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Gastrointestinal > GI 6 > Flashcards

GI 6 Flashcards

1
Q

What are short-term/acute effects of alcohol consumption?

A
  • Accidents/violence
  • Oesophagitis/gastritis
  • Acute pancreatitis
  • Aspiration
  • Overdose
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2
Q

What are the long-term/chronic effects of alcohol consumption?

A
  • Hypertension/cardiomyopathy/MI
  • Stroke
  • Neuropathies
  • Cerebellar degeneration
  • Dementia
  • Problems with stomach, liver, pancreas
  • Anaemia/bone marrow suppression
  • Osteoporosis
  • Endocrine/dermatologic/reproductive
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3
Q

What are the effects of foetal alcohol syndrome?

A
  • Growth deficiency
  • Mental retardation/intellectual impairment
  • Attentional learning disabilities
  • Behavioural problems
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4
Q

What are the 3 major effects of cirrhosis?

A

1) Reduced blood flow
2) Reduced metabolic function
3) Reduced plasma proteins

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5
Q

What would occur if NSAIDs were prescribed in liver disease?

A
  • Worsen renal impairment -> risk of hepatorenal syndrome
  • Worsening of CHF
  • Peptic ulcers cause high risk of GI bleed and perforation
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6
Q

What would you need to do if prescribing a NSAID to a patient with liver disease?

A

Always co-prescribe with a PPI; but NSAIDs should be avoided at all costs

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7
Q

Are opiates safe to prescribe in liver disease?

A

All should be avoided or used sparingly (sedative opiates cause severe confusion and respiratory depression), fentanyl may be the only safe opiate

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8
Q

What occurs with prescription of paracetamol in liver disease?

A
  • Reduced glutathione stores
  • Toxic drug intermediates not inactivated
  • Normal dose becomes dangerous
  • A very low dose can be given
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9
Q

What is Hy’s law?

A

To identify is a patient is at a high risk of drug-induced liver injury:

  • ALT/AST > 5xULN and
  • Bilirubin > 3mg
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10
Q

Which diuretic should be used in liver disease for oedema and ascites?

A

Spirinolactone: best drug, with fluid restriction, aim at 1kg/day weight loss

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11
Q

How can sedation be achieved in encephalopathic liver disease?

A

Small doses of phase II metabolised benzodiazepines (Lorazepam, Oxazepam, Lormetazepam)

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12
Q

What antibiotics should be avoided in liver disease?

A
  • Aminoglycosides nephrotoxic
  • Quinolones epileptogenic
  • Metronidazole reduced metabolism
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13
Q

What is fulminant hepatitis?

A

Fulminant hepatitis is a rare syndrome of massive necrosis of liver parenchyma and a decrease in liver size (acute yellow atrophy) that usually occurs after infection with certain hepatitis viruses, exposure to toxic agents, or drug-induced injury

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14
Q

When should you treat viral hepatitis?

A
  • HCV RNA present and genotype known
  • HBsAg and Hep B DNA present
  • Hep B: raised ALT and high HBV DNA
  • Chronic Hep C is treated right away (clinical priority)
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15
Q

What are the outcomes of liver injury?

A
  • Very resistant to injury and large functional reserve
  • Some can produce parenchymal necrosis but heal by restitution
  • Some can leave permanent damage
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16
Q

What are the causes of acute onset of jaundice?

A
  • Drugs
  • Viruses
  • Alcohol
  • Bile duct obstruction
17
Q

What are the 3 consequences of acute liver failure?

A

1) Complete recovery
2) Chronic liver disease
3) Death from liver failure

18
Q

What are the different types of jaundice?

A

1) Pre-hepatic - too much haem breakdown
2) Hepatic - liver cells injured or dead
3) Post-hepatic - bile cannot escape into the bowel

19
Q

What is cirrhosis of the liver?

A

Defined by bands of fibrosis separating regenerative nodules of hepatocytes; alteration of hepatic microvasculature

20
Q

What are the complications of cirrhosis?

A
  • Portal hypertension (-> oesophageal varices, caput medusa and haemorrhoids)
  • Ascites
  • Liver failure
21
Q

What are the outcomes of alcoholic liver disease?

A
  • Cirrhosis
  • Portal hypertension (varices and ascites)
  • Malnutrition
  • Hepatocellular carcinoma
  • Social disintegration
22
Q

What is non-alcoholic steatohepatitis (NASH)?

A
  • Non-drinkers
  • Pathologically identical to alcoholic liver disease
  • Occurs in patients with diabetes,obesity, hyperlipidaemia
  • On the increase
  • May lead to fibrosis and cirrhosis
23
Q

What is chronic drug-induced hepatitis?

A
  • Similar features to all other types of chronic hepatitis
  • May trigger an autoimmune hepatitis
  • Chronic active process
  • Causes are too many to list
24
Q

What are the storage diseases of the liver?

A
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1-antitrypsin deficiency
25
Q

What does the physiology of retching involve?

A
  • Rhythmic reverse peristalsis of the stomach and oesophagus
  • Forceful, involuntary, contraction of abdominal muscles and the diaphragm – cardiac portion of stomach pushed into the thorax
  • Upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
  • Pallor, sweating excessive salivation
26
Q

How is vomiting induced?

A

1) Release of mediators from enterochromaffin cells in mucosa
2) Depolarization of sensory afferent terminals in mucosa
3) Action potential discharge in vagal afferents to brainstem
4) Coordination of vomiting by VC in the medulla

27
Q

What is the vomiting centre (VC)?

A

A group of interconnected neurones within the medulla that are driven by a central pattern generator (CPG) that in turn receives input from the NTS

28
Q

What are the consequences of severe vomiting?

A
  • Dehydration
  • Loss of gastric protons and chloride
  • Hypokalaemia
  • Metabolic alkalosis, rarely acidosis
  • Oesophageal damage (Mallory-Weiss tear)
29
Q

Why is there an increased risk of osteoporosis in IBD?

A
  • Inadequate vitamin D and calcium status
  • Corticosteroid use
  • Age
  • Systemic inflammation
30
Q

What nutritional support strategies are used in the management of IBD?

A
  • Food fortification
  • Little and often pattern
  • High energy and nutrient dense options
  • Specific dietary counselling
  • Oral nutritional supplements
31
Q

What is exclusive enteral nutrition (EEN)?

A
  • Treatment option to induce remission in active Crohn’s disease
  • Involves withdrawal of all food and drink (except water) and replacement with enteral nutrition
  • Primary treatment option in children and adolescents
  • Consider in adults on an individual basis
  • Minimum adherence 4-6 weeks
32
Q

What is the first line dietary advice for IBS?

A
  • Food and symptom diary
  • Ensure adequate fluids and 3 meals/day
  • Eat smaller meals, slower, chew more
  • Take time to relax
33
Q

What is the second line dietary advice for IBS?

A

Low FODMAP diet; poorly digested and absorbed in the small bowel leading to fermentation and osmotic changes in the large bowel

34
Q

What is leuconychia?

A

White nails with lanulae undermarcated from hypoalbuminaemia

35
Q

What is Terry’s nails?

A

White proximally but distal 1/3 reddened by telangiectasis

Gastrointestinal (8 decks)

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