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CLASP- Alcohol Week > Alcohol > Flashcards

Alcohol Flashcards

1
Q

Methanol is toxic and not for consumption but where can it be found?

A

It is present in anti-freeze, solvents and some fuels. It may also be present in contaminated home brews.

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2
Q

What is methanol metabolised to form?

A

Formaldehyde and formic acid both which are toxic to the body.

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3
Q

What properties do both ethanol and methanol have?

A

Depressant (you’ll act drunk with both)

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4
Q

What are the potential harmful things methanol can do to the body?

A

Acidosis, blindness (destruction of the optic nerve) and renal failure

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5
Q

What is used to treat methanol poisoning? How does it work?

A

Ethanol- it is a competitive inhibitor so stops methanol being metabolised as they both are metabolised by alcohol dehydrogenase

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6
Q

Why shouldn’t you drink on an empty stomach?

A

There is limited alcohol absorption in the stomach so the longer food stays in the stomach the slower the alcohol will be absorbed. A full stomach slows gastric emptying and therefore alcohol absorption.

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7
Q

Name two drugs that increase gastric emptying and therefore alcohol absorption?

A

Antihistamines and metoclopramide

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8
Q

Aerated drinks are absorbed faster or slower?

A

Faster

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9
Q

Why do women tend to have a lower alcohol tolerance?

A

Women usually have higher levels of subcutaneous fat and as alcohol is water soluble it can’t be absorbed here. Men have a bigger pool for solution. In general women also have lower levels of alcohol dehydrogenase.

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10
Q

Why can some ethnic groups not handle alcohol? What groups?

A

Certain groups have constitutionally lower levels of alcohol dehydrogenase or aldehyde dehydrogenase. Aborigines, inuits and japanese.

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11
Q

What happens to certain ethnic groups when they drink?

A

Flushing, itching and feeling warm.

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12
Q

Describe the drug antabuse

A

It inhibits aldehyde dehydrogenase which makes drinking unpleasant, this helps alcoholics stop drinking even if they crave the alcohol.

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13
Q

Does drinking regularly improve alcohol tolerance?

A

Yes- it is possible to up regulate alcohol dehydrogenase activity. In heavy drinking alternative pathways are also activated.

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14
Q

Why does alcohol make you need to pee more?

A

Usually you are consuming more fluid. Alcohol also inhibits ADH so there is reduced water reabsorption and therefore clearer urine.

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15
Q

Does drinking occasional volumes of alcohol have overall health benefits?

A

No

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16
Q

Where does 90% of alcohol metabolism occur? Where does the rest occur?

A

The liver

Small volume in pancreas and brain

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17
Q

Describe simple alcohol metabolism

A

Ethanol converted to acetaldehyde by alcohol dehydrogenase. Acetaldehyde converted to acetate by aldehyde dehydrogenase.

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18
Q

Alcohol is generally removed from the blood at rate of ________ which is equivalent to ______

A

15mg/100ml/hr

1 UNIT PER HOUR

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19
Q

When does alcohol concentration usually peak?

A

60 minutes after consumption and it then decreases linearly.

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20
Q

The MEOS pathway is triggered in heavy drinking and results in excess hydrogen ions which have to be disposed of, this inhibits/ impairs three things which are?

A

Hepatic gluconeogenesis (you become hypoglycaemic)
Citric acid cycle
Fatty acid oxidation

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21
Q

Why do you become hungry when you drink? Who is this particularly relevant in?

A

Every stores in the liver can’t be used so blood sugar falls. Especially relevant in diabetics.

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22
Q

Explain alcoholic ketoacidosis?

A

Happens when you run out of glucose to metabolise (usually only occurs in malnourished states). As the body can’t use glucose it starts to burn fat and the by product is ketone bodies. If there is no insulin ketone bodies will begin to build in the blood stream.

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23
Q

Why are you dehydrated when hungover?

A

Inhibition of ADH means you haven’t been able to reabsorb as much water so have lost lots in urine

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24
Q

Why do you have sensation of a heavy heart beat when hungover?

A

Alcohol has negative inotropic effects (decrease heart contractility)

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25
Q

What is holiday heart syndrome?

A

It is associated with binge drinking, basically you get a SVT in an otherwise healthy heart with spontaneous resolution (the mechanism is unclear)

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26
Q

What can cause headaches apart from dehydration when hungover?

A

Congeners in alcohol- serotonin is produced from sulphites, tannins and phenols all present in red wine

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27
Q

There is no evidence for hangover cures but what may work?

A

Anything that speeds up the metabolism.

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28
Q

After how many units of alcohol do you begin to see fatty liver changes?

A

6 units

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29
Q

Explain what you might look for in the hands if you suspected alcoholism/ liver disease during general examination?

A

Palmar erythema- redness of palms usually related to underlying liver cirrhosis
Dupuytrens contracture- fingers permanently bent, this is not just caused by alcoholism and not all alcoholics have it

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30
Q

What condition in the lungs may alcoholics get?

A

Aspiration pneumonia- drinking too much suppresses the immune system and relaxes smooth muscle and there can then be migration of microbes due to vomiting or the gag reflex induced by drinking.

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31
Q

What heart condition can be caused by alcoholism?

A

Dilated cardiomyopathy

This is rare compared to it being caused by a genetic defect

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32
Q

What is dilated cardiomyopathy?

A

Heart is much bigger than normal but still weighs the same so is floppy and unable to pump blood effectively. Clinical features are generally symptoms of heart failure.

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33
Q

Why do you get a fatty liver when you drink?

A

Mitochondrial oxidation of fatty acids is reduced by alcohol. This causes decreased transport of fat out of hepatocytes due to intracellular tubular impairment

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34
Q

Define cirrhosis of the liver

A

The end stage of many liver diseases defined as a diffuse process characterised by fibrosis and conversion of the normal liver architecture into abnormal liver nodules.

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35
Q

Why does alcohol cause gastritis?

A

Alcohol irritates the gastric mucosa

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36
Q

What is a mallory weiss tear?

A

Repeated vomiting or retching from drinking alcohol causes a mucosal tear which will present as small amount of blood in the vomit. Most are small tears but if large you can get haemorrhage or oesophageal rupture.

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37
Q

Why do you get reflux oesophagitis and Barrett’s if you drink a lot of alcohol?

A

Alcohol is a smooth muscle relaxant meaning that the LOS is relaxed allowing reflux of gastric contents into the oesophagus. Repeated assault can result in metaplasia and Barretts.

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38
Q

Define Barretts oesophagus

A

Metaplastic change in the epithelium in the oesophagus from squamous epithelium to intestinal columnar epithelium.

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39
Q

Describe subdural haemotoma

A

This is related to repetitive trauma and alcohol related coagulopathies, blood collects between skull and brain.

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40
Q

What is the common mechanism of cirrhosis?

A

Hepatic stellate cells found in the space of Disse are activated and transformed into myofibroblasts under the influence of cytokines. These activated cells synthesis collagen leading to fibrosis.

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41
Q

Explain what portal hypertension is and why it relates to alcoholism

A

Note: portal hypertension can happen in other conditions.

Normal portal vein pressure is only 5-8mmHg. Alcoholism will damage the liver (fatty liver-> cirrhosis) and distortion of the liver architecture will result in increased pressure. As pressure rises the blood takes other paths with less resistance (porto-systemic anastamoses) and these anastamoses become engorged and dilated.

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42
Q

Describe symptoms of decompensated cirrhosis?

A

Jaundice, ascites, encephalopathy.

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43
Q

Why are oesophageal varices a problem in alcoholics?

A

As alcohol damages the liver, you get portal hypertension so blood collects in porto systemic anastomoses, one of these is in the oesophagus. As these veins are superficial they are prone to rupture and this can cause massive haemorrhaging. Ruptured oesophageal varices is usually catastrophic and is a medical emergency.

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44
Q

What is the most common primary malignancy of the liver?

A

Hepatocellular carcinoma

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45
Q

What is the most important risk factor in development of hepatocellular carcinoma?

A

Cirrhosis of any cause (can be alcoholics could be hepatitis etc)

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46
Q

What is caput medusae? What is it a sign of?

A

Distended veins around the umbilicus. Sign of portal hypertension

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47
Q

Three sites of porto systemic anastomoses?

A

Rectum, oesophagus and umbilicus

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48
Q

What are spider naevi? Why do you get them in liver disease?

A

Swollen blood vessels on skin surface. Happen due to excess oestrogen as the liver can’t break it down.

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49
Q

What is and why do you get gynaecomastia?

A

Swelling of breast tissue in men caused by oestrogen imbalance

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50
Q

What is and why do you get ascites?

A

Ascites is fluid within the peritoneal cavity due to Na and H2O retention, portal hypertension and low serum albumin. Abdominal swelling occurs and the presence of fluid is demonstrated by shifting dullness.

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51
Q

What is and why do you get hepatic encephalopathy?

A

In cirrhosis the blood bypasses the liver via collaterals and toxic metabolites pass directly to the brain, ammonia is the main cause.

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52
Q

Signs and symptoms of hepatic encephalopathy?

A

Patient may have disorder of personality, mood and intellect. May also be disorientated with slurred speech or be vomitting/ nauseous.

Signs include fetor hepaticus (sweet smelling breath), liver flap, constructional apraxia (can’t copy a drawing) and decreased mental function.

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53
Q

What is chronic pancreatitis a risk factor for?

A

Pancreatic cancer

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54
Q

The main cause of acute pancreatitis is ______ it can also be caused by ______ but the mechanism is not fully understood

A

gallstone blocking the ampulla of vater causing reflux of bile up the pancreatic duct
can be caused by excess alcohol also

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55
Q

2 signs that support severe necrotising pancreatitis?

A 
Periumbilical bruising (Cullens sign)
Flank bruising (Grey Turners sign)
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56
Q

8 complications of acute pancreatitis?

A

Systemic inflammatory response syndrome, multi organ dysfunction,
pancreatic fluid collections necrosis or abscess,
pleural effusions, pneumonia and ARDS
Metabolic complications
Jaundice
GI Bleeding
Acute kidney injury

57
Q

Management of acute pancreatitis?

A 
Initially need to rehydrate the patient
May need to remove gallstones
Pain relief
NG feeding
Anticoagulation with LMWH to prevent DVT as risk of portal vein thrombosis.
58
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas resulting in replacement of pancreas by scarred tissue and destruction of exocrine acini and islets

59
Q

2 main risk factors for chronic pancreatitis?

A

majority of cases in alcoholics but there is also an auto immune type

60
Q

How do those with chronic pancreatitis usually present?

A

Pain in the epigastrium often radiating through to the back
Pain may be episodic with short periods of severe pain or chronic and unremitting
Anorexia
Diabetes
Jaundice (fibrosed head obstructs the CBD)
Stearrhoea due to malabsorption

61
Q

Management and treatment of chronic pancreatitis?

A

In alcohol relate abstinence should be encouraged
In auto immune steroids are effective
Short term flare ups of pain can be treated with NSAIDS and an opiate eg tramadol
Chronic pain treated with tricyclic antidepressants eg amitriptyline and membrane stabalising agents
In those with severe or debilitating pain surgery may be an option
Creon needs to be given as an enzyme replacement to help with malabsorption issues.

62
Q

How many segments is the liver divided into? How many anatomical lobes is the liver divided into?

A

8 segments

4 anatomical lobes (these are visible on gross inspection- right, left, caudate and quadrate)

63
Q

In a restaurant today a standard glass of wine (175mls) is likely to contain approximately?

A

2 units of alcohol

64
Q

What is the alcohol guidelines for both men and women?

A

Don’t drink more than 14 units a week regularly

Have alcohol free days

65
Q

Treatments intended to manage ascites in cirrhosis aim to reduce?

A

Sodium levels

66
Q

What do portal tracts consist of?

A

Hepatic vein, hepatic artery, bile duct and lymphatic vessels.

67
Q

True or False? Alcohol is known to be associated with increased precipitation of uric acid

A

True

68
Q

What does ALT stand for?

A

Alanine aminotransferase

69
Q

The ligamentum teres within the falciform ligament is formed from which embryological structure?

A

Umbilical vein

70
Q

Where does aspiration pneumonia typically occur?

A

superior segment of the right lower lobe

71
Q

The legal age of drinking alcohol whilst at supervised at home is

A

5

72
Q

The liver enzyme AST is short for

A

Aspartate aminotransferase

73
Q

Jaundice as a result of alcoholic hepatitis is caused by an accumulation of

A

conjugated bilirubin

74
Q

Embryologically where is the liver derived from?

A

Foregut

75
Q

Microscopically hepatocytes are bordered by?

A

The space of disse

76
Q

What causes dupuytrens contracture?

A

scarring of the palmar fascia

77
Q

Define hazardous drinking

A

A pattern of consumption that increases the risk of harmful consequences for the user. It is not a diagnostic term. Drinking more than 14 units but less than 35 for females or less than 50 for men.

78
Q

Define Harmful drinking

A

A pattern of alcohol consumption that is causing mental or physical damage. Drinking more than 35 units for women or 50 units for men

79
Q

Define Alcohol dependence

A

A cluster of behavioural, cognitive and physiological factors that typically include a strong desire to drink alcohol and difficulties controlling its use.

80
Q

Name 4 complicated alcohol withdrawal symptoms

A

Seizures
Hallucinosis
Delirium Tremens (rapid onset of confusion)
Wernicke-Korsakoff Syndrome

81
Q

What drug can be used for medical assisted detoxification?

A

Chlorodiazepoxide

82
Q

What tends to increase after each alcohol withdrawal?

A

The severity of withdrawal symptoms

83
Q

Name 3 relapse prevention medications

A

Acamprosate
Naltrexone
Disulfiram

84
Q

Mechanism of acamprosate?

A

Acts on GABA and glutamate transmission correcting imbalance post withdrawal and reducing craving

85
Q

Mechanism of naltrexone?

A

Blocks opioid receptors reducing rewarding effect of alcohol

86
Q

Mechanism of disulfiram?

A

Causes unpleasant and dangerous reaction with alcohol acting a psychological deterrent

87
Q

Alcohol enhances ______ release producing rewarding effects

A

Dopamine

88
Q

At lower doses (<50mg/dl) alcohol is a ____1____ and activates arousal mechanisms in the _____2_____ but at higher doses this area is _____3_____ by alcohol

A

1) stimulant
2) brain stem reticular formation
3) depressed

89
Q

Alcohol is a ________ at GABAa receptors having a ________ effect on the CNS

A

positive allosteric modulator

depressive

90
Q

GABAa receptors are ____1_____ and when GABA binds to the GABAa receptor the channels opens and there is __2_____. As alcohol is a positive modulator at GABAa the chloride is increased so there is more hyper polarisation so more _____3______

A

1) chloride ion channels
2) hyperpolarisation
3) suppression of the CNS

91
Q

What is the drink drive limit in Scotland? How does this compare to the rest of the UK?

A 
Scotland = 0.05% 
RUK= 0.08%
92
Q

At what blood alcohol percentage will coma and death occur?

A

0.4%

93
Q

Name two drugs with cross tolerance with alcohol?

A

Benzodiazepines and anaesthetics

94
Q

How does alcohol react with NSAIDS?

A

increases risk of GI ulceration

95
Q

What are the direct, indirect and intangible costs of alcohol?

A

Direct- police and hospitals
Indirect- loss of productivity and working years
Intangible- peoples quality of life impacted by a persons drinking

96
Q

What fraction of alcohol is sold off trade and why?

A

3/4

this is probably due to price

97
Q

What accounts for most of the difference between drinking in Scotland vs England and Wales?

A

Spirits- particularly vodka

98
Q

In 2018 what was the average alcohol sold per adult per week?

A

19 units

99
Q

What are the three most effective strategies to decrease alcohol consumption?

A

Increase price, regulate marketing and decrease availability.

100
Q

Name and briefly describe 3 parliamentary acts to help target drinking in Scotland?

A

Licensing Act 2005- about protecting people by having more licensing boards etc
The Alcohol Act 2010: placed a ban on quantity discounts and put restrictions on alcohol display, promotions and advertising
Minimum Pricing: Introduced 1st May 2018, can’t sell a unit for less than 50p was designed to target off-trade sales as in 2017 47% of alcohol sold through off-trade was <50p per unit.

101
Q

How can alcohol cause seizures?

A

Seizures caused by alcohol withdrawal
Seizures can also be triggered by alcohol in those already with epilepsy so therefore they are susceptible. This is usually AM after acute intoxication

102
Q

Describe peripheral neuropathy in relation to alcohol

A

Nerve damage- patients get burning pain and weakness. Can be due to direct damage to nerves by alcohol or damage from nutritional deficiencies caused by alcohol

103
Q

Describe compression neuropathy in relation to alcohol

A

basically a trapped nerve due to temporary damage to the myelin sheath

104
Q

Describe myopathy in relation to alcohol

A

Acute- after binges patient has myalgia, proximal weakness, swollen tender muscles and raised CK, usually recover in weeks to months
Chronic- painless and develops over weeks to months with proximal weakness and atrophy, normal CK, recovery is long and incomplete.

105
Q

What causes Wernicke’s encephalopathy and how will the patient present?

A

Caused by thiamine deficiency and cytotoxic oedema in mamillary bodies. Presents as ocular dysfunction, ataxic fait and acute confusion.

106
Q

Treatment of Wernicke’s encephalopathy? Why is recognition important

A

Urgent thiamine replacement without this the signs can remain permanent and the patient will develop Korsakoff’s syndrome

107
Q

What is Korsakoff’s syndrome? How does it present?

A

It is cerebral atrophy resulting from wernicke’s encephalopathy. Presents as profound anterograde amnesia (no memory retention), variable retrograde amnesia (episodic memory) and confabulation.

108
Q

Treatment of Korsakoff’s syndrome?

A

Abstinence and nutrition are key but recovery chances unfortunately are low.

109
Q

Does alcohol increase risk of dementia?

A

Yes

110
Q

Out of fatty liver, alcoholic hepatitis and alcoholic cirrhosis which conditions are reversible?

A

Fatty liver is fully reversible, alcoholic hepatitis is potentially reversible but often progresses, alcoholic cirrhosis is irreversible

111
Q

Describe alcoholic fatty liver

A

This occurs in most heavy drinkers even after a single episode of heavy intake. Fat accumulates in hepatocytes due to abnormalities in the intermediate metabolism of lipids and carbohydrates. It is fully reversible with a couple of weeks of abstinence

112
Q

Describe alcoholic hepatitis

A

Can be asymptomatic or can be acute and life threatening. Signs of liver failure may be found and there is a high risk of progression to cirrhosis.

113
Q

Name 8 cancers alcohol increases the risk of

A 
1- oral
2- pharyngeal 
3- laryngeal
4- oesophageal
5- colorectal
6- hepatocellular carcinoma
7- female breast
8- pancreatic
114
Q

What is the only way to remove alcohol from the blood?

A

Time

115
Q

1g of pure alcohol contains how many calories?

A

7kcals

116
Q

How does alcohol increase the risk of deficiencies?

A

Reduces food intake
Impacts digestion by decreasing secretion of pancreatic enzymes and bile
Impacts absorption by damaging cells lining the stomach and SI
Impacts nutrient transport, storage and secretion as their is decreased liver stores of vitamins and increased excretion

117
Q

Name 6 common deficiencies caused by alcohol

A 
Thiamine 
Folate and B12
Niacin
Vit A
calcium 
Zinc
118
Q

Why do you get thiamine deficiency if you drink a lot of alcohol?

A

Levels are rapidly used due to poor intake in diet and there is increased demand as thiamine is used in ethanols metabolism

119
Q

What foods is thiamine usually found in

A

beans, nuts. yeast and meat

120
Q

What is thiamine important in?

A

nerve conduction and neural membranes

121
Q

Describe foetal alcohol spectrum disorders

A

Range of lifelong conditions from abnormal appearance, stunting, low body weight, low head size, poor coordination, learning difficulties, sight and hearing disorders. Foetal alcohol syndrome is the most severe form of FASD

122
Q

What tests should you do to test if a patient is drinking chronically? Why?

A

Test GGT, MCV and triglycerides. Ethanol induces GGT so it will be raised. MCV (mean corpuscular volume) is often raised in chronic alcohol excess, the mechanism is not fully understood. Triglycerides are raised due to synthesis in the liver.

123
Q

Even if someone smells of alcohol why must you check if their coma is due to alcohol?

A

Although alcohol may be the underlying cause the actual coma could be due to hypoglycaemia, injury from drinking, nutrient deficiency etc.

124
Q

What test should you do to determine if a coma is due to alcohol?

A

Serum osmolality

125
Q

Explain how serum osmolality helps you determine if a coma is due to alcohol?

A

All of the dissolved solvents contribute to serum osmolality. It can be calculated from concentrations of measured electrolytes (e.g. Na, K, Ca, glucose and urea). Usually Na dwarfs everything so serum osmolality = 2 x Na conc. So comatose patient comes in, measure electrolytes and these are normal so you calculate what serum osmolality should be. Then you compare this to the actual serum osmolality measured in the patient. If there is a gap between calculated and measured serum osmolality this suggests there is something else in the patient’s blood (e.g. alcohol) contributing to serum osmolality.

126
Q

Describe ALT

A

Alanine aminotransferase. Found in the liver and present in hepatocytes. It is released when they release their contents. It is a marker of liver damage/ hepatitis.

127
Q

Describe ALP

A

Found in the liver, bone, small intestine, kidneys and placenta. It is a measure of cholestasis in the liver but its unspecific. Can tell you about bone or liver metastases, you can look at GGT (only in the liver) to determine where the ALP is coming from.

128
Q

Describe GGT

A

Found in the liver, kidney, pancreas and prostate. Not used 1st line as too sensitive but used when unsure if rise in ALP is due to liver (cholestasis)

129
Q

Describe bilirubin

A

Red blood cells release contents at the end of working life including haemoglobin. Eventually the contents are broken down to unconjugated bilirubin. This is then conjugated in the liver and released in the duodenum as bile. Raised bilirubin causes jaundice.

130
Q

Describe albumin

A

Protein synthesised in the liver, it is decreased in liver failure. Due to its long half life (about 3 weeks) it is not terribly useful as a marker for current liver function.

131
Q

Describe prothrombin ratio

A

Clotting factors are synthesised in the liver. Half life is 3-4 days so gives better idea of current function. Also gives indication of patients bleeding tendency.

132
Q

5 differential diagnoses for patient with abdo pain and alcohol issues?

A

Acute pancreatitis, alcoholic hepatitis, peptic ulcers, ascites and peritonitis

133
Q

What tests do you do in someone with abdo pain and alcohol issues and why?

A

Amylase (and potentially lipase) as will be raised in acute pancreatitis. LFTs to determine liver involvement. Analysed ascitic fluid if present.

134
Q

What do you test for in patient with vomiting and alcohol issues?

A

Should determine the severity of the vomiting (are they losing ions and electrolytes etc) but doing U+Es, ABG, LFT and Amylase

135
Q

3 differential diagnoses for patient vomiting with alcohol issues?

A

Acute gastritis, oesophageal strictures, pyloric stenosis

136
Q

4 differential diagnoses for patient with haematemesis and alcohol issues?

A

Acute gastritis (have to have a LOT of alcohol to irritate stomach lining that badly), mallory weiss tear, peptic ulceration and oesophageal varices

137
Q

Biochemical investigations for patient with haematemesis and alcohol problems?

A

PTR, LFTs, U+E, lactate

138
Q

Why may you get opaque wet patches in the omentum with acute pancreatitis?

A

Release of enzymes beyond the pancreas leads to fat necrosis of the omentum.

CLASP- Alcohol Week (1 decks)

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