Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

104 Theme 2 > alcohol symposium > Flashcards

alcohol symposium Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does alcohol link to young people

A 
inc with age
parents don't discourage
recent drug use
drinkers at home
smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the impact of alcohol on health

A

early death
disease and injury
social, economic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

influences on alcohol consumption

A 
individual factors
family
culture and community
socioeconomics
country/laws
taxes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is methanol metabolised

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ethylene glycol metabolism

A

antifreeze poisoning
ethylene glycol
uses thiamine and pyridoxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does a unit mean

A

10ml or 8g pure alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

endocrine effect of alcohol

A 
Decreased testosterone (testicular atrophy)
Pseudo Cushings
Metabolic Syndrome and Dyslipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

thiamine deficiency via alcohol

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

effect of thiamine deficiency

A

cofactor in glycolysis and TCA

also in PPP

26
Q

what is the structure of the liver

A

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
Q

why is the liver biopsied

A

To make a diagnosis
Stage / grade the disease
To monitor treatment
To inform prognosis

percutaneous or venous approach

28
Q

what does a liver biopsy find

A

Microvesicular fatty change Extend of fibrosis Amount of MD bodies Intrahepatic cholestasis

29
Q

what are alcoholic liver diseases

A

Steatosis (fatty liver) macrovesicular microvesicular

Steatohepatitis ballooning of hepatocytes inflammation via neutrophils necrosis of hepatocytes Mallory Denk bodies

Fibrosis / cirrhosis

30
Q

steatosis - macrovesicular

A

single large fat droplets to osmicated fat (black droplets in varying size)
fat not seen under microscope, stained specially

31
Q

Steatosis - microvesicular

A

hepatocytes distended by large number of fat droplets surrounding central nuclei, also can have enlarged mt

32
Q

Steatohepatitis - ballooning

A

lack of cytoplasmic keratins (bigger and cytoplasm fragments in early stage of necrosis), plus clumped aggregates

33
Q

Steatohepatitis- inflammation

A

neutrophils (small purple dots surrounding hepatocytes)

heal by fibrosis and scarring

34
Q

Steatohepatitis - Mallory denk bd

A

dead hepatocytes clump together

35
Q

Fibrosis / cirrhosis

A

permanent long term and irreversible

little oxygen, lots of metabolism, red collagen fibres

36
Q

Fibrosis / cirrhosis mechanisms

A

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
Q

what is the end result of fibrosis

A

Macronodular cirrhosis/portal hypertension
nodules surrounded by thick fibrosis to inc PV pressure
can also lead to fibrosis

38
Q

portal hypertension consequences

A

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
Q

what are the types of drinking cultures

A

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
Q

why do people drink

A 
People drink alcohol for various reasons
e.g., Drinking Motives Questionnaire measures 
enhancement 
social
conformity
coping
41
Q

why do people not drink

A

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
Q

ca it be changed how people drink

A

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
Q

how does awareness effect drinking

A

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
Q

using unit-marked glasses affects IMB components

A

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
Q

population interventions: Dry January

A 
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
Q

Alcohol withdrawal

A

Physiological dependence
The ‘need’ to drink to avoid unpleasant symptoms - ‘Relief Drinking’
Delirium Tremens

47
Q

Symptoms of withdrawal

A 
Tremor/shaking
Sweating
Tachycardia
Nausea
Agitation
Seizures 
Visual hallucinations
48
Q

types of alcohol withdrawal

A

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
Q

what should be considered about alcohol withdrawal

A

Importance of alcohol history in all inpatients
High index of suspicion
Often occurs 2-3 days after admission
Look for corroborative evidence

50
Q

how is alcohol withdrawal managed

A

diazepam

chlordiazepoxide (RSCH and PRH)

51
Q

Alcohol Withdrawal Potential Hazards

A

Severe liver disease - precipitation of hepatic encephalopathy
Respiratory depression
Reluctance to prescribe more
Concomitant alcohol consumption

52
Q

What is delirium

A

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
Q

Other Causes of Delirium

A 
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
Q

what is WKS

A 
WERNICKE-KORSAKOFF SYNDROME
Wernicke’s Encephalopathy
Korsakoff’s Psychosis
THIAMINE
treated with oral or IV thiamine (check glucose first)
55
Q

Dietary sources of thiamine

A 
Wheat
Yeast
Nuts
Oatmeal
Potatoes
Pork
Marmite
intake 1mg, body stores 30mg
deficiency after a month of none
56
Q

use of thiamine

A 
Co-enzyme:
Glucose and lipid metabolism
Production of amino acids
Production of glucose derived
neurotransmitters
57
Q

THIAMINE: causes of deficiency

A

Alcoholism commonest cause
(inadequate intake, inhibition of active intestinal absorption by alcohol and malnutrition)
Chronic vomiting e.g. hyperemesis gravidarum
Famine

58
Q

signs of wernicke’s encephalopathy

A

Confusion
Eye Signs - opthalmoplegia and nystagmus
Ataxia
10% cases, under diagnosed

59
Q

results from wernicke’s encephalopathy

A

Brain damage:
Multiple small haemorrhages especially in upper brainstem, hypothalamus and thalamus, mamillary bodies
20% mortality if untreated

60
Q

what is Korsakoff’s Psychosis

A

Permanent brain damage
Severe short term memory loss
Confabulation

104 Theme 2 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions