Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Inflammatory & GI Diseases > GI System > Flashcards

GI System Flashcards

1
Q

What is the sub muscosa?

A

Connective tissue, allowing tract to distend & be elastic.
Contains larger blood & lymph vessels -> sends branches to muscosa & muscularis mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the muscularis externa?

A

Major smooth muscle comprised of 2 layers:
- Inner circular mayers
- Outer longtitudinal laters.
Responsible to mixing & propulsive movements.
Myenteric nevere plexus lives between 2 the 2 layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of the autonomic smooth muscle?

A

Self induced electrical activity in digestice smooth muscle. Electrical activity is induced by cells of Cajal.
Reaching the threshold to induce contraction depends on mechanical, neural& hormonal factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the receptors found in the GI tract?

A

Chemoreceptors, mechanoreceptors, osmoreceptors.
Stimulation results in neuronal reflexes or secretion of hormones which alter avidity of effector cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What hormones are released in the stomach?

A

Ghrelin
Gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Wht hormones are released in the duodenum?

A

Cholecytokinin
Sectretin
GIP
Motilin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What hormones are released in the pancreas?

A

Insulin
Glucagon
Pancreatic polypeptide
Amylin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What hormones are released in the small intestine?

A

GLP-1
GLP-2
Oxyntomodulin
PYY3-36

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does trypsinogen do?

A

Converted to active form trypsin by enterokinase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does chymotrypsinogen do?

A

Converted to active form chymotrysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does procarboxypeptidase do?

A

Converted to active form of carboxypeptidase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does pancreatic amylase do?

A

Only enzyme secreted throughout entire digestive system that can digest fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does pancreatic lipase do?

A

Only enzyme secreted throughout entire digestive system that can digest fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does bile contain?

A

Bile salts, Cholesterol, lecithin, bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is bile salts

A

Derivatives of cholesterol, convert fat globules into liquid emulsion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are carbohydrates absorbed?

A

1 - Polysaccharide starch & glycogen converted into disaccharide through action of salivary & pancreatic amylase.
2 - Maltase dissacha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where & how is stomach acid produced?

A

Produced in the parietal cells in the canaliuli. Stimulated by Histamine, gastrin ACh.
Gastrin production stimulated by vagal stimuli, this increases the pH & ingested protein & Ca2+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does somatostatin do in the stomach?

A

Increases mucus secretion, Increases bicarbonate, Increases blood flow & decrease acid production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Helicobacter Pylori (H.pylori)?

A

Bacteria that colonises itself beneath the mucus layer in the antrum -> chronic inflammation. decreased somatostatin, increased gastrin production -> increased acid.
Increased acid means chronic inflammation in duodenum. H.pylori moves into duodenum and causes a duodenal ulcer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is H.pylori identified?

A

Given radio labelled urea & CO2 produced in breath.
Stool sample needs to be stored at -20C before testing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the risk factors of PUD?

A

H.pylori is a major cause of PUD
NSAID common cause of PUD
More common in smokers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What drugs can induce dyspepsia?

A

NSAIDS
Sulfasalazine
Iron preparations
CC
Bisphosphinates.
Theophylline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the symptoms of gastric ulcer?

A

Pain on eating, epigastric pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the symptoms of Duodenal ulcer?

A

Localised pain occurring between meals and at night.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is GORD?

A

Condition caused by gastric juice & occasionally duodenal contents in oesophagus.
Defective Lower Oesophageal sphincter may be most important abnormality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What factors can cause the lowering pressure of the LOS?

A

Dietary factors
Smoking
Endocrine factors
Drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a hiatus hernia?

A

Where part of the stomach is pushed up through the diaphragm, prevents LOS from closing, allowing stomach contents to escape.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Drugs that can cause GORD?

A

Anticholinergics
B-2 Agonists
CCB
Diazepam
Nitrates
Alcohol
Progesterone
Oral Contraceptives
Theophylline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Drugs that cause ulcers?

A

NSAIDs
Bisphosphonates
Clindamycin
Cotrimoxazole
Doxycycline
K
Theophylline
Tetracyclic AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 4 groups of functional dyspepsia?

A

Ulcer like
Dysmotility like
Reflux like
Non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do you manage stomach & duodenal ulcers?

A

Identify & eradicate H.pylori
Stop inappropriate therapy
Decrease acid prod to reduce gastritis & enable mucosa to repair (H2 antagonist/ PPI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do you manage GORD?

A

Remove causative agents
Use of rafting products
Reduce acid prod to enable recovery of oesophageal mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the non-pharmacological advice for GORD?

A

Diet:
- Eat small meals
- Avoid food which decrease pressure of LOS
Avoid eating within 4 & drinking within 2 hours of going to bed
Avoid tight fitting cloths
Lose weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are Antacids?

A

Aluminium, magnesium, Sodium & Calcium salts.
These neutralise stomach acid but cause belching.
Rapid relief of symptoms of heartburn & indigestion.
Avoid long term use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the S/E of antacids?

A

Constipation with aluminium
- Al binds phosphates in the gut -> osteoporosis
- Al may be absorbed -> nephrotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are Alginates?

A

These come with antacids and form a high pH viscus mass (Raft) trapping air bubbles & CO2 from the reaction of antacid with stomach contents.
This raft floats to the top of the stomach and protects oesophageal mucosa from stomach contents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is Dimethicone?

A

Anti-foaming agent
Reduce the surface tension of intragastric air bubbles
Allow bubbles to escape -> reduce bloating feeling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are H2 antagonists?

A

Class of drugs that compete for H2 receptors on the parietal cells.
Can be overridden by a powerful stimulus such as a large meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the S/E of H2 antagonists?

A

Headache & dizziness.
Cimetidine - Gyno 0.2%
Nizatidine - Sweating, abnormal dreams
Cimetidine binds to CYP450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are PPI?

A

Drugs that are enteric coated to absorbed in the small intestine.
Prolonged suppression of acid secretion.
Heal uclers rapidly than H2 antagonists.
Superior treatment of reflux / GORD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the S/E of PPI?

A

Nausea, diarrhoea, flatulence, epigastric pain, dry mouth & headache.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When should you refer someone to the GP when taking PPI?

A

After 2 weeks treatment there’s no improvement.
Treatment required continuously for 4 weeks then refer
Pt is over 45 & present with new or changed symptoms.
Weight loss, loss of appetite, signs of anaemia, dysphagia .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What treatments should be used for dyspepsia, gastritis, PUD?

A

Removal of causative agents.
Dietary changes
Symptomatic treatment.
H2 antagonists/PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What treatments should be used for GORD?

A

Lifestyle & dietary changes
Alginate products / PPI
NOT H2 ANTAGONISTS .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is constipation?

A

Passage of hard stool less frequently than Pt own pattern.
Difficulty in opening bowl:
- Going <3X per week
- Straining to open bowls more than 25% of occasions.
- Hard or pellet like stool more than 25% of occasions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is chronic constipation classes as?

A

> 12 weeks in preceding 6 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What medications cause constipation?

A

Antacids.
Antispasmodics.
Antidepressants.
Iron tablets.
Diuretics.
Painkillers.
CCB.
Anti cholinergic
Ulcer healing.
Laxative abuse.

48
Q

What intestinal obstruction cause constipation?

A

Scarring from IBD, Diverticulitis
Adhesions
intestinal cancer
Abdominal hernia
Gallstones wedged in intestine
Volvulus
Foreign bodies
Haemorrhoids
Fissures.

49
Q

How would you diagnose constipation?

A

Medical history
History of symptoms:
- Normal patterns of shifting
- Other symptoms
- Frequency & consistency
- How long / Intense are the symptoms
- Impact on daily life.
Medication
Changes in diet & lifestyle

50
Q

What are the goals in constipation management?

A

Achieve individual normal frequency of shitting
Establish regular comfortable shit
Preventing laxative dependence
Relieving discomfort.

51
Q

Name some bulking agents

A

Ispaghula husk
Methylcellulose

52
Q

Name some stimulant laxatives

A

Bisacodyl
Senna
Dentron
Sodium picosulphate

53
Q

Name some faecal softeners

A

Docusate
Glycerol
Arachis oil

54
Q

Name some osmotic laxatives

A

Lactulose
Macrogols
Mg

55
Q

What is the acute treatment of constipation in Adults?

A

1 - Lifestyle + manage underlying cause
2 - Bulk forming (+/or) osmotic - macrogol
3 - Stimulant (Gradually reduce + stop after producing a soft, formed stool without straining at least >3X per week).

56
Q

What is the chronic treatment of constipation in adults?

A

1 - Lifestyle + manage underlying cause
2 - Bulk forming (+/or) osmotic - macrogol
3 - Stimulant
4 - Prucaptopride
Gradually titrate the laxative doses up/down aiming to produce soft, formed stool without straining >3X per week.

57
Q

What is the treatment constipation in pregnant people?

A

1 - Offer bulk forming
2 - ADD/Switch to osmotic
3 - Can consider a short course of stimulant
4 - Glycerol suppository.

58
Q

What is the treatment of constipation in someone who is breast feeding?

A

1 - Offer bulk forming
2 - ADD/Switch to osmotic
3 - Can consider a short course of stimulant (Senna/Bisacodyl)
4 - Glycerol suppository.

59
Q

What would you give for hard stool faecal impaction / Loading ?

A

1 - High dose of oral macrogol
2 - Stimulant reduce inadequate / slow
3 - Glycerol alone or with Bisacodyl suppositories
- Response still inadequate - Sodium phosphate / arachis oil retention enema.

60
Q

What is the treatment for opioid induced constipation?

A

Avoid bulk forming laxatives.
1 - Osmotic (or docusate) + stimulant
2 - Naloxegol :
- Peripherally acting mu-opioid receptor antagonist.
- Oral
3 - Mehtylnaltrexone :
- Pamora
- S/C
4 - Naldemdine :
- Pamora
- Oral

61
Q

What is the treatment of constipation in children?

A

1 - Macrogels & negotiated + non punitive b/h interventions suited to persons of development.
2 - Add stimulant
3 - Add lactulose

62
Q

What is the lifestyle advice you would give someone with constipation?

A

high fibre diet & sufficient fluid

63
Q

What is the pharmacology of bulk forming laxatives?

A

Mimic polysaccharides so increase osmolarity in the gut when broken which causes water retention. Water retention causes softening of stool. Promotion of peristalsis via stimulating colonic mucosal receptors this leads to ACh release. ACh activates muscarinic ACh receptors which increases peristalsis

64
Q

What is the pharmacology of Osmotic laxatives?

A

These are poorly absorbed so they act as osmotic agents which increase water retention. These are hyperosmolar agents, absorbed into stool by osmosis. Mg2 triggers release of cholecytokinin (CCK) this increases intestinal secretions & colonic motility. Which decreases transit time through the gut.

65
Q

What is the pharmacology of stimulant laxatives?

A

Stimulate local reflexes of the myenteric nerve plexus of the gut. Irritate nerve endings in wall of intestine. Motor effect on gut wall increases propulsion. Increase secretion of H20 into bowl, increases gut motility & decrease transit time.

66
Q

What is the pharmacology of Senna?

A

It is anthraquinone laxative. Combine with sugars -> glycosides. Glycosides molecules where sugars is attached to functional group via glycosidic bond. Glycosidic bonf hydrolysed by colonic bacteria to release irritant antracene glycoside, sennosides A&B. These are absorbed and have a direct action on the myenteric nerve plexus. Also postulated to increase PGE2 secretion and decrease colonic H20 absorption.

67
Q

What is the pharmacology of stool softeners?

A

Emollient laxatives. Work as a surface wetting agent / surfactant. Decrease surface tension allows H20/Fat to penetrate stool.

68
Q

What do PAMORA do?

A

Prevent opioid activator of intestinal mu-opioid receptor.

69
Q

What is the pharmacology if prucalopride?

A

5HT4 receptor agonist
Which causes an increase release of ACh which then increase parasympathetic drive which increase peristalsis

70
Q

What are the RED FLAG symptoms?

A

Pain on defication
Pt over 40
greater than 14 days
Associated fatigue
Presence of blood
Repeated failure of laxatives.

71
Q

What is chronic diarrhoea?

A

When its lasts more than 14 days

72
Q

What is the pathophysiology?

A

Change in balance between the absorption & secretion of water & electrolytes. Osmotic force drives water into the gut lumen.

73
Q

What is the mechanism of diarrhoea which is caused by bacteria??

A

Invasive:
Directly attack mucosal cells which cause diarrhoea.
Stools may contain puss & blood.
Non-Invasive:
Do not DMG gut
Bacteria produce enterotoxins that disrupt secretions

74
Q

What drugs cause diarrhoea?

A

Antibiotics
Laxatives
Metformin
Ferrous sulphate
NSAIDs
Cholestyramine
Antacids
Digoxin

75
Q

What is the treatment of acute diarrhoea in adults?

A

Prevention & reversal of fluid & electrolyte depletion
Management of dehydration ]
ORT
Eat bland food
Stool bulking fruits
Avoid alcohol, caffeine

76
Q

What is the pharmacology of Loperamide?

A

Binds to mu-opioid receptors in gut wall.
Doesnt cross BBB
–| ACh
ACh bind to muscarinic/nicotinic ACh receptors which increase parasympathetic activity.

77
Q

What are the red flags to refer?

A

Recent travel abroad
Blood/mucus in stool
Associated with severe vomiting and fever
Signs of dehydration.

78
Q

What medications should you stop taking while having diarrhoea for 24-48 hours?

A

ACE-i, ARB, Diuretics, Metformin.

79
Q

What is C.diff?

A

Board spectrum antibiotics upset the microbiome allowing C.diff to flourish.

80
Q

What is the treatment for C.diff?

A

Vancomycin 125-500mg every 6 hrs for 10 days

81
Q

What is the symptoms of IBS?

A

Abdominal cramping
Diarrhoea, constipation, alternating
Farting
Bloating
Urge to shit
Acid indigestion
Nausea
Lethargy
Eating may worsen symptoms
Passing mucus in the stool

82
Q

What are the red flags & referral of IBS?

A

Unintentional weight loss
Unexplained rectal bleeding
Loose stool for >6weeks in Pt over 60 yrs
Anaemia

83
Q

Describe the pathophysiology of CD?

A

Can affect any part of the GUT
Usually terminal ileium & ascending colon.
Affected areas are thickened, deep ulcer can appear, can progress to deep fissuring uclers

84
Q

What are the clinical features of both UC/CD?

A
  • Diarrhoea
  • Fever
  • Abdominal pain
  • N&V (More common in CD)
  • Malaise
  • Weight Loss (More common in CD)
  • Malabsorption
85
Q

What clinical features are unique to CD?

A
  • More debilitating that UC
  • Can be acute / insidious
  • Palpabke masses
  • Small bowel obstruction
  • Abcesses
  • Fistulas
86
Q

What are the complication of IBD

A
  • Osteopenia
  • Erythema Nodosum - Tender, hot red nodules, subside in a few days.
  • Pyoderma Gangrenosum
  • Ocular Episclritis - Intense burning & itching of blood vessels involved.
87
Q

What is P-ANCA present in?

A

-VE in CD
+VE in UC

88
Q

What is the MOA of CC?

A

Positively transporting themselves into target cells & binding the intracellular CC receptor du to being membrane bound to heat shock protein complex. When CC binds to GRalpha its activated of homodimer of 2 activated GR transported into nucleus of target cell. This –| promoter regions of genes such as NFKB & AP-1

89
Q

What is the MOA of azathioprine?

A

Azathioprine is converted to 6-MP. This is then activated by HGPRT &TPMT. 6-TGN is then slotted into DNA.
Another pathway forms Xanthine oxidase to form 6-Thiouric Acid. 6-Thio - GTP binds to Rac-1 instead of GTP. Activation of Rac-1 target genes such as MEK, NKFB, BCL-XL.

90
Q

What is the MOA of 5-aminosalcylates?

A
  • Have an action on both PG synthesis/cyclooxygenase pathway and supression of pro-inflammatory cytokines
  • Actions of PG synthesis comes VIA COX –|
  • Actions on supression of cytokines comes via –| of PPARgamma, NF.kB & other non-COX targets.
  • Can also scavange reactive oxygen metabolites. from superoxide anion generation by neutrophils which can in turn prevent DNA & tissue DMG.
91
Q

How does TNFα work?

A

TNFα activates macrophages to produce proinflammatory cytokines -> increase apoptosis of gut epithelial cells -> regulates T cells apoptosis -> paneth cell death vai necropoptosis.

92
Q

What mediators cause Crohns Disease?

A

TH1 - IFNγ, TNF, IL-6
TH17- IL-17A/F, IL-21, IL-22

93
Q

What mediators cause Ulerative collitis?

A

TH2 - IL-5, IL-6, IL-13, TNF
TH9 - IL-9
TH17 - IL17A/F, IL-21, IL-22

94
Q

What mediators cause resolution in healthy cells?

A

IL-10, TGF-β

95
Q

How does inflixumab work?

A

Human monoclonal antibodies that bind both soluble & trans membrane bioreactive forms of human TNFα -> prevents binding of TNFα to receptors -> –| biological activity of TNFα

96
Q

What is the MOA of Ustekinumab?

A

Monoclonal antibody targetting P40 subunit of IL-12 & IL-23. –| of IL-12 & IL-23 supress TH1 & TH17 cells linage of cytokines & chemokines in IBD

97
Q

Describe T-Cell homing IBD?

A
  • In IBD, T-cells migrate/home towards gut tissue when they accumulate in large numbers and secrete inflammatory mediators (IL-6, IL-23, TNFα)
  • T-cell homing to the gut requires an interaction between 2 molecules; one on the surfae of the T-cell and on the endothelial cell.
  • T-cell surface integrin, α4β7, is a gut specific adhesion molecule that specifically ineractis with mucosal vascular adression adhesion molecule (MAdCAM1) that is expressed in the endothelium.
  • T-cells are also reatined in the gut tissue through binding of the α4β7 integrin to the E-cadherin on the basal membrane of the epithelial cell.
98
Q

What is the MOA of Vedolizumab?

A

Anti α4β7 antibody blocking homing of T-cells to the inflammed gut.

99
Q

What is the signalling pathway for Sphingosine 1 - Phosphate?

A

S1P receptor controls egression of the immune cells from lymph nodes through a [ ] gradient on sphinosine 1 phosphate. S1PR1 agonists render lymphocytes sensing the S1P gradient and exiting lymph therefore causing a reduction in lymphocytes.

100
Q

What is the aim of UC therapy?

A
  • Reduce inflammation
  • Induce remission
  • maintain remission
  • Improve QOL
  • Minimise toxicity related to drugs
  • Maintain therapy used to maintain remission
101
Q

What is the treatment for proctitis UC?

A
  • Topical aminosalicylates
  • Add oral aminosalicylate if remmision not achieved in 4 weeks
  • For Pt that cannot tolerate aminosalicylates consider time limited oral/topical CC
102
Q

What is the treatment for proctosigmoiditits & distal colitis UC?

A
  • Topical aminosalicylates
  • If remissoin not achieved in 4 weeks consider high dose oral aminosalicylates or switching to high dose oral aminosalicylates + time limited topical CC
  • if this still doesnt work then oral aminosalicylates + oral CC
103
Q

What is the treatment for extenisve UC?

A
  • Topical aminosalicylates + high dose oral aminosalicylates
  • no remission in 4 weeks then stop troical treatment & offer time limited course of oral CC
  • For ppl who cannot tolerate aminosalicylates -> time limited oral CC
104
Q

What is the treatment to induce remission is moderate to severe UC?

A
  • Biologics & JAK
  • Infliximan & adalinumab
105
Q

What is the treatment to induce ression in acute hospitalised?

A
  • IV CC & assess likelihood of requireing surgery
  • Consider IV ciclosporin / surgery intolerant / decline / CI CC
106
Q

What is the treatment of proctitis & proctosigmoiditis - maintaining remmison in UC?

A
  • Topical aminosalicylate alone
  • Oral aminosalicylate + Topical aminosalicylate
  • Oral aminosalicylate if Pt decline topical treatment.
107
Q

What is the treatment to maintain remission in mild - moderate UC?

A
  • Offer low maintenance dose of oral aminosalicylate.
108
Q

What treatment should be used to maintain remission in all areas?

A
  • Consider mercaptopurine / azathioprine.
109
Q

What is the treatment for inducing remission in CD?

A

Monotherapy with traditional CC (Prednisolone, hydrocortisone IV)

110
Q

What is the treatment for inducing remission for add on therapy?

A
  • Consider + azathioprine / mercaptopurine to CC / budesonide to induce remission.
  • Consider adding MTX to CC / Budesonide in those who cant tolerate azathioprine / mercaptopurine or lower TPMT activity.
111
Q

What used in maintaining remission in CD?

A
  • Azathioprine / mercaptopurine
  • Consider MTX in those who need it.
112
Q

What are the S/E of aminosalicylates?

A
  • Headache, nausea, fever, rash, raised temp, decreased WBC
  • Pancreatitis
  • Hepatitis, pneumonia, skin reactions, haemolysis, inflammation of the kidney
113
Q

What should be checked before starting Thiopurines?

A
  • FBC, U&E, LFT
  • Screen of HCV, HIV, HBV / VZV
  • Vaccinated influenza & pneumococcal
114
Q

What should be monitored while on thiopurines?

A
  • FBC, U&E, LFT at least 2, 4 8 & 12 then 3 monthly
115
Q

What should the PT report if they’re on thiopurines?

A
  • Ulceration
  • Fever
  • Infection
  • Bruising
  • Bleeding
116
Q

What should you reduce the dose of azathioprine by when you are taking both allopurinol and azathioprine?

A

1/4

117
Q
A

Inflammatory & GI Diseases (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions