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Pharmacology > Lesson B8 - Pharmacology > Flashcards

Lesson B8 - Pharmacology Flashcards

1
Q

The major reason for the extensive use and abuse of

alcohol is

A

its ready availability and the permissive attitudes of society

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2
Q

alcohol is an old drug. It was the first sedative-hypnotic drug to be used by

A

ancient physicians. The use of fermented beverages can be traced back to 8000 B.C., when mead was
prepared from honey.

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3
Q

Traditionally, alcohol has been used for three major purposes.

A

In medicine as a sedative and hypnotic.
∙ For religious and other occasions, e.g. sacramental use by Christians and Jews.
∙ Recreational purposes.

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4
Q

The terms “alcohol” and “ethanol” are used

A

interchangeably

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5
Q

Ten to 13 ml of absolute alcohol is the amount metabolized by

A

the liver each hour.

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6
Q

Ethanol is absorbed rapidly from the

A

stomach and the upper small intestine (the major site of

absorption).

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7
Q

The overall absorption rate for a given dose of ethanol is affected by:

A

(a) Stomach-emptying time, or the time required for the alcohol to reach the small intestine.
(b) Ethanol concentration in the G.I. tract.

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8
Q

Ethanol distributes throughout the total body water and readily distributes across the

A

blood-brain barrier.

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9
Q

In pregnant women who drink alcoholic beverages, ethanol is readily transferred across the

A

placenta and distributes throughout the total body water of the fetus.

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10
Q

Over 95% of ethanol in the body is eliminated by biotransformation, primarily in the

A

liver

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11
Q

The remaining 5% is excreted in the

A

breath, urine and sweat.

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12
Q 
Aldehyde dehydrogenase (ADH) converts alcohol to acetaldehyde, and in turn aldehyde 
dehydrogenase converts acetaldehyde (ALDH) to
A

acetic acid. Acetic acid is then further
metabolized by a number of tissues. Disulfiram and calcium carbimide (drugs used to treat
alcohol abuse) inhibit aldehyde dehydrogenase, and as a result, acetaldehyde accumulates and
the individual will feel ill and presumably stop abusing alcohol to stop the adverse effects of
acetaldehyde.

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13
Q

The metabolism of alcohol is unusual as it occurs at a constant rate, irrespective of the blood
alcohol concentration. A constant amount of alcohol is metabolized each hour. This is because

A

ADH becomes rate-limiting or saturated at 20 mg of alcohol per 100 ml of blood (saturation is a
term used when a process is running at full capacity)

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14
Q

Ethanol is classified as a general central nervous system (CNS)

A

depressant.

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15
Q

Acute use of ethanol

more obviously affects the CNS, whereas

A

chronic, high-dose use affects many organ systems of

the body including the CNS, cardiovascular system, gastrointestinal tract and liver.

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16
Q

Chronic,

maternal use of high-dose ethanol can adversely affect the

A

fetus, including teratogenesis, which

can manifest as the fetal alcohol syndrome or fetal alcohol effects.

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17
Q

Ethanol produces dose-dependent depression of CNS function:

disinhibition → sedation → hypnosis → general anesthesia →

A

coma

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18
Q

Low dose: Disinhibition (inhibition of an inhibitory pathway in the CNS).
This is usually manifested by increased social
interaction, e.g

A

talking

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19
Q

High dose: Sedation → hypnosis → general anesthesia → coma →

A

death

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20
Q

A change in sleep pattern often occurs. The changes are an increase in slow-wave sleep and a

A

decrease in rapid-eye-movement sleep. A reduction in rapid-eye-movement sleep is associated with a feeling of having “slept poorly”.

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21
Q

The mechanism of action of alcohol is not understood. At high concentrations of alcohol, it was believed that the drug acted as a

A

general anesthetic

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22
Q

At lower alcohol

concentrations, alcohol binds to the GABA receptor and augments

A

GABA-mediated neuronal

transmission.

23
Q

Alcohol is a CNS depressant, but at low dose the response observed is one of

A

disinhibition.

24
Q

Drinkers feel gregarious,

A

jovial, relaxed and more self-confident.

25
Q

As the dose increases, the individual may demonstrate exaggerated

A

emotional responses

26
Q

Blackouts: This is the phenomenon where the drinker does not remember events while under
the influence of

A

alcohol

27
Q

Psychiatric effects: Low doses of alcohol (one to three drinks) causes relaxation, while heavy
drinking (five drinks or more) often leads to

A

depression, irritability and over-sedation

28
Q

Drinking and driving: Alcohol is one of the major causes of

A

automobile accidents.

29
Q

Violence: Individuals who drink heavily are more prone to violence than non-drinkers. Men
who are heavy drinkers are six times more likely to assault their wives/significant others than

A

non-drinkers

30
Q

The other risks associated with excessive use of alcohol is associated with

A

respiratory

depression, coma and death.

31
Q

Central nervous system: There are a number of neurological and mental disorders associated
with chronic alcohol

A

abuse. Alcohol damages the axons of the brain, resulting in fewer
connections between neurons. This causes alcoholic dementia. Dementia can be defined as a
global decrease in cognitive functioning, affecting memory, judgement, and thinking.

32
Q

Alcohol increases the metabolism of vitamin B1 (thiamine), resulting in thiamine deficiency.
There are two conditions which result from alcohol-induced thiamine deficiency –

A

Werniche’s
encephalopathy in which the patient becomes drowsy, confused and cannot walk properly, and
Korsakoff’s psychosis, a severe form of dementia.

33
Q

The peripheral nervous system is also subject to alcohol damage. Alcohol damages the axons
in the peripheral nervous system, resulting in a

A

peripheral neuropathy that is manifested by loss

of feeling in the feet and is often accompanied by burning pain and difficulty in walking.

34
Q

Chronic use of ethanol, especially in high doses, can lead to a state of drug dependence, often
referred to as

A

alcoholism. Ethanol drinking is a serious problem when it interferes with home
life, job or scholastic performance, finances or personal mental/physical health.

35
Q

Tolerance is defined as a state in which repeated administration of the same dose of drug
(ethanol) has progressively less effect, or a state in which the dose of drug needs to be increased
to obtain the same quantity of effect as was produced by

A

the original dose.

36
Q

During chronic use of ethanol, there is a decreased intensity of ethanol action or a shortened
duration of action. A larger dose of ethanol is needed to produce the original pharmacologic
effect. Recently, it has been reported that individuals can

A

develop tolerance more rapidly to
the ethanol-induced impairment of performance of a task when they perform that task repeatedly
under the influence of ethanol.

37
Q

Mechanism:

A
  1. Metabolic (dispositional, pharmacokinetic) tolerance due to increased ethanol metabolic
    rate. During chronic consumption of ethanol, the same dose produces a lower blood
    ethanol concentration or maintains the blood ethanol concentration above a certain level for
    a shorter time.
  2. Cellular (functional, pharmacodynamic) tolerance. The CNS adapts to the effects of
    ethanol.
38
Q

The consensus is that

A

cellular tolerance plays a greater role in the overall development of
tolerance. The extent or rate of development of tolerance depends on the individual, dose of ethanol, and frequency of ethanol administration.

39
Q

It is important to note that, normally, minimal tolerance develops to the

A

lethal dose of

ethanol.

40
Q

Physical dependence is defined as an abnormal physiologic state brought about by repeated
administration of a drug that leads to the appearance of a characteristic and specific group of
symptoms when drug administration is stopped or

A

decreased

41
Q

Cross-tolerance:

A
  1. between ethanol and sedative hypnotics

2. ethanol and general anesthetics

42
Q

The basis of physical dependence on ethanol primarily involves the CNS. Withdrawal from
ethanol (CNS depressant) produces

A

excitability of the CNS (arousal, stimulation).

43
Q

The ethanol withdrawal syndrome can be treated effectively by oral administration of
diazepam, a benzodiazepine-type sedative-hypnotic drug. The pharmacological basis for this
therapy involves the principle of

A

cross-dependence, in which the withdrawal syndrome
following cessation of use of a particular drug is suppressed by administration of a second drug
of the same or similar pharmacological classification.

44
Q

Psychological dependence is defined as a compulsion that requires periodic or continuous
administration of a drug to produce pleasure or to

A

avoid discomfort.

45
Q

The dependence liability is

A

moderate

46
Q

Acute use: Low doses of acute use lead to vasodilation (flushing) of the vessels to the skin,
resulting in a feeling of warmth. High doses of alcohol can depress the cardiovascular system
and lead to alterations in the

A

normal rhythm of the heart.

47
Q

Chronic use: Low chronic doses of alcohol can reduce the risk of coronary heart disease and

stroke. High chronic doses can lead to alcoholic cardiomyopathy (destruction of or poor heart
muscle) . In addition, there is an increased incidence of

A

hypertension and stroke.

48
Q

Low doses of alcohol will stimulate gastric secretion, and hence the use of a small dose of
alcohol before a meal to stimulate digestion and enhance appetite. Higher doses of alcohol will
irritate the lining of the stomach, causing inflammation and erosion (known as

A

gastritis).

49
Q

Chronic high doses of alcohol leads to alcoholic liver disease, a major cause of hospitalization
and deaths in North America. There are three stages to alcoholic liver disease.

A

In stage 1, the
liver cells accumulate fat, causing the liver to enlarge (fatty liver). This stage is usually
asymptomatic and is reversible if the alcohol is stopped. Stage 2 is alcoholic hepatitis. The liver
cells are damaged and inflamed. The stage of alcoholic hepatitis can be asymptomatic or there
can be severe liver function impairment. With abstinence, hepatitis is usually

50
Q

Epidemiologic and laboratory animal studies have demonstrated that ethanol is a

A

teratogen

51
Q

Chronic, maternal use of high-dose ethanol throughout pregnancy can produce teratogenic
effects in the embryo/fetus, which can manifest postnatally as the

A

Fetal Alcohol Syndrome.

52
Q

Drugs Used in the Treatment of Alcoholism: Disulfiram and Calcium Carbimide (Calcium
Cyanamide)

These drugs are used as pharmacological adjuncts to psychotherapy or group therapy, and are
referred to as alcohol-deterrent or alcohol-sensitizing drugs.

These drugs inhibit hepatic aldehyde dehydrogenase and result in

A

increased acetaldehyde
concentration if the patient drinks ethanol, thereby producing cardiovascular/respiratory changes
that are perceived as aversive.

53
Q

Alcohol and Drug Interactions

  1. Acute ethanol use during drug therapy (body contains ethanol).

)

A

1AIngestion of ethanol and other CNS depressants leads to an additive effect or
synergism of CNS depression.

B) Ethanol inhibits biotransformation (metabolism) of certain drugs

54
Q

Alcohol and Drug Interactions-Chronic ethanol use followed by drug therapy (no ethanol in body)

A

Ethanol causes proliferation (increase in growth) of the smooth endoplasmic reticulum of the
liver cell, leading to increased activity of the liver drug-metabolizing enzyme system. There will
be increased biotransformation of certain drugs (e.g. sedative-hypnotics, phenytoin), if there is
no co-existing ethanol-induced liver injury

Pharmacology (27 decks)

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