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Year 2 > CLASP Alcohol > Flashcards

CLASP Alcohol Flashcards

1
Q

Where may methanol be found sometimes

A

Home brew alcohol - it is toxic

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2
Q

What is methanol metabolised into

A

Formaldehyde (fixes tissue)

Then Formic acid (dissolves you)

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3
Q

Main symptom of methanol poisoning

A

Blindness

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4
Q

How is methanol poisoning treated

A

Ethanol +/- dialysis

Ethanol - competitive inhibitor

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5
Q

What enzyme metabolises both ethanol and methanol

A

Alcohol dehydrogenase

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6
Q

Why does drinking on a full stomach reduce alcohol absorption rate

A

Reduced gastric emptying - more metabolised in stomach instead of being absorbed into blood stream

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7
Q

Where is alcohol absorbed

A

Mainly small intestine, some in stomach

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8
Q

Which drugs increase gastric emptying therefore increase the rate of alcohol absorption into bloodstream

A

Antihistamines
Domperidone
Metoclopramide

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9
Q

Effect on absorption of drinking high conc alcohol

A

Reduced absorption - irritates gastric mucosa, delays emptying

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10
Q

Why do men have higher alcohol tolerance than women

A

Men are leaner - greater dilution volume

Women also have reduced alcohol dehydrogenase activity

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11
Q

Where is alcohol metabolised

A

Liver (mainly)
Pancreas
Brain

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12
Q

Where is alcohol excreted

A

Urine
Breath
Sweat
Stool

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13
Q

Rate of alcohol removal from body

A

15mg/100ml/hour = 1 unit/hour

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14
Q

When does alcohol concentration peak

A

1 hour after absorption

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15
Q

How does blood alcohol concentration decrease

A

Linearly

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16
Q

Which ethnic groups have reduced alcohol dehydrogenase

A

Aboriginis, eskimos

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17
Q

Why do some people flush and feel sick after alcohol

A

Low ALDEHYDE dehydrogenase enzyme - acetaldehyde builds up

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18
Q

Which drug can be used to manage chronic alcoholism

A

Aldehyde dehydrogenase inhibitor - disulfaram/anabutase - causes them to flush and be sick

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19
Q

Why do people who drink more have higher tolerance

A

Alcohol dehydrogenase upregulated

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20
Q

Which alternative pathway of alcohol metabolism is activated in chronic drinkers?

A

MEOS pathway - cytochrome P450 family of proteins

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21
Q

Which 3 biochemical processes are impaired in chronic alcoholism

A

Gluconeogenesis
Kerbs cycle
Fatty acid oxidation

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22
Q

Why may you be sore after a night of drinking

A

Krebs cycle inhibited - anaerobic metabolism - lactic acid builds up

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23
Q

What 2 processes start in the liver when blood glucose is low after a night of heavy drinking

A

Gluconeogenesis (using fat, proteins etc)

Glyocogenolysis

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24
Q

Why does alcohol make you gain weight

A

Impaired fatty acid oxidation
Excess lipid synthesis
plus calories in alcohol

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25
Q

How can DKA and alcoholic ketoacidosis be differentiated

A

DKA - massive hyperglycaemia

Alcoholic KA - little/no hyperglycaemia

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26
Q

The level of which neurotransmitter is increased by alcohol

A

GABA

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27
Q

How can you die from acute intoxication

A

Aspiration - unconscious, swallowing impaired, vomit and aspirate
Trauma - misadventures, falls, fights
Vomiting - metabolic alkalosis, mallory-weirs, boerhaave syndrome, acute pancreatitis

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28
Q

Release of what hormone is inhibited in alcohol

A

ADH

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29
Q

Why does alcohol give you a heavy heartbeat

A

-ve inotrope

therefore heart rate increases

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30
Q

What is holiday heart syndrome

A

Binge drinking causing spontaneous SVT

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31
Q

What contributes to a headache the day following

A

Congeners - substances used to make alcohol smell a certain way
Serotonin
Dehydration
Acetic acid

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32
Q

Why can alcohol cause heartburn the next morning

A

Smooth muscle relaxant - GORD

therefore also causes snoring/suppression of cough/gag

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33
Q

Brain injury caused by falling when drunk

A

Subdural haematoma

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34
Q

2 things that thiamine (B1) deficiency causes

A

Beri-beri

Wernicke-Korsikoff syndrome

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35
Q

Symptoms of wernicke korsakoff syndrome

A

Ataxia
Abnormal eye movements
Impaired consciousness/memory loss

36
Q

Confabulation

A

Seen in Wernicke Korsakoff syndrome (or just korsakoff) - can’t make new memories so make up lies to disguise this

37
Q

Why can you get neuropathy in alcoholism

A

Thiamine maintains peripheral nerves:

  • Foot drop
  • Wrist drop
  • Pain

More rarely - arrhythmias/CCF from CNX involvement

38
Q

Consequence of aspiration into lungs

A 
Acute inflammation (pneumonitis)
Later infection (pneumonia)
39
Q

What heart disease is assoc with chronic alcoholism, and what dies this pose a risk of

A

Dilated cardiomyopathy (big, heavy heart with normal wall thickness)

Arrhythmias, CCF

40
Q

Name of thiamine deficiency along with cardiac arrhythmias and CCF in alcoholics

A

Wet Beri Beri

41
Q

Initial liver disease after 1-2 days of heavy drinking

A

Alcoholic fatty liver (aka steatosis)

42
Q

Reason for increased intracellular fat seen in AFLD

A
  • More fatty acids delivered to liver
  • Alcohol converts NAD>NADH, stimulating lipid synthesis
  • Fatty acid oxidation is reduced
  • Reduced fat export by tubulins
43
Q

Liver disease seen after 3-4 weeks of heavy drinking

A

Alcoholic steatohepatitis (fat accumulation + inflammation)

direct toxicity of alcohol causes inflammation

44
Q

Symptoms of steatohepatitis

A

Fever
Jaundice
Tender liver

45
Q

What are all of these things seen in alcoholic steatohepatitis:

  • Acute inflammatory cells
  • Ballooning
  • Mallory bodies
A
  • lymphocytes
  • Fat inclusions in hepatocytes
  • Damaged intermediate filaments (stain dark purple)
46
Q

Which cells deposit scar tissue around hepatocytes in cirrhotic liver

A

Interstitial cells of Ito

47
Q

Where specifically is collagen deposited by cells of Ito and what does this leave behind

A

Space of Disse

Islands of functioning hepatocytes surrounded by bands of scar tissue

48
Q

Why do ‘islands of hepatocytes’ function poorly in cirrhosis

A

Reduced blood supply and capacity to metabolise it, so toxic waste build up

49
Q

Where is blood directed through if poor cirrhotic flow

A

Splenic vein
Oesophageal veins
Anorectal veins
Superficial veins

50
Q

How can hypoglycaemia be caused by alcohol

A

Reduced gluconeogenesis - dangerous in diabetics

51
Q

Type of cancer caused by barret’s

A

Adenocarcinoma

52
Q

What is a varied

A

Abnormally dilated vein

53
Q

In pancreatitis the lipase enzyme is prematurely activated and digests pancreatic cells, what is this process called?

A

Fat necrosis

54
Q

Normal intestinal epithelium?

A

Columnar epithelium with goblet cells

55
Q

In pancreatitis, enzymes come into contact with fat and turn it into soap, what is this process called?

A

Saponification

56
Q

Difference between Wernicke and Korsakoff syndrome

A

Wernicke - Walking - ataxia, abnormal eye movements (reversible)

Korsakoff - memory loss, confabulation (irreversible)

57
Q

In alcoholism, MCV is increased/decreased

A

Increased

58
Q

Why do triglyceride levels increase in excessive liver

A

Increased lipid synthesis in liver

59
Q

Tests to see if a patient is a chronic drinker

A 
Gamma GT (raised)
MCV (raised)
Triglycerides (raised)
60
Q

What tests are done when a patient comes into hospital in a coma

A 
Blood glucose (hypoglycaemia)
Serum osmolality
61
Q

Calculation for serum osmolality?

A

Roughly = 2 x Na conc

62
Q

How is serum osmolality used to determine if a patient is in an alcoholic coma

A

Osmolal gap = serum osmolality - calculated osmolality

Big gap = ethanol contributing

63
Q

tests if main complaint of patient is vomiting

A

U&E
LFT
Amylase
ABG

64
Q

U&E of an alcoholic who is vomiting

A

Low potassium
Low sodium
High urea and creatinine (reduced GFR)

65
Q

tests for a patient who presents with haematemesis

A

U&E
LFT
PTR
Lactate

66
Q

Why is urea classically raised in haematemesis

A

You’re absorbing your own blood, which contains proteins

67
Q

What poison is seen in antifreeze? Treatment

A

Polyethylene glycol (antifreeze)

Ethanol again

68
Q

What is the meyer-overton rule

A

As the number of carbons in an alcohol increases, so too does its ability to act as a general anaesthetic

69
Q

Cut off point for general anaesthetic effect of alcohol

A

hexanol-pentanol, then decreases

70
Q

What neurotransmitters does alcohol effect

A

Glutamate (excitatory)

GABA, Glycine (inhibitory)

71
Q

Ethanols effect on neurotransmitters causes what?

A

CNS depression

72
Q

Drink drive limit

A

0.05mg/100ml

73
Q

Definition of harmful alcohol use

A

Misuse for 1 month

74
Q

Criteria of alcohol dependence syndrome

A 
Strong compulsion to take alcohol
Difficulties in controlling alcohol use
Using alcohol despite evidence of harm
Preoccupation with alcohol use
Increased alcohol tolerance
Physiological withdrawal
75
Q

Screening tests to determine patient’s dependence on alcohol

A

FAST - before treatment

AUDIT Screen - after treatment

76
Q

What drugs help alcohol withdrawal

A

Chlordiazepoxide/Diazepam

Oxazepam

77
Q

What is Child Pugh score

A

Calculate prognosis in cirrhosis and assess suitability for drugs e.g. chlordiazepoxide

78
Q

Supportive treatment given to alcoholics

A

Oral thiamine

IM/IV Pabrinex (multi vitamins)

79
Q

What is thiamine used for in body

A

co-enzyme for krebs cycle

80
Q

Next step if alcohol withdrawal patient is delirious

A

Admit to hospital

IV pabrinex

81
Q

What happens 2-3 days into alcohol withdrawal

A

Delirium tremens

82
Q

What causes wernicke encephalopathy

A

Lactic acid in brain

83
Q

What causes korsakoff syndrome

A

Irreversible brain damage from lactic acid in brain

84
Q

Apart from Disulfarim, what can be given in chronic alcoholism

A

Acamprosate - reduces cravings

85
Q

What type of stroke commonly presents in drinkers

A

Haemorrhagic

86
Q

What neuro disease is common in drinkers

A

Amnesia

87
Q

Chronically, what arrhythmia might alcoholism lead to

A

Long QT syndrome

Year 2 (19 decks)

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