Random Q set 1 Flashcards

1
Q

What are the some possible side effects of amIODarone class III antiarrhymic?

A
thyroid dysfunction (b/c a lot of iodine in it)
corneal micro-deposits
blue-grey skin discoloration
drug-related hepatitis
pulmonary fibrosis
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2
Q

What are the typical symptoms of vertigo from vestibular dysfunction?

A

sudden onset
interferes w/ walking
N/V

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3
Q

What are the symptoms of damage to the posterior columns of the spinal cord?

A

ataxia
decreased TVP
hyporeflexia

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4
Q

WHat are some things that can cause damage to the posterior columns of the spinal cord?

A

syphilis

vit B12 deficiency

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5
Q

What are the symptoms of cerebellar dysfunction?

A

ataxia
imbalance
incoordination
nystagmus

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6
Q

What is the 68/95/99 rule?

A

68% falls within 1 SD
95% falls within 2 SD
99% falls within 3 SD

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7
Q

Ham is Thick Sarcomeres. What does this mean?

A

Z line for actin, I band is actin only.

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8
Q

When sarcomeres contract, which bands become smaller?

A
H band (only myosin)
I band (only actin)
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9
Q

A patient with exertional syncope & a murmur may have what?

A

aortic stenosis

specifically: systolic ejection-type, crescendo-decrescendo

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10
Q

Describe the symptoms of galactosemia.

A
following breastfeeding
vomiting
lethargy 
failure to thrive
**sometimes irreversible eye or liver damage 
OR cataracts
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11
Q

Describe the enzymes involved in galactose metabolism.

A

Galactose (galactokinase)–>Galactose 1P (Galactose-1-P uridyl transferase)–>UDP-galactose
Galactose–>Galactitol (via aldose reductase)

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12
Q

What is the most common enzyme deficiency that causes galactosemia?

A

Most common: Galactose-1-P uridyl transferase deficiency

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13
Q

What is the requirement for diagnosing schizoaffective disorder?

A

depressive & manic periods of time w/ psychotic features for majority of illness
+ >2 wks of psychotic features w/o mood symptoms.

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14
Q

What is schizophreniform disorder?

A

a disorder that has the psychotic features of schizophrenia, but lasts b/w 1-6 mo

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15
Q

What is fat embolism syndrome?

A

days after severe bone fractures, multiple fat emboli clog the pulmonary micro vessels
get resp distress, neurological impairment, petechiae (thrombocytopenia)

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16
Q

Lung tissue in a patient with fat embolism syndrome has black globs. Why are they black?

A

stained by osmium tetroxide

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17
Q

Explain why you get the symptoms you do w/ fat embolism syndrome?

A

resp distress-fat clogging vessels
neurology–fat clogging cerebral vessels
thrombocytopenia–platelets used by coating fat emboli
anemia–pulmonary hemorrhage or RBC aggregation

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18
Q

Which valve is most commonly affected in infective endocarditis from IV drug users?

A

tricuspid valve

get tricuspid regurgitation, early systolic murmur accentuated with inspiration

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19
Q

To access the cardia of the stomach for gastric banding surgery, which structure must you pass through?

A

lesser omentum

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20
Q

Describe the location & structure of the lesser omentum.

A
double layer
connects the liver to the stomach/SI
hepatogastric ligament
hepatoduodenal ligament
**inside:
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21
Q

What’s the deal with the falciform ligament?

A

attaches the liver to the anterior body wall
derivative of embryonic ventral mesentery
contains round ligament (old fetal umbilical vein)

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22
Q

What type of vision deficit does a Meyer’s loop temporal lobe lesion cause?

A

contralateral superior quadrantanopia

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23
Q

What does a lesion to the occipital cortex (only one side) produce?

A

contralateral homonymous hemianopsia w/ macular sparing

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24
Q

How do you get bitemporal hemianopsia?

A

with a lesion to the optic chiasm.

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25
Q

What is the MOA of entacapone?

A

used only in combination with levodopa

inhibits COMT peripheral degradation of levodopa

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26
Q

What is the MOA of tolcapone?

A

inhibits both peripheral & central degradation of levodopa.

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27
Q

A man takes antimalarial drugs & develops anemia, reticulocytosis, indirect hyperbilirubinemia. What could have caused this?

A

a man with G6PD deficiency can develop hemolysis w/ antimalarial drugs
would show Heinz bodies on peripheral smear

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28
Q

How is G6PD deficiency inherited?

A

X-linked recessive inheritance

29
Q

How does CO do its damage in the blood?

A

it binds heme competitively
has 220X higher affinity for it than O2
**causes a leftward shift of the oxygen dissociation curve, so that it is harder to let go of oxygen at targets sites=tissue hypoxia

30
Q

T/F Partial pressure of oxygen becomes lower w/ CO poisoning.

A

False. Doesn’t change. b/c has to do with the amount of oxygen dissolved in the blood, not the amount bound to hemoglobin

31
Q

You see a graph with increased CO & a steeper curve, also increased venous return & a steeper curve. WHat could cause this?

A

a chronic AV fistula

  • *causes decreased TPR=increased CO & venous return
  • *body compensates w/ increased sympathetic–>means increased CO
  • *steeper curve=lower TPR
32
Q

What is a good medication used to treat male pattern baldness?

A

finasteride–5 alpha reductase inhibitor

**male pattern baldness can be caused by increased DHT

33
Q

If you have an elderly person with chronic anemia…what deficiency might they have? How would you have to administer it?

A

probably Vit B12 deficiency
prob have to administer IV, unless dietary insufficiency
most often–malabsorption

34
Q

Describe the process of Vit B12 absorption?

A

R factor released in stomach binds VB12 & then in the duodenum, pancreatic protease releases it. Intrinsic factor (secreted by parietal cells in stomach) bind it for absorption in the terminal ileum.

35
Q

Drugs that affect the extrinsic pathway do what? Intrinsic pathway? Thrombin inhibitors?

A

Extrinsic pathway–elongates PT
Intrinsic pathway–elongates PTT
Thrombin inhibition–elongates TT

36
Q

What do factor 7a, factor 10a, and unfractionated heparin do to coagulation cascade measurements?

A

factor 7a: work on extrinsic pathway–>prolong PT
factor 10a: work on extrinsic & intrinsic–>prolong PT & PTT
unfractionated heparin: affect extrinsic, intrinsic, and thrombin, but only prolong PTT & TT

37
Q

WHat is the usual treatment for DVT?

A

3 months of anticoagulant therapy

beginning w/ heparin & transitioning to oral anticoagulant (warfarin)

38
Q

What are some signs of aortic regurgitation?

A
head bobbing (widened pulse pressure)
head throbbing (large stroke volumes to intracranial arteries)
palpitations (forceful ejections)
39
Q

What normally happens after 16-24 hours of fasting?

A

break down fats for energy, beta oxidation becomes higher & then acetyl coa goes into TCA
**if TCA gets backed up, acetyl coa is shunted to make ketone bodies

40
Q

Describe the energy produced by 1 round of beta oxidation v. 1 round of TCA?

A

beta oxidation: 1 NADH, 1 FADH2, 1 acetyl coa

TCA: 3 NADH, 1 FADH2, 1 GTP

41
Q

You have a kid who has fasted & has hypoglycemia, low ketones, vomiting, lethargy, enlarged liver, seizure. Which enzyme deficiency is quite possible?

A

hypoglycemia + no ketones w/ fasting
problem with beta oxidation
most common deficiency: acyl coa dehydrogenase (1st step)

42
Q

What should patients who overdose on beta blockers be given? MOA?

A

glucagon

  • *they activate cardiac myocytes via GPCR, adenylate cyclase activation & increased cAMP
  • *increases HR & contractility without touching the adrenergic receptors
43
Q

How does C. diphtheria get its ability to make its exotoxin?

A
via lysogenization (Bacteriophage integrates its tox gene)
then it can make the diphtheria AB exotoxin
44
Q

WHat is a severe thing that C. diphtheria can cause?

A

severe pseuodmembranous pharyngitis

45
Q

What does the neurotoxin released by C. tetani do?

A

inhibits inhibitory neurons ability to release GABA & glycine
get constant firing

46
Q

What’s the deal with cryptococcus neoformans?

A

affects immunocompromised patients, like HIV+ pts
yeast with polysaccharide capsule (antiphagocytic)
affects lungs first, and likes to disseminate to the CNS

47
Q

When the neural tube doesn’t close in the ____ week of gestation, you get NTDs, particularly in which locations?

A

4th week of gestation
anterior & posterior neuropores
folic acid supplementation reduces these risks

48
Q

How does a maternal rubella infection present?

A

low grade fever
maculopapular rash w/ cephalocaudal progression
posterior auricular & suboccipital LAD
In Mom, can result in polyarthalgia or polyarthritis

49
Q

What can happen to children exposed to rubella during pregnancy?

A

sensorineural deafness
cataracts
cardiac malformation-patent ductus arteriosus

50
Q

As the fluid runs along the tubules in the kidney, which substance increase their conc’n? secreted…

A

PAH (90% secreted)
Creatinine (20% secreted)
Urea

51
Q

As fluid runs along the tubules of the kidney, which substances decrease their conc’n? reabsorbed…

A

Bicarb

Glucose (super reabsorbed), AA

52
Q

Ceftriaxone is used to treat gonococcal urethritis. But doesn’t work as well for nongonococcal urethritis. Why?

A

NGU: chlamydia, u. urealyticum
Chlamydia: lacks peptidoglycan
urealyticum: lacks cell wall entirely.
**better to use macrolides & tetracyclines

53
Q

WHat is phenotypic mixing?

A

two viruses infect a cell & make a thing with proteins of one & genome of the other (no real genetic exchange). Their progeny don’t have these characteristics.

54
Q

With an ischemic stroke, when do you see red neurons on histo?

A

12-24 hours after the stroke

55
Q

What does the retinoblastoma protein do?

A

regulates the entry from G1-S phase of the cell cycle

CDK4 can cause phosphorylation & inactivation of Rb, allowing unchecked cell cycle

56
Q

What is the basic structure of capitation?

A

physicians paid per enrollee, not per service

57
Q

What is the idea behind minimal alveolar conc’n?

A

measure of the potency of an inhaled anesthetic
MAC is the amount of anesthetic when 50% of people can’t feel painful stimuli
lower the MAC–>higher the potency

58
Q

Which syndromes show mild proteinuria & RBC casts?

Which syndromes show heavy proteinuria & no RBC casts?

A
Nephritic syndrome (including glomerulonephritis): mild proteinuria, RBC casts
Nephrotic Syndrome: heavy proteinuria, no RBC casts
59
Q

What are the lab values for iron deficiency anemia?

A

low ferritin, high transferring, microcytic anemia, hypo chromic

60
Q

What are the first symptoms reported for primary biliary cirrhosis?

A

pruritis at night (severe)

middle-aged women

61
Q

What are the symptoms of Horner’s syndrome?

A

ptosis
miosis (constricted pupil)
anhidrosis
enopthalmos (shrunken eyeball)
**damage to sympathetic trunk, ipsilateral signs.
**can be from pan coast tumor in the apex of the lung (can also cause brachial plexus problems)

62
Q

What is ataxia telangectasia?

A

aut rec disorder w/ bad DNA repair enzymes

hypersensitive to ionizing radiation (gamma & xray)

63
Q

What are the symptoms of ataxia telangectasia?

A

ataxia b/c of cerebellar atrophy
oculocutaneous telangectasia
immunocompromised–>recurrent sinopulmonary infections.
risk for cancer

64
Q

What is the pathogenesis & clinical manifestation of chronic granulomatous disease?

A

X-linked impaired NADPH oxidase so you can’t get a respiratory burst & intracellular phagocytic killing
get a lot of catalase + infections & granulomas

65
Q

How do you diagnose chronic granulomatous disease?

A

nitroblue tetrazolium test– don’t see normal blue pigment

dihydrorhodamine flow cytometry–don’t see fluorescent green pigment

66
Q

Give some examples of some non depolarizing NMJ blockers. What does neostigmine do to these?

A

pancuronium
tubocurarine
**neostigmine counteracts these w/o delay

67
Q

Give an example of a depolarizing NMJ blocker. What does neostigmine do to this?

A

succinylcholine
if neostigmine is used during phase 1, augments the effect.
if used in phase 2, dampens.

68
Q

Why is ornithine so important to the urea cycle?

A

Need to get ornithine into the mitochondria to combine with carbamoyl phosphate to become citrulline & get back into the cytosol. Then you eventually get urea.

69
Q

If your urea cycle isn’t working…which dietary restriction would you consider?

A

stop the protein

b/c with your urea cycle messed up could get too much ammonia