivating an aminoglycoside-modifying enzymes. makes a protein that modifies the antibiotic to decrease te binding ability

Pseudomonas = resist by decreasign anitbiotic entry into the bacterium

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13
Q

what 3 things affect the RAAS pathway?

A

macula densa, intrarenal barroreceptor, and beta adrenergic receptor pathways (thorugh B1 on the JG cells) -> norepi binds and causes release in renin

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14
Q

how does a Bblockers (like propanolol) affect the RAAS

A

decr. symp input, so inhibits renin release

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15
Q

high fructose in urine, but otherwise asymptomatic. what’s missing?

A

fructokinase

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16
Q

what will an absent galactose- 1 phosphate ruridyl transferase cause?

A

galactosemia. auto recessive. neonatal jaundice, bleeding diatheis feeding intolerance, hypotension, and death =[

Tx: eliminate all milk products from diet. feed with soy based formula

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17
Q

Don’t have aldolase B….what happens?

A

normally, aldolase B converts fructose 1 phosphate to DHAP and glyceraldehyde.

Tx. must eliminate dietary fructose. infants present with failure to thrive, hepatomegaly and cirrhosis

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18
Q

acid alpha glucosidase (or acid maltase) deficinecy causes what?

A

glycogen storage disease !!, pompe dz.

presents with hepatomegaly, cardiomegaly, and increased risk for cirrhosis

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19
Q

what lab findings will you find with post strep GN?

A
high ASO titers
high antiDNase titers
decreases C3
decreased total complement
presence of cryoglobulins
(C4 is usually normal)
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20
Q

what does coadministration with clavulanate do?

A

it is a beta lactamase inhibitor. it expands the ability (for ex. amoxicillin) to include strains of b-lactamase synthesizing bacteria….

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21
Q

what are GABAa and GABAc receptors?

A

ion channels. influx of cl-

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22
Q

what re GABAb receptors?

A

linked to G protein

23
Q

name 3 things that bind to GABAa and facilitate the inhibitory action of GABA n the CNS

A

bensodiazepines, barbiturates, and alcohol

24
Q

where is GABAc located?

A

retina

25
Q

what has positive heterophil antibodies

A

Mono!

26
Q

what cofactor is needed for the synthesis of tyrosine, dopa, serotonis, and NO?

A

BH4 = teetrabydrobiopterin

27
Q

what is serotonin synthesized from?

A

tryptophan

28
Q

go through the pathway to make Epi from phenylalanine

A

phen –> tyrosine–> dopa –> dopamine –> NE –> epi.

29
Q

what is niacin made from?

A

tryptophan

30
Q

what is the porphyrin in heme made from?

A

glycine

31
Q

what is gaba made from?

A

glutamate

32
Q

what is NO (and creatine and urea) made from?

A

arginine

33
Q

what is melanin made from?

A

Dopa!

34
Q

what is a cofactor needed to make NE from dopamine?

A

Vitamin C!

35
Q

what is melatonin made from?

A

serotonin!

36
Q

what CV abnorm. do you see with digeorge? (2)

A

tetro of fallot
interrupted aortic arch
(and persistant truncus arteriosus)

37
Q

what CV abnorm. do you see with friedreich ataxia?

A

hypertrophic cardiomyopathy

38
Q

what CV abnorm. do you see with Kartagener’s?

A

situs inversus

39
Q

what CV abnorm. do you see with Marfan’s? (2)

A

cystic medial necrosis (aortic dissection or aneurysm)
mitral valve prolapse
(and aortic regurg)

40
Q

what CV abnorm. do you see with tuberous sclerosis?

A

valvular obstruction due to cardiac rhabdomyomas =[

41
Q

what CV abnorm. do you see with Turner’s? (2)

A

aortic coarctation

bicuspid aortic valve

42
Q

what CV abnorm. do you see with fetal alcohol syndrome?

A

VSD, (PDA, ASD, ToF)

43
Q

what CV abnorm. do you see with congenital rubella?

A

PDA, (septal defects, pulm artery stenosis)

44
Q

what CV abnorm. do you see with maternal DM?

A

transposition of the great vessels

45
Q

what CV abnorm. do you see with prenatal lithium exposure?

A

Ebstein anomaly

46
Q

what CV abnorm. do you see with Williams syndrome?

A

Supravalvular aortic stenosis

47
Q

what is the mechanism of buproprion?

A

mixed dopamine and norepi reuptake inhibitor

48
Q

foot drop. what is injured and where?

A

common peroneal nerve. from trauma to the leg near the head of the fibula

49
Q

reddish pink periodic acid schiff + granules in the periportal hepatocytes are…?

A

unsecreted, polymerized A1AT.
will develop panacinar emphysema (from destruction of alveolar walls from elastases)
and cirrhosis and HCC

50
Q

borrelia burgdorferi

A

Lyme

51
Q

treponema pallidum

A

syphilis

52
Q

patchy skin anesthesia, hypopigmentation, bacteria invading Schwann cells

A

mycobacterium leprae

53
Q

in what kind of pts does lepromatous leprosy occur? (the bad one)

A

pts with a weak Th1 response. macrophages are never given the signal to kill the mycobacterial organisms….