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CLASP MB2 > Alcohol Biochemistry; Pharmacology > Flashcards

Alcohol Biochemistry; Pharmacology Flashcards

1
Q

Gamma GT

A

Found in bile canaliculi.

When ethanol is metabolised -p450 enzymes and Gamma GT are induced

Very sensitive

Marker of how much they are drinking

Gamma GT levels can rise due to other causes however

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2
Q

Raised MCV

A

Increased percentage of immature red blood cells.

Chronic alcohol excess

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3
Q

Raised triglycerides

A

Alcohol excess.

Increased synthesis in liver

Blood looks milky when centrifuged.

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4
Q

What tests would you run if the patient is drinking chronically?

A

Gamma GT
MCV
Triglycerides

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5
Q

What tests would you run if the patietn is in a COMA?

A

Glucose and serum osmolality

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6
Q

What is the glucose test useful/important for?

A

Do not want to miss HYPOGLYCAEMIA

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7
Q

Serum osmolality

A

All dissolved solutes contribute to serum osmolality.

Can calculate from concentration of measured electolytes.

e.g. Na, K, Ca, Urea, Glucose

Serum osmolality = 2 x[Na]

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8
Q

What is the equation for calculated serum osmolality

A

2 x [Na]

In practice sodium dwarfs everything else

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9
Q

What is the reference interval for serum osmolality

A

275-295mmol/kg

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10
Q

Sometimes there is a gap between measured (in clinic) and calculated serum osmolality. What is this gap called?

A

OSMOLOL GAP

(most cases due to ethanol)

Clinicians know that theres something else in patient’s blood contributing to osmolality but not measured.

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11
Q

What tests would you do for abdominal pain?

A

Amylase (pancreatitis)
LFTs
(Ascetic fluid analysis)

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12
Q

ALT (alanine aminotransferase)

A

Found in liver

Present in hepatocytes

Marker of liver DAMAGE.

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13
Q

Alk phos (alkaline phosphatase)

A

> Rise comes from liver (bile canaliculi)/bone (osteoblasts)
Check GAMMA GT
Kidney - proximal tubules

Think BONES if only this is elevated and other LFTs are normal.

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14
Q

Why is albumin not a good marker for current synthesis?

A

Half life is 3 weeks.

Systemic inflammatory response

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15
Q

Prothrombin ratio

A

Clotting factos synthesised in liver

Half life of 3-4 days

Better indicator of liver function.

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16
Q

What kind of bilirubin does an obstruction lead to

A

Conjugated hyperbilirubinaemia

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17
Q

Tests for Vomiting?

A

U&Es, LFTs, Amylase, ABG

Acute gastritis
Oesophageal stricture
Pyloric stenosis

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18
Q

When vomiting, acidosis or alkalosis?

A

Metabolic alkalosis

Losing acid from stomach when vomiting
Very low chloride

For every hydrogen ion you lose – you gain a bicarbonate
Raised bicarbonate = metabolic alkalosis
Hence ABGs are used.

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19
Q

What may occur in pyloric stenosis if the patient is vomiting?

A

Only losing fluid from stomach (due to stenosis of pyloric - little fluid lost from duodenum (bicarb))

Losing more acid

Metabolic alkalosis

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20
Q

What tests would you run for Haematemesis

A

U&Es, LFT, PTR, Lactate

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21
Q

GI bleed. What happens to the red blood cells?

A

They are absorbed and then go into portal circulation

Urea produced (protein in RBCs)

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22
Q

What is secreted when losing blood volume?

A

Secretion of aldosterone
Retains sodium and water

Also secrete ADH

  • reabsorption of water
  • pee out less
  • concentrated urine
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23
Q

Methanol and ethylene glycol are both…

A

toxic alcohols

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24
Q

Why are methanol and ethylene glycol toxic?

A

Very acidic metabolites

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25
Q

What is ethylene glycol present in?

A

Antifreeze

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26
Q

Methanol toxicity

A

–> Formaldehyde –> formic acid

Acidosis is toxic.

Blindness

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27
Q

Alcohol is initially metabolised by

A

Alcohol dehydrogenase in the stomach.

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28
Q

Does eating before you drink slow down absorption?

A

Yes.

the longer the food is in the stomach, the longer it is metabolised before getting to the small bowel.

Full stomach slows gastric emptying.

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29
Q

Which drugs increase gastric emptying rate and increase absorption?

A

Antihistamines
Metoclopramide

Absorb alcohol much faster.

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30
Q

The higher the concentration of alcohol, the…

A

slower is it absorbed

Spirits irritate gastric mucosa and delay emptying

Aerated drinks are absorbed faster

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31
Q

Women become intoxicated more quickly than men, why? (generally)

A

Lower levels of alcohol dehydrogenase

Higher subcutaneous fat percentage

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32
Q

Metabolism of ethanol

A

Ethanol (alcohol dehydrogenase) –> acetaldehyde (aldehyde dehydrogenase) –> acetate + CO2 + H2O

90% occurs in liver
Small volume in pancreas and brain

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33
Q

How fast is alcohol removed from blood?

A

15mg/100ml/hour

1 unit an hour roughly

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34
Q

When does alcohol concentration peak?

A

60 mins after consumption and the decreases linearly.

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35
Q

Aborigines, Inuits, Japanese have low levels of

A

alcohol dehydrogenase

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36
Q

Flushing & feeling sick

A

Aldehyde responsible.

Often south east asians

Deficient or ineffective varian of aldehyde dehydrogenase

Antabuse mimics this

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37
Q

What happens when you drink a lot?

A

Increased tolerance

Possible to up regulate alcohol dehydrogenase

Heavy drinkers - analogous and alternative pathways are activated

Induction of CP450

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38
Q

MEOS pathway induction

A

Heavy drinkers

Production of hydrogen ions (REDOX).

Disposed of by:

  1. Inhibition of hepatic gluconeogenesis
  2. Citric acid cycle
  3. Fatty acid oxidation impairment

Higher resting energy expenditure

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39
Q

Effects of alcohol (general)

A

Cortex - disinhibition, talkativeness, anxiolytic

Limbic system - memory loss, confusion, disorientation

Cerebellum - loss of muscular coordination, slurred speech

Reticular formation (upper brainstem) - consciousness

Lower brain stem - control of breathing and blood pressure

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40
Q

Effects of alcohol by concentration

A

< 100 - excitement, fun, disinhibited, still in some control

100-200 - slurring of speech.blurred vision, falls, wide emotions

> 200 - stupor. difficult to rouse. loud SNORING

Dangerous if brain stem is inhibited - decreased consciousness and breathing.

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41
Q

at what age are you legally allowed to drink alcohol at home?

A

5 years old.

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42
Q

Where does ADH take effect?

A

Distal tubules
Promotes water reabsorption.

Concentrates urine

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43
Q

Effect of alcohol on ADH?

A

Inhibits ADH

Reduced water reabsorption and clearer urine

DEHYDRATION.

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44
Q

Alcohol effect on heart (acute)

A

Negative inotrope

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45
Q

Holiday heart syndrome

A

Associated with binge drinking
Most commonly an SVT

Spontaneous resolution

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46
Q

Hangover

A

Congeners (substances other than alcohol in the drink)

Serotonin - produced from sulphites, tannins, phenols

Dehydration

Acetic acid

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47
Q

Heart burn due to alcohol

A

Muscle relaxant

Smooth muscle in sphincter relaxes –> reflux/ heart burn

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48
Q

Snoring after alcohol consumpton

A

Relaxation of smooth muscle in pharynx/oropharynx

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49
Q

Grey turner’s sign

A

Bruised flanks

sign of pancreatitis

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50
Q

Cullen’s sign

A

“Bruised umbilicus”

sign of pancreatitis

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51
Q

Ethanol is what type of alcohol

A

Aliphatic

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52
Q

How many hydrogen bond acceptors/donors does ethanol have?

A

1 of each

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53
Q

Does ethanol have stereoisomers?

A

No

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54
Q

What is the strongest bond in ethanol?

A

hydrogen bond

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55
Q

Ethanol’s partition coefficient in octane/water?

A

-0.08

Very close to zero

i.e. miscible in BOTH water and organic solvents

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56
Q

The intoxicating effect of n-alcohols increases exponentially as…

A

the number of carbon atoms within the molecule increases from 1 (methanol) to 5 (pentanol)

Reaches a maximum at 6 (hexane) to 8 (octane) and above this decreases.

57
Q

When does the intoxicating effect of n-alcohols reach a max?

A

6-8 carbon atoms (hexane-octanol) then decreases.

58
Q

Lipid solubility and membrane disordering effect of n alcohols. Is there a “cut off”?

A

Lipid solubility and membrane disordering increases exponentially

59
Q

What is GABA

A

Gamma Aminobutyric acid

60
Q

Potentiation of Inhibitory Neurotransmission is mediated by?

A

GABA, or glycine

61
Q

Inhibition of Excitatory neurotransmission is mediated by?

A

Glutamate

62
Q

Enhancement of inhibition and suppression of excitation is anticipated to cause..

A

CNS depression

Major action of ethanol

63
Q

What structure mediates FAST excitatory and inhibitory neurotransmission in the CNS?

A

Ligand-Gated Ion channels.

64
Q

Cys-Loop LGICs general structure

A

Pentamer of subunits
Each subunit has 3 functional modules

i) Extracellular domain//

– binding site for neurotransmitter and competitive antagonists

ii) transmembrane domain

– forms the central ion channel and is also the binding site for allosteric regulators, including ethanol and general anaesthetics

iii) intracellular domain

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

65
Q

GLIC

A

proton activated bacterial homologue of Cys loop receptors

66
Q

Drink drive limit in Scotland?

A

50mg EtOH per 100mL of blood

= 10.9mM

“0.05g per 100ml”

67
Q

Effect of ethanol on Glutamate receptors of the NMDA

A

Ethanol inhibits their function.

68
Q

Effect of ethanol on GABAa receptors

A

Ethanol enhances function.

69
Q

Effect of alcohol on Strychnine-sensitive glycine receptors

A

Ethanol enhances their function

70
Q

Alcohol dependence syndrome

3 or more of?

A
  • Strong desire or compulsion to take alcohol
  • Difficulties in controlling use
  • Persistent use despite clear evidence of harm
  • Preoccupation with substance use
    o Where do I get my next drink?
  • Increased tolerance
  • Psychological withdrawal state
    o People keep using the substance to avoid withdrawal symptoms
71
Q

Dependence syndrome - treatment

A
  • Medically Assisted Alcohol Withdrawal (MAAW)

– Community - chlordiazepoxide/ diazepam

– Inpatient - Oxazepam

72
Q

Oxazepam is used in patients with

A

Known liver damage.

73
Q

Complications of alcohol withdrawal

A

> Minor/major withdrawal (4-12 hours)

> withdrawal seizures (60% of heavy drinking population)

> Delirium tremens (3-10 days)

> Wernicke-Korsakoff syndrome

74
Q

How many days after withdrawal from alcohol do DTs (delirium tremens) arise?

A

3-10 days

75
Q

Delirium tremens

  • signs
  • management
A

> Lillipution hallucination
- objects/people shrunken in size

> Formication
- sensation of insects on skin

Management

  • inpatient detox
  • BENZODIAZEPINE reducing regime
  • anticonvulsants, antipsychotics
  • Pabrinex
76
Q

Is Wernicke’s encephalopathy reversible?

A

Yes

Korsakoff’s is not.

77
Q

Is Korsakoff’s syndrome reversible?

A

NO

urgent treatment

78
Q

Antabuse/Disulfiram

A

Inhibits acetaldehyde dehydrogenase

Hangover effects experienced as soon as alcohol is consumed.

79
Q

Alcoholic hallucinosis

A

Chronic drinkers

During or shortly after periods of heavy drinking

  • acoustic hallucinations
  • delusions
  • mood disturbances

can progress to frank (clinically obvious) psychotic illness

80
Q

Wernicke Korsakoff syndrome

A

Thiamine deficiency

Ocular disturbances (6th nerve spasm, double vision)

Nystagmus (involuntary eye movement)

Ataxia

Mental state changes

Confabulation

Apathy, indifference

81
Q

When does BAC peak?

A

~30-60 minutes after consumption

82
Q

Does anything help speed up alcohol excretion/metabolism

A

Nothing except time.

83
Q

1g of alcohol = kcals

A

7 kcals

84
Q

Beriberi

A

Dry - nervous system. Weakness, numbness, polyneurpathy , paralysis

Wet - CV system. Increased HR, SOB, high output cardiac failure

85
Q

Korsakoff’s syndrome

A

Mental disorder

Retrograde amnesia
Then anterograde and current memory

86
Q

Most common cancer associated with alcohol?

A

Breast cancer.

Also bowel, liver, oral/oesophageal and stomach cancer.

Breakdown products of alcohol are carcinogenic

Acetaldehyde is carcinogenic

As alcohol increases, less metabolised on first pass through liver and circulating alcohol then metabolised by ADH (alcohol dehydrogenase) at other sites.

Acetaldehyde unable to be converted to acetate at these sites due to absence of AlDH (aldehyde dehydrogenase)

87
Q

Can alcohol be transferred to breast milk?

A

Yes.

Could severely affect baby’s liver as it has not yet fully developed.

88
Q

Foetal alcohol spectrum

A
  • low interlligence
  • abnormal appearance
  • low body weight
  • behavioural problems
  • sight and hearing problems
  • severity and nature linked to amount consumed and developmental stage
89
Q

If drinking in first trimester, what are risks?

A

Miscarriage and high rate of premature birth

Low birth weight

90
Q

Percent of NHS spending on hospitals

A

12% towards alcohol related illness.

91
Q

Alcohol withdrawal

  • Mild
  • Moderate
  • Severe
A

Mild (12-36hrs from last drink)– fine tremor, sweating, anxiety, hyperactivity, ^HR, ^BP, fever, anorexia, nausea, retching

Moderate (12hrs to 5 days) – coarse tremor, shaking agitation, confusion, disorient ation, paranoia, seizures (especially 24-48hrs), hallucinations

Severe (12 hrs – 7+ days) – more severe and prolonged, risk of DTs around 48 hrs – severe agitation, anxiety, confusion, delusions, hallucinations (tactile visual – crawling beesties). Circulatory collapse and death can occur

92
Q

Alcohol withdrawal seizures

A

Sudden cessation/reduction in alcohol in 12-24 hours

Generalised tonic-clonic

Clustered over few hours

93
Q

Epileptic seizures in alcoholics

A

Alcohol ingestion precipitates seizures in susceptible individuals

Usually morning AFTER acute intoxication

Any pattern - Tonic-clonic vs focal

94
Q

Alcohol - effect on nerves and muscles

A

> Peripheral neuropathy - sensorimotor axonal polyneuropathy “glove and stocking”

> Burning, pain, weakness

  • direct damage to peripheral nerves from alcohol
  • nutritional deficiencies
  • Compression neuropathy
95
Q

Compression neuropathy

A

Temporary damage to myelin sheath - Saturday night palsy

Radial nerve compression at humeral head

96
Q

Wernicke’s encephalopathy

A

Thiamine deficiency and cytotoxic oedema in maxillary bodies

  • ocular dysfunction
  • ataxic gait
  • acute confusion

Urgent recognition needed.

Without treatment it can end in development of Korsakoff’s syndrome

97
Q

Korsakoff’s syndrome

A

Cerebral atrophy from WE

  • Profound anterograde amnesia

Variable retrograde amnesia - episodic memory

COnfabulation

98
Q

Alcoholic cardiomyopathy

A

8-9 units/day for 5+ years

Alcohol impairs ventricular function

Prolonged exposure leads to chronic inflammation/ fibrosis of myofibrils

Arrhythmias

AF, SVT - acute

Chronic –> Long QT
Dilated cardiomyopathy

99
Q

Alcohol related steatosis

A

> Heavy drinkers

> Common presentation - abnormal LFTs

> Hepatocytes swell with triglycerides

> Reverses with cessation

100
Q

Alcohol related hepatitis

A

> Acute
Parenchymal inflammation and hepatocyte damage

> Jaundice, coagulopathy, liver failure

> Severe AH has 50% mortality

> Renal failure, bleeding, infections likely

101
Q

Alcohol related Cirrhosis

A

> Progressive fibrosis -> architectural distortion –> Cirrhosis ± portal hypertension

Compensated
Decompensated

102
Q

Compensated Alcohol related cirrhosis

A

Normal Liver function

Normal physical function

103
Q

Decompensated alcohol related cirrhosis

A

Impaired synthetic function

Ascites

Encephalopathy

104
Q

Portal hyperetnsion

A

Variceal bleeding

Ascites

SBP - spontaneous bacterial peritonitis (25-40% in hospital mortality)

Hepatic encephalopathy

HEPATOCELLULAR CARCINOMA

Nutritional decline

105
Q

Treatment for alcohol abuse - liver disease

A

ABSTINENCE

Vitamins
Nutrition
Endoscopic
Pharmacological - beta blockers, lactulose, rifamixin

Radiological - TIPPS

Surgical - transplant (last line)

106
Q

Oestrogen levels are…in alcohol drinkers

A

INCREASED

Important in post-menopausal women

107
Q

Brief intervention

A

Identification and Brief Advice

feedback on the person’s alcohol use and any related harm
 clarification as to what constitutes low-risk consumption
 information on the harms associated with risky alcohol use
 benefits of reducing intake
 motivational enhancement to support change
 analysis of high-risk situations for drinking
 coping strategies and the development of a personal plan to reduce consumption
—

Alcohol Support Services

assessment and engagement
 care planning and case management
 withdrawal management
 addressing physical and psychiatric co-morbidity
 psychosocial interventions
 pharmacotherapy for relapse prevention
 recovery, aftercare & reintegration

108
Q

Government role in reducing impact of alcoholism

A

Lowered drink drive limit

Increased taxation

Minimum unit pricing

Health warnings on packaging.

109
Q

Management of withdrawal

A

Symptom trigger withdrawal therapy

Regular assessment of patient - signs and symptoms

Scored at predefined times

Decide amount of benzodiazepine to give patient

110
Q

Foetal alcohol syndrome - facial features

A 
> Epicanthal folds
> Flat nasal bridge
> Small palpebral fissures
> Railroad track ears
> Upturned nose
> Smooth philtre
> Thin upper lip
111
Q

Types of “cost” due to alcohol

A

Direct - borne by government, health/socail care, police, justice, unemployment, welfare

Indirect - borne by society; losses in productivity, premature death

Intangible - pain, suffering, loss of income

112
Q

Binge drinking

Men & women

A

Men - 8 units in one sitting

Women - 6 units in one sitting

113
Q

The extent to which alcohol is available is strongly associated with…

A

alcohol consumption and alcohol related harm

Higher densities of off-sales outlet largely found in most deprived areas of Scotland.

114
Q

How much is in a unit?

A

10mls of pure alcohol (8g)

115
Q

Aspiration pneumonia typically occurs in

A

Superior segment of the right lower lobe.

116
Q

Ligamentum teres formed from which embryological structure?

A

Umbilical vein

117
Q

What may be used to assess perfusion in a patient with a severe GI bleed?

A

Lactate

118
Q

Liver enzyme AST

A

Aspartate aminotransferase

119
Q

Facial flushing and general feeling of unwell is caused by

A

Aldehyde

120
Q

Dupuytren’s contracture caused by?

A

Scarring of palmar fascia

121
Q

Severe hepatitis is associated with?

A

Hepatorenal syndrome

122
Q

Useful screening tool for alcohol dependence disorder?

A

AUDIT

123
Q

Alcoholic liver disease presenting with Upper GI bleed. What gives most useful info about liver synthetic function

A

Prothrombin time

124
Q

Portal hypertension is most associated with…

A

splenomegaly

125
Q

Fibrosis/cirrhosis of the liver is mediated by which type of cell?

A

Interstitial cells of Ito

126
Q

Which microscopic feature is not present within a portal tract?

A

Hepatocyte

127
Q

Alcohol can increase/decrease HDL?

A

Increase blood HDL levels

128
Q

Alcoholic hepatitis - jaundice caused by

A

CONJUGATED bilirubin

129
Q

Normal metabolic pathway the substance from which bilirubin is formed is…

A

Biliverdin

130
Q

Which biochemical findings is commonly seen in patients with established alcoholic liver disease (ALD) (cirrhosis)?

A

Hyperbilirubinaemia

131
Q

Alcohol causes a diuresis because of

A

Decreased ADH levels

132
Q

Microscopically, hepatocytes are bordered by

A

The space of Disse

133
Q

Which clotting factor is NOT made in the liver

A

VIII

134
Q

Death certification part 2 refers to

A

Conditions contributing to but not directly responsible for death

135
Q

Effects of domperidone on alcohol absorption?

A

Leads to faster rate of absorption

136
Q

Normal LFTs, normal GGT, AST and ALT with HIGH Alk phos - what should be considered?

A

Bone disease

137
Q

Treatments intended to manage ascites in cirrhosis aim to reduce what levels?

A

Sodium levels

Sodium restriction

138
Q

Diabetic ketoacidosis

A

> No available energy source

> Mobilise free fatty acids to form ketone bodies from which energy can be produced.

> Ketone body - acetoacetate

> No insulin - sugar is there, just not utilised.

High sugar levels, but high ketone bodies.
Smells like acetone

CLASP MB2 (1 decks)

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