alcohol symposium Flashcards

(60 cards)

1
Q

how many adults drink and don’t drink

A

80% drank in the last year (48% in the last week) and 20% didn’t
proportion drinking inc with age

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2
Q

what is the CMO guidance for alcohol units

A

low risk <14 over >3 days
inc risk men 14-50, women 14-35
high risk men >50, women >35, risk of alcohol related health problems

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3
Q

how does alcohol consumption link to income

A

non drinkers inc as household income dec

proportion of adults drinking >14u dec with income

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4
Q

how does alcohol link to young people

A
inc with age
parents don't discourage
recent drug use
drinkers at home
smoking
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5
Q

what is the impact of alcohol on health

A

early death
disease and injury
social, economic

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6
Q

influences on alcohol consumption

A
individual factors
family
culture and community
socioeconomics
country/laws
taxes
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7
Q

Policies to limit consumption and reduce harm

A

taxation (affordability, raise revenue)
regulation and legislation (promotion, price, driving)
eg minimum unit pricing, sensible on strength, cumulative impact zone

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8
Q

how is ethanol metabolised

A

water soluble, distribution to lean body mass only
some endogenous production
10% lost via breath/urine, rest metabolised (liver, some brain, pancreas and stomach)
ethanol to (via alcohol DH) acetaldehyde to (via Aldehyde DH) acetate

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9
Q

Alcohol dehydrogenase polymorphisms

A

Several isoforms of this enzyme present with variable activity depending on genetic makeup, gender and other factors.
Eg individuals of Asian descent who have the B2 ADH isoform metabolise ethanol 20% faster than northern Europeans who posses the B1 ADH.

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10
Q

what is alcohol dehydrogenase’s effect on redox state

A
reduce NAD+ to NADH
Increases: 
lactate:pyruvate ratio
beta-hydroxybutyrate:acetoacetate ratio 
Decreases:
Glycolysis
Citric acid cycle – ketogenesis
Fatty acid oxidation
Gluconeogenesis
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11
Q

toxic and metabolic effects of alcohol

A

Oxidant stress
Lipid peroxidation, associated with both acute tissue damage & fibrosis
Free radicals attack cellular & mitochondrial DNA causing deletions & mutations

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12
Q

how is methanol metabolised

A

methanol to (alcohol DH) formaldehyde to (aldehyde DH) formic acid to (folate) CO2 and H20

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13
Q

ethylene glycol metabolism

A

antifreeze poisoning
ethylene glycol
uses thiamine and pyridoxine

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14
Q

what does a unit mean

A

10ml or 8g pure alcohol

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15
Q

how does ethanol link to driving

A

legal limit in UK
blood ethanol <80mg/dL
<2-3 units in women and <3-4 in men
measured via breath

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16
Q

blood ethanol and symptoms

A

sporadic -euphoria, gregariousness, incoordination to slurred speech, drowsiness, lethargy, vomiting to coma and respiratory depression
chronic - less effect, euphoria and mild emotional/motor changes later to drowsiness, have to drink a lot more to become lethargic, coma

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17
Q

what is alcohol ketoacidosis

A

metabolic acidosis (inc anion gap)
binge with little nutritional intake
Glycogen depletion/inhibited gluconeogenesis
Lipolysis and ketones increased, Insulin suppressed
Extracellular volume depletion/dehydration/stress - increase counter regulatory hormones further supressing insulin

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18
Q

how does alcohol cause hypoglycaemia

A

decreased intake of glucose (CHO)
depletion of glycogen
blockade of gluconeogenesis
CNS damage as may be thiamine deficiency

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19
Q

endocrine effect of alcohol

A
Decreased testosterone (testicular atrophy)
Pseudo Cushings
Metabolic Syndrome and Dyslipidaemia
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20
Q

nutrition issues with alcohol

A
Low calcium (diet, decreased vitamin D)
Low phosphate (diet, increased PTH)
Low Mg, K (diet, urinary loss, hyperaldosteronism)
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21
Q

Typical Liver Function alcohol effects

A

Gamma Glutamyl Transferase (GGT) increased by enzyme
Transaminases (ALT and AST) increased by hepatocellular damage
Globulin increased in cirrhosis
Bilirubin & INR increased and albumin decreased by liver failure

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22
Q

thiamine deficiency via alcohol

A

Ethanol interferes with GI absorption
Hepatic dysfunction, which hinders storage and activation
Malnourishment

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23
Q

other relevant blood tests for alcohol effects

A

Macrocytosis – raised MCV in a full blood count
Raised serum ferritin concentration
Hyperuricaemia
Hypertriglyceridaemia
Increased carbohydrate-deficient transferrin or CDT

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24
Q

how does alcohol causes hypertension

A

impairment of the baroreceptors
increase of sympathetic activity
stimulation of RAAS
increase in plasma cortisol
increase of intracellular calcium with subsequent increase in vascular reactivity
endothelial e.g. inhibition of endothelium-dependent NO production

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25
effect of thiamine deficiency
cofactor in glycolysis and TCA | also in PPP
26
what is the structure of the liver
hepatic lobules with portal triads (portal vein, hepatic arteriole and bile duct) central vein, sinusoids flow mixed blood from triad giving hepatocytes time to interact with blood as it flows to central vein flows via zones 1, 2, 3 (o2 dec, met activity inc) most vulnerable to injury
27
why is the liver biopsied
To make a diagnosis Stage / grade the disease To monitor treatment To inform prognosis percutaneous or venous approach
28
what does a liver biopsy find
Microvesicular fatty change Extend of fibrosis Amount of MD bodies Intrahepatic cholestasis
29
what are alcoholic liver diseases
Steatosis (fatty liver) macrovesicular microvesicular Steatohepatitis ballooning of hepatocytes inflammation via neutrophils necrosis of hepatocytes Mallory Denk bodies Fibrosis / cirrhosis
30
steatosis - macrovesicular
single large fat droplets to osmicated fat (black droplets in varying size) fat not seen under microscope, stained specially
31
Steatosis - microvesicular
hepatocytes distended by large number of fat droplets surrounding central nuclei, also can have enlarged mt
32
Steatohepatitis - ballooning
lack of cytoplasmic keratins (bigger and cytoplasm fragments in early stage of necrosis), plus clumped aggregates
33
Steatohepatitis- inflammation
neutrophils (small purple dots surrounding hepatocytes) | heal by fibrosis and scarring
34
Steatohepatitis - Mallory denk bd
dead hepatocytes clump together
35
Fibrosis / cirrhosis
permanent long term and irreversible | little oxygen, lots of metabolism, red collagen fibres
36
Fibrosis / cirrhosis mechanisms
inflammation and necrosis cause increase in cytokines and growth factors (TGF-beta, MCP-1) that activate fibroblasts/myofibroblasts to deposit collagen (Disse’s space) centrilobular fibrosis - reversible septal fibrosis - increasingly irreversible
37
what is the end result of fibrosis
Macronodular cirrhosis/portal hypertension nodules surrounded by thick fibrosis to inc PV pressure can also lead to fibrosis
38
portal hypertension consequences
impaired intestinal function and malabsorption splenomegaly with anaemia and thrombocytopenia portal bypass circulations - haemorrhoids, caput medusae (paraumbilical veins engorged), oesophageal veins (varices) ``` vasodilatation and compensatory inc in CO toxic metabolites (NH3, fatty acids, biogenic amines) bypass the liver and may cause portosystemic (hepatic) encephalopathy ```
39
what are the types of drinking cultures
in “wet” drinking cultures, there is integration of alcohol into daily life as a consumer commodity like any other; in dry drinking cultures, alcohol is marginalized as an especially powerful and hazardous commodity
40
why do people drink
``` People drink alcohol for various reasons e.g., Drinking Motives Questionnaire measures enhancement social conformity coping ```
41
why do people not drink
short term - poisoning, accidents/injury, violence, antisocial behaviour long term - cirrhosis, cancers, stroke, premature death + suicide also hangovers, ALDH-2 deficiency, religion and culture
42
ca it be changed how people drink
efforts focus on motives for drinking and not drinking gain framed or loss framed eg IMB or psychosocial (need social context and factors eg health, fitting in, reputation and image)
43
how does awareness effect drinking
people tend to have poor knowledge and lack the requisite skills to stop so personalised feedback on drink pouring - improves knowledge - enhances behavioural skills - reduces alcohol intake
44
using unit-marked glasses affects IMB components
cluster-randomised-controlled trial and follow-up survey greater use of glasses resulted in - better knowledge of guidelines - better capacity to monitor intake - better attitudes toward using guidelines ... but no significant reductions in intake
45
population interventions: Dry January
``` Abstinence challenges allow people to - perform behavioural experiments - boost motivation - enhance behavioural skills Benefits of not drinking majority report better sleep, concentration, saving money + a minority report weight loss Enduring effects 40% drink less 6 months later (50% return to previous drinking) and greater sense of control over drinking ```
46
Alcohol withdrawal
Physiological dependence The ‘need’ to drink to avoid unpleasant symptoms - ‘Relief Drinking’ Delirium Tremens
47
Symptoms of withdrawal
``` Tremor/shaking Sweating Tachycardia Nausea Agitation Seizures Visual hallucinations ```
48
types of alcohol withdrawal
Planned: in community or in hospital/detox facility Unplanned: known alcohol problems + another medical problem or alcohol history not known in patient presenting with a separate problem
49
what should be considered about alcohol withdrawal
Importance of alcohol history in all inpatients High index of suspicion Often occurs 2-3 days after admission Look for corroborative evidence
50
how is alcohol withdrawal managed
diazepam | chlordiazepoxide (RSCH and PRH)
51
Alcohol Withdrawal Potential Hazards
Severe liver disease - precipitation of hepatic encephalopathy Respiratory depression Reluctance to prescribe more Concomitant alcohol consumption
52
What is delirium
Disturbance of consciousness Change in cognition or a perceptual disturbance (hallucination) Tendency to fluctuate Behaviour overactive or underactive Other features: disorganized thinking, poor memory, delusions and mood lability
53
Other Causes of Delirium
``` Any infection Drug side effect Hypoxia Drug overdose Alcohol intoxication Wernicke encephalopathy Hypoglycaemia Meningitis / encephalitis Psychiatric illness Head injury Constipation (elderly) Hepatic encephalopathy Etc…etc…. ```
54
what is WKS
``` WERNICKE-KORSAKOFF SYNDROME Wernicke’s Encephalopathy Korsakoff’s Psychosis THIAMINE treated with oral or IV thiamine (check glucose first) ```
55
Dietary sources of thiamine
``` Wheat Yeast Nuts Oatmeal Potatoes Pork Marmite intake 1mg, body stores 30mg deficiency after a month of none ```
56
use of thiamine
``` Co-enzyme: Glucose and lipid metabolism Production of amino acids Production of glucose derived neurotransmitters ```
57
THIAMINE: causes of deficiency
Alcoholism commonest cause (inadequate intake, inhibition of active intestinal absorption by alcohol and malnutrition) Chronic vomiting e.g. hyperemesis gravidarum Famine
58
signs of wernicke's encephalopathy
Confusion Eye Signs - opthalmoplegia and nystagmus Ataxia 10% cases, under diagnosed
59
results from wernicke's encephalopathy
Brain damage: Multiple small haemorrhages especially in upper brainstem, hypothalamus and thalamus, mamillary bodies 20% mortality if untreated
60
what is Korsakoff’s Psychosis
Permanent brain damage Severe short term memory loss Confabulation