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CLASP > Alcohol > Flashcards

Alcohol Flashcards

1
Q

what is methanol metabolised into

A

formaldehyde then formic acid

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2
Q

what can acidosis from methanol poisoning cause

A

blindness

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3
Q

how do you treat methanol toxicity

A

alcohol +/- dialysis

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4
Q

how does alcohol treat methanol toxicity

A

competitive inhibition- both metabolised by alcohol dehydrogenase

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5
Q

how many units a week

A

14

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6
Q

where is alcohol mostly absorbed and what is it soluble in

A

the small bowel, water

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7
Q

what is ethanol metabolised by

A

alcohol dehydrogenase

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8
Q

what can delay alcohol gastric emptying

A

eating, spirits irritate gastric mucosa and delay emptying

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9
Q

what can speed up gastric emptying

A

antihistamines and metoclopramide

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10
Q

what type of alcohol is absorbed faster

A

20-30% aerated

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11
Q

what is a common sign of alcohol withdrawal

A

seeing spiders

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12
Q

why do men have higher tolerances

A

as women have more adipose tissue, alcohol is distributed in fat free mass. women also have less alcohol dehydrogenase

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13
Q

what is ethanol metabolised to

A

acetaldehyde and then aldehyde dehydrogenase then CO2 and h20

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14
Q

what causes hangover

A

acetaldehyde

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15
Q

where does alcohol metabolism occur

A

90% in the liver, small volume in the pancreas and brain

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16
Q

at what rate is alcohol removed from the body

A

15mg/100ml/hour, one unit per hour, conc decreases linearly

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17
Q

when is alcohol conc at its highest

A

60 mins after consumption

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18
Q

why do some ethnic groups have lower tolerance

A

lower levels of dehydrogenase

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19
Q

what is antabase

A

drug which makes drinking unpleasant, inhibits aldehyde dehydrogenase

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20
Q

what is acetaldehyde metabolised

A

aldehyde dehydrogenase

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21
Q

how do you increase your alcohol tolerance

A

increase alcohol dehydrogenase activity, analgous and alternative pathways activated: MEOS pathway, induction og CP450

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22
Q

what are the consequences of activating alternative pathways in alcohol metabolism

A

MEOS pathway- increased production of hydrogen ions which are removed via the krebs cycle, switch to anaerobic metabolism which produces lactic acid faster, inhibits citric acid cycle and hepatic gluconeogenesis

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23
Q

what happens to hepatic gluconeogenesis with alcohol

A

is inhibited, get hypoglyceamic, hungry

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24
Q

what happens to fatty acid oxidation with alcohol

A

impaired- excess ketogenesis and lipid synthesis- makes you fat

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25
Q

what is alcoholic ketoacidosis

A

no gluconeogenesis, impaired fatty acid oxidation, makes ketones instead, excess NADH

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26
Q

compare diabetic and alcohol ketoacidosis

A

diabetic- hyperglycaemia, high ketones

alcoholic- hypoglycaemia, high ketones

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27
Q

how does alcohol act as a depressant

A

increases levels of GABBA- inhibitor of neurotransmitters

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28
Q

affects of alcohol via the cortex

A

dis-inhibition, talkative, anxiolytic

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29
Q

affects of alcohol via the limbic system

A

memory loss, confusion, disorientation

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30
Q

affects of alcohol via the cerebellum

A

loss of muscular coordination, slurred speech

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31
Q

affects of alcohol via the reticular formation (upper brain stem)

A

consciousness

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32
Q

affects of alcohol via the lower brain stem

A

breathing and blood pressure

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33
Q

what are signs of high alcohol blood content

A

stupor, difficult to rouse, loud snoring

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34
Q

what happens to ADH when drinking

A

inhibited

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35
Q

why do you get a heavy heartbeat when hungover

A

alcohol is a negative inotrope

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36
Q

describe holiday heart syndrome

A

binge drinking- healthy heart, supra-ventricular tachycardia, spontaneous resolution

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37
Q

why do you get a headache

A

dehydration and acetic acid

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38
Q

describe the symptoms of mild alcohol withdrawal and their onset

A

(12-13 hrs from last drink) fine tremor, sweating, anxiety, hyperactivity, increased HR and/or BP, fever, anorexia, nausea, retching

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39
Q

describe the symptoms of moderate alcohol withdrawal and their onset

A

(12 hrs - 5 days) coarse tremor, shaking, agitation, confusion, disorientation, paranoia, seizures (especially 24-48 hours), hallucination

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40
Q

describe the symptoms of severe alcohol withdrawal and their onset

A

(12 hrs to 5 days) severe agitation, confusion, delusions, hallucinations, circulatory collapse, death

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41
Q

how is alcohol withdrawal treated

A

diazepam

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42
Q

how is the dosage of diazepam decided

A

regular symptom assessment

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43
Q

what does alcohol cause the release of from the reward centres of the brain

A

dopamine and serotonin

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44
Q

what types of seizure are associated with alcohol consumption

A

alcohol withdrawal can cause seizures

can cause epileptic seizures in susceptible individuals

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45
Q

how does alcohol affect nerves and muscles long term

A

peripheral neuropathy, compression neuropathy, myopathy,

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46
Q

what does peripheral neuropathy feel like and how is it caused by alcohol

A

‘glove and stocking’ burning pain and weakness

direct damage to peripheral nerves, nutritional deficiencies (thiamine)

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47
Q

what is compression neuropathy and what causes it

A

temporary damage to myelin sheath- radial nerve compression at humeral head

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48
Q

describe acute myopathy after binges

A

myalgia, proximal weakness, swollen tender muscles, raised CK

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49
Q

how long does acute myopathy take to recover

A

weeks to months

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50
Q

describe chronic myopathy

A

develops over weeks to months, painless, proximal weakness and atrophy, normal CK, low K, PO4

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51
Q

define wernickes encephalopathy

A

thiamine deficiency and cytotoxic oedema in mamillary bodies

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52
Q

what are the symptoms of wernicke encephalopathy

A

ocular dysfunction, ataxic gait, acute confusion

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53
Q

how is WE syndrome treated

A

thiamine replacement

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54
Q

what happens if WE syndrome isn’t resolved

A

develops into korsakoffs syndrome

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55
Q

define korsakoffs syndrome

A

cerebral atrophy resulting from WE

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56
Q

what are the symptoms of korsakoff syndrome

A

loss of shirt term memory, episodic memory, confabulation, lack insight

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57
Q

how is korsakoff syndrome treated

A

abstinence and nutrition, chances of recovery low

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58
Q

what other brain problems can alcohol cause

A

dementia, storke (haemorrhagic), depression, head injury, cerebellar disease

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59
Q

describe the relationship between alcohol and cardiovascular mortality

A

j shaped curve

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60
Q

how does excessive drinking over a long period cause cardiomyopathy

A

alcohol impairs ventricular function (calcium homeostasis), mitochondrial effects, signal transduction). prolonged exposure leads to chronic inflammation/ fibrosis of myofibrils muscle fibres)

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61
Q

what acute arrhythmias can be cause by alcohol

A

AF, SVT ‘holiday heart’

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62
Q

what chronic arrhythmias can be caused by alcohol

A

long QT- electrolyte imbalance

atrial and ventricular arrhythmias due to dilated cardiomyopathy

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63
Q

how old are the majority of people who die from alcohol liver disease

A

<60

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64
Q

describe the simple pathological process of cirrhosis

A

regular heavy drinking- fat accumulation in hepatocytes- inflammation- fibrosis- cirrhosis

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65
Q

does alcohol related steatosis reverse with cessation

A

yes

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66
Q

what happens to hepatocytes in alcohol related steatosis

A

swell with triglycerides

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67
Q

is alcohol related hepatitis acute or chronic

A

acute

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68
Q

describe the pathology of alcohol related hepatitis

A

parenchymal inflammation and hepatocyte damage

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69
Q

what conditions are associated with alcohol related hepatitis

A

jaundice, coagulopathy, liver failure

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70
Q

what are people with alcohol related hepatitis at high risk of

A

renal failure, bleeding, infections (if severe mortality <50%)

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71
Q

how do you treat alcohol related hepatitis

A

abstinence, nutrition

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72
Q

what is associated with portal hypertension

A

variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy,

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73
Q

what is the process leading to hepatic encephalopathy

A

portosystemic shunting through collaterals, failure to clear toxins/ ammonia from blood, crosses blood brain barrier

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74
Q

what is the treatment for ecephalopathy

A

lactulose and rifampicin

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75
Q

treatments for alcohol related cirrhosis

A

abstinence, vitamins, nutritionm endoscopic, beta blockers, radiological (TIPPS), transplant

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76
Q

why does alcohol cause cancer

A

Alcohol -> acetaldehyde (carcinogenic) -> acetate
Most alcohol -> acetaldehyde by ADH in liver

As alcohol increases, less metabolised on first pass through liver, and circulating alcohol then metabolised by ADH at other sites eg oral mucosa. Acetaldehyde unable to be converted to acetate at these sites due to absence of AlDH

is a soovent, makes it easier for carcinogens to enter cells

deficiencies in essential nutrients

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77
Q

why (theory) does alcohol increase risk of breast cancer

A

as increases oestrogen levels (post- menopausal women)

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78
Q

what are the pharmacological interventions for alcohol missuse

A

acamprosate- reduces cravings

naltrexone- reduces desire for alcohol

disulfiram- aversion drug therapy

nalmefene- opioid antagonist

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79
Q

how is alcohol excreted

A

lungs, sweat and urine

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80
Q

where is the primary metabolism site of alcohol

A

liver

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81
Q

how is alcohol removed from the blood

A

oxidation process

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82
Q

eating slows absoption of alcohol, how does this decrease drunkness

A

as increases first pass metabolism in the liver, less reaches systemic circulation

83
Q

how many calories in 1g of alcohol

A

7kcal

84
Q

how does alcohol increase risks of deficiencies

A

replaces food/ alters appetite

decreases secretion of pancreatic enzymes and bile

damages cells lining stomach and intestines limiting absorption

ethanol metabolism relies of thiamine

decreased liver stores of vitamins

85
Q

what is vitamin B1, describe it and where its found

A

thiamine- water soluble essential nutrient found in e.g cereals, beans, nuts, yeast and meat

86
Q

what is thiamine important for

A

ATP production, normal nerve conduction and maintenance of neural membranes

87
Q

why do thiamine levels get low in alcoholism

A

poor intake,
decreases phosphorylation in the gut to active co enzyme,
reduced storage in fatty liver,
inhibited intestinal absorption,
increased metabolic demand (needed for ethanol metabolism)

88
Q

what are the three clinical thiamine deficiency signs

A

dry beriberi, wet beri beri, wernicke-korsakoff syndrome

89
Q

describe dry beriberi

A

nervous system- polyneuropathy, weakness, numbness, paralysis- usually in lower limbs

90
Q

what is wet beriberi

A

CV system- increased HR, SOB, high cardiac output failure

91
Q

what is ataxia

A

inability to coordinate voluntary movements

92
Q

what vitamin deficiencies are associated with alcoholism

A

thiamine (B1)

water soluble vits (B+C)= folate and B12, niacin

fat soluble vits (A,DE,K)- vit a

minerals- increased urinary excretion of Ca- osteoporosis

93
Q

what does a folate and B12 deficiency result in

A

megaloblastic anaemia

94
Q

what is niacin

A

pellagra- diarrhoea, dermatitis, dementia, and death

95
Q

what vitamin deficiency causes night blindness

A

vit a

96
Q

what cancers can be caused by alcohol

A

breast, bowel, liver, mouth/ throat, oesophageal and stomach

97
Q

describe foetal alcohol syndrome

A

physical (abnormal appearance, stunting, low body weight and head size, poor coordination)

mental (low intelligence, learning difficulties)

sight and hearing problems

98
Q

what type of bonds does alcohol form

A

hydrogen- low affinity as only one hydrogen donor/ acceptor

99
Q

blood goes hypotonic when drinking alcohol, why don’t red blood cells swell

A

as alcohol gets into the cytoplasm

100
Q

how does alcohol act as a depressant on a cellular level

A

enhancement of inhibitory enhancement of inhibitory neurotransmission or depression of excitatory transmission

enhancement of neuronal membrane conductances leading to hyperpolarisaton

101
Q

name the two important receptors that alcohol affects and whether they inhibit or excite neurotransmission

A

glycine and GABAa receptors (inhibitory)

subtypes of glutamate receptor (excitatory)

102
Q

explain excitatory and inhibitory neurotransmitters and alcohol

A

alcohol potentiates inhibitory neurotransmission by GABA (y-aminobutyric acid) or glycine

and

inhibits excitatory neurotransmission by glutamate

103
Q

what mediates fast excitatory and inhibitory neurotransmission in the CNS

A

ligand gated ion channels

104
Q

what receptor family does glycine and GABAa belong to

A

cys-loop family

105
Q

what is the main inhibitory neurotransmitter in the CNS

A

GABA

106
Q

where does GABA and glutamate act

A

ionotropic receptors

G protein coupled receptors

107
Q

which ionotropic glutamate receptor is sensitive to alcohol

A

NMDA

108
Q

what is the main excitatory neurotransmitter in the CNS

A

glutamate

109
Q

summaries alcohols affect on GABA and glutamate

A

simultaneous enhancement of GABAergic inhibitory neurotransmission and a suppression of excitatory glutamateric transmission leading to overall CNS depression

110
Q

what is the reward system of the brain (activated by alcohol and most drugs)

A

mesolimbic dopaminergic pathway

111
Q

how do drugs cause dependence via the reward system- which method does alcohol use

A

exciting ventral tegmental area neurones stimulating the release dopamine which inhibits neurones in the nucleaus accumbens

enhancing release of dopamine from the ventral tegmental area neurone terminals or preventing its reuptake

inhibiting nucleus accumbens neurones (how alcohol does it)

112
Q

describe the neuroadaption that causes the symptoms of alcohol withdrawal

A

to compensate for CNS depression (after prolonged usage of alcohol) NMDA receptor expression is upregulated in the brain and GABAa receptors are down regulated

during alcohol withdrawal there is an imbalance between excitatory (upregulated) and inhibitory (downregulated) influences- anxiety, dysphoria, seizures

113
Q

how long must a pattern of use that is causing damage physical or mental health persist for until it is classified harmful use

A

for a least 1 month or occurred repeatedly

114
Q

name the criteria for dependence syndrome (3 or more= diagnosis)

A

strong desire or compulsions

difficulties in controlling use

persistent use despite clear evidence of harm

preoccupation with substance use

increased tolerance

psychological withdrawal state (many forms)

115
Q

what are the components needed to treat alcohol dependence

A

medical treatment, psychology of change, social context

116
Q

what supportive treatments should be gives for alcohol dependence

A

oral thiamine for low risk

IM/IV pabrinex for high risk

nutrition, hydration, anti emetics, anti- diarrhoeals

117
Q

what are the complications of alcohol dependence

A

withdrawals (4-12hrs), withdrawal seizures (60%) *30-40% progress to status epilepticus), delirium tremens (3-10 days), wernicke-korsakoff syndrome

118
Q

what is the main characteristic of korsakoff

A

confabulation

119
Q

what drug to support after seizures

A

diazepam

120
Q

what is delirium tremens

A

severe from of withdrawal that includes sudden and severe mental and/or nervous system changes A MEDICAL EMERGENCY

121
Q

what are the symptoms of deririum tremens

A

confusion, hallucinations, autonomic hyperactivity, tachycardia, sweating, HTN, pyrexia, tremors, seizures

122
Q

when does delirium tremens occur

A

72-96 hrs after last drink

123
Q

how do you manage delirium tremens

A

inpatient detox, benzodiazepine (to prevent seizures), pabrinex (vitamin injection), anticonvulsants, antipsychotics, antiemetics, fluids

124
Q

what are the triad of symptoms of wernickes encephalopathy

A

ophtalmoplegia (eye paralysis), ataxia (lack of voluntary coordination), confusion

125
Q

what does alcohol and BZD cause

A

ataxia and nystagmus (involuntary eye movement)

126
Q

what medications can be used to prevent relapsing

A

acamprosate and naltrexone (1st line)

disulfiram 2nd line

127
Q

what does disulfiram do

A

makes patient suffer allergy like symptoms when they drink

128
Q

what psychological programme is used to prevent relapsing

A

12 step programme AA, trauma focused therapies, brief interventions

129
Q

what is the minimum pricing

A

50p per unit of alcohol

130
Q

where does aspiration pneumonia typically occur

A

superior segment of the right lower lobe

131
Q

which of these microscopic features is not present within a portal tract; artery, vein, hepatocyte, lymphocyte, bile ducts

A

hepatocyte

132
Q

why does alcohol cause diuresis

A

decreased ADH levels

133
Q

jaundice as a result of alcoholic hepatitis is caused by an accumulation of what

A

conjugated bilirubin

134
Q

is hyperbilirubinaemia (resulting in clinical jaundice) associated with alcoholic liver disease

A

yes

135
Q

facial flushing and a generl feeling on being unwell is caused by what

A

aldehyde

136
Q

name a drug that increases the rate of alcohol absorption

A

domperidone (anti emetic)

137
Q

what cell type mediates fibrosis cirrhosis of the liver

A

hepatic stellate cells / interstitial cells of ito

138
Q

what is a patient with normal GGT, AST and ALT but raised Alk Phos most likely to have

A

bone disease

139
Q

what syndrome is severe hepatitis associated with

A

hepatorenal syndrome

140
Q

which of the following of signs is not associated with acute pancreatitis;
caput medusa, grey turners sign, cullens sign, renal failure, resp failure

A

renal failure

141
Q

true or false; ethanol is sometimes used to treat patients with a raised osmolal gap

A

true

142
Q

what causes dupuytrens contracture

A

scarring of the palmar fascia

143
Q

what is portal hypertension associated with: splenomegaly, +ve courvoisier’s sign, +ve murphys sign, hepatomegaly, cullens sign

A

splenomegaly

144
Q

name a medication used for medically assisted alcohol withdrawal

A

chlordiazepoxide

145
Q

what biochem test can be used to assess perfusion in a severe upper GI bleeding

A

lactate

146
Q

what does alcohol do to the precipitation of uric acid

A

increases it

147
Q

what embryological remnant forms the falciform ligament

A

umbilical vein

148
Q

what is the timescale for delerium tremens

A

3-10 days

149
Q

which clotting factor is not made in the liver

A

8

150
Q

what borders hepatocytes

A

the spaces of disse

151
Q

where is haemoglobin broken down

A

the liver and spleen

152
Q

haemoglobin is broken down in to haem and globin, what is haem then broken down into

A

iron and biliverdin

153
Q

what breaks down haem into iron and biliverdin

A

oxygenase

154
Q

what then breaks down biliverdin into what

A

reductase

unconjugated bilirubin

155
Q

how is unconjugated bilirubin transported to the liver

A

with albumin (not water soluble)

156
Q

how and where is bilirubin conjugated

A

at the liver by glucuronyl transferase

157
Q

what is bilirubin conjugated with

A

glucuronic acid

158
Q

what does conjugated bilirubin do

A

goes into gall bladder to make bile salts

159
Q

why is bile needed

A

excretion of; lipophilic toxins, bilirubin, cholesterol

immune function IgA

emulsify dietary fat

160
Q

what enzyme do statins target

A

Hmg-CoA reductase

161
Q

what does HmG-CoA reductase do

A

rate controlling enzyme for pathway controlling production of cholesterol

162
Q

what happens to bile after it leaves gall bladder

A

converted to urobilinogen and stercobilinogen and finally stercobilin

10-15% reabsorbed by enterohepatic circulation

163
Q

what does AST stand does

A

asparate transaminase (aminotransferase)

164
Q

what is AST an imprtant part of

A

amino acid metabolism

165
Q

what does ALT stand for

A

alanine aminotransferase

166
Q

ALK raised in isolation would most likely be what

A

bone disease

167
Q

what does raised ALP and GGT suggest

A

biliary disease- obstructive post hepatic jaundice

168
Q

what does raised AST but not ALT suggest

A

liver damage

169
Q

what does raised GGT and abnormal AST and ALT suggest

A

alcohol

170
Q

what are biological markers of chronic alcohol consumption

A

Gamma GT
MCV (mean corpuscular volume)
triglycerides raised (increased synthesis in the liver)

171
Q

what is the osmolal gap and how does it show if a patient had ingested alcohol

A

a difference between measured (inc. dissolved solutes in blood) and calculated serum (electrolytes) osmolarity

solutes contribute to osmolarity

172
Q

what is ALT a marker of

A

liver damage

173
Q

where is ALP found

A

liver, bone, small intestine, kidneys, placenta

174
Q

where is gamma GT found

A

liver (cell membranes of bile ducts), kidneys, pancreas, prostate

175
Q

what does albumin show in relation to alcohol

A

albumin falls in the systemic inflammatory response- capillary permeability associated with inflammation causes redistribution

176
Q

what is better than albumin at showing liver synthesis

A

prothrombin ratio

177
Q

what does prothrombin ratio show

A

clotting factors synthesised in the liver - liver synthesis and patients bleeding tendency

178
Q

what are the differential diagnosis of abdominal pain in patient with alcohol issues

A

acute pancreatitis, alchoholic hepatitis, peptic ulceration +/- perforation, ascites +/- peritonitis

179
Q

what investigations should be done for abdominal pain in patient with alcohol issues

A

amylase, liver function tests, ascitic fluid analysis

180
Q

what are the differential diagnosis of vomiting in apatient with alcohol issues

A

acute gastritis, oesophageal stricture, pyloric stenosis

181
Q

how do you check to severity of vomiting in a patient with alcohol issues

A

U&E, ABG, LFT, Amylase

182
Q

does acid increase or decrease hydrogen ions in the gut

A

increases

183
Q

does alcohol increase the hydrogen ion and CO2 concentration of the blood

A

increase CO2

decrease H+

184
Q

what are the differentials in a patient with haematemesis and alcohol issues

A

acute gastritis, mallory-weiss tear, peptic ulceration +/- perforation, oesophageal varices

185
Q

what investigations should be done in a patient with haematemesis and alcohol issues

A

prothrombin ration, LFTs

186
Q

what signs show acute drinker

A

osmolality/ osmolal gap

187
Q

what tests should be done into a GI bleed

A

U&E, LFT, PTR, lactate

188
Q

what in relation to alcohol activated GGT

A

The mechanism by which alcohol is converted to aldehyde by alcohol dehydrogenase induces GGT

189
Q

does MCV increase or decrease with chronic drinking

A

decreases

190
Q

what can be used to treat hyponutremia

A

aldosterone antagonst e.g. spironolactone

191
Q

what ions will be low after excessive vomiting

A

sodium and potassium

192
Q

which LFT can reflect enzyme induction

A

GGT (very sensitive)

193
Q

how do triglycride levels change in the blood with chronic alcohol consumption

A

increase in the blood due to increased triglyceride synthesis in the liver

194
Q

metabolic acidosis is harder to compensate in pateints with what

A

pyloric stenosis- hydrogen ions cannot re-enter stomach from small intestines

195
Q

what does serum osmolarity measure

A

the amount of solutes in the fluid portion of the blood

196
Q

what happens to lipid solubility and intoxicating potential as alcohol chain length increases

A

lipid solubility increases

intoxicating potential increases up to chain length of 6 then after 8 decreases

197
Q

what are cys-loop receptors comprised of

A

a pentamer of subunits with 3 functional nodules; the extracellular, transmembrane and intracellular domains

198
Q

which functional nodule of the cys loop receptor contains an allosteric binding site which can accomodate alcohol and general anaesthetics

A

transmembrane

199
Q

what does the extracellular component of a cysloop do

A

provides a binding site for neurotransmitter and competitive antagonists

200
Q

what does the intracellular component of the cysloop do

A

interacts with the cytoskeleton and harbours sites for channel regulation by phosphorylation

201
Q

does alcohol mix best with water or organic solvents

A

mixes with both equally well

202
Q

why are alcohols longer than 8 less intoxicating

A

as physically dont fit into sites

203
Q

what type of receptors are GABBA A

A

ligand gated cys loop receptors

CLASP (3 decks)

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