use of medicines - GI Flashcards

1
Q

DRUG CAUSES OF CONSTIPATION

A
  1. opiates
  2. calcium channel blockers (verapamil)
  3. anticholinergic drugs (benzhexol, tricyclic antidepressants)
  4. iron
  5. lithium
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2
Q

dense dietary sources of fibre

A

figs - 4 per day is sufficient
all bran
wholemeal and wholegrain

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3
Q

comparison of laxative timecourse

A

bulk forming - 1-3days

stimulant laxatives - 6-8hrs (semi solids)

osmotic laxatives - 1-3 hours (watery evacuation) - so torrential that sometimes can kill. hypokalaemia perhaps.

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4
Q

FLUIID REPLACEMENT IN INFECTIOUS DIARRHOEA

A
  1. Rehydrate with oral rehydration therapy (isosomotic electrolyte solutions e.g. dioralyte)
  2. Composition of oral rehydration solutions
    Na 60 mmol, K+ 20 mmol, Cl- 60 mmol glucose 90 mmol (glucose helps absorb electrolytes)
  3. If very volume deplete use IV fluids that will replace sodium and potassium
    initially 0.9% sodium chloride solution; normal saline (150mM (millimolar) NaCL)
    added potassium, guided by serum electrolytes to replace water losses use 5% dextrose solution (can’t give plain water as the osmotic pressure will cause haemolysis)
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5
Q

how does loperamide act

A

an opioid that is pretty gut selective. causes the constipation (anti diarrhoea) but doesn’t have the effects of pain relief, euphoria, or nausea.

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6
Q

important negatives if you want to make a diagnosis of IBS

A
weight loss
PR blood loss
abdo masses
anaemia
raised inflammatory markers

its important to check these are negative as they would indicate something more insidious.
just for reference - positive symptoms for IBS
A. Abdominal pain
B. Bloating
C. Change in bowel habit

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7
Q

use of aminosalicylates

A

These drugs act on the distal small bowel and large bowel
Salicylate is delivered to these parts of the bowel where it has a topical anti-inflammatory action by inhibiting prostaglandin production

all the -salazines. SULPHASALAZINE, MESALAZINE, OLSALALAZINE

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8
Q

2 steroid sparing immunosuppressants

A

methotrexate - is an antimetabolite and antifolate drug.

azathioprine - Consequently, blocking the synthesis of purine also hinders DNA synthesis and thus inhibits the proliferation of cells, especially fast-growing cells without a method of nucleotide salvage (“recycling”), such as lymphocytes.

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9
Q

upper limit of normal for bilirubin

A

around 20. over 60mmol/l and in caucasians you’ll see the jaundice.

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10
Q

Hx: Qs to ask the Jaundiced patient

A
  • Duration
  • Previous attacks
  • Pain (gallstones)
  • Chills, fever, systemic symptoms (cholangitis)
  • Itching
  • Exposure to drugs (prescribed, ‘natural’, recreational)
  • Biliary surgery
  • Anorexia, weight loss
  • Colour of urine and stool
  • History of injections or blood transfusions
  • Contact with other jaundiced patients
  • Occupation (alcohol, animal contact, industrial exposure)
  • Travel (malaria, recent travel to endemic areas)
  • Sexual contacts and prior hepatitis immunisation
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11
Q

what is Gilberts Syndrome

A

Gilbert’s syndrome (/ʒiːlˈbɛər/ zheel-bair), often shortened to GS, also called Gilbert–Meulengracht syndrome, is a genetic liver disorder and the most common hereditary cause of increased bilirubin and is found in up to 5% of the population (though some gastroenterologists maintain that it is closer to 10% in Caucasian people).

Gilbert’s syndrome is a phenotypic effect, characterized by mild jaundice due to increased unconjugated bilirubin, that arises from several different genotypic variants of the gene for the enzyme responsible for changing bilirubin to the conjugated form.

Gilbert’s syndrome is characterized by a 70–80% reduction in the glucuronidation activity of the enzyme, (UGT1A1). The UGT1A1 gene is located on human chromosome 2

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12
Q

causes of jaundice

A

check OHCM

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13
Q

Investigation of Hepatic Jaundice

A
Blood tests (liver screen)
• HBsAg
• Anti–HCV
• Ferritin
• Caeruloplasmin - wilson's, almost never presents over the age of 40.
• α-1-antitrypsin
• Autoantibodies / Immunoglobluins
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14
Q

what happens in acute liver failure

A

• Development of encephalopathy & coagulopathy within 12 weeks of the onset of jaundice in absence of pre-existing liver disease

• Common (55%)
– Paracetamol 40%
– Acute viral hepatitis 13% (A, B & E)
– Idiosyncratic drug reactions 12% (isoniazid, phenytoin, sulphonamides, PTU)

• Rare (30%)
– Autoimmune hepatitis
– Herbal supplements
– Mushroom poisoning
– Budd-Chiari syndrome
– Pregnancy-related liver failure
– Heat stroke or rhabdomyolysis
– Herpes hepatitis
– Ischaemic hepatitis
– Malignant infiltration
– Fulminant Wilson’s disease

• ?cause (15%)

• Only effective treatment for ALF is Transplantation
– Assess & manage appropriately – Referral
– Safe transfer

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15
Q

what is Non-Ulcer dyspepsia

A

Dyspepsia is common and most of the time NO cause is found
Can be related to:
• Reflux
• Dysmotility
and treatment is symptomatic
• (may need to perform ph & manometry studies to exclude achalasia)

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16
Q

how do PPIs work

A
  • Irreversible inhibition of H+/K+ATPase
  • Reduction in gastric acid production
  • Effective (Cochrane review)
  • Billion dollar drug
  • Examples; Omperazole, Lansoprazole
  • S.E; headaches, abdo pains & diarrhoea (c.diff/infection in cirrhosis)
17
Q

when would you use a dopamine antagonist antiemetic

A

in this lecture’s example it is used in acute pancreatitis
• Action is on D2 receptors
• Block CTZ
• Used in neoplastic disease, radiation sickness, drug induced vomiting, general anaesthetics and cytotoxics
• Not effective for motion sickness
• Examples; Metoclopramide, Domperidone,
• S.E; extrapyramidal specially in the young, elevate prolactin levels

18
Q

antiemetic used for chemo sickness

A

5-HT3 Antagonist
• Gastric prokinetic activity
• Very effective but expensive
• Used in cytotoxic chemotherapy or radiotherapy
• Well tolerated
• Examples; Ondansetron, Granisetron
• S.E; constipation , rash, flushing, headache, hypersensitivity reaction

19
Q

what antiemetic would you use for vertiginous nausea

A
  • Centrally acting, on brainstem and vestibular afferents
  • Good for any cause of N&V mainly in vestibular disorders e.g vertigo, tinnitus, Meniere’s disease, motion sickness
  • Examples; Cinnarizine, Cyclizine
  • SE: drowsiness, dry mouth, sometimes blurred vision
20
Q

what is a Mallory Weiss syndrome

A

Mallory–Weiss syndrome or gastro-esophageal laceration syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe alcoholism, retching, coughing, or vomiting.

21
Q

Management of acute GI bleed

A
  • Protect airway, give 100%O2
  • 2 large IVI access
  • Bloods for FBC,U&E,LFT, glucose, clotting, CXM 6 units
  • IV colloid whilst awaiting blood, (O Rh-ve)
  • CVP, urinary catheter, HCU/ITU
  • 15 mins vital obs, including pulse, BP, CVP, UO
  • Urgent endoscopy
  • If risk of rebleed then iv PPI infusion
  • Surgical intervention