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104: Theme 2 > Alcohol Symposium > Flashcards

Alcohol Symposium Flashcards

1
Q

What is the importance of solubility of alcohol?

A
  • it is water-soluble
  • those with a higher BMI (fat) will have a higher blood alcohol levels
  • hence why females usually have higher blood alcohol than men?
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2
Q

How is alcohol metabolised?

A

Ethanol –> Acetalhdye –> Acetate

  • Alcohol dehydrogenase major enzyme pathway way for both reactions
  • P4502E1 (at higher levels of alcohol) and Catalase can convert Ethanol to Acetaldehyde
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3
Q

What is a common alcohol dehydrogenase polymorphisms?

A
  • individuals of Asian descent who have B2 ADH isoform, metabolise ethanol 20% faster than northern Europeans who posses the B1 ADH polymorphism
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4
Q

What is the effect of alcohol on the redox state?

A
  • Increases lactate: pyruvate ratio
  • Increase beta-hydroxybutyrate: acetoacetate ratio
  • this reduces the conversion of NAD to NADH
  • inhibition of: glycolysis, citric acid cycle, fatty acid oxidation. gluconeogenesis
  • all resulting in hypoglycaemia
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5
Q

What is the effect of alcohol on lipid levels?

A
  • stimulates fatty acid synthesis: these are then esterified and with glycerol and stored as triglycerides

Oxidant stress

  • lipid peroxidation which is associated with acute tissue damage and fibrosis
  • free radicals attack cellular and mitochondrial DNA causing deletions and mutations
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6
Q

Describe the metabolism of Methanol

What is the resultant impact?

A
  • metabolised using alcohol dehydrogenase to give Formic acid
  • Formic acid converted to CO2 and H2O in the presence of Folate
  • if there is a folate deficiency or excess Formic acid this can cause blindness
  • dialysis may be needed to remove the methanol from the bloodstream
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7
Q

Explain how Ethylene glycol (antifreeze) is metabolised

What is its resultant impact?

A
  • Oxalic acid binds to calcium which deposits in renal tubules –> acute renal failure
  • Glycolic acid causes a metabolic acidosis: requires IV NaHCO3
  • can use ethanol and fomepizole as ca competitive inhibitor of ethylene glycol
  • may need dialysis
  • treat with calcium and thiamine and pyridoxine
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8
Q

How much is 1 unit of alcohol?

A

= 10mL or 8g of pure alcohol

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9
Q

What is the effect of ethanol on individuals?

A
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10
Q

What is alcohol ketoacidosis?

A
  • Metabolic acidosis with an increased anion gap.
  • Typically chronic alcoholics who binge with little nutrition intake.

Caused by:

  • Extracellular volume depletion
  • Glycogen depletion
  • Increased NADH/NAD ratio
  • Insulin suppressed
  • Lipolysis and ketones increased (beta-hydroxybutyrate)
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11
Q

What is the treatment of alcoholic ketoacidosis?

A
  • IV glucose
  • IV fluids to overcome dehydration
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12
Q

What are the endocrine effects of alcohol?

A
  • Decreased testerone- testicular atrophy
  • Pseudo Cushing
  • Metabolic syndrome and Dyslipidemia
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13
Q

What are nutritional issues associated with alcohol

A
  • Low calcium: linked to diet, decreased vitamin D
  • Low phosphate: linked to diet, increased PTH
  • Low Mg, K: linked to diet, urinary loss, hyperaldosteronism
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14
Q

What are typical Liver function tests?

A
  • Gamma Glutamyl Transferase (GGT) increased by liver enzyme induction
  • Transaminases (ALT and AST) increased by hepatocellular damage
  • Globulin increased in cirrhosis
  • Bilirubin & INR increased and albumin decreased by liver failure and escape into the peritoneal cavity (ascites)
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15
Q

What are other relevant blood tests that may be used when alcohol is involved?

A
  • alcohol causes Macrocytosis – seen in raised MCV in a full blood count
  • Raised serum ferritin concentration
  • Hyperuricaemia: high purine content in alcoholic drinks, competition with ketone bodies and lactate for excretion
  • Hypertriglyceridaemia
  • Increased carbohydrate-deficient transferrin ( have they actually stopped drinking, this would be high days after a binge)
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16
Q

How does alcohol cause hypertension?

A
  • impairment of the baroreceptors
  • increase of sympathetic activity
  • stimulation of the renin-angiotensin-aldosterone system
  • an increase in plasma cortisol
  • an increase of intracellular calcium with subsequent increase in vascular reactivity
  • endothelial e.g. inhibition of endothelium-dependent nitric oxide production
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17
Q

What is the cause of Thiamine deficiency?

A
  • Ethanol interference with GI absorption
  • Hepatic dysfunction, which hinders storage and activation of thiamine
  • Malnourishment
18
Q

What three enzymes is thiamine an important co-factor for?

A
  • Pyruvate dehydrogenase in glycolysis: leads to a build-up of pyruvate and depleted production of Acetyl-CoA
  • alpha- Ketoglutarate dehydrogenase in the TCA: leads to accumulation of GABA and glutamate
  • Transketolase enzymes in the Pentose Phosphate pathway: important for the formation of amino ribose-5-phosphate –> nucleic acids, complex sugars and coenzymes
19
Q

What are the zones of the liver?

How are they organised?

A
  • this is the functional classification of sections of the liver that pertain to its oxygen supply
  • Zone 1: Peritoneal, near the portal tract- high oxygen
  • Zone 2: Transitional
  • Zone 3: Centrilobular- site of drug and xenobiotic metabolism

most susceptible to

  • hypoxia
  • to detoxification injury
  • passive congestion in heart failure
20
Q

What is the need for a liver biopsy?

A
  • To make a diagnosis
  • Stage/grade the disease
  • To monitor treatment
  • To inform prognosis
21
Q

What key things are monitored/ looked for in a liver biopsy?

A
  • Microvesicular fatty change
  • Extend of fibrosis
  • Amount of MD bodies
  • Intrahepatic cholestasis
22
Q

What are the three main consequences of alcoholic liver disease?

A
  • Steatosis: macrovesicular and microvesicular
  • Steatohepatitis: ballooning of hepatocytes, inflammation (puts of neutrophils), necrosis of hepatocytes, Mallory Denk bodies
  • Fibrosis/ cirrhosis (irreversible): first seen in Zone 3 in the perivenular area then speeds to more oxygenated Zone 1
23
Q

What are Mallory Denk bodies?

A
  • red structures that are cytokeratin scaffolding of the hepatocytes destroyed by the inflammatory process
  • not specific to alcoholic liver disease, but often presents itself and adds to confirmation of the diagnosis
24
Q

What are the consequences of long-standing cirrhosis?

A
  • likely hood of getting Hepatocellular carcinoma increases

Portal hypertension:

  • collaterals found largely in the oesophagus: oesophageal
  • varices rupture is life-threatening, the umbilical vein: seen as caput medusa
25
Q

What are the symptoms of alcohol withdrawal?

A
  • Tremor/shaking
  • Sweating
  • Tachycardia
  • Nausea
  • Agitation
  • Siezures
  • Visual hallucinations
26
Q

What are CAGE questions?

A
  • Cut down alcohol, have you ever thought to do so
  • Annoyed of others criticism of your drinking
  • Guilty about your drinking habits
  • Eye opener, drink in the morning to get yourself going

Yes to two of these needs further investigation for potential alcohol dependency

  • use the AUDIT questionnaire to do so
27
Q

What is treatment/ management of alcohol withdrawal?

what are the potential hazards of these treatments?

A
  • CHLORDIAZEPOXIDE – used at BSUH
  • DIAZEPAM

Hazards

  • Severe liver disease - precipitation of hepatic encephalopathy
  • Respiratory depression
  • Reluctance to prescribe more
  • Concomitant alcohol consumption ( cant be taken the same time as alcohol)
28
Q

What is the classic triad of Wernicke’s Encephalopathy?

A
  • Confusion
  • Eye Signs- ophthalmoplegia (inhibited eye movement) and nystagmus (rapid eye movements)
  • Ataxia

Only seen in 10% of cases

29
Q

What are three indicators/ results of Korsakoff’s psychosis?

A
  • Permanent brain damage
  • Severe short term memory loss
  • Confabulation
30
Q

What treatment is given to Wernicke-Korsakoff syndrome?

A
  • PABRINEX: -Thiamine 250mg + others
  • Give IV for 2-5 days depending on the response, do this before giving dextrose or feeding them
  • Rarely causes anaphylaxis
  • Continue oral thiamine and other vitamins after initial treatment
  • check glucose levels hypoglycaemia trumps low thiamine, but you usually give them together.
31
Q

What is the relationship between alcohol and violence?

A
  • 1/3 of domestic violence is alcohol-related
  • 1/5 of calls to childlike are related to parents alcohol consumption
  • RTA- 1in 7 of those killed on UK roads
  • 53% of violent crime in England (2014)
32
Q

What is Sensible on Strength?

A
  • local action in Brighton that reduces maximum strength alcohol at off-licence stores
  • increase training to staff with dealing with anti-social behaviour
  • it seemed to have worked
33
Q

What is the Cumulative Impact Zone initiative in Brighton and Hove?

A
  • if your starting a business that may be selling alcohol in an area that already does so, you might not be allowed to, in order to reduce the impact in specific areas
34
Q

What are the two distinctions of drinking cultures?

A
  • Wet: normalized
  • Dry: don’t usually drinking, when they do drink it can be in excess, is a commodity that people do need to be protected from
35
Q

What are the 3 main motives for drinking alcohol?

A

Enhancement: to feel better, to do things otherwise impossible

Social: to be sociable, to celebrate parties

Coping: because it makes you forget your problems

Conformity: because others do so, to fit in

36
Q

How can we change how people drink using different motives for drinking?

A
  • Using the IMB model
  • give them information, this will inform and potentially change their motivation
  • and this will also change the behavioural skills to change their drinking behaviour
37
Q

How is community alcohol detox managed?

A
  • Benzodiazepines (chlordiazepoxide)
  • Vitamins tablets – Vitamin B complex / Thiamine / Vit BPC
  • Pabrinex IM
  • Relapse prevention meds – Acamprosate
  • 2 week CBT based group
  • Further weekly groups
  • 1:1 care coordination
  • AA / NA / CA groups
38
Q

What are mild/ moderate signs of alcohol dependence?

A

usually occurs within 6-8 hours after a fall in blood alcohol level

  • Insomnia and fatigue
  • Tremors
  • Mild anxiety/restlessness/agitation
  • N&V
  • Headache
  • Excessive sweating
  • Palpitations
  • Craving for alcohol
39
Q

What is the progression of alcohol withdrawal in dependent individuals?

A
  • Signs of physical dependence within 6-8 hours
  • Alcoholic Hallucinations: 12-24 hours after reduced alcohol consumption (crawling insects, snakes and rats)
  • Alcohol withdrawal seizures: 6-48 hours (lasting 2-3 days), 80% occur within 48 hours, largely in patients with long history of chronic alcoholism
  • Delirium Tremens: 48-96 hours after reduced alcohol consumption
40
Q

What occurs in Delirium Tremens?

A
  • Hallucinations
  • Heightened anxiety
  • Severe agitation
  • Delusions
  • Tachycardia
  • Hypotension
  • Hypothermia
  • Tachypnoea
  • Altered electrolytes – hypokalaemia / Hypomagnesemia
41
Q

How is a non-medical detox managed?

A
  • Planned reduction
  • Drink diaries
  • Stabilisation
  • Gradually reduce
  • Consider the form of alcohol, strength and size of the vessel
  • which drinks should you not have, plan day based on that

104: Theme 2 (7 decks)

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