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BSO8 > Disorders of the oesophagus, stomach and small intestine > Flashcards

Disorders of the oesophagus, stomach and small intestine Flashcards

1
Q

What is GORD?

A

Symptomatic passage of gastric contents -> lowers oesophagus

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2
Q

What is the incidence of GORD?

A

1 in 10 Australians

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3
Q

What are the risk factors for GORD?

A

Decreased tone of lower oesophageal sphincter
Impaired mucosal defences
Increased intra-abdominal pressure

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4
Q

What causes decreased tone of the lower oesophageal sphincter?

A

Caffeine, fatty foods, hiatal hernia

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5
Q

What causes impaired mucosal defences?

A

Smoking, alcohol

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6
Q

What causes increased intra-abdominal pressure?

A

Pregnancy, obesity, ascites, lifting and bending

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7
Q

What is the pathophysiology of GORD?

A

Chronically low pH induces inflammation of lower oes. mucosa

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8
Q

What are the potential outcomes of GORD?

A

Healing with no residual effects
Healing with fibrosis (obstruction, dysphagia)
Blood loss -> iron deficiency anaemia
Oesophageal ulceration
Metaplasia = barrett’s mucosa

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9
Q

What is barrett’s mucosa?

A

Stratified squamous epithelium replaced by simple columnar epithelium

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10
Q

What is barrett’s mucosa considered to be?

A

A pre-malignant transformation (regular endoscopic review required)

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11
Q

What are the clinical features of GORD?

A

Heartburn: epigastric and/or retrosternal pain
- Agg factors: big meals, acidic foods, bending and lifting, lying supine
- Rel factors: Antacids
Dyspepsia
Dysphagia, odynophagia

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12
Q

What is the management of GORD?

A

Reduction of predisposing factors
Endoscopy to directly visualise mucosa and structural changes (e.g. hiatal hernia)
Biopsy for Barrett’s mucosa

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13
Q

What are the three medications for GORD?

A

Histamine H2-receptor antagonists
- Ranitidine, cimetidine
Proton Pump inhibitors
- Esomeprazole, pantoprazole
Antacids
- Mylanta, gaviscon, quick-eze

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14
Q

How do Histamine H2-receptor antagonists work?

A

Inhibits action of histamine at H2-receptors on gastric parietal cells

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15
Q

How do proton pump inhibitors work?

A

Inhibits H+/K+ ATPase pump

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16
Q

How do antacids work?

A

Neutralises HCl in oesophageal lumen

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17
Q

What is a peptic ulcer?

A

Ulceration in any part of the GIT exposed to gastric secertions

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18
Q

What is the incidence of peptic ulcers?

A

10-20% of Australians

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19
Q

Where are the most common sites for peptic ulcers?

A

Duodenal ulcers are more common than gastric- - 4:1
Duodenal ulcers: D1, gastric ulcers: lesser curvature
Usually solitary, coexist in 10% of cases

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20
Q

What is the appearance of peptic ulcers?

A

Circular punched-out lesion (1-3cm)
Ulcer extends into the muscularis and has a fibrous base

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21
Q

What is the bacteria that is linked to peptic ulcers?

A

H. pylori
90% of duodenal ulcers and 70% gastric ulcers

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22
Q

What are the pathogenic properties of H. pylori?

A

Produces urease - allows survival in low pH
Helical structure and flagella - burrowing capacity
Release of bacterial toxins and reactive oxygen species - direct damage to mucosa
Recruitment of neutrophils, mast cells and macrophages results in release of inflammatory cytokines (further injury)

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23
Q

What are other factors contributing to peptic ulcers?

A

NSAIDS
Smoking
Familial factors

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24
Q

How can NSAIDS cause peptic ulcers?

A

Reduce prostaglandin content of mucosal cells
Aspirin directly damage cell membranes

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25
Q

How can smoking cause peptic ulcers?

A

Generation of reactive oxygen species -> mucosal damage
Reduces the healing rate once an ulcer has formed

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26
Q

How can familial factors cause peptic ulcers?

A

Determine susceptibility to ulcers and site formation
Risk increases 3-fold if first degree relative has an ulcer

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27
Q

What are the clinical features of peptic ulcers?

A

Epigastric pain
- Periodicity of several weeks, disappears then returns
- Relationship to food: eating can either agg or relieve pain
Anorexia, dyspepsia, nausea, vomiting
Can be asymptomatic esp. in elderly

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28
Q

What are the complications of peptic ulcers?

A

Healing with fibrosis can cause pyloric stenosis (prevention of food into small intestine)
Blood vessel erosion can lead to:
- Iron deficiency, anaemia, melena and haematemesis

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29
Q

What is the management of peptic ulcers due to H. pylori?

A

Eradication with antibiotics, usually combined with proton pump inhibitor

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30
Q

What is the management of peptic ulcers without H. pylori?

A

Histamine H2 receptor antagonists or PPI used

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31
Q

What is the general management for all ulcers?

A

Cease smoking
Modify NSAID therapy
Regular endoscopic review

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32
Q

How do antibiotics work?

A
  1. Inhibition of cell wall synthesis
  2. Disruption of cell membrane
  3. Inhibition of protein synthesis
  4. Interference with metabolic processes
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33
Q

What are the preferred antibiotics for H. pylori?

A

Clarithromycin - inhibits protein synthesis
Amoxycillin - broad spectrum penicillin that inhibits cell wall synthesis
Metronidazole - prevents DNA replication

34
Q

What is coeliac disease?

A

Genetically-determined, abnormal, hypersensitivity reaction to gluten or its peptide derivative, gliadin

35
Q

What are some sources of gluten?

A

Wheat, oats, barley, rye

36
Q

What is the incidence of coeliac disease?

A

Most common cause of malabsoption in temperate climates
1:300 to 1:3000

37
Q

What is the genetic component of coeliac disease?

A

25% of patients have affected family members
Genes HLA-DQ2, HLA-DQ8 are found in up to 95% of cases
- Genes also associated with other auto-immune diseases such as type 1 diabetes

38
Q

What is the pathophysiology of coeliac disease?

A

Proximal bowel most effected esp. duodenal-jejunal flexure
1. Type 4 (cell mediated) hypersensitivity reaction
2. Immune cells infiltrate lamina propria
3. T-lymphocytes release inflammatory cytokines
4. Plasma cells produce IgA antibodies
5. Damage to mucosa and atrophy of villi
6. Elimination of gluten -> epithelium returns to normal

39
Q

What are the clinical features of coeliac disease in childhood?

A

Usually occurs several months after weaning
Irritability, failure to thrive, abdominal distension
Voluminous, pale stool

40
Q

What are the clinical features of coeliac disease in adulthood?

A

Can vary from silent, mild to florid disease
WEight loss, diarrhoea
Abdominal discomfort, excessive flatus
Fatigue
Amenorrhea

41
Q

What are complications of coeliac disease?

A

Generalised malabsorption
- Range of nutritional deficiencies
Ulcerative jejuno-ileitis
- Can perforate, bleed and scar (strictures)
Increased risk of GIT cancers
- Small bowel lymphoma, small bowel carcinoma
Skin disorders
- Dermatitis, herpatiformis

42
Q

What is the diagnosis of coeliac disease?

A

Blood tests: elevated IgA antibodies
Endoscopy with small bowel biopsy (SSBx)
Atrophy of villi? infiltration of immune cells
- +’ve blood test but - ‘ve SBBX
“potential coeliac disease”
- +’ve blood test +’ve SBBx but no SSx
“silent coeliac disease”

43
Q

What is the primary form of management of coeliac disease?

A

Patient education and dietary modification are mainstau management

44
Q

What is jaundice?

A

A yellow appearance of the skin, sclerae and mucous membranes produced by extra bilirubin

45
Q

What other disorder can also cause jaundice?

A

Extra-hepatic disroders (e.g. cholelithiasis) can also cause jaundice

46
Q

What is bilirubin and how can it cause yellow skin?

A

Waste product of RBC breakdown - usually metabolised in the liver and excreted as bile pigment
Hepatic injury (amongst other disorders) can cause bilirubin to accumulate in the body

47
Q

What are normal and abnormal levels of bilirubin?

A

Normal: <17 micromol/L
Deposition in tissues begins: 35-50 micromol/L
Detectable clinically when blood level > 50 micromol/L

48
Q

What is neonatal jaundice?

A

Occurs in 60% of full-term and 80% pre-term babies within the first week of life

49
Q

What is viral hepatitis?

A

Hepatitis virus types A, B, C, D and E
Hepatitis F and G now known to exist
Other viruses: epstein barr virus, cytomegalovirus

50
Q

What is the pathophysiology of viral hepatitis?

A

Virus induces an acute inflammatory reaction, leading to widespread hepatocyte necrosis
Usually liver begins to recover before SSx disappear
Occasionally, severe destruction of whole lobes results in acute hepatic failure
Chronic hepatitis with cirrhosis is particularly associated with HBV and HCV

51
Q

What is hepatitis virus HAV?

A

Transmission: faecal-oral route
Severity: Usually mild, worse in older patients
Chronicity: Very rare
Vaccination: Yes

52
Q

What is hepatitis virus HBV?

A

Transmission: Parenteral, sexual contact, perinatal
Severity: Mild to severe (mortality -10%)
Chronicity: Common
Vaccination: Yes

53
Q

What is hepatitis virus HCV?

A

Transmission: Parenteral, perinatal, possibly sexual
Severity: Usually mild
Chronicity: very common
Vaccination: not available

54
Q

What are the clinical features of acute hepatitis?

A

Stage 1: Preclinical
- Asymptomatic, but virus actively replicating
- Spread during this phase a concern
Stage 2: Prodrome/Pre-icteric
- Anorexia, nausea, vomiting, malaise, headache
- Mild fever, diarrhoea, upper abdominal discomfort
Stage 3: Icteric
- Jaundice develops
- Possibly tender hepatomegaly
- HBV: polyarthralgia affecting small joints, skin rash
Stage 4: Convalescent
- Symptoms subside over a course of several weeks

55
Q

What is the management for hepatitis?

A

Hep A - bed rest
Diet: should be low in fats but relatively high in proteins
Avoid hepatic insults: drugs, esp alcohol

56
Q

How to reduce spread of hepatitis?

A

No sharing needles
Not donating blood or body organs
Advising healthcare workers of health status
Covering wounds appropriately
Carefully disposing of blood stained material
Pracitising safe sex

57
Q

What is the most important cause of liver disease in western societies?

A

Alcohol

58
Q

What does alcohol do in the liver?

A

Causes induction of oxidases
- Enzymes that aid metabolism but damage hepatocytes with chronic exposure

59
Q

What is the pathophysiology of alcoholic liver disease?

A

Stage 1: Fatty liver
Stage 2: Alcoholic hepatitis
Stage 3: Cirrhosis

60
Q

What is involved in stage 1 of alcoholic liver disease?

A

Destruction of rough ER in hepatocytes reduces the amount of lipoproteins synthesised and secreted -n this causes cells to become swollen with lipids
Mild to moderate changes are reversible
Clinical features: +/- hepatomegaly

61
Q

What is involved in stage 2 of alcoholic liver disease?

A

Usually superimposed hepatitis on fatty liver
Hepatocyte necrosis induces the infiltration of inflammatory cells
Clinical features: tender hepatomegaly, fever, jaundice, ascites
Severe cases: heavy drinking bout may induce encephalopathy

62
Q

What is involved in stage 3 of alcoholic liver disease?

A

Irreversible: arises due to chronic inflammation and progressive fibrosis
Regenerating hepatocytes do not conform to normal cytoarchitecture (nodule formation)
Structural change obstructs nutrient flow (impaired hepatocyte function)
Death occurs due to complications (hepatocellular failure, portal hypertension)

63
Q

What are other causes of cirrhosis?

A

Alcohol 60-70% of cases
Non-alcoholic fatty liver disease
- Obesity, insulin resistance, hyperlipidemia
Viral and auto-immune hepatitis
Cholestasis
Metabolic disorders
- Haemochromatosis

64
Q

What are the cirrhosis clinical features?

A

Jaundice, RUQ pain, hepatomegaly (liver shrinks in advanced stages), foetor hepaticus
Constitutional symptoms: fever, anorexia, nausea, vomiting, weakness, fatigue, weight loss

65
Q

What are the complications of cirrhosis?

A

Portal hypertension and hepatocellular failure

66
Q

What are the manifestations of portal hypertension?

A

Ascites
Splenomegaly
Varicose veins

67
Q

What is ascites?

A

Accumulation of fluid in peritoneal cavity
Abdominal distension with shifting dullness to percussion

68
Q

What are some other causes of ascites?

A

Liver carcinoma, cardiac failure

69
Q

What is splenomegaly and how is it a manifestation of portal hypertension?

A

Enlarged spleen
Occurs due to passive congestion

70
Q

What is the complication of varicose veins as a manifestation of portal hypertension?

A

Oesophageal (haemorrhage risk)
Rectal
Caput medusae

71
Q

What are the manifestations of hepatocellular failure?

A

Hepatic encephalopathy
- Failure to metabolise neurotoxic wastes from gut bacteria
Coagulation defects
- Failure to produce coagulation factors
Endocrine changes
- failure to deactivate hormones
Peripheral oedema
- failure to produce albumin

72
Q

What is hepatic encephalopathy?

A

Loss of brain function when liver doesn’t remove toxins
Changes in intellect, mood, alertness
Asterixis (flapping tremor), hyper-reflexia, babinski

73
Q

What is the management of alcoholic liver disease?

A

Cease alcohol
Improve nutrition
Carefully monitor medications
Treat complications: ascites, encephalopathy, varices
No treatment to reverse cirrhosis

74
Q

What is the prognosis of alcoholic liver disease?

A

Poor overall - most people present in the later stages of the disease (5 year survival rate - 25%)
If liver function is good, 50% patients survive for 5 years and 25% for 10 years

75
Q

What is the most common gallbladder disorder in the Western world?

A

Cholelithiasis (gallstones)

76
Q

How many people is Cholelithiasis estimated to affect?

A

11% of population

77
Q

What are the risk factors for cholelithiasis?

A

In adults <40 years, stones are more common in women (no difference in elderly)
Obesity, increased age, multi-parity, diabetes, diets high in refined sugar, ileal disease

78
Q

What types of gallstones are there?

A

Cholesterol
- Most common in western countries
- Linked to disturbed cholesterol balance
Pigment variety
- More common in developing countries
- Correlation with infection

79
Q

What is the pathophysiology of cholesterol gallstones?

A

Solubility of cholesterol in bile is determined by the ratio:
- Cholesterol: bile salts: phospholipids
Many factors can alter this ratio
- Crystal begin to form when bile is supersaturated with cholesterol - “lithogenic bile”

80
Q

What are the clinical features of cholesterol stones?

A

Most gallstones are asymptomatic, especially if the stone remains in the GB
Only 25% of stones have enough calcium to be radio-opaque
Pure cholesterol stones: often solitary
May be more than 3cm in length
More likely for patient to present with a complication

81
Q

What are the gallstone complications?

A

Acute cholecystitis
- Acute inflammation from chemical irritation
Chronic cholecystitis
- GB walls become fibrotic and shrunken following repeated bouts of acute inflammation
Mucocele development
- GB distended with mucoid watery fluid
Infection
- Bacterial infection (e coli)
Increased risk for carcinoma
Choledocholithiasis
- Impaction of gallstone in bile duct
Acute pancreatitis
- Obstruction of hepatopancreatic ampulla generates back-pressure

82
Q

What is the management of gallstones?

A

If asymptomatic, leave alone
Otherwise:
Surgery (cholecystectomy)
- Open or laparoscopic
Oral bile acid therapy
- Ursodeoxycholic acid
- Chemical dissolution of stones
- Not suitable for all patients
Extra-corporeal shockwave lithotripsy
- Application of high frequency sound waves to fracture the stones
- Followed by a course of bile salts to dissolve the fragments

BSO8 (8 decks)

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