Disease

Question 1

Black stools (melaena)

Answer 1

GI bleeding

Question 2

Steatorrhoea

Answer 2

Greasy frothy yellow stools

Fat malabsorption

Question 3

Grey stools

Answer 3

Biliary tract obstruction (lack of bile in stools)

Question 4

Appendicitis

Answer 4

Inflammation of appendix

Obstruction of proximal lumen of appendix, usually by hard mass of faeces, stones, tumour, parasite, inflammation, oedema

Appendix then distends with fluid secreted by its mucosa, pressure increases and blood supply is impaired. Formation of purulent exudate further expands appendix.

24-36 hrs tissue is necrotic and perforation may occur if not removed

Classified as simple, gangrenous, perforated

S&S- upper abdo pain, then becomes intense over right lower quadrant, aggravated by moving, rebound tenderness, nausea, vomiting, low grade temp

Complications- perforation, peritonitis, abscess

Diagnose- abdo USS, X-ray, IV pyelogram, urinalysis, pelvic exam, WBC

Treatment- IV fluids, antibiotics, surgery-laparoscopic/laparotomy usually when ruptured , analgesia

Question 5

Acute abdomen

Answer 5

Causes- inflammation, CVS problem- (hypovolaemia, occlusion of blood flow), gynae problem -(ruptures ectopic, PID, infectious diseases, obstruction/perforation, GI bleed

S&S- sudden onset severe pain, distended abdo, rigidity, nausea, vomiting, diarrhoea, constipation, flatulence, melaena , haematemesis, hypovolaemic shock

Question 6

Peritonitis

Answer 6

Acute inflammation of the peritoneum

Caused by enteric bacteria entering peritoneal cavity through perforated ulcer, ruptured appendix, perforated diverticulum, necrotic bowel, gallbladder rupture, peritoneal dialysis, abdominal trauma

Peritoneal cavity that is usually sterile gets contaminated by infection or chemical irritant

Bacterial peritonitis caused by infection with e-Coli, klebsiella, proteus, pseudomonas or gonorrhoea. Inflammation releases histamine causing vasodilation and increased capillary membrane. Polymorphonuclear leukocytes infiltrate peritoneum to phagocyte bacteria

S&S- severe abdo pain with guarding, inflammation inhibits peristalsis resulting in paralytic ileus, bowel sounds diminish, abdominal distension, nausea and vomiting, fever, malaise, tachycardia, tachypnoea, restlessness, disorientation, oliguria, board like rigid abdomen

Complications- abscess formation, fibrous adhesions and obstruction, septicaemia, septic shock, paralytic ileus

Diagnostics- WBC, blood cultures, X-ray, liver and renal function, serum electrolytes, abdominal paracentesis

Treat- antibiotics, analgesia, surgery-laparotomy, peritoneal lavage (Washington our of peritoneum), Jackson-Pratt drain, IV fluids and electrolyte replacement, place on bed rest in fowlers, intestinal decompression via nasogastric tube or if prolonged a jejunostomy -food and fluids witheld till intestinal motility has returned

Question 7

Gastroenteritis

Answer 7

Inflammation of stomach and small intestines

Usual via contaminated food or fluid via faecal oral route. Rotavirus or nova virus

Manifest by

1. Bacteria (staph, clostridium perfringens, e-coli) excrete exotoxins causing damage and inflammation, impair intestinal absorption and cause secretion of significant amounts of electrolytes and water into bowel creating diarrhoea
2. Invasion and ulceration of mucosa by bacteria (salmonella, shigella, e-coli) producing microscopic ulceration, bleeding, fluid exudates and water/electrolyte secretion

S&S- diarrhoea, anorexia, nausea, vomiting, bowel distension, abdominal pain and cramping, borborygmi (hyperactive bowel sounds), headache, malaise, dry skin, poor skin turgor, fever

Complications- electrolyte and acid base imbalance, metabolic alkalosis with vomiting, metabolic acidosis with diarrhoea, hypokalaemia

Diagnosis- stool sample, colonoscopy, serum osmolarity, electrolytes, ABG’s

Treatment- replace fluid and electrolyte loss, oral rehydration, gastric lavage (if botulism), plasmapheresis, dialysis (haemorrhagic colitis)

Question 8

Protozoal bowel infection

Answer 8

Parasites infecting bowel via faecal-oral route. Giardiasis is most common, cryptosporidiosis, amoebiasis

Giardiasis- transmission overcrowding or poor sanitation. Asymptomatic but can be diarrhoea, cramps, bloating, nausea, vomiting, fever, fatigue, wt loss

Amoebiasis- caused by entamoeba histolytica. Food or water contaminated by faeces, person-person contact. Enters intestine where it lives causing ulceration and inflammation. Trophozoites of some strains may spread via blood to liver, lungs or brain. Manifest cramps, diarrhoea containing blood/mucous

Cryptosporidiosis- faecal-oral route. Contaminated water. Organism attaches to bowel epithelium. Manifests watery diarrhoea, low grade fever, malaise, nausea, vomiting, abdo cramps

Diagnosis- stool sample, sigmoidoscopy, small bowel biopsy

Treatment- antiparasitic medication

Question 9

Helminthic disorder

Answer 9

Parasitic worms - roundworms (trichinosis), flukes, tapeworms, threadworms (strongyloides stercoralis), hookworm (anclostoma duodenale)

Enters body in undercooked food

Diagnosis- stool sample, presence of parasites eggs on perianal skin, FBC (anaemia with hookworm and eosinophilia), elevated CK with trichinosis

Treatment- aldendazole or mebendazole (vermin)

Question 10

Ulcerative colitis

Answer 10

Risk factors- family hx, meds, diet

Affects mucosa and submucosa of colon and rectum, insidious onset, usually distal colon affected

Begins at rectosigmoid area of anal canal and progresses proximal.

Microscopic mucosal haemorrhage occurs and abscesses develop, spread laterally leading to necrosis and sloughing of bowel mucosa, further tissue damage is caused by inflammation and leads to atrophy, narrowing and shortening of the colon

S&S- diarrhoea with blood and mucous, mild (4 stools), severe (6-10 stools), stools with anaemia, hypovolaemia, malnutrition, arthritis, uveitis, skin lesions, may affect liver, kidney and biliary

Complications- haemorrhage, toxic mega colon, colon perforation, risk of colorectal cancer

Question 11

Chron’s

Answer 11

Chronic inflammatory disease affecting GI tract. Can affect any portion of the GI tract but usually terminal ileum or ascending colon

Begins with small Aphthoid lesion of the mucosa and submucosa of the bowel, progress to deep ulcerations, granulomatous lesions and fissures

Fibrotic changes in bowel wall cause thickening and decreased flexibility and lead to local obstruction, abscess and fistula between loops of bowel or bowel and other organs. Malabsorption May develop due to prevention of absorption of nutrients

S&S- persistent diarrhoea, don’t contain blood, abdominal pain and tenderness, palpable right lower quad mass, fever, fatigue, malaise, wt loss, anaemia

Complications- intestinal obstruction, fistula, recurrent UTI

Diagnostic- colonoscopy, X-ray, stool sample, FBC, ESR, CRP, serum albumin, LFT

Treatment- anti-inflam (sulfasalazine), immune suppressors if severe, corticosteroids, hydrocortisone, inflixumab (suppress tumour necrosis factor), alter diet, surgery if bowel obstruction or perforation (colectomy, ostomy), probiotics, herbal remedies

Question 12

Coeliac/ tropical sprue

Answer 12

Chronic primary disorder of small intestines where absorption of nutrients especially fats is impaired.

Two forms- coeliac and tropical sprue

Flattening of villi and thus no surface to absorb nutrients and digestive enzyme production is reduced.

Coeliac- chronic immune medicated malabsorption disorder with sensitivity to the gliadin fraction of gluten

Involves particular genetic make up with genes HLA-DQ2 and HLA-DQ8
Intestinal mucosa damaged by immunological response. Gliadin acts as antigen prompting inappropriate T cell mediated immune response resulting in loss of intestinal folds

S&S- abdominal bloating, cramps, diarrhoea, steatorrhoea, anaemia, tetany, vitamin deficiencies, muscle wasting, osteomalacia

Complications- GI malignancies, intestinal lymphoma, intestinal ulceration

Tropical sprue- unknown cause, but may be bacterial or toxins

Similar pathophysiology to coeliac but without gluten

S&S- sore tongue, diarrhoea, wt loss, folic acid deficiency, Vit B12 and iron deficiency

Diagnosis- endoscopy, biopsy, serology for antibodies, stool sample, serum levels of protein , albumin, cholesterol, electrolytes, iron, Hb, haematocrit

Treat- vitamin and mineral supplements for deficiency, gluten free diet

Question 13

Lactase deficiency

Answer 13

Lactose is the primary carbohydrate in milk and milk products. Lactase is needed to break down and absorb it. Leads to lactose intolerance and malabsorption

Undigested lactose ferments in intestines forming gases creating bloating and flatus. Lactic acidosis and fatty acids produced by fermentation irritate bowel and u digested lactose draws water to intestines= diarrhoea

Diagnose- lactose breath test

Question 14

Polyps

Answer 14

Mass of tissue arising from bowel wall and protruding into lumen, have the potential to turn malignant

Most are adenomas

Disruption of normal cell division and maturation lead to formation of polyp (tightly packed epithelial cells)

Named by the way they attach to the wall- sessile (raises nodule), or pedunculated (attached by stalk)

Adenomas bigger than 1cm have higher risk of being malignant

S&S- asymptomatic or have rectal bleeding, diarrhoea or mucous discharge

Question 15

Colorectal cancer

Answer 15

Risk factors- age >50, polyps, family hx, IBD, exposure to radiation, high fat diet (produces anaerobic bacteria that converts bile acids into carcinogens)

Hereditary non-polyposis colorectal cancer=lynch syndrome

Start as adenomatous polyp that develop into adenocarcinoma and spreads by direct extension to involve entire bowel. Can also involve lymph node then spreads to liver, lungs, brain, bones and kidneys

S&S- usually produces symptoms once advanced- rectal bleeding, change in bowel habits, pain, anorexia, wt loss

Complications- bowel obstruction (due to narrowing from lesions), perforation , direction extension of tumour to adjacent organs

Prevention- diet high in fruit and vegetables and low in fats

Screening- check for blood in faeces in >50 yr olds

Diagnostic- sigmoidoscopy, colonoscopy, biopsy, FOBT (faecal occult blood test), FBC (anaemia), carcinoembryonic antigen (CEA)- tumour marker, X-ray, CT, MRI (metastasis in lung)

Treat- laser photocoagulation, surgery (stage 1&2), surgery and chemo (stage 3), colostomy, radiation (after surgical resection for rectal tumours)

Question 16

Hernia

Answer 16

Defect in abdominal wall allowing abdominal contents to protrude out of abdominal cavity

Classified by location-
Indirect inguinal hernia caused by improper closure of the tract developing as the testes descend into the scrotum before birth. A sac comprising of abdominal contents protrudes through internal inguinal ring into inguinal canal

Direct inguinal hernia- acquired defect resulting from weakness of the posterior inguinal wall

Femoral hernia- defects in which peritoneal sac protrudes through the femoral ring (usually obese or pregnant women)
S&S- lump, swelling, bulge in groin, may cause sharp pain or dull ache radiating to scrotum

Umbilical hernia- may be congenital or acquired as tissue closing the umbilical ring weakens allowing protrusion of abdominal contents. Usually multiple pregnancies, obese, ascites, large intra-abdominal tumours. Tend to enlarge steadily and contain omentum.
S&S- sharp pain on coughing or straining, dull aching sensation. Strangulation/obstruction is common complication (bowel involved can not retract and tissue dies)

Incisional or ventral hernia-occur at previous surgery sites or abdominal muscle tears due to inadequate healing.
Contributing factors- age, poor wound healing, infection, obesity, inadequate nutrition, vigorous coughing
S&S- asymptomatic, bulge at site

Treatment- herniorhaphy

Question 17

Intestinal obstruction

Answer 17

Failure of intestinal content to move through bowel lumen

Mechanical obstructions- problems outside intestines (scar tissue/hernia), problems within (tumour, IBD, obstruction of the lumen)

Functional obstructions paralytic ileus- peristalsis fails to propel content due to muscular or neurogenic impairment

Partial or complete, named by area of intestine affected

When obstructed gas and fluid accumulate proximal to and within obstructed section distending bowel. Water and sodium are drawn into bowel lumen, interferes with peristaltic movement leading to atony and compromises blood flow to mucosa=necrosis. Gangrene bowel may perforate leading to peritonitis

Bowel distension, vomiting and third spacing of fluids in bowel and peritoneal cavity leads to massive loss of fluids and electrolytes leading to hypovolaemia, hypokalaemia, renal insufficiency and shock

S&S- cramping, vomiting with faecal matter if low or distal obstruction, high pitched tinkling bowel sounds, possible visible peristalsis, abdominal distension with distal obstructions and paralytic ileus, tender abdo, hypovolaemia (tachycardia, tachypnoea, hypotension, temp, oliguria)

Complications- hypovolaemia/shock, multiple organ dysfunction, renal insufficiency, septic, pulmonary ventilation impaired due to pressure on diaphragm

Diagnosis- X-ray, CT, WBC, serum amylase, serum osmolality, electrolytes, ABG

Treatment- gastrointestinal decompression, surgery-laparotomy

Question 18

Diverticular disease

Answer 18

Small outpouchings of the colon occurring in rows in GI tract except rectum. Possibly caused by highly refined foods low in fibre, decreases exercise and delaying defecation

Form when increased pressure within bowel lumen causes bowel mucosa to herniate through defects in the colon wall. Circular and longitudinal muscles thicken or hypertrophy in area of diverticula which narrows bowel lumen increasing intraluminal pressure

S&S- left sided abdominal episodic pain, diarrhoea, constipation, narrow stools, bleeding in stools, weakness and fatigue

Complications- haemorrhage, diverticulitis (inflammation in and around diverticula- food causing hard mass and impairing blood flow and brings bacteria)

Complications of diverticulitis- bowel obstruction, fistula, haemorrhage, scarring and fibrosis

Diagnosis- barium enema, X-ray, sigmoidoscopy, colonoscopy, WBC, FBE, stool sample for blood

Treatment- antibiotics, high fibre diet, avoid foods with small seeds, bowel rest, surgery

Question 19

Stomatitis-HSV

Answer 19

HSV, candida, canker sore, ulcerative gingivitis

Inflammation of oral mucosa, can be caused by HSV, fungal or trauma, tobacco.

Common side effect of cancers

S&S- painful lesions

Question 20

Oral cancer

Answer 20

Squamous cell carcinoma, most common lower lip, tongue and floor of mouth

Presents as inflamed areas with irregular borders

Caused by smoking, alcohol, chewing tobacco

Tumours deepen as they advance affecting deeper tissues

S&S- oral lesion, difficulty speaking/swallowing/chewing, loose teeth, earache, swollen lymph, bleeding, sensory or motor nerve compromise

Treatment- surgery, radiation, chemo

Question 21

GORD

Answer 21

Backward flowing of gastric content into oesophagus=heartburn

risk factors- smoking, obesity, pregnancy

Transient relaxation of lower oesophageal sphincter and/or increased pressure within stomach

Contributing factors- increased gastric volume, positioning , increased gastric pressure (obesity, preg, tight clothes)

S&S- burning, retrosternal pain- can radiate to jaw, metallic taste, chronic cough, exacerbation of asthma

Complications- oesphagitis, oesophageal ulcer, peptic ulcer, haemorrhage, Barrett’s oesophagus, oesophageal cancer

Diagnosis- barium swallow, upper endoscopy, 24hr ambulatory ph monitoring, oesophageal monometry

Treatment- antacids, proton pump inhibitors, H2 receptor, metoclopramide, dietary change (avoid acid/fatty foods, avoid large meals), elevate head of bed, smoking cessation, alcohol avoidance, stress reduction, wt loss, surgery-laparoscopic fundoplication (gastric fundus wrapped around distal oesophagus)

Question 22

Hiatal hernia

Answer 22

Part of stomach protrudes through oesophageal hiatus of the diaphragm into the thoracic cavity

Sliding hiatal hernia-gastro-oesophageal junction and fundus of the stomach slide upward through oesophageal hiatus.

Contributing factors- weakness gastro-oesophageal diaphragmatic anchors, shortening of the oesophagus, increased intra-abdominal pressure

Paraoesophageal hiatal hernia- junction between oesophagus and stomach remain in its normal position below the diaphragm while part of the stomach herniates through the oesophageal hiatus. Can become strangled and impair blood flow to herniated tissue

S&S- reflux, heartburn, feeling of fullness, substernal chest pain, dysphagia, occult bleeding, indigestion

Diagnosis- barium swallow, upper endoscopy

Treat- surgery- nissen fundoplication, meds for GORD

Question 23

Oesophageal cancer

Answer 23

Oesophageal tumours= adenocarcinoma or squamous cell carcinoma

Usually asymptomatic until late stage

Risk factors- smoking and chronic alcohol use-squamous cell, obesity, GORD, Barrett’s oesophageal-adenocarcinoma

S&S- dysphagia, wt loss, anaemia, GORD like symptoms, regurgitation, anorexia, chest pain, persistent cough, hoarseness

Complications- tracheoesophageal fistula leading to aspiration, pneumonia, SOB

Diagnosis- barium swallow, upper endoscopy, chest X-ray, CT, MRI, FBC, serum albumin, LFT

Treatment - surgery- oesophagectomy, radiation, chemo. If too advanced then palliative care- brachytherapy, chemo, oesophageal stenting

Question 24

Gastritis

Answer 24

Inflammation of stomach lining from irritation of the gastric mucosa

Acute gastritis- disruption of mucosal barrier by local irritant (NSAIDS, aspirin, steroids, alcohol, caffeine) allows hydrochloric acid and pepsin to come into contact with gastric tissue creating irritation, inflammation and erosion- usually self limiting

Erosive/stress induced gastritis- severe form of acute gastritis. Usually complication of life threatening event such as shock, severe trauma, major surgery, sepsis, burns or head injury. Of occur after major burn are called curlings ulcers, post head injury is called Cushings ulcers
Ischaemia of gastric mucosa from sympathetic vasoconstriction and tissue injury due to gastric acid

S&S- mild- anorexia ore pigs stricken pain relieved by belching. Severe- abdominal pain, nausea, vomiting, gastric bleeding

Chronic gastritis- progressive disorder that begins with superficial inflammation and leads to atrophy of gastric tissues, involved glands of mucosa are disrupted and destroyed and inflammation involves deep portions of mucosa

Type A- autoimmune gastritis- body produces antibodies to parietal cells and to intrinsic factor, antibodies destroy gastric mucosa resulting in atrophy and loss of hydrochloride acid and pepsin
Type B- more common- incidence increases with age, chronic infection of the gastric mucosa by H-pylori, outer most layer thins and atrophies providing less effective barrier to hydrochloric acid and pepsin

S&S- asymptomatic until atrophy is advanced then vague gastric distress, epigastric heaviness, anaemia, Vit B12 def, blood vomit, pain 1-2hrs post meals

Diagnosis- FBE, serum Vit B12, endoscopy

Treatment- proton pump inhibitors, H2 receptor antagonist, gastrointestinal rest

Question 25

Peptic ulcers

Answer 25

Break in mucosal lining of GI tract where it comes into contact with gastric juice

Risk factors- chronic H-pylori infection, NSAIDS/aspirin, smoking, unclean food/water, advanced age, family hx, crowded unsanitary living conditions

Develops when mucosa barrier is unable to protect mucosa from damage by hydrochloric acid and pepsin. H-pylori bacteria produce enzymes that reduce efficacy of mucosal gel in protecting gastric mucosa. Host inflammation response to bacteria contribute to epithelial damage

NSAIDS interrupt prostaglandin synthesis which helps maintain mucosa barrier

Can be in oesophagus, stomach or duodenum

S&S- pain relieves by eating, blood in stools, heartburn, regurgitation, pain 3-4hrs post eating

Complications- haemorrhage, obstruction, perforation

Zolliner-Ellison syndrome- gastrin secreting tumour of the pancreas, stomach or intestines. Increased gastrin level from tumour increases hydrochloric acid and pepsin secretion leading to mucosa ulceration

Diagnosis- CT, endoscopy, biopsy, urea breath test (tests for H-pylori), gastric analysis

Treatment- antibiotics, proton pump inhibitors, H2 receptor antagonist, antacids, sucralfate, prostaglandin analogues, surgery

Question 26

Stomach cancer

Answer 26

Risk factors- H-pylori, genetic, chronic gastritis, pernicious anaemia, gastric polyps, carcinogenic factors in diet, lack of hydrochloric acid (achlorhydria)

Adenocarcinoma, most frequently in distal part of stomach

Begins as local lesion then progresses to mucosa and submucosa

S&S- usually advanced before symptoms, early satiety, anorexia, indigestion, vomiting, ulcer like pain unrelieved by antacids, wt loss

Diagnosis- FBE, X-ray, CT, barium swallow, endoscopy, biopsy

Treatment- surgery-partial gastrectomy, total gastrectomy if whole stomach involved by not spread further, radiation, chemo

Complications of stomach removal- dumpiest g syndrome, anaemia (rapid emptying reduces absorption), Vit B12 def (stomach produces intrinsic factor that absorbs B12)

Question 27

Choleslithiasis (gallstones)

Answer 27

Formation of stones within gallbladder or duct system

Risk factor- age, fam hx, obesity, rapid wt loss, female, preg, fasting

Caused by abnormal bile composition, biliary stasis/obstruction (slow emptying of gallbladder), inflammation of gallbladder (excess water and bile salt reabsorption)

Most consistent with cholesterol, excess cholesterol in bile is due to obesity, high kilojoules/ high cholesterol diet, drugs that lower serum cholesterol levels

S&S- epigastric fullness, gastric distress after eating large meal, stones that are obstructing cystic duct lead to distension and increased pressure behind stone (biliary colic-pain in epigastric region/RUQ-May radiate to back/shoulder), begins suddenly after meal and lasts 5hrs, nausea/vomiting

Complications- obstruction of bile duct leads to bile reflux into liver=jaundice, pain and liver damage, pancreatitis

Cholecystitis- inflammation of gallbladder. Obstruction leads to increased pressure within gallbladder leading to Ischaemia of gallbladder wall and mucosa, inflammation follows=pain, anorexia, nausea, vomiting, fever,

Complications- empyema, gangrene, perforation-peritonitis, fistula, obstruction of small intestine by stone

Diagnostic- serum bilirubin, FBC, WBC, serum amylase, serum lipase, X-ray, ultrasound, oral cholecystogram, gallbladder scans

Treatment- surgery-laparoscopic cholecystectomy, fat intake limited, fat soluble vitamins and bile salts, lithotripsy (shock wave to dissolve stone)

Question 28

Hepatocellular failure

Answer 28

Impaired protein metabolism= low albumin= oedema in peripheral tissues and acsites and low clotting factor (liver makes clotting factors)=risk of bleeding, disrupted lipids and fat soluble vitamins, impaired steroid hormones=feminisation in men and irregular menses in women

Question 29

Jaundice

Answer 29

Bilirubin accumulates in tissues. When haemoglobin is broken down it produces biliverdin that gets converted to fat soluble bilirubin (unconjugated) which binds with albumin and transported to liver to water soluble conjugated bilirubin and excreted in bile

Haemolytic jaundice- excess RBC destruction that liver can’t handle= raised unconjugated bilirubin levels

Hepatic jaundice- impaired liver cell function disrupts conversion an excretion of bilirubin. Conjugated and unconjugated rose (clay stools, dark urine)

Obstruction of bile- impairs excretion and conjugated levels elevate (clay stools, dark urine)

Question 30

Portal hypertension

Answer 30

Impaired blood flow through liver increases pressure in portal vein system that drains GI tract

Dilated veins of GI and abdominal wall lead to formation of collateral vessels in oesophagus, stomach and rectum

Splenomegaly

Ascites (pressure forces fluid out of vessels into peritoneal cavity, low albumin level reduces osmotic draw back into vessels)

Gastrointestinal bleeding- esophageal bleeds, melaena

Portal systemic encephalopathy- impaired consciousness due to accumulation of toxic waste in blood as it bypasses congested liver. Cerebral oedema develops late in liver failure- leads to intracranial pressure, cerebral perfusion decrease and brain hypoxia

Hepatorenal syndrome- acute renal failure due to disrupted blood flow to kidneys

Question 31

Hepatitis

Answer 31

Hep B=DNA
Hep A,C,E,B-associated delta=RNA

Hepatitis A (infectious hepatitis)- transmitted faecal-oral by contaminated food/water/direct contact with infected person. Incubation of 4 weeks, once jaundice presents minimal risk of spread

Hepatitis B- can create acute, chronic, fulminating and carrier states. Spread by blood and body fluids.
Risk factor for liver cancer.
Liver cells damaged by immune response to antigen.
S&S- nausea, vomiting, malaise, photophobia, muscle pain, headache

Hepatitis C- transmitted through blood, can cause liver cancer, cirrhosis

Hepatitis Delta- can only occur in person with HBV via double exposure or superinfection. Spread body fluids/blood

Hepatitis E- rare, faecal contamination of water supplies in developing areas

Toxic hepatitis- substances (paracetamol), toxins and alcohol damage cells

Hepatobilliary hepatitis- cholestasis (interruption of normal flow of bile)

S&S- prodromal phase- malaise, anorexia, fatigue, muscle and body aches, may develop nausea, constipation, vomiting and diarrhoea, mild RUQ pain(liver pain), rigors and fever.
Icteric phase- jaundice, pruritus (due to bile salts), clay stools (bile pigment not excreted in bowel but excreted in kidneys so dark urine)
Convalescent phase- symptoms improve, decrease serum enzymes, reduced liver pain

Diagnosis- LFT’s, GGT, LDH, SBR, antigen year, liver biopsy

Treatment- prevent with vaccine (hep A x2 doses, hep B x3 doses), exposure prophylaxis of immunoglobulin, hep C- interferon alpha/ribavirin (antiviral)

Question 32

Cirrhosis

Answer 32

End stage chronic liver disease, irriversible leads to liver failure

Risk of bleeding cause liver responsible for clotting production

Results from alcoholism/laennec’s, chronic hep B/C, prolonged obstruction of biliary duct, long term severe right heart failure

Functional liver tissue is gradually destroyed and replaced by fibrous scar tissue, functional liver metabolism is lost. Fibrous tissue creates constrictive tissue bands that disrupt blood and bile flow, blood no longer flows through liver to inferior vena cava creating portal hypertension

Alcoholic cirrhosis- alcohol causes metabolic changes in liver. Triglycerides and fatty acid synthesis increase formation of lipoproteins decreases, leading to fatty infiltration of hepatocytes. If continued alcohol use then causes inflammation and necrosis, fibrosis and destruction of liver tissue. Liver shrinks

Biliary cirrhosis- retained bile damages and destroys liver cells close to interlobular bile ducts leading to inflammation, fibrosis and formation of regenerative nodules

Post-hepatic cirrhosis- damage from chronic hep B/C- liver shrinks and extensive liver cell loss and fibrosis

S&S- few in early stages, dull aching pain in RUQ, fever, malaise, nausea, vomiting, diarrhoea, anorexia, then as progresses portal hypertension, splenomegaly, ascites, oesophageal varies, portal systemic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, jaundice, men decrease body hair/testicular atrophy, women dysmenorrhoea/amenorrhea, haemorrhage, anaemia

Diagnosis- LFT, FBC, coags, WBC, electrolytes, bilirubin, serum albumin, serum glucose, serum ammonia, abdominal ultrasound, endoscopy

Treatment- aimed at slowing progression
Avoid alcohol and hepatotoxic drugs, diuretics, lactulose/neomycin (concert ammonia into ammonium ion that can’t be absorbed and excreted in faeces), beta blocker to prevent varicose bleeding, iron and folic acid (anaemia), Vit K, PRBC if bleeding acute, antacids
Nutrition- sodium and fluid restriction, vitamin replacement, liver transplant

Complication management-

• paracentesis (aspiration of fluid from peritoneum)
• balloon tamponade (balloon inserted nasogastric and blown up to exert pressure on bleeders
• transjugular intrahepatic portosystemic shunt (relieves portal hypertension)

Question 33

Liver cancer

Answer 33

Hepatocellular carcinoma or cholangiocarcinoma (bile duct)

Damage to cellular DNA due to hepatitis, or repeated cycles of cell necrosis and regeneration that facilitate DNA mutation

Grow rapidly and metastasis early

S&S- insidious, weakness, anorexia, wt loss, fatigue, malaise, jaundice, abdominal pain, mass in RUQ, ascites, liver failure as tumour progresses (4mth survival)

Diagnosis- CT/MRI, biopsy, serum alphafetoprotein (AFP)

Treatment- small resections, liver transplant (tumour May return in new liver), radiation, chemo, direct continuous hepatic arterial infusion with implanted pump

Question 34

Pancreatitis

Answer 34

Inflammation of pancreas. Release of pancreatic enzymes into tissue of pancreas itself leading to haemorrhage and necrosis

Caused by alcohol abuse and gallstones

Acute pancreatitis- interstitial oedematous pancreastitis (self limiting) and necrotising pancreatitis (inflammation and haemorrhage=necrosis)

Gallstones may obstruct pancreatic duct or cause bile reflux activating pancreatic enzymes in pancreatic duct system

Alcohol causes duodenal oedema and May increase pressure and spasm of the sphincter of oddi, obstructing pancreatic outflow, increasing pancreatic enzyme production and raising pressure within the pancreas

Trauma, tissue Ischaemia, pregnancy, pancreatic tumours, infectious agents, elevated calcium/lipid levels, some medications

Pancreatic enzyme gets released and trypsin digests pancreatic tissue and activates phospholipase A which digests cell membrane. Leads to proteolysis, oedema, vascular damage, haemorrhage and necrosis. Cell damage/necrosis release vasoactive substances that increase vascular permeability and cause oedema. Large volumes of fluid shift from blood to retroperitoneal space, peripancreatic space and abdominal cavity

S&S- continuous severe epigastric pain and abdominal pain radiating to back and slightly relieved by sitting up, pain irritated by fatty food and alcohol. Nausea, vomiting, abdominal distension, rigidity, decreases bowel sounds, tachycardia, hypotension, temp, cold/clammy, jaundice, retroperitoneal bleeding, epigastric mass

Complications- intravascular volume depletion, acute tubular necrosis, renal failure, ARDS, pancreatic necrosis, abscess, shock, multiple organ failure

Chronic pancreatitis- irreversible and leads to pancreatic insufficiency

Risk factors- alcoholism, CF

Alcohol increases insoluble protein that calcify and block pancreatic ducts and flow

Stones may block flow

Leads to fibrotic changes and loss of exocrine function=malabsorption

If endocrine function is disrupted may lead to diabetes

S&S- recurrent episodes of epigastric pain and left abdominal pain, as progresses interval between pain decreases, anorexia, nausea, vomiting, wt loss, flatulence, constipation, steaorrhoea,

Complications- malabsorption, malnutrition, peptic ulcer, pancreatic abscess, diabetes, pancreatic cancer

Diagnosis- ultrasound, CT, endoscopy retrograde cholangiopancreatography, magnetic endoscopic retrograde cholangiopancreatography, fine needle aspiration

Treatment- IV fluids, NBM, narcotics, antibiotics if infection, pancreatic enzyme supplements, proton pump inhibitors, H2 receptor antagonist, low fat diet, no alcohol, surgery if gallstones

Question 35

Pancreatic cancer

Answer 35

Adenocarcinoma, slow onset

Risk factors- smoking, industrial chemical exposure, chronic pancreatitis, diabetes, obesity

Tumours in head of pancreas (only one that can be ressected) obstruct bile flow and cause jaundice, clay stools, dark urine, pruritus

Tumours in body of pancreas- press on coeliac ganglion causing increase pain on eating or supine position

Tumours in tail pancreas- no symptoms until metastasis

Treatment- whipples (dissect head of pancreas, entire duodenum, distal third of stomach, portion of jejunum and lower half of common bile duct), radiation, chemo

S&S- anorexia, wt loss, flatulence, nausea, dull epigastric pain, pain increases as tumour grows

Question 36

Bile salt deficiency

Answer 36

Need to emulsify fats

Conjugated bile salts synthesised from cholesterol in liver

Can result from liver disease and bile obstructions

Poor intestinal absorption of lipids causes fatty stools, diarrhoea, loss of fat soluble vitamins (A,D,E,K)

Vit A- night blindness
Vit D- decreases calcium absorption, bone osteoporosis, fractures
Vit K- prolonged prothrombin time, purpure, petechiae
Vit E- uncertain

Question 37

Liver disease

Answer 37

Liver responsible for clotting production

Reduction of clotting factors associated with level of liver damage

Factor VII first to decline then protein C, factor II and X. Factor IX are less affected and don’t decline till liver damage well advanced as well as protein S

Factor V deficiency directly correlates with amount of liver damage