Neuro 4 Flashcards
chronic consumption of etoh has what reproductive effects
- gynecomastia 2. testicular atrophy 3. mental retardation 4. congenital malformation 5. fetal etoh syndrome
___________________ is the leading cause of metal retardation and congenital malformation
chronic etoh consumption
__________________ 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)
fetal etoh syndrome
GI effects of chronic etoh consumption
- liver disease 2. chronic pancreatitis 3. gastritis 4. small intestine damage
________________ plays a signficant role in the chronic alcohol associated liver dz
TNF-a
why is chronic etohism a common cause of chronic pancreatitis
etohism promotes the formation of protein plugs and calcium carbonate stones
small intestine damage secondary to chronic etoh consumption leads to
- diarrhea 2. weight loss 3. MVI deficiencies
chronic consumption of alcohol effects on blood?
- IDA from GI bleeding 2. folic acid def –> anemia 3. cause of several hemolytic syndromes
endocrine and electrolyte effects of chronic alcohol consumption
- disrupts steroid hormone balance 2. ascites 3. edema 4. effusions 5. hypoglycemia 6. ketosis
chronic alcohol consumption depletes what enzyme?
glutathione
an acutely intoxicated (etoh) pt will need _______________________ doses of anesthetic drugs
decreased
a chronic etoh consumer, (but not acutely intoxicated) will need _______________ doses of anesthetic drugs
increased
alcohol can potentiate the effects of which drug classes?
- vasodilators 2. oral hypoglycemics 3. sedative-hypnotics
acute consumption of etoh will inhibit the metabolism of what drugs d.t decreased enzyme activity and decreased hepatic blood flow?
- phenothiazine 2. tricyclic antidepressants 3. sedative-hypnotics
T/F: prolonged intake of etoh without liver damage, can enhance the metabolism of other drugs
TRUE
consumption of 3 or more etoh drinks/day increases the risk of _________________ from therapeutic high/toxic levels of __________________
hepatotoxicity; acetaminophen
BAC of 50-100 (.05 - .1) will have what clinical effect?
- sedation 2. subjective “high” 3. slower reaction times
BAC of 100 - 200 will have what clinical effects
- impaired motor fx 2. slurred speech 3. ataxia
BAC of 200 -300 will have what clinical effects?
- emesis 2. stupor
BAC of 300 -400 will have what clinical effects
coma
BAC > 400 will have what clinical effects
respiratory depression, death
_________________ is used in the industrial production of synthetic organic compounds and as a consituent of many commerical solvents
methanol
methanol can be absorbed via what ways?
- skin 2. respiratory tract 3. GI
how is methanol eliminated in humans
via the oxidation of formaldehyde, formic acid, and CO2
with methanol, metabolism is slow, thus it could be ______________ hours before toxicity develops
6-30
s/sx of mild methanol toxicity
- inebriation 2. gastritis 3. elevated osmolal gap
with mild methanol toxicity, 97% of patients will have an osmolal gap in the range of ___________ to _____________
+10; -10
what osmolal gap value is considered a “critical value”
15
with methanol toxicity, the presence of ______________, _________________, and _____________ = medical emergency that requires prompt treatment
low blood pH; elevated anion gap; greatly elevated osmolal gap
severe s/sx of methanol toxicity
- 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
tx of methanol/ethylene glycol toxicity
- 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
what meds are used to tx methanol toxicity
- Fomepizole 2. IV ethanol
dialysis would be used as a tx option for methanol toxicity in severe cases, blood levels > ____________ mL/dL
50
MOA of fomepizole
alcohol dehydrogenase inhibitor
what med is approved for methanol and ethylene glycol poisoning
fomepizole
after 48 hours on fomepizole, the dose has to be _________________
increased; d/t med rapidly inducing its own metabolism via CYP450
what med can be given as alternative to fomepizole in methanol and ethylene glycol poisoning
IV ethanol
how does IV ethanol work in the tx of methanol poisoning
ethanol has higher affinity for alcohol dehydrogenase than methanol, therefore it decrease the formation of the methanols toxic metabolites
ethylene glycol is used as heat exchangers in what products
- antifreeze 2. industrial solvents
ethylene glycol is metabolized to toxic ______________ and _____________
aldehydes and oxalates
describe the three stages of ethylene glycol OD
- first few hours - transient excitation followed by CNS depression 2. hours 4-12 - severe metabolic acidosis 3. after 12 hours - delayed renal insufficiency
what is epilepsy
a heterogenous symptom complex disorder characterized as chronic recurrent seizures
___________________ is a finite episode of brain dysfunction resulting from abnormal discharge of cerebral
seizure
when seizures occur with acute underlying disorders, how should therapy be directed
toward the disorder
existing anti-seizure drugs provide adequate seizure control in about __________ of patients
2/3
anti-seizure drugs act by one of 3 mechanisms, what are the 3 mechanisms?
- enhancement of GABAergic (inhibitory) transmission 2. reduction of excitatory (usually glutamatergic) transmission 3. modification of ionic conductance
presynaptic targets for anti-seizure drugs diminishing the (excitatory) glutamate release
- Na 1.6 voltage gated sodium channels 2. Kv 7 voltage gated calcium channels 3. alpha2delta Ca+ channels
what is the mechanism of action of carbamazepine for seizures
blocks pre synaptic voltage gated sodium channels to decrease synaptic release of glutamate
MOA of phenytoin/fosphenytoin
blocks presynaptic voltage gated Na channels to decrease synaptic release of glutamate
anti-seizure post-synaptic targets at excitatory (glutamate) synapses are:
- AMPA receptors 2. T-type calcium voltage gated channels 3. Kv7 voltage gated potassium channels
