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4TH YEAR - CPTP > Week 5 - Dyspepsia & Altered Bowel Habit > Flashcards

Week 5 - Dyspepsia & Altered Bowel Habit Flashcards

1
Q

Name 3 examples of drugs that undergoes substantial first pass metabolism in the liver?

A

Aspirin, Isosorbide dinitrate, Glyceryl trinitrate, Levodopa, Lidocaine, Morphine, Propranolol, Salbutamol

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2
Q

How can liver disease alter the response of drugs in the body?

A

o Impaired drug metabolism
o Hypoproteinemia → especially drugs that bind to albumin to get around the body
o Reduced clotting
o Hepatic encephalopathy
o Fluid overload → worsens liver function itself.
o Hepatotoxic drugs

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3
Q

Name 3 common hepatotoxic drugs…

A

Paracetamol, Isoniazid, statins, methotrexate, phenytoin, aspirin, alcohol, oral contraceptives, antibiotics

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4
Q

Name some antibiotics to be avoided in liver disease?

A

Chloramphenicol, Erythromycin, Tetracycline, pyrazinamide, Griseofulvin, Nalidixic acid, Nitrofurantoin

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5
Q

Antibiotics to be avoided in liver disease

Why is Erythromycin avoided in liver disease?

A

Erythromycin estolate - causes cholestasis

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6
Q

Antibiotics to be avoided in liver disease

Why is Tetracycline avoided in liver disease?

A

Tetracycline - dose related hepatotoxicity

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7
Q

Antibiotics to be avoided in liver disease

Why is pyrazinamide avoided in liver disease?

A

Antituberculous therapy in combinations, pyrazinamide → hepatotoxic

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8
Q

Antibiotics to be avoided in liver disease

Why is nalidixic acid avoided in liver disease?

A

Nalidixic acid – increase incidence of adverse effects

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9
Q

Antibiotics to be avoided in liver disease

Why is Nitrofuratonin avoided in liver disease?

A

Nitrofurantoin - prolonged use can cause liver problems e.g. jaundice

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10
Q

Antibiotics to be avoided in liver disease

Why is Chloramphenicol avoided in liver disease?

A

Chloramphenicol - higher risk of bone marrow suppression (markedly increased half life)

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11
Q

What is the effect of Hepatic Disease on Pharmacokinetics?

•

A

Hepatic disease may lead to:

Drug accumulation → Its not being metabolized properly and active metabolites are circulating in the system

Failure to form an active or inactive metabolite

Increased bioavailability after oral administration

Alteration in drug protein binding, and kidney function (low albumin)

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12
Q

What is the definition of hepatic drug clearance?

A

Hepatic drug clearance can be defined as the volume of blood perfusing the liver that is cleared of the drug per unit of time.

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13
Q

What are the 3 major parameters that determine drug elimination by the liver?

A
  1. Blood flow (Q) through the liver -> reflects drug delivery to liver
  2. The fraction of drug (f) in the blood that is free or unbound to plasma proteins and capable of interacting with hepatic enzymes
  3. Intrinsic clearance (Clint) is the intrinsic ability of the liver to metabolize drug in the absence of flow limitations and binding to cells or proteins in the blood.
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14
Q

What is the formula for hepatic clearance?

A 
Hepatic clearance = 
	Cl(hep) = Q X E
	             = Q X (Ci – Co)
Q = blood flow
E = extraction
Clhep  = hepatic clearance
Ci  = conc. of drug in portal circulation
Co = conc. of drug in hepatic outflow
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15
Q

What is the extraction ratio (ER)?

A

The fraction or percentage of the drug removed from the perfusing blood during its passage through the organ

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16
Q

How do we class extraction ratio (ER)?

A
  1. High (>0.7),
  2. Intermediate (0.3-0.7) or
  3. Low (<0.3),
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17
Q

How does ER relate to bioavailability? How does this effect cirrhotic patients?

A

Drugs with high hepatic ER have a large first-pass effect, therefore low oral bioavailability.

In cirrhotic patients, therefore the initial and maintenance doses of oral drugs have to be reduced.

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18
Q

How do you alter drug doses of drugs metabolised in the liver in patients with hepatic impairment?

A

Reduced dose = (Normal dose X bioavailability) / 100

Normal dose = starting dose in patient without liver dysfunction

Bioavailability = drug’s bioavailability in a healthy person (1-ER)

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19
Q

How should you prescribe high extraction drugs in liver impairment?

A

High extraction drugs given ORALLY, initial and maintenance dose should be reduced in patients with impaired blood flow

High extraction drug given IV, normal initial dose but maintenance dose should be reduced according to hepatic blood flow

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20
Q

How should you prescribe low extraction drugs, with low albumin binding in liver impairment?

A

For drugs with a low extraction ratio (first pass metabolism ≤30%) and low binding to albumin…

Reduce maintenance dose or increase dosing interval.

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21
Q

How should you prescribe low extraction drugs, with high albumin binding in liver impairment?

A

For drugs with a low extraction ratio with high binding to albumin (≥90%)
o Reduce initial dose if low albumin
o Adjust maintenance dose based on clinical effect or drug level

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22
Q

What is the best practise for prescribing to patients with liver disease?

A

Use drugs eliminated by routes other than liver
Avoid hepatotoxic drugs
Avoid sedatives, diuretics, drugs which cause constipation –> precipitate encephalopathy
Avoid drugs that interfere with haemostasis e.g. aspirin, warfarin
Drugs that cause Na retention e.g. NSAID’s or steroids exacerbate fluid overload and ascites

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23
Q

In summary, what are the main pharmacokinetic alterations in liver disease?

A

Drug accumulation & ↑ oral bioavailability (Absorption)

Formation of active & inactive metabolites (Metabolism) Reduced protein binding (Distribution & Excretion)

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24
Q

How does dyspepsia present?

A

Spectrum of usually intermittent upper GI symptoms including :
• Epigastric pain
• Heartburn
• May include bloating, nausea, vomiting

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25
Q

What is a Peptic ulcer?

A

Acid related ulcer in the lining of the stomach or duodenum

Ulceration can be seen in mucosa

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26
Q

What is the pathophysiology of peptic ulcers?

A

Layer of mucus in our stomachs to protect our cells from the stomach acid (HCL) → a disruption in the mucous layer is what leads to problems like ulceration.

Parietal Cells that secrete HCl into the stomach are targets for pharmacological therapy. PPIs target the pump that actively exchanges potassium ions for hydrogen ions and lowers the pH in the stomach.

Inhibiting the pump will increase the pH

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27
Q

What are the factors that increase risk of ulceration?

A 
Increased acid production
•	Gastrin
•	Parasympathetic stimulation
•	Pepsin 
•	H. Pylori
•	Histamine
Decreased Mucosal protection
•	Mucin / HCO3- secretion
•	H. Pylori
•	Prostaglandin inhibition (Cox)
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28
Q

What are the common causes of PUD?

A

Helicobacter pylori infection – 60 - 95% (most common)

NSAIDS use 5% ical
o Reduced mucin/HCO3 production – COX I inhibitory effect

Long term steroid use

Alcohol & Smoking

Severe physiological stress → Major burns / CNS trauma / surgery, medillness - ITU

Hypersecretory states – Zollinger Ellison syndrome

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29
Q

What is the most common cause of PUD?

A

Helicobacter pylori infection – 60 - 95% (most common)
o Common childhood infection
o Inflammation / Increased acid production

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30
Q

What is the difference in the pain associated with duodenal and peptic ulcers?

A

Both cause epigastric pain

Gastric Ulcer – worse with / shortly after meals

Duodenum U – relieved during meals, worse 2-3h after meals or at night

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31
Q

What are the common pharmacological causes of Dyspepsia?

A 
o	NSAIDs – gastritis and peptic ulcers
o	Steroids – gastritis and peptic ulcers
o	Calcium antagonists - gastritis
o	Nitrates - Reflux
o	Theophyllines - gastritis
o	Bisphosphonates – oesphageal erosion and ulceration.
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32
Q

What are the Emergency Presentations related to PUD and dyspepsia?

A 
UGI bleeding
o	Haematemesis
o	Melaena
o	Haemodynamic compromise
o	Severity scoring → BLATCHFORD score &amp; Rockall score

Acute abdomen
o Perforation – gastric / duodenal

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33
Q

What are the differentials for dyspepsia?

A

Ulcer, Gastric cancer, Reflux disease, Gallstones, Chronic pancreatitis, Myocardial infarction

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34
Q

What are the common investigations in patients with dyspepsia? (apart from FBC, etc.)

A 
H. pylori tests
o	Faecal antigen test 
o	Carbon 13 urea breath test
o	Serum H.pylori antibody test
o	Endoscopic biopsy samples – rapid urease test - CLO

Endoscopy

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35
Q

What are the different ways of testing for H. Pylori?

A

o Faecal antigen test
o Carbon 13 urea breath test
o Serum H.pylori antibody test
o Endoscopic biopsy samples – rapid urease test

36
Q

What is the general advise given to patients with dyspepsia?

A
  • Stop smoking
  • Reduce alcohol intake
  • Lose weight
  • Increase exercise
  • Reduce fatty/spicy foods
  • Eat small regular meals
  • Raising head of the bed
37
Q

What is the mechanism of acid suppression therapy– PPI?

A
  • PPI becomes activated by acid in the canaliculus and irreversibly binds to the proton pump, blocking its action.
  • Receptors are still active, but cannot stimulate acid production as the pump is blocked.
  • Inactive PPI diffuses out of blood vessels and across the parietal cell to the canaliculus.
38
Q

Name 2 antacids…

A

Aluminium hydroxide
Magnesium carbonate
Magnesium trisilicate

39
Q

What is the mechanism of action of antacids?

A

o Antacids are made of alkaline Al3+ and Mg2+ salts
o Raise the pH of the stomach
o Neutralising stomach acid
o Bind to and inactivate pepsin

40
Q

What are the adverse effects of antacids?

A

o Constipation

o Diarrhoea

41
Q

What are the contraindications of antacids?

A

Aluminium hydroxide and Magnesium hydroxide should not be given to patients with hypophosphataemia
H2-receptor antagonist

42
Q

Name 2 H2-receptor antagonists…

A

Cimetidine and Ranitidine (better tolerated)

43
Q

What is the mechanism of action of H2-receptor antagonists?

A

H2 receptor antagonists competitively block the action of histamine on the parietal cell by antagonising the H2 receptor

44
Q

name 2 PPIs

A

Omeprazole and Lansoprazole

45
Q

What is the mechanism of action of PPIs?

A

PPIs cause irreversible inhibition of H+/K+ ATPase responsible for H+ secretion from parietal cells

46
Q

What are the problems with PPIs?

A

o C. difficile diarrhoea risk with PPIs + Antibiotics
o Electrolyte disturbance with PPIs
o Drug – drug interactions →PPI vs. Clopidogrel

47
Q

When should the H2-receptor antagonist cimetidine be avoided?

A

Cimetidine should be avoided in patients on warfarin, phenytoin, theophylline (inhibits the P450 enzyme system hepatic metabolism)

48
Q

What are the H. pylori eradication therapies?

A

Triple therapy
o PPI, amoxicillin and clarithromycin
o PPI, amoxicillin and metronidazole

Quadruple therapy
o Eradication failure:
• Omeprazole, 2 antibiotics (tetracycline and metronidazole) and bismuth chelate

49
Q

What is the treatment of PUD?

A

Heal the ulcer
o Antisecretory medications
o Post treatment repeat endoscopy

H. pylori eradication
o Antibiotics and PPI – triple therapy

Stop NSAID use if applicable

Surgery
o If failed medical / endoscopic management in UGI bleed or if there are complications

50
Q

What are the 4 types of laxatives?

A

Bulk forming, Osmotic, Stimulant and Faecal softeners

51
Q

Name some examples of osmotic laxatives…

A
  • Lactulose – semi synthetic disaccharide (not absorbed from the GI Tract),
  • Macrogol
52
Q

Name some examples of bulk forming laxatives…

A

Bran, Methylcellulose, Ispaghula husk

53
Q

Name some examples of stimulant laxatives…

A

Senna, Danthron, Bisacodyl and Sodium picosulphate

54
Q

Name some examples of faecal softeners…

A

Liquid paraffin and Docusate sodium

55
Q

What is the mechanism of action of bulk forming laxatives?

A

Increase volume of non- absorbable material in the gut

Distend the colon and stimulate peristaltic movement

56
Q

What is the mechanism of action of osmotic laxatives?

A

Increase water content in the bowl via osmosis

Distend the colon and stimulate peristaltic movement

57
Q

What is the mechanism of action of stimulant laxatives?

A

Increase gastrointestinal peristalsis

Increase water and electrolyte secretion by the mucosa

58
Q

What is the mechanism of action of faecal softeners?

A

Promote defecation by softening the stool (Docusate sodium)

Promote defecation by lubricating the stool (Liquid paraffin)

59
Q

What are the contraindications of bulk forming laxatives?

A

Dysphagia, intestinal obstruction, colonic atony, faecal impaction

60
Q

What are the contraindications of osmotic laxatives?

A

Intestinal obstruction

61
Q

What are the contraindications of stimulant laxatives?

A

Intestinal obstruction

62
Q

What are the contraindications of faecal softeners?

A

Should not be administered to children under 3 years old

63
Q

What are the adverse effects of bulk forming laxatives?

A

Flatulence, abdominal distension and gastro intestinal obstruction

64
Q

What are the adverse effects of osmotic laxatives?

A

Flatulence, cramps and abdominal discomfort

65
Q

What are the adverse effects of stimulant laxatives?

A
  • Short term: cramps and abdominal discomfort
  • Long term use: damage to the nerve plexuses
  • Can cause deterioration of normal intestinal function
66
Q

What are the adverse effects of faecal softeners?

A

Long term use of liquid paraffin can impair absorption of fat soluble vitamins (Vitamin A and Vitamin D)

67
Q

What type of ulcer is likely if epigastric pain is relieved by eating?

A

Duodenal ulcer

68
Q

How does NICE recommend you to manage patients with persistent dyspepsia?

A

< 55 years “Test and Treat”
• Test for H. pylori – C13 Urea breath test or stool antigen (2 week washout post PPI)
• 4 weeks full dose PPI

> 55 years with unexplained, persistent symptoms – URGENT endoscopy referral
• Don’t prescribe PPI pre-endoscopy → as need to be off acid suppression medication for > 2 weeks prior to endoscopy

69
Q

What test is used to test a biopsy sample for H. pylori?

A

CLO test

Endoscopic biopsy samples – rapid urease test

70
Q

Why are duodenal ulcer relieved by eating?

A

Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum.
Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum

71
Q

Why are gastric ulcers exacerbated by eating?

A

A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach.

72
Q

How often are duodenal ulcers and gastric ulcer associated with H. pylori?

A

Duodenal - 90% association

Gastric - 60% association

73
Q

How does H. pylori effect risk of cancer?

A

Increases carcinoma incidence by x3

74
Q

What is the therapy for a H. pylori ulcer?

A

Triple therapy
Omeprazole, amoxicillin and clarithromycin

Then continue PPI for 8 weeks

75
Q

How long do you continue PPI for after triple therapy?

A

8 weeks

76
Q

What are the side effects of PPIs

A

Low magnesium

Increased risk of C difficile and infective diarrhoea
o Suspend PPI in patients receiving course of antibiotics

Acute interstitial nephritis

Microscopic colitis

77
Q

What is the therapeutic pathway for non-ulcer dyspepsia?

A
  • Test and treat for HP
  • 4 weeks low dose PPI
  • If symptoms recur step down PPI/H2RA to lowest dose to control symptoms.
78
Q

What is the Blatchford score?

A

Gives an idea of how risky a GI bleed is

Low risk = 0, Anything higher is high risk

79
Q

What is the Rockall score?

A

Measures risk of mortality and re-bleeding

80
Q

What should you do when prescribing NSAIDS in those with past dyspepsia?

A

Give PPI cover

81
Q

Which NSAIDS are better and why?

A

COX1 and COX2 both convert arachadonic acid into pGs and other mediators.

COX-2 are better than non-selective

COX-2 inhibits the proinflammatory pathways

Non-selective will also inhibit COX-1 which increases GI side effects.

82
Q

If a patient has suspected c-diff, what is your first treatment?

A

Admit in isolation

83
Q

Which pharmacological treatments increase risk of c-diff, what should you do to prevent this?

A

PPI + Abx

Suspend PPI when you prescribe Abx

84
Q

What are the causes of constipation?

A 
Primary
•	Hirschsprung’s disease
•	Rectocele/ prolapse
•	Impaired pelvic floor relaxation
Secondary
•	Medication: Opiates/ CCB/ Iron
•	Neurological: PD/MS/MD/spinal lesions
•	Dietary: Low fibre diet and immobility
•	Mechanical: Ca/stricture/painful sphincter
•	Metabolic: High and low calcium, Low K+, Low Mg, uraemia
•	Endocrine: Hypothyroidism, diabetes 
•	Psychiatric: depression, anxiety, somatization, eating disorders
85
Q

When cant you use stimulant or bulk forming laxatives?

A

Intestinal obstruction

86
Q

What non-pharmacological management is advised in constipated patients?

A

Well-balanced diet high in fibre
Cutting down on white bread, cakes and sugar.
Drinking at least 6 to 8 glasses of water a day.
Prunes and plum juice can also be beneficial.
Regular exercise

4TH YEAR - CPTP (19 decks)

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