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z Clinical Sciences 2 > Topic 6 Gastrointestinal Conditions > Flashcards

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
Q

What is coeliac disease

A

Loss of mature intestinal villous epithelium caused by hypersensitivity to gluten

26
Q

CM of coeliac disease

A 
Seizures and tetany 
Bone resorption
Rickets and clubbing in children 
Steatorrhoea
Loss of fat soluble vitamins,
Poor blood clotting
Anaemia
27
Q

How does coeliac disease work

A

Gluten protein → immunological GIT response (T-cell mediated autoimmune response) →breakdown of mucosal cells and loss of villi→ reduces surface area → malabsorption

28
Q

CM of hepatitis

A

Biliary disruption leads to range of CM (subclinical to coma dependent on extent of hepatocyte destruction), inflammation, cirrhosis

29
Q

Outline hepatitis A

A

Transmitted via faecal-oral route
On decline
Effective vaccine available.

30
Q

Outline hepatitis B

A

Transmitted by direct contact with blood and body fluids.

Vaccine available.

31
Q

Outline hepatitis C

A

Epidemic proportions (needles, blood to blood).

32
Q

Outline hepatitis D

A

Transmitted by blood products and IV drug use.

Requires Hep B so Tx Hep B vaccination.

33
Q

Outline hepatitis E

A

Transmitted via faecal-oral route by contaminated food and water

34
Q

CM of liver disease

A 
Most have no signs
Fatigue
Pain
Weight loss
Loss of appetite
35
Q

Dx of liver disease

A

Blood tests (prothrombin time test- how fast blood clots)
CT
MRI
Liver biopsy

36
Q

Tx of liver disease

A 
No drug therapy
Lifestyle changes (low-fat diet, weight loss, reduce alcohol, exercise)
37
Q

What is jaundice

A

Abnormally high bilirubin blood level

38
Q

Aetiology of jaundice

A

Bilirubin formed when RBCs breakdown. Exceeds liver’s ability to metabolise bilirubin causing blood levels to rise.

39
Q

CM of jaundice

A

Yellowish discolouration of skin

Sclera

40
Q

Types of jaundice

A

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
Q

Aetiology of gallstones

A

Caused by buildup of substances found in bile – cholesterol, calcium and bilirubin

42
Q

Risks of gallstones

A

Medication to reduce cholesterol (increase excretion, increase risk of stones)

43
Q

Factors which contribute to gallstones

A

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
Q

CM of gallstones

A

??

45
Q

Tx of gallstones

A

Low fat diet
Ursodeoxycholic acid
Laparoscopic cholecystectomy

46
Q

Dx of gallstones

A 
History
CM
Ultrasound
Cholangiogram
Raised bilirubin
47
Q

Types of gallstones

A

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
Q

What is acute pancreatitis

A

Release and activation of pancreatic enzymes into pancreatic tissue and surrounding tissues, causing autodigestion, necrosis & haemorrhage.

49
Q

Causes of acute pancreatitis

A 
Cholelithiasis
Alcohol
Hyperlipidemia
Infections
Trauma and surgery
Drugs
50
Q

CM of acute pancreatitis

A

Acute and dramatic onset
Epigastric and abdominal pain
Abdominal distention and reduced bowel motility
Cullen’s sign - superficial oedema andbruisingin the subcutaneous fatty tissue around the umbilicus
Grey Turner’s sign - bruisingbetween last rib and top of hip
Signs of shock - decrease BP increase Pulse, RR diaphoretic

51
Q

Dx of acute pancreatitis

A

CM
History
Raised serum amylase and lipase
CT scan

52
Q

Tx of acute pancreatitis

A 
Rest gut (nil by mouth)
Fluid resuscitation 
Support
Analgesia
Metoclopromide
Broad-spectrum antibiotics
Anxiolytic
Hypnotic
53
Q

What is chronic pancreatitis

A

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
Q

CM of chronic pancreatitis

A

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
Q

Dx of chronic pancreatitis

A

CM
History
CT scan

56
Q

Tx of chronic pancreatitis

A

Low fat diet
Abstain from alcohol
Insulin
Pancreatic enzyme supplement

z Clinical Sciences 2 (5 decks)

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