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The Patient - Semester 2 > The Patient - Semester 2 GI > Flashcards

The Patient - Semester 2 GI Flashcards

1
Q

How much small intestine in average human?

A

20m

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2
Q

Path from mouth to rectum?

A

Mouth –> pharynx –> oesophagus –> stomach –> small intestine –> large intestine –> rectum

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3
Q

What is mumps and where does it infect?

A
  • Viral infections that involves salivary glands.
  • It binds to receptors and cells in glands.
  • Can also infect testes and make patient sterile.
  • Can also infect pancreas.
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4
Q

How does swallowing occur?

A
  • Sensors in mouth and back of throat
  • Relay info to brain which is fed to medulla oblongata
  • Processed so impulses and action potentials fed back to throat allow swallowing.
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5
Q

Two main nerves involved in swallowing process?

A
  • Trigemirial

- Facial

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6
Q

What is dysphagia?

A

Difficulty swallowing.

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7
Q

What is the oesophagus hiates?

A

An opening in the diaphragm - there can sometimes be weakness at this point resulting hiatus hernia which can cause acid reflux.

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8
Q

What is barrets oesophagus

A
  • Usually lined with squamous epithelial cells under high power microscope
  • Oesophagus and stomach are separated by the lower oesophageal sphincter –> a muscle sealing stomach and top and bottom
  • This stops stomach acid from entering oesophagus.
  • If stomach contents do move up epithelium - squamous cells are replaced by abdominal cells.

MAJOR ISSUE as cells replaced with are pre cancerous - these individuals are at higher risk of colenocarcinoma

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9
Q

What is the purpose of mucous cells?

A

Act as a barrier across the surface of the stomach.

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10
Q

What is the purpose of G cells?

A

Enteroendocrine secretes gastrin which stimulates acid production.

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11
Q

What is the purpose of chief cells?

A

secrete pepsinogen/lipase

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12
Q

What is the purpose of parietal cells?

A

(aka oxyntic cells) they secrete HCl

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13
Q

What is pepsinogen?

A
  • Pepsinogen is the inactive form of pepsin.
  • When pepsinogen is exposed to acid it cleaves pepsinogen to pepsin (active)
  • Now have enzyme to digest proteins.
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14
Q

How is acid secreted into stomach?

A

1) Smell of food triggers receptors and stimulates stomach.
2) Binds to receptors on parietal cells and this causes release of H+ into lumen.
3) Gastrin released from G cells which binds to receptor on parietal cell and causes release of HCl
4) When you eat, stomach stretches causing a release of histamine. This binds to receptor on parietal cell again causing release of acid –> if we block this we can reduce release of acid.

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15
Q

How do H2 receptor antagonists work?

A

Drugs bind to histamine receptor therefore less acid is released to lumen. e.g. Ametidine

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16
Q

How do PPI’s work?

A

Example omeprazole.

  • this irreversibly binds to proton pump and targets SH groups of pump to prevent acid being released.
  • They prevent H+ release so only Cl- released fro, cell to lumen.
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17
Q

How is self digestion prevented in the stomach?

A

1) Mucus foveolar cells –> secreted and its alkaline nature neutralises HCl
2) Tight junctions–> lock epithelial cells together. Restricts movement of the acid.
3) High cell turnover rate - damaged cells replaced

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18
Q

What would happen if there was a breakdown in the mucus barrier?

A
  • Epithelial cells would then be exposed to the HCl and pepsin –> this would then produce a gastric/duodenal ulcer.
  • Duodenal = upper part of digestive system.
  • Damage may extend deeper overtime into wall of GI tract (can result in haemorrhage or excessive bleeding)
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19
Q

What is a perforated ulcer?

A
  • Complete erosion through tract wall which allows contents of GI tract to move out and into peritoneal cavity (where intestines are held)
  • This can lead to peritonitis and hospitalisation.
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20
Q

What is a fatal consequence of peritonitis?

A

Sepsis.

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21
Q

What is Helicobacter Pylori?

A

A flagellated bacteria which infects gastric mucosa. (leads to a decrease in barrier efficacy)

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22
Q

What is the treatment for Helicobacter Pylori ?

A

2 antibiotics and a PPI.
Omeprazole, Carithromycin and Amoxicillin
or
Omperazole, Clarithromycin and metrondiazole

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23
Q

What is the most proximal part of the small intestine called?

A

Duodenum.

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24
Q

What is peristalsis?

A

Group of muscles called circular muscles and longitudal muscles contract which moves food down.

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25
Q

How is diarrhoea treated?

A

Reduce peristalsis activity so the faeces is exposed to epithelial cells for longer therefore more absorption occurs.

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26
Q

How is contraction controlled?

A

Controlled by nerves and neurones inside the MP (myenteric plexus)

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27
Q

Loperamide (Imodium) mechanism of action?

A
  • Mechanism of action = binds to opioid receptors of the MP and reduces contraction of the muscles.
  • However may cause constipation.
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28
Q

Purpose of bile acids?

A
  • Emulsify lipids and allow their absorption.

- Also needed for lipid soluble vitamins A, D, E, K which we need day to day.

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29
Q

Gastrointestinal adaptations:

A

1) Plicae (folds) - covered in finger like projections called villi which are also covered in microvilli.
2) epithelium = 1 cell thick
3) Enzymes- lots of them to convert non absorbable macromolecules to absorbable small molecules.

Glucose and galactose via sodium glucose transporter 1 SGLT 1
- Sodium Na+ dependent.

Fructose transported by GLUT5

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30
Q

How is protein digested?

A
  • Proteins too large therefore chopped into small molecules.
  • Small peptides transported by PEPT1 transporter (H+ dependent)
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31
Q

How are hydrophilic absorbed?

A
  • Absorption via uptake transporters is extremely efficient

- Hence why drugs are based on natural products e.g. peptide based drugs

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32
Q

Examples of PEPT1 substrates?

A
  • Cephalosporins
  • Penicillins
  • Enalapril
  • alphamethyldopaphenylalanine
  • Valacyclovir
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33
Q

Examples of Organic Cation transporter substrates (OCTN2)?

A
  • Quinidine
  • Verapamil
  • Imatinib
  • Valproic acid
  • alphamethyldopaphenylalanine
  • Valacyclovir
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34
Q

Examples of Organic Anion Transporting polypeptide (OATP2B1) substrates:

A
  • Pravastatin
  • Rosuvastatin
  • Atorvastatin
  • Fexofenadine

(remember statins)

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35
Q

How can transporters be detrimental to drug absorption?

A
  • Efflux transporters (eject compound from cell) thereby reducing drug absorption.
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36
Q

What are P-glycoproteins?

A

Efflux pumps.

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37
Q

What are some examples of Pgp substrates?

A
  • HIV PI
  • Immunosupressants
  • Antibiotics
  • Cardiotonics (digoxin)
  • VERY DIFFICULT TO GIVE CANCER DRUGS ORALLY
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38
Q

All oral anticancer drugs are substrates for Pgp efflux pump.
True or False?

A

True

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39
Q

Is Doxorubicin a Pgp substrate?

A

Yes -

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40
Q

Name 2 Digoxin drug drug interactions

A

Digoxin and ritonavir
Digoxin and atorvastatin

Both increase digoxin AUC

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41
Q

What is Dyspepsia?

A

Persistant or recurrent pain or discomfort in upper abdomen.

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42
Q

Causes of Dyspepsia?

A
  • Lifestyle factors
  • Medication
  • Disease
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43
Q

What is GORD and what are the symptoms?

A

Gastro Oesophageal Reflux Disease.

Complications resulting from reflux gastric contents into oesophagus, oral cavity or lung such as stricture, barrets oesophagus and oesophageal carcinoma.

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44
Q

Causes of GORD:

A
  • Obesity
  • Genetic
  • Lifestyle
  • Medication
  • Age
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45
Q

What are peptic ulcers?

A
  • Open sores on the inside lining of oesophagus, stomach and upper portion of small intestine.
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46
Q

Causes of peptic ulcer?

A
  • H pylori
  • NSAIDS
  • Lifestyle factors
  • Genetics
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47
Q

Definition of peptic ulcer:

A

Breach in continuity of epithelial lining of more than 5mm in diameter associated with inflammation.

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48
Q

What is the difference between a gastric ulcer and a duodenal ulcer?

A

GASTRIC ULCER –>

  • Pain radiates to back
  • Mainly occurs at night
  • Aggravated by food
  • Loss of weight

DUODENAL ULCER–>

  • Eipgastric pain
  • Anytime - empty stomach
  • Relieved by food/antacids
  • Weight gain
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49
Q

Management of ulcers?

A
  • Medicine management
  • Smoking cessation
  • Avoid acidic food and drink
  • avoid eating late in evening
  • Weight reduction
  • Reduce stress
50
Q

What is ALARMS?

A 
Warning signs for ulcers:
A = anaemia 
L = loss of weight 
A = Anorexia 
R = Recurrent 
M = melaena 
S = swallowing problems
51
Q

What are the required assessments for ulcers?

A
  • Medicine review
  • Blood test
  • H pylori testing
  • X ray
  • Endoscopy
52
Q

What are antacids used for and what are some of their side effects?

A

Ulcer

  • they neutralise stomach acid
  • Simple cheap and effective
  • Dosage = PRN
  • Side effects –>
    magnesium = laxative effect
    aluminium = constipation
    calcium containing = possible rebound acid secretion.
53
Q

Can sodium bicarbonate be prescribed on its own?

A

No - but present in some other preparations.

To be avoided if patient is on a salt restricted diet.

54
Q

Interactions of antacids:

A
  • May impair action of drugs taken at same time
  • can damage enteric coating by raising the pH
  • Rarely may affect pH dependent renal excretion
55
Q

What is an alginate?

A
  • Drug given in combo with an antacid

- Increase viscosity of stomach contents

56
Q

How does an alginate work?

A

Forms raft that floats on top of stomach contents.

57
Q

What is the daily dose of H2 receptor antagonists ?

A

BD

58
Q

Are H2 receptor antagonists available OTC?

A

Yes - they are generally safe and well tolerated. example Ranitidine (Zantac)

59
Q

Name some interactions of H2 receptor antagonist Cimetidine:

A
  • Warfarin
  • Theophylline
  • Sildenafil
  • Phenytoin, carbamazepine, valproate,
60
Q

Are PPI’s available OTC?

A

Yes

61
Q

Indications of PPI’s

A
  • Dyspepsia
  • GORD
  • Treatment of gastric and duodenal ulcers
  • NSAID prophylaxis
62
Q

Side effects of PPI’s

A

Headache, constipation, diarrhoea, dizziness

MHRA warning - SCLE (sub cutaneous lupus erythematosus)

63
Q

What are some of the consequences of long term PPI use?

A
  • gastric cancer
  • H pylori infection
  • Pneumonia
  • Clostridium difficile infection
  • Bacterial overgrowth and reduced calcium absorption leading to hip fracture.
64
Q

Name some interactions of PPI’s:

A
  • antiretro virals
  • methotrexate
  • citalopram
  • predicted to decrease efficiency of clopidogrel
65
Q

Helicobacter pylori always castes gastritis, true or false?

A

True

66
Q

How is H. Pylori detected?

A
  • Antibody response detectable in serum, salvia or urine.

- Antigen detectable in stool

67
Q

Testing that is required for H Pylori:

A
  • Urea breath test kits
  • Stool antigen test
  • Mucosal biopsies
  • Lab based serology
68
Q

Antibiotics can surpress H Pylori growth and give a false negative. True or false?

A

True

69
Q

Rules of testing for H Pylori:

A

Testing should not be performed within 4 weeks of treatment with antibacterials or 2 weeks with PPI drugs.

70
Q

Consequences of NSAIDS:

A

Variety of GI injuries including PUD bleeding and ulceration.

71
Q

What is the mechanism of NSAID induced ulcers:

A
  • Inhibition of prostaglandins synthesis impairs mucosal defences (erosive breach of epithelial layer)
  • Acid attack deepens breach into frank ulceration
72
Q

What is the indirect mechanism of NSAID induced ulceration:

A

Reduced gastric blood flow and reduced mucus production leads to decreased cell repair.

73
Q

Management against NSAID induced GI injury:

A
  • Stop NSAID if possible
  • Test for H Pylori
  • Treat with full dose of PPI or H2 receptor antagonist for 8 weeks.
74
Q

Name a medication that prevents NSAID induced PUD.:

A

Misoprostol

75
Q

Misoprostol mechanism of action?

A

Prostaglandin analogue - less well tolerated than PPI’s

- Also a drug used to terminate pregnancy

76
Q

What are the two examples of Inflammatory Bowel Disease?

A
  1. Crohn’s disease

2. Ulcerative colitis

77
Q

What is the peak age of diagnosis in Inflammatory Bowel Disease?

A

10 - 25

78
Q

Most common side effect o Inflammatory Bowel Disease?

A

Diarrhoea

79
Q

What is IBD?

A

Inflammation of the gastric mucosa

80
Q

Difference between Crohns disease and ulcertaive colitis:

A

CD = whole of GI tract from mouth to anus and affects all layers

UC = affects mucosa of colon and rectum
only mucosal and submucosal layers involved.

81
Q

Causes of Inflammatory Bowel Disease?

A

Precise mechanism unknown - likely to be a combo of factors such as:

  • Genetic
  • Environmental
  • Gut microbes
  • Smoking
  • Infection
  • Diet
  • Medication
82
Q

IBD signs and symptoms?

A 
Abdo pain 
Diarrhoea 
Fatigue 
Anaemia 
Weight loss 
Fever

(Can get extraintestinal manifestation) e.g. swollen joints, eye problems

83
Q

Consequence of Crohns:

A

Strictures: narrowed segments of bowel –> leads to blockages

Fistulas: abnormal channels lined with granulation tissue –> form between intestine and skin

84
Q

Investigations required for Crohns:

A
  • Blood test (full blood count, thyroid function, liver function, urea and electrolytes, inflammatory markers)
  • Stool culture
  • Faecal calprotectin (distinguishes between CD and UC)
  • Endoscopy
  • Colonoscopy
  • Biopsies
  • Abdo imaging.
85
Q

What is the CDAI?

A

Crohns Disease Activity Index

86
Q

Aims of management of IBD?

A
  • Achieving remission
  • Mainting remission
  • Improving QoL
87
Q

What are the 5 treatments for IBD?

A
  • Corticosteroids
  • Aminosalicylates
  • Immunomodulating agents
  • Antibiotics
  • Novel treatments
88
Q

How are Corticosteroids used in IBD treatment?

A
  • Induce remission
  • Reduce inflammation
  • Oral or IV used
  • Mustn’t be stopped abruptly –> adrenal supression
Oral = prednisolone 40mg daily 
IV = acute severe, hydrocortisone 100mg ads
89
Q

Do corticosteroids prevent progression of IBD?

A

No - they just induce remission.

90
Q

Side effects of corticosteroids:

A
  • GI side effects
  • Fluid and electrolyte balance
  • Increased appetite
  • Hypertension
  • Infection risk
  • Risk of development of osteoporosis
91
Q

How are aminosalicylates used in IBD treatment?

A
  • anti inflammatory action
  • Induce and maintain remission
  • Mostly used for UC
  • Can give topical and oral together if required.
92
Q

Give two examples of aminosalicylates

A

Sulfasalazine

Mesalazine

93
Q

Monitoring requirements for aminosalicylates:

A
  • Renal Function

- Blood dyscresias

94
Q

How are thiopurines used in IBD treatment?

A
  • Induce and maintain remission
  • First line Immunomodulators for IBD
  • Can take 3-6 months for full effects
95
Q

Example of thiopurine:

A

Azathioprine (prodrug)

Weight based dosing

96
Q

What are TMPT levels?

A

Thiopurine methyl transferase.

Must be recorded when taking thiopurines.

97
Q

What other immunomodulators are used in IBD apart from thiopurine?

A
  • Methotrexate (mainly for maintenance in CD) once weekly
    (sometimes coprescribed with folic acid)
  • Tacrolimus- induces remission in mild moderate UC
  • Ciclosporin induces remission in severe UC
98
Q

What biologics are used in IBD and what is there mode of action?

A

E.g. Infliximab

  • Monoclonal antibodies
  • Work by binding to tumour necrosis factor a
  • Inhibit inflammatory effects in gut
99
Q

How is infliximab administrated?

A

IV

100
Q

Future therapies of IBD?

A
  • Faecal microbiota transplant
  • Probiotics
  • New biologics
101
Q

What is the WHO definition of diarrhoea?

A

Passage of 3 or more loose liquid stools per day

102
Q

How is diarrhoea categorised?

A

Acute < 14 days
Persistant > 14 days
Chronic > 28 days

103
Q

Causes of diarrhoea?

A
  • Increased osmotic load in gut lumen
  • Increased intestinal motility
  • Increased secretion

Other causes= drugs, parasites, anxiety
ecoli, salmonella

104
Q

When would you refer an adult with diarrhoea?

A 
Symptoms:
>72 hours in healthy adults 
>48 hours in elderly 
>24 hours in diabetics 
- Associated severe vomiting 
- blood/mucus in stools
- ADR 
- Weightloss
- Rectal pain
105
Q

What treatment is available for diarrhoea?

A
  • Oral rehydration therapy
  • Loperamide
  • Morphine
  • Diphenoxylate
  • Adsorbents
  • Antibiotics
106
Q

How does oral rehydration therapy work?

A
  • enhances absorption of water and electrolytes
  • contain alkalinising agent to counter acidosis
  • Must be slightly hypo-osmolar
107
Q

What ingredients do oral rehydration therapies usually contain?

A
  • Na and K to replace essential ions

- Citrate and/or bicarbonate to prevent acidosis

108
Q

How does loperamide work?

A
  • it is a synthetic opioid analogue
  • Reduces peristalsis so faeces stays in gut for longer
  • Cant be used In active ulcerative colitis
  • MHRA ALERT - serious cardiac ADR
109
Q

When are antibiotics used in diarrhoea treatment?

A

Only if confirmed infection in stool sample

110
Q

How does morphine work in diarrhoea treatment ?

A

Direct action on intestinal smooth muscle

111
Q

How does diphenoxylate work in diarrhoea treatment?

A

Synthetic derivative of pethidine

112
Q

How does absorbents work in diarrhoea treatment?

A

absorb microbial toxins and microorganisms e.g. kaolin

113
Q

What is the rotavirus vaccine?

A

A live oral vaccine that protects young children against gastroenteritis infection.

2 doses:

  • First at 2 months of age
  • 2nd at 3 months (at least 4 weeks after last one)
  • Course should be completed before 25 weeks of age
114
Q

What is clostridium difficile?

A
  • Spore producing, anaerobic, gram positive anaerobic bacterium.
  • Caused by antibiotics
115
Q

Clostridium difficile antimicrobial treatment?

A
  • Oral metronidazole 400mg ads
  • Oral vancomycin - sever disease oral 125mg every 4 hours
  • probiotics, faecal microbiota transplant and iv immunoglobulin used also
116
Q

How many types of stool classified in Bristol stool chart?

A

1-7

117
Q

What are the two cases of constipation?

A

Functional - no anatomical cause known

Secondary - induced by particular condition or medicine

118
Q

Constipation treatment?

A

Lifestyle intervention:

  • Diet (fibre)
  • Fluids
  • Lifestyle measures

LAXATIVES

119
Q

What are the four type of laxatives available? Explain.

A
  1. Bulk forming - increase faecal mass to stimulate peristalsis e.g. methyl cellulose
  2. Stimulant - increase intestinal motility via muscle contractions e.g. Senna
  3. Osmotic - draw water into intestine by osmosis e.g. macrogel powders.
  4. Faecal softening - stimulate peristalsis by increasing Faecal mass
    e. g. glycerol suppositiory
120
Q

What is coeliac disease?

A
  • Autoimmune disease
  • Affects small bowel
  • NOT ALLERGIC REACTION
121
Q

How is coeliac diagnosed?

A

Serology or endoscopy

The Patient - Semester 2 (4 decks)

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