Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRAIN BATTACK > CH41: Alcohol, Drugs, Toxins and Chemical Agents > Flashcards

CH41: Alcohol, Drugs, Toxins and Chemical Agents Flashcards

1
Q

Neurotransmitters and modulating agents attach to receptors at synapses are able to increase or decrease the permeability of ion channels and stimulate or inhibit second cytoplasmic messengers. Give examples. (p. 1210)

A

L dopa: dopamine
Tryptophan: serotonin
Choline: acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

No particular aspect of alcohol metabolism has been found to account for the development of addiction with the possible exception of (p. 1211)

A

aldehyde dehydrogenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Energy liberated by oxidation of alcohol (p. 1211)

A

7cal/g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q 
Determine state of these alcohol levels (p. 1211)
30
50
100
200
300
400
A 
30 mild euphoria
50 mild incoordination
100 obvious ataxia
200 confusion and reduced mental activity
300 stuporous
400 deep anesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Drugs that have eh effect of disulfiram but less potent (p. 1212)

A

sulfonyluroeas
metronidazole
furazolidone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Refers to the period of severe intoxication for which the patient later has no memory– even though the state of consciousness was not grossly altered during that interval (p. 1213)

A

blackout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Can be a therapeutic option for blood alcohol concentrations more than 500mg/dL (p. 1214)

A

hemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Characteristic of methyl alcohol intoxication (p. 1214)

A

damage to retinal ganglion cells (scotomata)

bilateral degeneration of the putamen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Major constituent of antifreeze (p. 1214)

A

Ethylene glycol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Finding in ethylene glycol toxicity that may aid in the diagnosis (p. 1214)

A

Hippurate crystals (that can also be found in toluene ingestions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of alcohol intoxication (p. 1214)

A

Fomepizole (IV 4-methylpyrazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Characteristic tremor of Alcohol Withdrawal (p. 1215)

A

fast frequency 6-8 Hz, slightly irregular, variable in severity, tending to diminish when the patient is in quiet surroundings and increase with motor activity or emotional stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Most common hallucinations of alcohol withdrawal (p. 1216)

A

Human voices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic auditory hallucinosis vs Paranoid schizophrenia (p. 1216)

A

the alcoholic illness develops in close relation to a drinking bout and the past history rarely reveals schizoid personality traits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Withdrawal seizures from peak at around what time (p. 1216)

A

13 and 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F During period of withdrawal, he patients are sensitive to stroboscopic stimulation; almost half of he patients respond with generalized myoclonus or convulsive seizure (p. 1216)

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Frequency of EEG findings is rum fits (p. 1217)

A

No greater than in normal persons in shapr conrast to the EEGs of nonalcoholic patients with recurrent seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of Withdrawal seizures (p. 1218)

A

diazepam or sodium phenobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How many percent of cases of delirium tremens end fatally (p. 1217)

A

15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Early phase of alcohol withdrawal is associated with these metabolic abnormalities (p. 1218)

A

drop in serum magnesium
hypokalemia
rise in arterial pH
low pCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

These drugs should be avoided because it may decrease the threshold to seizures in patients with alcohol withdrawal (p. 1219)

A

phenothiazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T/F Alcoholic dementia lacks a distinctive, well- defined pathology (p. 1220)

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Requisite for successful treatment of alcohol dependence (p. 1221)

A

Total abstinence from alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drugs for alcohol dependence (p. 1221)

A

Disulfiram- dont give to patients with cardiac or advanced liver disease
Naltrexone
Acomprosate
Topiramate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute opioid poisoning clinical findings (p. 1223)

A 
Unresponsiveness
Shallow respirations
Slow respiratory rate or periodic breathing
Pinpoint pupils
Bradycardia
Hypothermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cause of death in opioid overdose (p. 1223)

A

Respiratory depression with asphyxiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Treatment of opioid overdose (p. 1223)

A

Naloxone 0.4 to 0.5mg repeated every 2 mins o a dose of 15mg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The desensitization of opioid receptors mainly these accounts for tolerance through a mechanism of uncoupling of the receptor from the G protein complex (p. 1224)

29
Q

Treatment of Opioid Abstinence syndrome (p. 1225)

A

Methadone substitution- habituation
Clonidine
Naloxone/ Naltrexone

30
Q

Opioid complicaions (p. 1226)

A

occlusion of cerebral arteries
amblyopia
transverse myelopathy
peripheral neuropathy

31
Q

MRI findings in opioid users (p. 1226)

A

Widespread white matter hyperintensity involving supra and infratentorial structures; predilection for CST and below the IC; with sparing of subcortical U fibers and grey matter structures

32
Q

Increases the potency of drugs (p. 1227)

A

higher lipid solubility

lower plasma PH

33
Q

MOA of Barbiturates (p. 1227)

A

suppress neuronal transmission, presumably by enhancing GABA inhibition at pre and post receptor sites to reduce excitatory potentials

34
Q

Fast acting barbiturates (p. 1227)

A

Pentobarbital, secobarbital

35
Q

Potential fatal dose of phenobarbital (p. 1227)

A

6 to 10g
lethal overdose at 60mgdL for Pb
10mgdL for pentobarbital and amibarbital

36
Q

Treatment for barbiturates overdose (p. 1227)

A

Hemodialysis and hemofiltration with charcoal

37
Q

MOA of Benzodiazepines (p. 1228)

A

Act in concert with GABA to open chloride ion channels and hyperpolarize postsynaptic neurons and reduce their firing rate. Primary actions are on: cerebral cortex and limbic system

38
Q

MOA of Flumazenil (p. 1228)

A

binding o CNS diazepine receptors and thereby blocking the activation of GABAergic synapses

39
Q

Selective 5HT1A receptor serotenergic agonist (p. 1229)

40
Q

Of all the phenothiazines, this has the tendency to cause akathisia (p. 1230)

A

Molindone

Treatment: Propanolol

41
Q

Treatment for post-phenothiazine dyskinesia (p. 1230)

A

Amantadine

42
Q

Treatment for Neuroleptic Malignant Syndrome (p. 1231)

A

Bromocriptine

Dantrolene

43
Q

Most common adverse effect of all MAO inhibitors (p. 1231)

A

Postural hypotension

44
Q

Contraindicated when taking MAO inhibitors (p. 1232)

A 
phenothiazines
CNS stimulants
TCA and serotonergic antidepressants
sympathomimetic amines
tyramine- containing foods
45
Q

Presently are the most effective drugs for the treatment of patients with depressive illness (p. 1232)

A

TCA

Serotonergic drugs

46
Q

Treatment of Serotonin Syndrome (p. 1233)

A

Discontinuation of medication

Cyroheptadine

47
Q

Neuro findings of Lithium intoxication (p. 1233)

A 
fast frequency action tremor or asterixis
Nausea
Loose stools
Fatigue
Polydypsia and polyuria
48
Q

Cocaine withdrawal syndrome (p. 1234)

A 
insomnia
restlessness
anorexia
depression
hyperprolactenemia
dopaminergic sensitivity
49
Q

Marijuana activates this receptor, mainly on GABA-ergiv neurons in the hippocampus, amygdala and cortex (p. 1235)

50
Q

The source of recurrent inhibition of spinal and brainstem motor neurons preferentially affected by Tetanus Toxin (p. 1236)

A

Renshaw Cell

51
Q

Differentiate stiffman syndrome and tetanus (p. 1237)

A

In Tetanus, the physiologic silent period that occurs 50 to 100ms after reflex contraction is loss

52
Q

Treatment for Tetanus (p. 1237)

A

Antitoxin
10day course of Penicillin
Metronidazole
Tetracycline

53
Q

How to give tetanus immunity (p. 1238)

A

Toxoid every 10 years

If has a threat, one dose then 6 weeks after

54
Q

Most common clinical type of diphtheria (p. 1238)

A

faucial- pharyngeal form

55
Q

Characterized by early oropharyngeal symptoms, ciliary paralysis with retained pupillary response to light, subacute evolution of a delayed symmetrical sensorimotor peripheral neuropathy (p. 1238)

A

Diphtheria

56
Q

Has been useful in reversing the weakness of limn and extraoccular muscles in Botulism (p. 1239)

A

Guanidine hydrochloride

57
Q

Workup for lead poisoning (p. 1241)

A

Lead lines at the metaphysis of long bones
Basophilic stippling in red cells
Basophilic stippling of bone marrow erythroblasts

58
Q

Confirmation of Lead toxicity (p. 1241)

A

Lead excretion with calcium disodium edetate given in three doses (25mg/kg)
500mg in 24hrs means there is toxicity

59
Q

Treatment for Lead toxicity (p. 1242)

A

2,3 dimercaprol

oral penicillamine

60
Q

Transverse lines 1 to 2mm in width above the lunula of each fingernail (p. 1243)

A

Mees lines

found in arsenic

61
Q

Treatment for arsenic toxicity (p. 1243)

A

Dimercaprol

62
Q

Cock gait. Which element is in excess (p. 1244)

A

Manganese

Treatment: L dopa

63
Q

Pathologic findings in Mercury poisioning (p. 1244)

A

Striking degeneration of the granular layer of the cerebellar cortex with relative sparing of the Purkinje cells and neuronal loss and gliosis of the calcarine cortex

64
Q

Treatment for Mercury poisoning (p. 1245)

A

Penicillamine or Dimercaprol

65
Q

Symptoms reversing organophosphate poisoning (p. 1245)

A

Atropine and Pralidoxime

66
Q

Biopsies in patients who had Cisplatin (p. 1247)

A

Primary axonal degeneration

67
Q

MOA of neuropathy for patients taking Paclitaxel and Docetaxel (p. 1247)

A

Inhibitors of depolymerization of tubulin

68
Q

Most frequent side effect of Calcineurin inhibitors (p. 1249)

BRAIN BATTACK (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions