Topic 6 Gastrointestinal Conditions Flashcards

1
Q

What is Crohn’s disease

A

Chronic inflammatory bowel disease that affects lining of small and large bowel

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2
Q

CM of Crohn’s disease

A
Pain - RLQ 
Lesions affecting sub mucosa of small intestine and proximal colon
Marked granulomatous inflammatory response with resulting scarring
Inflexible bowel
Colicky pain
Weight loss
Fatigue
Diarrhoea
Fluid and electrolyte imbalance
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3
Q

Dx of Crohn’s disease

A

History

Endoscopy

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4
Q

Tx of Crohn’s disease

A

Anti inflammatory drugs
Infliximab (monoclonal antibody)
Surgery

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5
Q

Risk factors of Crohn’s disease

A

Smoking increases susceptibility and exacerbates condition

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6
Q

What is ulcerative colitis

A

Ulceration of large bowel and rectum

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7
Q

Aetiology of ulcerative colitis

A

Crypts of lieberkuhn ulcerate, develop abscess and become necrotic leading to pseudo polyps and faecal peritonitis.
Begins at rectum or sigmoid colon and travels proximally
Small erosions form and develop into ulcers, abscess form, inflammation, pus, necrosis of cells.

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8
Q

CM of ulcerative colitis

A
Bleeding
Cramping
Pain
Urge to defecate
Diarrhoea 
Anorexia
Weakness
Fatigue
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9
Q

Tx of ulcerative colitis

A

Diet (avoid caffeine, milk, gas forming foods)
Anti-inflammatory drugs
Nicotine
Surgical resection (ileostomy or colostomy)

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10
Q

Risk associated with ulcerative colitis

A

Increased risk of colon cancer as bowel wall thickens by inflammatory process

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11
Q

Prevention of ulcerative colitis

A

Smoking

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12
Q

What is GORD

A

Chronic disease when bile irritates the oesophageal lining

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13
Q

CM of GORD

A

Heartburn pain

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14
Q

Tx of GORD

A

Avoid large meals and irritants
Sleep with shoulders slightly elevated
Medications to reduce gastric acid (antacids, PPIs, Sucralfate)

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15
Q

Dx of GORD

A

Clinical manifestations
Endoscopy
Barium swallow

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16
Q

Types of ulcers

A

Curlings: stress like ulcer due to hypo perfusion

Cushing: associated with head injury caused by hypersecretion of gastric acid due to stimulation of vagal nuclei as a result of increased ICP

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17
Q

CM of ulcers

A

Burning sensation in mid-epigastric region

Perforation → peritonitis and haemorrhage → shock

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18
Q

Dx of ulcers

A
History
Radiological examination
Endoscopy and biopsy
Gastrin levels 
Intermittent epigastric pain 
Anorexia
Vomiting
Weight loss
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19
Q

Tx of ulcers

A
Lifestyle modifications (smoking cessation, diet high in vitamin A and fibre)
Endoscopic heater probes
Antacids (alkaline)
Peppermint oil (calming effect on gut)
Local anaesthetics
Basic compounds
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20
Q

Complications of ulcers

A

Perforation of ulcer
Acute bleeding
Mortality
Obstruction as result of oedema from inflammation or scarring

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21
Q

What is lactose intolerance

A

Deficiency in enzyme lactase that digests lactose (into glucose and galactose) hence lactose is not absorbed across the intestinal wall.

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22
Q

CM of lactose intolerance

A
Dehydration (fluid remains in intestine)
Gas
Cramps
Pain
Osmotic diarrhoea
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23
Q

Dx of lactose intolerance

A

Lactose-tolerance test which monitors glucose levels after ingestion (no rise in lactose intolerant person)

24
Q

Tx of lactose intolerance

A

Avoid milk

Lactose free diet

25
What is coeliac disease
Loss of mature intestinal villous epithelium caused by hypersensitivity to gluten
26
CM of coeliac disease
``` Seizures and tetany Bone resorption Rickets and clubbing in children Steatorrhoea Loss of fat soluble vitamins, Poor blood clotting Anaemia ```
27
How does coeliac disease work
Gluten protein → immunological GIT response (T-cell mediated autoimmune response) →breakdown of mucosal cells and loss of villi→ reduces surface area → malabsorption
28
CM of hepatitis
Biliary disruption leads to range of CM (subclinical to coma dependent on extent of hepatocyte destruction), inflammation, cirrhosis
29
Outline hepatitis A
Transmitted via faecal-oral route On decline Effective vaccine available.
30
Outline hepatitis B
Transmitted by direct contact with blood and body fluids. | Vaccine available.
31
Outline hepatitis C
Epidemic proportions (needles, blood to blood).
32
Outline hepatitis D
Transmitted by blood products and IV drug use. | Requires Hep B so Tx Hep B vaccination.
33
Outline hepatitis E
Transmitted via faecal-oral route by contaminated food and water
34
CM of liver disease
``` Most have no signs Fatigue Pain Weight loss Loss of appetite ```
35
Dx of liver disease
Blood tests (prothrombin time test - how fast blood clots) CT MRI Liver biopsy
36
Tx of liver disease
``` No drug therapy Lifestyle changes (low-fat diet, weight loss, reduce alcohol, exercise) ```
37
What is jaundice
Abnormally high bilirubin blood level
38
Aetiology of jaundice
Bilirubin formed when RBCs breakdown. Exceeds liver’s ability to metabolise bilirubin causing blood levels to rise.
39
CM of jaundice
Yellowish discolouration of skin | Sclera
40
Types of jaundice
Pre hepatic jaundice - excessive RBC destruction Intra hepatic jaundice - problem with synthesis of bilirubin by the liver Post hepatic jaundice - obstruction to bile flow Obstructive jaundice - extrahepatic obstruction (bile duct blocked by a gallstone or tumour, intrahepatic obstructive caused by hepatocyte dysfunction)
41
Aetiology of gallstones
Caused by buildup of substances found in bile – cholesterol, calcium and bilirubin
42
Risks of gallstones
Medication to reduce cholesterol (increase excretion, increase risk of stones)
43
Factors which contribute to gallstones
1 - abnormalities in bile 2 - stasis of bile (causes sludge formation) 3 - inflammation of the gallbladder More often in females as oestrogen reduces synthesis of bile
44
CM of gallstones
??
45
Tx of gallstones
Low fat diet Ursodeoxycholic acid Laparoscopic cholecystectomy
46
Dx of gallstones
``` History CM Ultrasound Cholangiogram Raised bilirubin ```
47
Types of gallstones
Acute cholecystitis – obstruction by cholelithiasis, concentrated bile causes irritation and inflammation of mucosa Chronic cholecystitis - repeated attacks, infection due to destruction of mucosa. May lead to gangrene and perforation of gallbladder
48
What is acute pancreatitis
Release and activation of pancreatic enzymes into pancreatic tissue and surrounding tissues, causing autodigestion, necrosis & haemorrhage.
49
Causes of acute pancreatitis
``` Cholelithiasis Alcohol Hyperlipidemia Infections Trauma and surgery Drugs ```
50
CM of acute pancreatitis
Acute and dramatic onset Epigastric and abdominal pain Abdominal distention and reduced bowel motility Cullen’s sign - superficial oedema and bruising in the subcutaneous fatty tissue around the umbilicus Grey Turner’s sign - bruising between last rib and top of hip Signs of shock - decrease BP increase Pulse, RR diaphoretic
51
Dx of acute pancreatitis
CM History Raised serum amylase and lipase CT scan
52
Tx of acute pancreatitis
``` Rest gut (nil by mouth) Fluid resuscitation Support Analgesia Metoclopromide Broad-spectrum antibiotics Anxiolytic Hypnotic ```
53
What is chronic pancreatitis
Progressive destruction of pancreas Calcifying - often due to alcoholism Obstructive - cystic fibrosis and ductal stenosis Progressive fibrosis resulting in reduction on enzymes and insulin
54
CM of chronic pancreatitis
Same as acute but less severe steatorrhea weight loss fatigue flatulence and abdominal distention (bacterial fermentation of unabsorbed food) oedema anaemia bleeding disorders (vitamin K malabsorption) Metabolic bone disease (Vitamin D deficiency) neurologic manifestation hypocalcemia
55
Dx of chronic pancreatitis
CM History CT scan
56
Tx of chronic pancreatitis
Low fat diet Abstain from alcohol Insulin Pancreatic enzyme supplement