2 Alcohol – 2
T | F | |
---|---|---|
1. Heavy alcohol consumption increases the risk of pharyngeal carcinoma. | ![]() |
![]() |
2. Convictions for driving with blood level over 80 mg/L are strongly suggestive of alcohol dependence. | ![]() |
![]() |
3. Binge drinking is more harmful than regular drinking. | ![]() |
![]() |
4. Alcoholic liver disease is more common in bus conductors than in the general population. | ![]() |
![]() |
5. Chronic alcohol intake enhances GABA (gamma-aminobutyric acid)-benzodiazepine receptor function. | ![]() |
![]() |
6. The microsomal ethanol oxidizing system metabolizes only 5–10% of the alcohol consumed. | ![]() |
![]() |
7. Cloninger’s type 1 alcoholism is predominantly genetically determined. | ![]() |
![]() |
8. Acute alcohol intoxication elevates gamma glutamyl transpeptidase (GGT) levels. | ![]() |
![]() |
9. In the EEG (electroencephalogram), there is a pattern associated with alcohol use. | ![]() |
![]() |
10. Withdrawal delirium is an essential feature of alcohol dependence syndrome. | ![]() |
![]() |
11. Auditory hallucinations occur in alcohol withdrawal. | ![]() |
![]() |
12. In delirium tremens, cogwheel rigidity may suggest nicotinic acid deficiency. | ![]() |
![]() |
13. Approximately 10% of chronic heavy drinkers develop seizures. | ![]() |
![]() |
14. Alcoholic hallucinosis characteristically occurs when alcohol intake is reduced. | ![]() |
![]() |
15. Confabulation is a feature of Korsakoff’s psychosis. | ![]() |
![]() |
16. In Korsakoff’s psychosis, semantic memory is impaired. | ![]() |
![]() |
17. Increased fast activity in the EEG is a characteristic feature of hepatic encephalopathy. | ![]() |
![]() |
18. 80% of survivors of Wernicke’s encephalopathy suffer from Korsakoff’s syndrome. | ![]() |
![]() |
19. In chronic alcoholism suicide risk is increased only in the depressed. | ![]() |
![]() |
20.The Minnesota model of treatment for alcoholism recommends strict daily limits on alcohol consumption rather than abstinence. | ![]() |
![]() |
21. Acamprosate is an NMDA (N-methyl-D-aspartic acid) antagonist. | ![]() |
![]() |
22. Alcohol detoxification cannot usually be done at home in a 65-year-old man. | ![]() |
![]() |
23. Disulfiram can cause peripheral neuritis. | ![]() |
![]() |
24. In the management of alcoholism, group therapy is more effective than individual therapy. | ![]() |
![]() |
25. Marchiafava–Bignami syndrome is associated with demyelination of the corpus callosum. | ![]() |
![]() |
ANSWERS
True: The gastrointestinal effects of heavy alcohol consumption include gastritis, vomiting, Mallory–Weiss tear, stomach and duodenal ulcers, cirrhosis of the liver, pancreatitis and an increased risk of cancer of the mouth, pharynx, oesophagus, stomach and liver. Garro and Lieber concluded that excess drinking increases the risk of cancer of the oropharynx by threefold, cancer of the oesophagus by twofold and cancer of the larynx by fourfold. Those who smoke or abuse other drugs are at even higher risk (DSM-IV 1994, p. 200; Chick & Cantwell 1994, p. 81; Johnstone et al 2004, p. 370).
Offenders with exceptionally high blood levels of alcohol, i.e. over 150 mg/L, or who have previous drink-driving convictions are particularly likely to be alcohol dependent. Drink-driving offences are also common in patients with other alcohol-related problems. This question is about convictions being strongly suggestive, not about one single conviction being diagnostic (Ghodse 2002, p. 159; Johnstone et al 2004, p. 372).
Binge drinkers can be identified by dividing number of units of alcohol consumed in the last week by usual drinking frequency. Binge drinking, and particularly frequent binge drinking, is more likely than regular moderate drinking to be associated with alcohol-related problems. Many of the binge drinkers have low average consumption. This has resulted in the ‘second order prevention paradox’.
True: Bus conductors and bus drivers’ mates have a higher risk than the general population of developing alcoholic liver disease. Bus drivers are not considered a high-risk group (Chick & Cantwell 1994, p. 115).
False: The indirect effect of alcohol on the GABA-A receptor is responsible for sedating, sleep-inducing, anticonvulsant and muscle-relaxant effects of alcohol. Chronic alcohol intake decreases GABA-benzodiazepine receptor function. This may be causally related to dependence (King 2004, p. 494; Sadock & Sadock 2005, p. 1171).
True: The microsomal ethanol oxidizing system (MEOS) metabolizes 5–10% of the alcohol consumed. Its activity increases with tolerance (Ghodse 2002, p. 149; King 2004, p. 492; Sadock & Sadock 2005, p. 1171).
Type 2 is genetically determined, starts before age 20, affects mostly males and is associated with severe alcoholism, criminality and other substance misuse (Gelder et al 2006, p. 441).
False: Acute alcohol intoxication does not raise GGT levels. Regular moderate drinking in the preceding weeks raises the levels slightly. The heavier the drinking, the higher the levels (Ghodse 2002, p. 149).
False: There is no particular pattern associated with alcohol use. There is increased fast activity, decreased alpha activity and decreased EEG coherence in alcoholics and even their alcohol-naïve offspring. This may reflect higher arousal levels and may be a possible marker of susceptibility to alcoholism. Acute ingestion of alcohol increases alpha activity and slows alpha frequency. Higher blood levels increase theta activity. Chronic alcohol use may be associated with a lower voltage and slightly faster resting EEG. Withdrawal is associated with increased higher frequency beta activity. Delirium tremens is associated with dominant fast activity. A state of subacute encephalopathy with seizures has been described in chronic alcohol users who are not withdrawing, associated with prominent slowing and periodic lateralized paroxysmal discharges (Chick & Cantwell 1994, p. 97; Sadock & Sadock 2005, p. 185).
False: Withdrawal delirium is not a criterion for ICD-10 diagnosis of dependence syndrome, although withdrawal symptoms are (ICD-10 1992, p. 79).
True: Transient visual, tactile or auditory hallucinations or illusions occur in alcohol withdrawal (DSM-IV, p. 198; Gelder et al 2000, p. 489).
True: Nicotinic acid deficiency can manifest in 3 ways:
True: Approximately 10% of hospitalized alcoholics develop seizures – ‘rum fits’. Causes include direct toxic effect of alcohol, alcohol withdrawal, hypoglycaemia and head injury. An epileptic fit for the first time in an adult should alert to the possibility of alcohol dependence. Withdrawal fits can occur without other gross features (Ghodse 2002, p. 153; Johnstone et al 2004, p. 373).
In contrast, in alcohol withdrawal and delirium tremens the hallucinations are transient and disorganized. They are mainly visual, but also auditory and tactile. Delirium tremens is also associated with altered consciousness (Gelder et al 2000, p. 490; Johnstone et al 2004, p. 368).
True: Confabulation is the unconscious filling of gaps in memory by imagined or untrue but often plausible experiences, occurring in clear sensorium. It is associated with organic pathology, e.g. neurodegenerative conditions, dementias, amnesic disorders and psychotic disorders. It is not synonymous with lying or factitious disorders where symptoms are deliberately distorted or feigned. It is more common in damage to diencephalic structures than in bilateral hippocampal damage. In Korsakoff’s syndrome it is most often seen in the acute stages but is not universal. The provoked or momentary type is more common and usually has reference to the recent past, sometimes a memory that is displaced. The spontaneous or fantastic type does not have a stimulus and has been linked to frontal lobe damage. Suggestibility may facilitate confabulation (Lishman 1997, p. 30).
Korsakoff’s syndrome is characterized by severe impairment of episodic memory. Other deficits, although they may exist, are comparatively modest (Hodges 1994, pp. 5, 19; Lishman 1997, p. 30).
False: The EEG is useful in the diagnosis, prognosis and monitoring of severity of hepatic encephalopathy. EEG changes appear even before psychological abnormalities. First there is alpha slowing and appearance of 5–7-Hz theta waves, most prominently in the frontal and temporal regions. As consciousness deteriorates, alpha waves are increasingly replaced by theta. Then the characteristic triphasic waves appear. This is followed by a decrease in amplitude, blunting of triphasic waves and periods of flattening. Similar changes occur also in uraemia, hypokalaemia, anoxia, vitamin B12 deficiency and raised intracranial pressure (Lishman 1997, p. 564).
True: In Victor et al’s (1971) series of 245 patients 84% developed a typical amnesic syndrome (Gelder et al 2000, p. 491; Gelder et al 2006, p. 328).
False: The Minnesota model, 28-day programme or 12-step programme is a refined and expanded version of the 12-step principles of Alchoholics Anonymous. It is usually used in private residential treatment programmes. Like the AA, the focus is on abstinence (Gelder et al 2000, p. 507; Sadock & Sadock 2005, p. 1151).
Acamprosate is an analogue of taurine and structurally resembles GABA. Some believe that acamprosate stimulates GABAergic inhibitory neuro-transmission (Gelder et al 2006, p. 448; Johnstone et al 2004, p. 375; King 2004, p. 495; Sadock & Sadock 2005, p. 1187).
False: Indications for inpatient detoxification include severe symptoms, medical/psychiatric complications, a history of withdrawal seizures or DT, comorbid severe mental illness, frail and elderly patients, intercurrent acute physical illness, failure of previous outpatient detoxification and lack of social support (Chick & Cantwell 1994, p. 132; Wright et al 2005, p. 431).
False: There is no evidence that the results of group psychotherapy differ in general from those of individual therapy of similar form and duration and used for the same problem. Moreover, different styles of group therapy produce almost similar results (Gelder et al 2006, p. 449; Johnstone et al 2004, p. 377).
True: Marchiafava–Bignami syndrome involves extensive demyelination of the corpus callosum and adjacent subcortical white matter, optic tracts and cerebellar peduncles. The clinical features include dysarthria, ataxia, epilepsy and impaired consciousness. Dementia and limb paralysis are seen in the more slowly progressive forms. Mortality is high and recovery is rare. The cause may be nutritional and/or alcohol-related (Gelder et al 2006, p. 437; Lishman 1997, p. 586).