Modules 4.1 & 4.2 Flashcards
What is vomiting (emesis) and its pathophysiology?
- forceful expulsion of chyme from GIT
1. Vomiting center triggered, triggers cranial nerves and hypersalivation
2. glottis closes before deep inspiration and diaphragm contracts
3. abdo. muscles contract upwardly, antiperistaltic waves inc. pressure and push chyme out of mouth
What are the 5 classes of antiemetics ?
- Dopamine antag. (Block dopamine D2 receptors in the CTZ to inhibit nausea and vomiting), Domperidone
- Antimuscarinics (muscarinic receptors in the vestibular apparatus and cortical pathways at CTZ) Hyosine
- Antihistamines (H1 receptors in the vestibular apparatus and vomiting centre)
- -sertrons (serotonin (5-HT3) receptors on vagal nerve fibres. for chemo induced vomiting)
- Neurokinin-1 antagonists (Block substance P on vagal afferents)
What is diarrhoea?
- inc. fluidity and movement of stool
- daily stool production in excess of 250g which is over 70% water
- treatment: slow down gastrointestinal motility or help to absorb the excessive fluids, BUT can only treat underlying cause
What are the 4 types of diarrhoea?
- Osmotic: non-absorbable substances are drawing water into the lumen (lactose intolerance)
- Secretary: IT secretes more water than can be absorbed leading to inc. stool volume, caused by infection
- Inflammatory: due to intestinal inflam. from infection or disease, presence of blood in stool
- Motility: accelerated passage of food or absorption disorders (IBS)
What is constipation and its treatment?
- Infrequent bowel movements <3 per week
- Laxatives are used to treat (osmotic, stimulant, lubricant, faecal softeners, bulk forming)
What do the different types of GIT pain represent?
Burning: inflam/ulcer in UGIT
Dull: stretching/swelling of liver capsule
Cramping: stretching of intestines
Colicky: comes and goes, smooth muscle spasm in response to severe inflammation (gallstone obstruction)
What is the pathophys. of bacterial GIT infections?
- attachment to epi. cell and produces of exotoxins, reduces absorptive capacity of epi. and stimulates water and mucous secretion
- results is inflammatory diarrhoea
- Salmonella, campylobacter and E. coli
What is the pathophys. of viral GIT infections?
- Infect enterocytes of SI, causing damage or death to cells
- hence reduced absorptive capacity of water and electrolytes
What is appendicitis and its pathophys?
- Inflam. and infection of appendix
1. Obstruction of lumen by facealith
2. Fluid builds in appendix, wall becomes inflamed and purulent exudate forms causing swelling
3. increased pressure leads to ischaemia and necrosis of appendiceal wall
4. toxins escape into surrounding area, causing peritonitis and possible abscess development
5. Localized infection/peritonitis and inc. pressure in appendix causes inc. necrosis and gangrene
What is peritonitis?
- Bacterial infection of the peritoneal cavity or chemical irritants enter cavity causing irritation and muscle spasm
- Triggers inflam. response, peritoneum becomes more permeable, causing fluid shift and may result in hypovolemic shock
What is Ulcerative colitis?
- Inflamed mucous membrane of colon and rectum, causing ulceration
- Mucosa becomes oedmatous, and ulcers develop
- granulation tissues form trying to heal but is fragile and bleeds easy, affects colon absoprtion
- Sulphasalazine, anti-inflam to inhibit PG
What is Crohn’s disease?
- inflammation of mucosal layer of the ileum
- creates ‘rubber hose’ like wall, leaving a narrow lumen that gets obstructed easily
- impairs ability of small intestine to process food, stimulates motility and decreased absorption ability
- Can cause ulcer and abscess formation
What is a GIT ulcer?
- break in tissue lining,
What is GORD?
- periodic flow of gastric contents into
oesophagus - depends on competence or pressures of the lower oesophageal sphincter
- frequent GORD leads to inflammation/ulceration of mucosa
- Treatment: antacids, H2-receptor antag, PPIs
What is PUD?
- gastric and duodenal ulcers, mucosal erosion which exposures blood vessels, smooth muscle, sensory nerves
- caused by overexposure to gastric juices on mucosa and weakened mucosal protection
- H. pylori detection
What are the 7 LFTs? (Liver function testing)
- Bilirubin (Blood related)
- Albumin (Synthesis function)
- Prothromin time (PT) (Synthesis function)
- Alanine Aminotransferase (ALT) (Liver injury)
- Aspartate Aminotransferase (AST) (Liver injury)
- Alkaline Phosphatase (ALP) (Biliary tract)
- Gamma-Glutamyl Transferase (GGT) (Biliary tract)
What does bilirubin do?
- Breakdown product of haemoglobin, produced by liver
- Inc. levels due to haemolysis, liver injury
What do Albumin and PT do?
Albumin: transports substances and maintains oncotic pressure,
- low levels due to cirrhosis or nephrosis
PT: measures blood clotting ability and produces clotting factors,
- low levels indicate liver dysfunction,
What do ALT and AST do?
ALT: liver specific enzyme, inc. levels indicated liver cell injury
AST: found in liver, skeletal and cardiac muscle, inc. levels due to liver injury
What do ALP and GGT do?
ALP: found in liver and is involved in dephosphorylation process
- inc. levels due to bone disease or biliary obstruction
GGT: found in liver kidney and pancreas, involved in AA transport
- inc. levels same
What are the major altercations of liver disease?
- damage/death of hepatocytes
- dec. metabolic activity of liver
- portal HTN
- impeded bile excretion
- pain
What is hepatitis?
- liver inflammation due to damage, inflammation, alcohol intoxication and infection
What are consequences of prolonged impaired metabolic liver activity?
- Failed liver gluconeogenesis
- inability to convert ammonia into urea, causing hepatic encephalopathy
- Dec. albumin production, causing oedema and ascites
- Altered metabolism of sex hormones, (gynaecomastia)
- Failure to produce bile and bilirubin, causes jaundice
What is the hepatic portal vein?
- Drains blood body to be filtered in the liver
- Converges from left gastric ( drains from oesophagus and stomach), splenic (splee, stomach and pancreas), Inf. mesenteric (distal colon and rectum) and sup, mesenteric vein (SI, cecum, A. colon and T colon).
What is portal HTN?
- Inc. pressure in portal system leads to blood flow resistance through liver
- Blood seeks alternative routes (collateral circulation) to return to systemic circulation leading to varices
- Varices can be around the spleen, stomach area (caput medusae), oespohagus or rectum (haemorrhoids)
What is the pathophys of jaundice?
- Bile from liver to duodenum is blocked, accumulates in liver
- Bile salts and bilirubin to ‘spill’ into bloodstream
- Elevated bilirubin and bile salts cause itching, yellowish skin and damage hepatocytes
- 2.5mg/100ml bilirubin levels
How is bilirubin metabolised?
- Red blood cell is broken down in spleen and releases bilirubin and iron from haem portion of haemoglobin
- Transported to liver by albumin
- Unconjugated bilirubin in converted into by adding glucuronic acid (Water soluble)
- Conjugated bilirubin excreted into bile, stored in gallbladder and released into duodenum
- Either converted into urobilinogen, reabsorbed and reused, converted into urobilin for urine excretion or stercobilin into faeces
What are the types of liver cancer?
Originating in hepatocytes (hepatocarcinoma) or bile ducts (cholangiocarcinoma)
What is cirrhosis?
- Replacement of health liver tissue with fibrotic tissue leading to impaired liver function
- Causes portal HTN, Varices, Splenomegaly, Ascites, Jaundice, Hepatic encephalopathy, gynecomastia, testicular atrophy, inc. bleed, peripheral oedema, hypoalbuminemia, thrombocytopenia, hepatorenal and hepatopulmonary syndrome
What are (Cholelithiasis) gallstones?
- Emulsification of cholesterol by bile salts, creating crystals in bile ducts
- ## Occurs due to cholesterol concentration inc. or bile salts dec., or bile is in gallbladder for too long and cholesterol overconcentrates
What is acute pancreatitis?
- Tissue damage in pancreas provoking inflammatory response, causing inflamed pancreas
What is CF in regards to the pancreas?
- Affect chloride transport, which affects water movement and secretions become sticky and slow moving, blocking delivery of digestive enzymes to duodenum
