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YEAR 3 TCD > WEEK 16 > Flashcards

WEEK 16 Flashcards

1
Q

At low levels of consumption, alcohol is converted to ______ and _____ for excretion via the _______, _______ and _________

A
  • CO2
  • H2O
  • urine
  • lungs
  • sweat
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2
Q

At higher levels of consumption, ethanol is converted to acetaldehyde by ___________ in gastric mucosal cells and ________ and then undergoes lipogenesis to form fatty acids and glycerol. These can accumulate in hepatocutes leading to inflammation (_________) that impairs liver function.

A
  • alcohol dehydrogenase
  • hepatocytes
  • hepatitis
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3
Q

There are many mechanisms by which alcohol damages the human body: it is directly _____, the metabolite ___________ is carcinogenic, it induced _____ change, inflammation and fibrosis in the liver, it induces enzymes like ______, and it prevents absorption and storage of essential nutrients (particularly __ vitamins).

A
  • toxic
  • acetaldehyde
  • fatty
  • cp450
  • B
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4
Q

Describe the 5 steps of liver disease

A
  1. Fatty liver — fats are deposited in the cytoplasm of the hepatocyte
  2. Hepatitis — hepatic leucocytosis and loss of function
  3. Fibrosis — reversible deposition of pericellular fibrous bands
  4. Cirrhosis — irreversible nodules that comprise a hypo plastic hepatocyte surrounded by fibrous tissue
  5. Hepatocellular carcinoma — genetic changes inside the cell
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5
Q

Alcohol is a CNS ______ at low levels of consumption

A

Stimulant

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6
Q

Alcohol is _________, allowing it to easily cross the BBB and act on neurones

A

Lipophilic

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7
Q

At very high levels of consumption, alcohol acts on ________ centres in the brainstem

A

Respiratory

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8
Q

Alcohol is a CNS __________ at high levels of consumption, acting via ____ receptors

A
  • depressant
  • GABA
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9
Q

Chronic alcohol consumption interferes with absorption and utilisation of vitamin B1 (__________), which is essential for CNS ______ metabolism

A
  • thiamine
  • glucose
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10
Q

Name 4 pre-hepatic causes of jaundice

A
  • haemolytic anaemia
  • drugs
  • Gilbert’s syndrome
  • Crigler-Najjar syndrome (rare)
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11
Q

Name hepatic causes of jaundice

A
  • viral infection
  • alcohol
  • NAFLD
  • autoimmune disorders (primary biliary cholangitis, primary sclerosing cholangitis)
  • malignancy of biliary system (HCC, cholangiocarcinoma, gallbladder cancer)
  • metabolic (haemochromatosis, Wilson’s disease)
  • drugs
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12
Q

Name 5 drugs that can cause jaundice

A
  • ciprofloxacin
  • co-amoxiclav
  • phenytoin
  • erythromycin
  • nitrofurantoin
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13
Q

Name 4 post-hepatic causes of jaundice

A
  • gallstones
  • surgical strictures
  • extra-hepatic malignancy (pancreatic cancer)
  • pancreatitis
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14
Q

What stigmata of chronic liver disease may you see as a result of high oestrogen levels?

A
  • Palmar erythema
  • Spider naevi
  • Gynaecomastia
  • Loss of secondary body hair (in males)
  • Male genital atrophy
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15
Q

What stigmata of chronic liver disease may you see as a result of low albumin?

A

Leukonychia

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16
Q

What stigmata of chronic liver disease may you see as a result of portal hypertension?

A
  • caput medusae
  • dilated anterior abdominal wall veins
  • ascites
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17
Q

What else may you see in chronic liver disease?

A
  • signs of hepatic encephalopathy including a liver flap (asterixis)
  • muscle loss (sarcopenia)
18
Q

What symptoms may indicate an obstructive jaundice?

A
  • dark urine
  • pale stools
  • itching
19
Q

What is jaundice and what are normal plasma bilirubin levels?

A

NICE defines jaundice as the yellow pigmentation of the skin, sclera and mucous membranes resulting from raised plasma bilirubin. Normal plasma bilirubin levels are <21mmol/L

20
Q

What is bilirubin?

A

A breakdown product of Haem molecules in red cells

21
Q

Describe the pre-hepatic metabolism of red cells

A
  • as red cells in the blood reach the end of their lifecycle (approx 120 days) they are phagocytosed by macrophages
  • this breaks haemoglobin down to Haem and globin
  • Haem is then broken down into iron and protoporphyrin
  • protoporphyrin is then broken down into unconjugated bilirubin (not water-soluble)
  • this mainly takes place in the spleen
  • albumin in the blood then binds to unconjugated bilirubin and transports it to the liver
22
Q

Describe the hepatic metabolism of red cells

A
  • Unconjugated bilirubin is taken up by hepatocyte in the liver and is conjugated by an enzyme called uridine glucoronyl transferase, creating conjugated bilirubin = water soluble
  • here the conjugated bilirubin is secreted into bile duct and stored in the gallbladder as bile
23
Q

Describe the post hepatic metabolism of red cells

A
  • when you eat, particularly fatty food, bile is excreted from the gallbladder into the duodenum
  • conjugated bilirubin in the bile is converted into urobilinogen by microbes in the small intestine
  • some of this urobilinogen is reabsorbed into the blood, converted into urobilin and either sent back to the liver or excreted by the kidneys giving urine its yellow colour
24
Q

What is a Whipple procedure?

A

—> Aka pancreaticoduodenectomy

The Whipple procedure is an operation to treat tumors and other conditions in the pancreas, small intestine and bile ducts. It involves removing the head of the pancreas, the first part of the small intestine, the gallbladder and the bile duct.

It’s often used to treat pancreatic cancer that hasn’t spread beyond the pancreas.

25
Q

If a pancreatic cancer is obstructing and non-respectable, what can be done to relieve symptoms?

A

ERCP with biliary stent insertion

26
Q

What is Librium?

A

Librium is a brand name for chlordiazepoxide, a long-acting benzodiazepine that NICE recommends for the treatment of symptoms associated with acute alcohol withdrawal

27
Q

Benzodiazepines can be effective at reducing the psychological and physiological response to agitation. However this can be unhelpful for many reasons, such as what?

A
  • It may mask the signs of the underlying condition.
  • It may reduce the physiological response where this is actually a helpful response to the physical effects of the condition.
  • It may cause respiratory depression; this could be a serious problem if the patient is unwell due to an underlying cardio-respiratory problem in particular.
  • It may cause CNSD depression (see for example problems if the underlying problem was encephalitis or similar).
  • It may limit the patient’s ability to give an accurate history that may help in diagnosis and management.
  • It may worsen delirium.
  • It may increase the risk of falls.
28
Q

What are some physical symptoms of alcohol withdrawal?

A
  • Anxiety
  • Nausea / vomiting
  • Insomnia
  • Craving for alcohol
  • Tremor
  • Sweating
  • Palpitations
  • Diarrhoea
  • Confusion
  • Hallucinations
  • Seizures
29
Q

What is excessive alcohol a risk factor for, which could cause a GI bleed?

A
  • Oesophagitis
  • Mallory Weiss tears
  • Gastritis and peptic ulceration
  • Oesophageal varices ( although these are less common than the above)
  • (Rarely oesophagogastric malignancy)
30
Q

Alcohol acts on several neurotransmitter pathways in the brain including acting at _________, __________, ____, and ____ receptors.

A

Alcohol acts on several neurotransmitter pathways in the brain including acting at dopamine, serotonin, GABA, and NMDA receptors.

31
Q

The symptoms of alcohol withdrawal are thought to arise because chronic excessive alcohol use __________ inhibitory activity (via GABA receptors) and __________ excitatory activity (via NMDA receptors). Continuous alcohol use maintains the status quo. However, abrupt cessation of alcohol use unmasks this maladaptive response, leading to an overall over-excitation of the central nervous system

A

The symptoms of alcohol withdrawal are thought to arise because chronic excessive alcohol use enhances inhibitory activity (via GABA receptors) and inhibits excitatory activity (via NMDA receptors). Continuous alcohol use maintains the status quo. However, abrupt cessation of alcohol use unmasks this maladaptive response, leading to an overall over-excitation of the central nervous system

32
Q

Alcohol withdrawal: describe autonomic hyperactivity

A

starts <6 hours, resolves <24-48 hours (insomnia, tremulousness, mild anxiety, gastrointestinal upset, anorexia, headache, diaphoresis, palpitations)

33
Q

Alcohol withdrawal: describe withdrawal seizures

A

<12-48 hours (generalised tonic-clinic seizures; occurring as a singular seizure or brief flurry of seizures over a short period; in patients with a long history of chronic alcoholism therefore usually happen in the 4-5th decades of life; withdrawal-associated seizures are not usually recurrent or prolonged and so these features should prompt further investigation into structural or infectious aetiologies; if untreated, 1/3 patients experiencing alcohol withdrawal seizures will progress to delirium tremens)

34
Q

Alcohol withdrawal: describe alcoholic hallucinosis

A

starts <12-24 hours, resolves <24-48 hours (usually visual but may be auditory or tactile; patients are aware that they are hallucinating)

35
Q

Alcohol withdrawal: describe delirium tremens

A

complicates 5% alcohol withdrawal states; starts 48-96 hours, resolves <1-5 days (unlike alcoholic hallucinosis, delirium tremens is a syndrome of severe alcohol withdrawal that is associated with abnormal vital signs, fluid status, and electrolyte levels; another discerning feature is that patients with alcoholic hallucinosis are usually alert whereas delirium tremens clouds the sensorium; it carries a 5% mortality even with prompt identification and management- death is usually from dysrhythmia, pneumonia, or a failure to identify the underlying illness that led to alcohol sensation in the first place such as pancreatitis or hepatitis)

36
Q

In hospital, the tools used to assess severity of withdrawal can include the ________________________(MD+Calc) or the _________________ (GAS). We also screen all patients for the presence of hazardous alcohol consumption using tools such as the _______________________________(MD+Calc) to identify patients at risk of withdrawal during their admission.

A

In hospital, the tools used to assess severity of withdrawal can include the Clinical Institute Withdrawal Assessment (CIWA) (MD+Calc) or the Glasgow Alcohol score (GAS). We also screen all patients for the presence of hazardous alcohol consumption using tools such as the Alcohol Use Disorders Inventory Test (AUDIT) (MD+Calc) to identify patients at risk of withdrawal during their admission.

37
Q

What might opthalmoplegia, nystagmus or memory disturbance suggest?

A

Wernicke’s encephalopathy

38
Q
A

Last option

39
Q
A
  • ataxia
  • impaired memory
  • visual changes
  • confabulation
40
Q
A
  • liver cirrhosis
  • delirium tremens
  • seizures
  • cardiomyopathy
41
Q
A
  • diarrhoea
  • back pain
  • constipation
  • new onset diabetes
  • abdominal pain
  • nausea/vomiting

(Not PR bleed — indicates bowel cancer. Not bloating — indicates ovarian cancer)

42
Q
A
  • haemolytic anaemia
  • Gilbert’s disease

YEAR 3 TCD (15 decks)

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