Management of Diarrhoea and Constipation Flashcards

1
Q

Diarrhoeas

A

Acute < 14 days
Persistent > 14 days
Chronic > 30 days

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2
Q

Inflammatory diarrhoea

A

Viral, bacterial, parasitic infection
Radiation injury
IBD

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3
Q

Inflammatory diarrhoea symptoms

A

Mucoid and bloody stool
Tenesmus (urge to empty bowels when they are empty)
Fever
Crampy abdominal pain

Histology of GI tract = abnormal

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4
Q

Non-inflammatory diarrhoea

A

Osmotic
Secretory

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5
Q

Non-inflammatory diarrhoea symptoms

A

Watery
Frequent stool > 10-20 times a day
High volume depletion

Histology of GI tract = preserved

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6
Q

Osmotic diarrhoea

A

Presence of unabsorbed solute
Small stool volume
Stops/improves with diet
Maldigestion

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7
Q

Secretory diarrhoea

A

Altered transport of ions across mucosa
Increased secretion; decreased absorption
Not affected by diet

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8
Q

Infectious bacterial diarrhoea causes

A

E.coli
Campylobacter
Salmonella
C.Diff
Listeria
Vibrio cholerae

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9
Q

Infectious viral diarrhoea causes

A

Rotavirus
Norovirus
Adenovirus
Astrovirus

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10
Q

Infectious protozoal diarrhoea causes

A

Entamoeba histoltica
Giardia lamblia
Cryptosporidium

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11
Q

Non-infectious CV drugs causing diarrhoea

A

Digoxin
Quinidine
Propranolol
ACE inhibitors

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12
Q

Non-infectious GI drugs causing diarrhoea

A

Antacids (Mg salts)
Laxarives
H2 antagonists

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13
Q

Non-infectious endocrine drugs causing diarrhoea

A

Oral hypoglycaemic agents
Thyroxine

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14
Q

Non-infectious antibiotics causing diarrhoea

A

Amoxicillin
Cephalosporins
Erythromycin

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15
Q

Absorption

A

Water follows movement of electrolytes and glucose

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16
Q

Cl- transport in intestine

A

Na+/K+/2Cl- cotransporter
Actively driven by low intracellular Na+
Na+ and water enter lumen by paracellular transport

17
Q

Vibrio cholerae

A

Cholera toxins enter cells
Activates G protein > activates adenyl cyclase
Increases cellular cAMP > activation of PKA
Phosphorylation of Cl- channel
Increased efflux of Cl- and water
Diarrhoea

18
Q

Increased motility

A

Reduction in intestinal transit time = inadequate absorption

Cholinergic drugs - Pilocarpine

Anticholinesterase activity drugs - Donepezil

19
Q

Anti-motility drugs

A

Diphenoxylate + atropine
Codeine phosphate
Racecadotril

20
Q

Diphenoxylate MOA

A

μ opioid receptor on neuronal varicosities
Activation decreases ACh release
Peristalsis decrease
Segmental contraction increase

21
Q

Racecadotril MOA

A

δ opioid receptor decreases cellular cAMP levels
Decreased Cl- and water
Enkephalins are endogenous activators
Prodrug - metabolised to thiorphan
Thiorphan is enkephalinase inhibitor

22
Q

Opiates side effects

A

Rebound constipation
CNS affects
opioid dependance

23
Q

Constipation

A

Heterogeneous disorder

Primary
Secondary

24
Q

Constipation symptoms

A

< 3 bowel movements per week
Straining
Lumpy/hard stool
Sensation of anorectal obstruction
Manoeuvring required to defaecate

25
Q

Primary constipation

A

Normal transit
Slow transit (colonic inertia)
Pelvic floor dysfunction
IBS

26
Q

Secondary constipation

A

Medications
Metabolic disorders
Endocrine disorders
Psychiatric (anxiety, depression)

27
Q

Drug induced constipation

A

Anticholingeric activity
-Antidepressants
-Antihistamines
-Antimuscarinics
-Antipsychotics
-Antiparkinsonian agents

Opioids

Laxative misuse

28
Q

Constipation treatment

A

Laxatives
-Osmotic
-Stimulant
-Bulk-forming
-Faecal softeners

29
Q

Linaclotide

A

14 amino acid synthetic
Activates Guanylate Cyclase C GC-C
Increases cellular cGMP and activation of PKG
Phosphorylation of Cl- channel
Increased efflux of Cl- and water

30
Q

Lubiprostone

A

Prostones
Derived from functional natural fatty acids
Activates Cl- channel (CIC-2)
Increased efflux of Cl- and water
May restore mucosal barrier function

31
Q

Linaclotide & Lubiprostone side effects

A

Diarrhoea
Nausea
Vomiting
Abdominal pain