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GI Flashcards

0
Q

What do G-cells secrete and where are they found?

A

Gastrin which stimulates H+ release.

Found in Antrum, duodenum and pancreas.

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1
Q

What do parietal cells do?

A

Secrete intrinsic factor & gastric acid

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2
Q

What do D-cells secrete?

A

Somatostatin which act on parietal cells

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3
Q

What do chief cells secrete and where are they found?

A

Secrete pepsinogen and are only found in the fundus

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4
Q

What is diarrhoea?

A

> 3 loose stools in one day.

Acute = 14 days

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5
Q

What occurs in secretory diarrhoea and what can cause it?

A

Increase in active secretion ± reduced absorption. It continues when fasting and produces high volume, normal osmolality stools.

Can be caused by Cholera

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6
Q

What is osmotic diarrhoea and what can cause it?

A

Osmotic potential of the gut lumen is increased drawing in more fluid –> high osmolality.

Can be caused by Sorbitol, coeliac disease, lactose intolerance

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7
Q

What is exudative diarrhoea and what causes it?

A

Presence of pus, mucus and blood in stools.

Can be caused by Crohn’s and UC

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8
Q

What is dysentary?

A

Blood and mucus in the stools with abdominal pain

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9
Q

What are the symptoms of C.diff?

A

Post Abx, foul smelling and cramps

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10
Q

What is ETEC?

A

Travellers diarrhoea, watery stools that last several days

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11
Q

What are 2 examples of viral gastroenteritis and in what groups are they most common?

A

Rotavirus- <5 y.o.

Notovirus- adults

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12
Q

What is a parasitic cause of diarrhoea and what are its symptoms?

A

Giadiasis

Parasite in areas of poor sanitation, causes bloating, cramps, flatulence and diarrhoea

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13
Q

How can pancreatitis or pancreatic insufficiency cause diarrhoea?

A

The body cannot break down and absorb lipids causing steatorrhoea

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14
Q

What is in oral rehydration solution and what is its osmolality?

A

Water, sodium chloride and glucose
UK- 240 mOsm/L
WHO- 245 mOsm/L

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15
Q

How much fluid should be replaced per loose stool?

A

200ml

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16
Q

What drugs can cause diarrhoea and how?

A

ABx- increase motility and altering gut flora
NSAIDs- irritation and inflammation of the gut
Digoxin- Ion imbalance
Orlistat- Fat in the gut
Metformin
Mg- osmotic effect

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17
Q

How does loperamide work?

A

Acts on opioid receptors in the bowel, decreasing bowel motility and increases anal sphincter tone

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18
Q

What are red flag symptoms in GORD?

A

Dysphagia
Haematemesis, malaena or anaemia
Weight loss
Anorexia

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19
Q

What can cause dysphagia?

A

Oesophageal/peptic stricture, long-term GORD–> adenocarcinoma

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20
Q

What is the treatment for H. pylori?

A

Triple therapy:

  • PPI (omeprazole)
  • Clarithromycin
  • Amoxicillin
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21
Q

How can H.pylori be diagnosed?

A

Urea breath test
Stool antigen
Serology IgG

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22
Q

What is barratts oesophagus?

A

Z-line is higher up and there is metaplasia of the oesophagus from squamous to columnar epithelium

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23
Q

What is a peptic ulcer and where are they most common?

A

Break in the mucosal surface >5mm in size.

Most common on the lesser curvature of the stomach

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24
Q

What is Zollinger-Ellison syndrome?

A

Gastrin secreting tumour –> can cause ulcers

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25
Q

How do NSAIDs increase the risk of peptic ulcers?

A

They decrease COX-1 levels which therefore reduces prostaglandins.

Prostaglandins stimulate mucus secretion so there’s decreased mucosal protection

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26
Q

What are the indicators for endoscopy of peptic ulcer disease?

A

Any red flags
>55 + previous PU or surgery
Pernicious aneamia
Long-term NSAIDs

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27
Q

What effect does H.pylori have?

A

Predominantly affects the antrum and decreases somatostatin (D-cells) which increases gastrin and H+ levels

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28
Q

Treatments for PUD/DUD?

A

Lifestyle modifications
Neutralise acids- antacids
Reduce irritancy- alginates
Promote mucosal defence- Misoprostol, Sucralphate
Gastric stimulants- Metaclopramide, Domperidone
Decrease H+ production- PPIs, H2- receptor antagonists

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29
Q

What is Sucralphates mechnism of action?

A

Protects damaged musoca and stimulates HCO3- production

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30
Q

How does Misoprostol work?

A

It’s a synthetic prostaglandin –> increases mucus secretion

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31
Q

What is the mechanism of action of metaclopramide and domperidone?

A

Increase peristalsis in the jejunum and duodenum and stimulate GIT muscarinic receptors reducing nausea

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32
Q

How do H2-receptor antagonists work and give an example?

A

Ranitidine

Suppress H+ secretion and gastrin by blocking the action of Histamine on the H2 receptors of parietal cells

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33
Q

What is metabolic syndrome?

A

Central obesity + 2 or more of:

  • TGs >1.7mmol/L
  • HDL 130 systolic and >85 diastolic
  • Glucose >7mmol/dL
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34
Q

What are secondary causes of obesity?

A

Hypothyroidism
Prada-willi syndrome
GH insufficiency
Hypothalamic dysfunction

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35
Q

What is Orlistat?

A

Intestinal lipase inhibitor –> reduces fat absorption

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36
Q

How is metformin used to treat obesity?

A

It reduces appetite and inhibits hepatic gluconeogenesis

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37
Q

How is GLP-1 related to obesity?

A

It is secreted post food ingestion and promotes satiety and reduces appetite.

It delays gastric emptying and reduces liver glucose output as it reduces glucagon and increases insulin levels

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38
Q

What are the important subregions of the hypothalamus and what do they do?

A

Lateral- low glucose so it stimulates hunger
Ventromedial- high glucose so it stimulates satiety
Arcuate nucleus- Leptin, an adipostat–> high levels = high fat = reduced hunger

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39
Q

What gene codes for Leptin?

A

Ob gene

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40
Q

What is an example of an anorexigenic peptide and what receptor does it bind to?

A

a- MSH and it binds to the Melanocortin 4 receptor (MC4R)

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41
Q

What is an example of an orexigenic peptide and what receptor does it bind to?

A

AGRP (Agouti) and it binds to the MC4R

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42
Q

What is Ghrelin?

A

Peptide produced by the fundus of the stomach indicating hunger.

Levels are low in obese people

43
Q

What does dopamine have to do with food and where is it produced?

A

Produced by the Ventral Tegmental area and is part of the reward circuit –> people learn to want palatable fatty foods.

44
Q

What cells are glucose dependant?

A

RBCs
Lymphocytes
Brain
Skeletal muscle

45
Q

What are fatty acid dependent organs?

A

Liver
Renal cortex
Myocardium
Skeletal muscle

46
Q

What tissues can utilise ketone bodies?

A

Renal cortex and Mycardium –> preferentially
Brain in starvation
Skeletal muscle

47
Q

What can cause acute pancreatits?

A

Gallstones
Alcohol
Trauma

48
Q

What are the main functions of the pancreas?

A

Both exocrine and endocrine functions

49
Q

What controls the exocrine functions of the pancreas?

A

Vagus nerve
Hormones –> CCK = secretion from lipids in chyme
Secretin = HCO3- secretion in low pH
Inhibitory hormones –> Amylin, pancreatic polypeptide

50
Q

What does Secretin do and where is it secrete from?

A

Control HCO3- levels and is secreted by duodenal endocrine cells in response to low pH.

51
Q

Wha effect does CCK have?

A

In the presence of lipids it causes contraction of the gall bladder and relaxation of the spincter of oddi –> bile influx and acinar cell production of enzymes (Trypsin)

52
Q

What investigations would you perform to diagnose pancreatitis?

A 
Serum amylase (>3x normal), FBC, U&Es, inflammatory markers.
CXR (for perforation), Abdo USS and CT <---
53
Q

What is chronic pancreatitis?

A

Long-term inflammation with irreversible structural changes, can be due to previously injured pancreas

54
Q

What is the pathological process of pancreatitis?

A

Blockage of the duct –> reflux of digestive enzymes into the pancreas.
Fibrosis, scarring

55
Q

What is Bile?

A

Lecithin plus bile salts e.g. cholic acid and glycocholic acid

56
Q

How are bile acids secreted?

A

As Bile salts (conjugated to taurine/glycine). The salt is ionised in the duodenum and acids degraded by flora –> reabsorbed

57
Q

What is bilirubin formed from?

A

Degradation of Haem (by the reticuloendothelial system- liver/spleen)

58
Q

What are the steps in the degradation of haem?

A

Haem –> Biliverdin –> Billirubin –> bilirubin glucoronide –> Stercobilin & Urobilinogen

59
Q

How is bilirubin transported and where does it go?

A

It is transported bound to albumin travelling to the liver where it enters hepatocytes and binds to ligandin

60
Q

Why does jaundice occur?

A

Bilirubin is conjugated –> bilirubin glucoronide. This is actively transported to bile canaliculi and into the bile.

This requires energy –> fails with liver damage –> Jaundice as levels build up

61
Q

What are the main types of gallstones and what are they made of?

A

Cholesterol stones- Cholesterol supersaturation and reduced bile salts
Black Pigment stones- Calcium bilirubinate. Assoc. w/ haemolytic disease
Brown pigment stones- Calcium/FA salts +bilirubin

62
Q

What are the main predisposing factors to gallstones?

A

Fat, fair, female, fertile and >40.

Obesity
Crohn’s of the terminal ileum.
Diabetes

63
Q

What is the presentation of gallstones?

A

Biliary colic- stone lodged in cystic duct
Acute cholangitis - obstruction of the GB –> inflmmation
Obstructive jaundice - Hepatic duct blocked
Gallstone ileus- large gallstone erodes from GB into duodenum

64
Q

Presentation of biliary colic/ mucocoele of the GB?

A

Upper rt. quadrant pain; restless, colicky, precipitated by fatty foods,
N&V and possibly jaundice

65
Q

What is Charcot’s triad and what is it associated with?

A

Fever, RUQ pain, Jaundice

Assoc. w/ cholangitis (infection of the bile duct)

66
Q

Where can cholestasis have referred pain and why?

A

To the rt. shoulder to irritation of the diaphragm

67
Q

What characterises Crohn’s disease?

A

Inflammatory disease- full thickness
Any part of the GI
Skip lesions
Granuloumatous

68
Q

What are the macroscopic features of Crohn’s?

A 
Skip lesions
Ulceration
"cobble stoning"
Strictures, fissures
Fistula formation
69
Q

What affect does smoking have in IBD?

A

Decreases the risk or UC

Increases risk of Crohn’s

70
Q

Presentation of Crohn’s?

A 
Intermittent pain, bloating, diarrhoea
Discomfort
Bleeding/anaemia
Wt. loss
Aphthous ulcers
/\ ESR & CRP
71
Q

What are the endoscopic findings of UC?

A

Diffuse, continuous erythema with rectal involvement

Mucosal islands- pseudopolyps

72
Q

What are the endoscopic findings of Crohn’s disease?

A

Large ulcers, cobblestone appearance, Strictures/fissures, fistulae

73
Q

On a barium x-ray, are haustra more likely to be absent in UC or CD?

A

UC

74
Q

What is tenesmus?

A

Feeling of needing to defacate all the time

75
Q

Which IBD is characterised by granulomas?

A

Crohn’s disease

76
Q

Where is the discomfort or pain most commonly felt in IBD?

A

Lower left quadrant in UC

Lower right quadrant in crohn’s.

77
Q

What is the pathophysiology of Crohn’s disease?

A

Abnormal immune response to gut flora –> Cell mediated:

Th1 –activates –> Macrophage –> Fibrosis & Tissue damage

There is infiltration of the bowel wall by neutrophils & granulomas (macrophage aggregates)

78
Q

What is ulcerative colitis?

A

Inflammatory disease only affecting the mucosal layer of the rectum ± colon.

It has a continuous distribution and is non- granulomatous

79
Q

What is the pathophysiology of UC?

A

Innate immune response:

Th2 – IL 4, 5 & 10 –> B-lymphocytes –> plasma cell –> antibodies

80
Q

What is backwash ileitis?

A

When some of the faecal matter is ‘backwashed’ through an incompetent ileo-caecal valve causing UC in the terminal ileum.

81
Q

How does UC present?

A 
Diarrhoea with blood and mucus
Abdo cramps
Pain (lowet lt. quadrant)
Tenesmus
Fever, wt loss
82
Q

What are the investigations for IBD?

A 
Stool examination
FBC
Inflammatory markers
U&Es
LFTs (1' sclerosing cholangitis)
AXR
Endoscopy/colonoscopy
83
Q

What are complications of UC?

A 
Primary sclerosing cholangitis
Bowel cancer
Toxic megacolon
Ankylosing spondylitis
Erythema nodosum
Uveitis
Pyoderma gangrenosum
84
Q

What is primary sclerosing cholangitis?

A

Inflammation and obstrucion of the bile ducts both intra- and extrahepatically

–> Cirrhosis, failure and cancer

85
Q

What are the microscopic/biopsy findings in UC?

A
  • Acute & chronic inflammatory cells in the lamina propria
  • Neutrophils in crypt epithelium and lumen
  • Distorted crypts and loss of mucin
86
Q

What symptoms can occur as a result is ileal disease?

A

B12 deficiency
Bile salt malabsorption –> colon irritation
Steatorrhoea –> malabsorption of Vit A, D, E & K
Protein losing enteropathy –> obstructed lymphatics)

87
Q

What is Hirschsprung’s disease?

A

Ganglion cells migrate into the gut from neural crest –> absent from the neural plexus

= Spasm of a section of bowel, \/ peristalsis ==> slower transit & obstruction (preceding section may be dilated)

88
Q

What GI symptoms are associated with cystic fibrosis?

A

Meconium ileus
Pancreatic atrophy
Biliary cirrhosis

89
Q

Where is Crohn’s most common?

A

Ileum ~ 80%

90
Q

What do colonic biopsy specimens typically show in CD?

A

Cryptitis, crypt abscesses, branching of crypts, atrophy of glands ad loss of mucin in goblet cells

91
Q

What autoantibodies can be tested for in UC?

A

P-ANCA +ve and ASCA -ve

92
Q

What autoantibodies can be used to diagnose crohn’s?

A

ASCA

93
Q

What are aminosalicylates and what is the 1st line choice?

A

They are the first line drug for inducing and maintaining remission of symptoms in ulcerative colitis

E.g. Mesalazine

94
Q

What are some of the side effects of ASAs?

A

Diarrhoea
Headache
Nausea
Rash

95
Q

What are corticosteroids used for in IBD and what are the typical examples?

A

Inducing remission , but NOT maintenance.
Prednisolone- both
Budesonide- Crohn’s
Beclomatasone- UC

96
Q

What are the side effects of corticosteroids?

A 
Cushingoid:
Buffalo hump
Moon face
cataracts
/\ abdo fat
Thin skin, easy bruising and poor wound healing
Muscle wasting
Hypertension
Osteoporosis
97
Q

What should be given alongside corticosteroids?

A

Calcium, vitamin D, Bisphonates

98
Q

What are the drugs which are used as ‘Steroid-sparing’?

A

Thiopurine

Azathiopurine

99
Q

When are the thiopurines indicated?

A
  • When aminosalicylates cannot be tolerated or ineffective.
  • 2+ steroid courses in 12months
  • Relapse if steroid <15mg
  • relapse w/in 6/52 of steroid course
  • following cyclosporin induction of remission in UC
100
Q

How does cyclosporin induce remission of UC?

A

It’s a calcineurin inhibitor –> \/ No. T-cells

101
Q

When is cyclosporin indicated?

A

Rescue therapy –> IV steroids have failed to induce remission

102
Q

What is methotrexate?

A

Drug used in the induction and maintenance of remission in Crohn’s disease

103
Q

What are the biological therapies for IBD?

A

Infliximab

Adalimumab

104
Q

What is the mechanism of action of the monoclonal antibody drugs?

A

They target membrane bound TNF-a and kill the host cell by complement induced lysis –> anti-inflammatory action

105
Q

What are the indications for `infliximab?

A

Resistant crohn’s

UC where ciclosporin is contra-indicated/inappropriate

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