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Justin Lyle Cards > Neuro 4 > Flashcards

Neuro 4 Flashcards

1
Q

chronic consumption of etoh has what reproductive effects

A
  1. gynecomastia 2. testicular atrophy 3. mental retardation 4. congenital malformation 5. fetal etoh syndrome
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2
Q

___________________ is the leading cause of metal retardation and congenital malformation

A

chronic etoh consumption

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3
Q

__________________ is d/t chronic etoh consumption, where etoh crosses the placental barrier, and the fetus must rely on moms enzymes for elimination (which are low)

A

fetal etoh syndrome

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4
Q

GI effects of chronic etoh consumption

A
  1. liver disease 2. chronic pancreatitis 3. gastritis 4. small intestine damage
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5
Q

________________ plays a signficant role in the chronic alcohol associated liver dz

A

TNF-a

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6
Q

why is chronic etohism a common cause of chronic pancreatitis

A

etohism promotes the formation of protein plugs and calcium carbonate stones

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7
Q

small intestine damage secondary to chronic etoh consumption leads to

A
  1. diarrhea 2. weight loss 3. MVI deficiencies
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8
Q

chronic consumption of alcohol effects on blood?

A
  1. IDA from GI bleeding 2. folic acid def –> anemia 3. cause of several hemolytic syndromes
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9
Q

endocrine and electrolyte effects of chronic alcohol consumption

A
  1. disrupts steroid hormone balance 2. ascites 3. edema 4. effusions 5. hypoglycemia 6. ketosis
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10
Q

chronic alcohol consumption depletes what enzyme?

A

glutathione

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11
Q

an acutely intoxicated (etoh) pt will need _______________________ doses of anesthetic drugs

A

decreased

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12
Q

a chronic etoh consumer, (but not acutely intoxicated) will need _______________ doses of anesthetic drugs

A

increased

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13
Q

alcohol can potentiate the effects of which drug classes?

A
  1. vasodilators 2. oral hypoglycemics 3. sedative-hypnotics
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14
Q

acute consumption of etoh will inhibit the metabolism of what drugs d.t decreased enzyme activity and decreased hepatic blood flow?

A
  1. phenothiazine 2. tricyclic antidepressants 3. sedative-hypnotics
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15
Q

T/F: prolonged intake of etoh without liver damage, can enhance the metabolism of other drugs

A

TRUE

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16
Q

consumption of 3 or more etoh drinks/day increases the risk of _________________ from therapeutic high/toxic levels of __________________

A

hepatotoxicity; acetaminophen

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17
Q

BAC of 50-100 (.05 - .1) will have what clinical effect?

A
  1. sedation 2. subjective “high” 3. slower reaction times
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18
Q

BAC of 100 - 200 will have what clinical effects

A
  1. impaired motor fx 2. slurred speech 3. ataxia
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19
Q

BAC of 200 -300 will have what clinical effects?

A
  1. emesis 2. stupor
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20
Q

BAC of 300 -400 will have what clinical effects

A

coma

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21
Q

BAC > 400 will have what clinical effects

A

respiratory depression, death

22
Q

_________________ is used in the industrial production of synthetic organic compounds and as a consituent of many commerical solvents

A

methanol

23
Q

methanol can be absorbed via what ways?

A
  1. skin 2. respiratory tract 3. GI
24
Q

how is methanol eliminated in humans

A

via the oxidation of formaldehyde, formic acid, and CO2

25
Q

with methanol, metabolism is slow, thus it could be ______________ hours before toxicity develops

A

6-30

26
Q

s/sx of mild methanol toxicity

A
  1. inebriation 2. gastritis 3. elevated osmolal gap
27
Q

with mild methanol toxicity, 97% of patients will have an osmolal gap in the range of ___________ to _____________

A

+10; -10

28
Q

what osmolal gap value is considered a “critical value”

A

15

29
Q

with methanol toxicity, the presence of ______________, _________________, and _____________ = medical emergency that requires prompt treatment

A

low blood pH; elevated anion gap; greatly elevated osmolal gap

30
Q

severe s/sx of methanol toxicity

A
  1. odor of formaldehyde on the breath 2. visual distrubances 3. metabolic acidosis 4. can cause blindness 5. bradycardia 6. prlonged coma 7. seizures 8. resistant acidosis 10. sudden respiratory arrest
31
Q

tx of methanol/ethylene glycol toxicity

A
  1. dialysis in severe cases 2. support respiration 3. suppress metabolism of methanol by alcohol dehydrogenase 4. bicarbonate - to counteract metabolic acidosis 5. fomepizole or IV ethanol
32
Q

what meds are used to tx methanol toxicity

A
  1. Fomepizole 2. IV ethanol
33
Q

dialysis would be used as a tx option for methanol toxicity in severe cases, blood levels > ____________ mL/dL

A

50

34
Q

MOA of fomepizole

A

alcohol dehydrogenase inhibitor

35
Q

what med is approved for methanol and ethylene glycol poisoning

A

fomepizole

36
Q

after 48 hours on fomepizole, the dose has to be _________________

A

increased; d/t med rapidly inducing its own metabolism via CYP450

37
Q

what med can be given as alternative to fomepizole in methanol and ethylene glycol poisoning

A

IV ethanol

38
Q

how does IV ethanol work in the tx of methanol poisoning

A

ethanol has higher affinity for alcohol dehydrogenase than methanol, therefore it decrease the formation of the methanols toxic metabolites

39
Q

ethylene glycol is used as heat exchangers in what products

A
  1. antifreeze 2. industrial solvents
40
Q

ethylene glycol is metabolized to toxic ______________ and _____________

A

aldehydes and oxalates

41
Q

describe the three stages of ethylene glycol OD

A
  1. first few hours - transient excitation followed by CNS depression 2. hours 4-12 - severe metabolic acidosis 3. after 12 hours - delayed renal insufficiency
42
Q

what is epilepsy

A

a heterogenous symptom complex disorder characterized as chronic recurrent seizures

43
Q

___________________ is a finite episode of brain dysfunction resulting from abnormal discharge of cerebral

A

seizure

44
Q

when seizures occur with acute underlying disorders, how should therapy be directed

A

toward the disorder

45
Q

existing anti-seizure drugs provide adequate seizure control in about __________ of patients

A

2/3

46
Q

anti-seizure drugs act by one of 3 mechanisms, what are the 3 mechanisms?

A
  1. enhancement of GABAergic (inhibitory) transmission 2. reduction of excitatory (usually glutamatergic) transmission 3. modification of ionic conductance
47
Q

presynaptic targets for anti-seizure drugs diminishing the (excitatory) glutamate release

A
  1. Na 1.6 voltage gated sodium channels 2. Kv 7 voltage gated calcium channels 3. alpha2delta Ca+ channels
48
Q

what is the mechanism of action of carbamazepine for seizures

A

blocks pre synaptic voltage gated sodium channels to decrease synaptic release of glutamate

49
Q

MOA of phenytoin/fosphenytoin

A

blocks presynaptic voltage gated Na channels to decrease synaptic release of glutamate

50
Q

anti-seizure post-synaptic targets at excitatory (glutamate) synapses are:

A
  1. AMPA receptors 2. T-type calcium voltage gated channels 3. Kv7 voltage gated potassium channels

Justin Lyle Cards (27 decks)

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