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.
1
Q
What do parietal cells do?
A
Secrete intrinsic factor & gastric acid
2
Q
What do D-cells secrete?
A
Somatostatin which act on parietal cells
3
Q
What do chief cells secrete and where are they found?
A
Secrete pepsinogen and are only found in the fundus
4
Q
What is diarrhoea?
A
> 3 loose stools in one day.
Acute = 14 days
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
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
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
8
Q
What is dysentary?
A
Blood and mucus in the stools with abdominal pain
9
Q
What are the symptoms of C.diff?
A
Post Abx, foul smelling and cramps
10
Q
What is ETEC?
A
Travellers diarrhoea, watery stools that last several days
11
Q
What are 2 examples of viral gastroenteritis and in what groups are they most common?
A
Rotavirus- <5 y.o.
Notovirus- adults
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
13
Q
How can pancreatitis or pancreatic insufficiency cause diarrhoea?
A
The body cannot break down and absorb lipids causing steatorrhoea
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
15
Q
How much fluid should be replaced per loose stool?
A
200ml
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
17
Q
How does loperamide work?
A
Acts on opioid receptors in the bowel, decreasing bowel motility and increases anal sphincter tone
18
Q
What are red flag symptoms in GORD?
A
Dysphagia
Haematemesis, malaena or anaemia
Weight loss
Anorexia
19
Q
What can cause dysphagia?
A
Oesophageal/peptic stricture, long-term GORD–> adenocarcinoma
20
Q
What is the treatment for H. pylori?
A
Triple therapy:
- PPI (omeprazole)
- Clarithromycin
- Amoxicillin
21
Q
How can H.pylori be diagnosed?
A
Urea breath test
Stool antigen
Serology IgG
22
Q
What is barratts oesophagus?
A
Z-line is higher up and there is metaplasia of the oesophagus from squamous to columnar epithelium
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
24
What is Zollinger-Ellison syndrome?
Gastrin secreting tumour --> can cause ulcers
25
How do NSAIDs increase the risk of peptic ulcers?
They decrease COX-1 levels which therefore reduces prostaglandins.
Prostaglandins stimulate mucus secretion so there's decreased mucosal protection
26
What are the indicators for endoscopy of peptic ulcer disease?
Any red flags
>55 + previous PU or surgery
Pernicious aneamia
Long-term NSAIDs
27
What effect does H.pylori have?
Predominantly affects the antrum and decreases somatostatin (D-cells) which increases gastrin and H+ levels
28
Treatments for PUD/DUD?
Lifestyle modifications
Neutralise acids- antacids
Reduce irritancy- alginates
Promote mucosal defence- Misoprostol, Sucralphate
Gastric stimulants- Metaclopramide, Domperidone
Decrease H+ production- PPIs, H2- receptor antagonists
29
What is Sucralphates mechnism of action?
Protects damaged musoca and stimulates HCO3- production
30
How does Misoprostol work?
It's a synthetic prostaglandin --> increases mucus secretion
31
What is the mechanism of action of metaclopramide and domperidone?
Increase peristalsis in the jejunum and duodenum and stimulate GIT muscarinic receptors reducing nausea
32
How do H2-receptor antagonists work and give an example?
Ranitidine
Suppress H+ secretion and gastrin by blocking the action of Histamine on the H2 receptors of parietal cells
33
What is metabolic syndrome?
Central obesity + 2 or more of:
- TGs >1.7mmol/L
- HDL 130 systolic and >85 diastolic
- Glucose >7mmol/dL
34
What are secondary causes of obesity?
Hypothyroidism
Prada-willi syndrome
GH insufficiency
Hypothalamic dysfunction
35
What is Orlistat?
Intestinal lipase inhibitor --> reduces fat absorption
36
How is metformin used to treat obesity?
It reduces appetite and inhibits hepatic gluconeogenesis
37
How is GLP-1 related to obesity?
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
38
What are the important subregions of the hypothalamus and what do they do?
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
39
What gene codes for Leptin?
Ob gene
40
What is an example of an anorexigenic peptide and what receptor does it bind to?
a- MSH and it binds to the Melanocortin 4 receptor (MC4R)
41
What is an example of an orexigenic peptide and what receptor does it bind to?
AGRP (Agouti) and it binds to the MC4R
42
What is Ghrelin?
Peptide produced by the fundus of the stomach indicating hunger.
Levels are low in obese people
43
What does dopamine have to do with food and where is it produced?
Produced by the Ventral Tegmental area and is part of the reward circuit --> people learn to want palatable fatty foods.
44
What cells are glucose dependant?
RBCs
Lymphocytes
Brain
Skeletal muscle
45
What are fatty acid dependent organs?
Liver
Renal cortex
Myocardium
Skeletal muscle
46
What tissues can utilise ketone bodies?
Renal cortex and Mycardium --> preferentially
Brain in starvation
Skeletal muscle
47
What can cause acute pancreatits?
Gallstones
Alcohol
Trauma
48
What are the main functions of the pancreas?
Both exocrine and endocrine functions
49
What controls the exocrine functions of the pancreas?
Vagus nerve
Hormones --> CCK = secretion from lipids in chyme
Secretin = HCO3- secretion in low pH
Inhibitory hormones --> Amylin, pancreatic polypeptide
50
What does Secretin do and where is it secrete from?
Control HCO3- levels and is secreted by duodenal endocrine cells in response to low pH.
51
Wha effect does CCK have?
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
What investigations would you perform to diagnose pancreatitis?
```
Serum amylase (>3x normal), FBC, U&Es, inflammatory markers.
CXR (for perforation), Abdo USS and CT <---
```
53
What is chronic pancreatitis?
Long-term inflammation with irreversible structural changes, can be due to previously injured pancreas
54
What is the pathological process of pancreatitis?
Blockage of the duct --> reflux of digestive enzymes into the pancreas.
Fibrosis, scarring
55
What is Bile?
Lecithin plus bile salts e.g. cholic acid and glycocholic acid
56
How are bile acids secreted?
As Bile salts (conjugated to taurine/glycine). The salt is ionised in the duodenum and acids degraded by flora --> reabsorbed
57
What is bilirubin formed from?
Degradation of Haem (by the reticuloendothelial system- liver/spleen)
58
What are the steps in the degradation of haem?
Haem --> Biliverdin --> Billirubin --> bilirubin glucoronide --> Stercobilin & Urobilinogen
59
How is bilirubin transported and where does it go?
It is transported bound to albumin travelling to the liver where it enters hepatocytes and binds to ligandin
60
Why does jaundice occur?
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
What are the main types of gallstones and what are they made of?
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
What are the main predisposing factors to gallstones?
Fat, fair, female, fertile and >40.
Obesity
Crohn's of the terminal ileum.
Diabetes
63
What is the presentation of gallstones?
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
Presentation of biliary colic/ mucocoele of the GB?
Upper rt. quadrant pain; restless, colicky, precipitated by fatty foods,
N&V and possibly jaundice
65
What is Charcot's triad and what is it associated with?
Fever, RUQ pain, Jaundice
Assoc. w/ cholangitis (infection of the bile duct)
66
Where can cholestasis have referred pain and why?
To the rt. shoulder to irritation of the diaphragm
67
What characterises Crohn's disease?
Inflammatory disease- full thickness
Any part of the GI
Skip lesions
Granuloumatous
68
What are the macroscopic features of Crohn's?
```
Skip lesions
Ulceration
"cobble stoning"
Strictures, fissures
Fistula formation
```
69
What affect does smoking have in IBD?
Decreases the risk or UC
| Increases risk of Crohn's
70
Presentation of Crohn's?
```
Intermittent pain, bloating, diarrhoea
Discomfort
Bleeding/anaemia
Wt. loss
Aphthous ulcers
/\ ESR & CRP
```
71
What are the endoscopic findings of UC?
Diffuse, continuous erythema with rectal involvement
| Mucosal islands- pseudopolyps
72
What are the endoscopic findings of Crohn's disease?
Large ulcers, cobblestone appearance, Strictures/fissures, fistulae
73
On a barium x-ray, are haustra more likely to be absent in UC or CD?
UC
74
What is tenesmus?
Feeling of needing to defacate all the time
75
Which IBD is characterised by granulomas?
Crohn's disease
76
Where is the discomfort or pain most commonly felt in IBD?
Lower left quadrant in UC
| Lower right quadrant in crohn's.
77
What is the pathophysiology of Crohn's disease?
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
What is ulcerative colitis?
Inflammatory disease only affecting the mucosal layer of the rectum ± colon.
It has a continuous distribution and is non- granulomatous
79
What is the pathophysiology of UC?
Innate immune response:
Th2 -- IL 4, 5 & 10 --> B-lymphocytes --> plasma cell --> antibodies
80
What is backwash ileitis?
When some of the faecal matter is 'backwashed' through an incompetent ileo-caecal valve causing UC in the terminal ileum.
81
How does UC present?
```
Diarrhoea with blood and mucus
Abdo cramps
Pain (lowet lt. quadrant)
Tenesmus
Fever, wt loss
```
82
What are the investigations for IBD?
```
Stool examination
FBC
Inflammatory markers
U&Es
LFTs (1' sclerosing cholangitis)
AXR
Endoscopy/colonoscopy
```
83
What are complications of UC?
```
Primary sclerosing cholangitis
Bowel cancer
Toxic megacolon
Ankylosing spondylitis
Erythema nodosum
Uveitis
Pyoderma gangrenosum
```
84
What is primary sclerosing cholangitis?
Inflammation and obstrucion of the bile ducts both intra- and extrahepatically
--> Cirrhosis, failure and cancer
85
What are the microscopic/biopsy findings in UC?
- Acute & chronic inflammatory cells in the lamina propria
- Neutrophils in crypt epithelium and lumen
- Distorted crypts and loss of mucin
86
What symptoms can occur as a result is ileal disease?
B12 deficiency
Bile salt malabsorption --> colon irritation
Steatorrhoea --> malabsorption of Vit A, D, E & K
Protein losing enteropathy --> obstructed lymphatics)
87
What is Hirschsprung's disease?
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
What GI symptoms are associated with cystic fibrosis?
Meconium ileus
Pancreatic atrophy
Biliary cirrhosis
89
Where is Crohn's most common?
Ileum ~ 80%
90
What do colonic biopsy specimens typically show in CD?
Cryptitis, crypt abscesses, branching of crypts, atrophy of glands ad loss of mucin in goblet cells
91
What autoantibodies can be tested for in UC?
P-ANCA +ve and ASCA -ve
92
What autoantibodies can be used to diagnose crohn's?
ASCA
93
What are aminosalicylates and what is the 1st line choice?
They are the first line drug for inducing and maintaining remission of symptoms in ulcerative colitis
E.g. Mesalazine
94
What are some of the side effects of ASAs?
Diarrhoea
Headache
Nausea
Rash
95
What are corticosteroids used for in IBD and what are the typical examples?
Inducing remission , but NOT maintenance.
Prednisolone- both
Budesonide- Crohn's
Beclomatasone- UC
96
What are the side effects of corticosteroids?
```
Cushingoid:
Buffalo hump
Moon face
cataracts
/\ abdo fat
Thin skin, easy bruising and poor wound healing
Muscle wasting
Hypertension
Osteoporosis
```
97
What should be given alongside corticosteroids?
Calcium, vitamin D, Bisphonates
98
What are the drugs which are used as 'Steroid-sparing'?
Thiopurine
| Azathiopurine
99
When are the thiopurines indicated?
- 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
How does cyclosporin induce remission of UC?
It's a calcineurin inhibitor --> \/ No. T-cells
101
When is cyclosporin indicated?
Rescue therapy --> IV steroids have failed to induce remission
102
What is methotrexate?
Drug used in the induction and maintenance of remission in Crohn's disease
103
What are the biological therapies for IBD?
Infliximab
| Adalimumab
104
What is the mechanism of action of the monoclonal antibody drugs?
They target membrane bound TNF-a and kill the host cell by complement induced lysis --> anti-inflammatory action
105
What are the indications for `infliximab?
Resistant crohn's
| UC where ciclosporin is contra-indicated/inappropriate
