GI disorders Flashcards
What innate physical barriers do we have that protect us from food poisoning?
Sight Smell Memory Saliva Gastric acid Small intestine secretions Colonic mucus Anaerobic environment Peristalsis/segmentation
What causes xerostomia and what might it result in?
Severe illness and/or dehydration results in reduced salivary flow which then leads to microbial overgrowth in the mouth and dental caries
Can lead to parotitis caused by Staph aureus
What is achlorhydira?
Do not produce gastric acid. More suceptible to shigellosis, cholera and salmonella.
What microorganisms are resistant to gastric acid?
STB Helicobacter pylori Hep A Polio Coxsackie Norovirus
How does the small intestine maintain a sterile environment?
Secretions - proteolytic enzymes, bile Lack of nutrients Anaerobic environment Shedding epithelial cells Rapid transit (peristalsis)
What protects the colon?
Anaerobic environment
Mucus layer
What is the innate cellular protection in the body?
Neutrophils Macrophages Natural killer cells Tissue mast cells Eosinophils
What cellular protection does the body have against worms?
Eosinophils
When might eosinophilia occur?
Asthma
Hay fever
Parasitic infections
How do mast cells cause massive fluid loss?
Gut infections can activate complement recruite mast cells which release histamine. This causes vasodilation and increased capillary permeability. In untreated cholera, can lose up to 1 l/hr. 60% mortality if untreated
Where do carbon particles localise if injected intravenously?
Lungs
Liver
Spleen
What is a portal system?
2 capillary systems in series eg. hepatic portal system, hypothalamo-hypophyseal portal system
Where are the 2 capillary systems in the hepatic portal system?
Villus and hepatic lobule
What are kupffer cells?
Macrophages in the liver
What might cause liver failure?
Viral hepatitis Alcohol Drugs eg paracetomol Industrial solvents Mushroom poisoning
What does liver failure increase susceptibility to?
Infections
Toxins, drugs, hormones
Increased blood ammonia due to failure to clear
What does high ammonia in the body cause?
hepatic encephalopathy
What can result from hepatic fibrosis?
Leads to portal venous hypertension -> portosystemic shunting and therefore toxin shunting -> oesophageal varicose, haemorrhoids and caput medusae
What adaptive cellular defences do are bodies have?
B lymphocytes
T lymphocytes
Where is GALT usually distributed?
Tonsils
Peyer’s patches
Appendix
Why is there a lot of lymph tissue at the ileocaecal valve?
Lots of bacteria in large intestine which is harmful to the small intestine (likely if valve incompetent) Lymph there to provide appropriate defence if necessary
What is mesenteric adenitis?
Common cause of right iliac fossa pain in children can easily be mistaken for appendicitis. Caused mostly by adenovirus/coxsackie virus
How might typhoid fever kill patients?
Causes inflamed Peyer’s patches in terminal ileum which can perforate
How is appendicitis caused?
Lymphoid hyperplasia at the appendix base can lead to obstructed outflow - stasis=infection
May also be caused by obstruction by faecolith
When is purulent appendicitis most common?
During epidemics of chickenpox in children
What processes are affected by liver disease?
Bile production Carb, protein and lipid metabolism Protein synthesis Vitamin D synthesis Detoxification Vitamin and mineral storage Phagocytosis
What do liver function tests assess?
Hepatocellular damage through aminotransferases and gamma-glutamyl transpeptidase
Cholestasis through bilirubin and alkaline phosphate
Synthetic function though albumin and prothrombin time
What are the 3 classifications of jaundice?
prehepatic (haemolytic)
hepatic (parenchymal)
Post hepatic (cholestatic)
What is pre-hepatic jaundice?
Excessive haemolysis - liver unable to cope with excess bilirubin
What is found in the blood of a patient with pre-hepatic jaundice?
Unconjugated hyperbilirubinaemia Reticulocytosis Anaemia Increased LDH Decreased haptoglobin
What causes pre-hepatic jaundice?
Genetics - red cell membrane defects, haemoglobin abnormalities, metabolic defects
Congenital hyperbilirubinaemias
Immune, mechanical, acquired defects, infections, drugs, burns
What is hepatocellular jaundice?
Deranged hepatocyte function. An element of cholestasis
What are the lab findings of hepatocellular jaundice?
Mixed unconjugated and conjugated hyperbilirubinaemia
Increased liver enzymes - reflects liver damage
Abnormal clotting
What causes hepatocellular jaundice?
Congenital - Gilbert's syndrome, Crigler-Najjar syndrome Hepatic inflammation Drugs Cirrhosis Hepatic tumours
What is post-hepatic/cholestatic jaundice?
Obstruction of the biliary system - intra/extahepatic
Passage of conjugated bilirubin blocked
What are the lab findings of post-hepatic/cholestatic jaundice?
Conjugated hyperbilirubinaemia Bilirubin in urine No urobilinogen in urine Increased canalicular enzymes Increased liver enzymes (mild hepatocyte damage)
What are the potential causes of intrahepatic post-hepatic jaundice?
hepatitis
drugs
Cirrhosis
Primary biliary cirrhosis
What are the potential causes of extrahepatic post-hepatic jaundice?
Gallstones Biliary stricture Carcinoma Pancreatitis Sclerosing cholangitis
What are the stages of damage in hepatitis?
Acute -> chronic
Acute hepatocyte breakdown - aminotransferase release, jaundice
Prolonged /chronic damage - synthetic failure, decreased albumin, decreased clotting factors
What are the potential causes of hepatitis?
Viral
Autoimmune
Drugs
Hereditary
What is the pathology of alcoholic liver diseae?
Fatty changes
Alcoholic hepatitis
Cirrhosis
What are the potential complications of alcoholic liver disease?
Hepatocellular carcinoma Liver failure Wernicke-Korsakoff syndrome Encephalopathy Dementia Epilepsy
What is liver cirrhosis?
Liver cell necrosis followed by nodular regeneration and fibrosis, resulting in increased resistance to blood flow and deranged liver function
What are the potential causes of liver cirrhosis?
Alcohol Hep B & C Biliary cirrhosis Autoimmune hepatitis Haemochromatosis Wilson's disease
What are the clinical features of liver cirrhosis?
Liver dysfunction: -Jaundice -Anaemia -Bruising -Palmar erythema -Dupuytren's contracture -Portal hypertension Spontaneous bacterial peritonitis
What causes GIt ischaemia?
Arterial disease, systemic hypotension or intestinal venous thrombosis
What investigation results confirm a diagnosis of liver cirrhosis?
Increase ALT/AST/ALP Increased bilirubin Decreased Albumin Deranged clotting Decreased Na+
What is the management of liver cirrhosis?
Stop drinking
Treat complications
Transplantation
What are the specific causes of primary biliary cirrhosis and what are the clinical features and treatment?
Chronic obstruction of the bile ducts
Jaundice, pruritis, xanthelasma, hepatosplenomegaly
Supportive treatment then liver transplant
What is the genetic inheritance of hereditary haemochromotosis?
Autosomal recessive
Abnormal iron transport -> iron depostion
What are the clinical features of hereditary haemochromatosis?
Heart - cardiomyopathy Pancreas - diabetes Pituitary - hypogonadism Liver - hepatitis/cirrhosis Skin - hyper pigmentation
Treat by venesection
What is the pattern of inheritance of Wilson’s disease?
Autosomal recessive. Dissordered copper transport -> deposition
What are the clinical features of Wilson’s disease?
Liver - hepatitis -> cirrhosis
Basal ganglia - tremor, dysarthria, dementia
Kidney - tubular degeneration
Eyes - Kayser-Fleischer rings
Treat with penecillamine
Describe alph 1 antitrypsin deficiency.
Autosomal recessive Deficient alpha 1 antitrypsin Liver cirrhosis Emphysema Transplant needed
Define portal hypertension
Portal venous pressure in excess of 20mmHg, resulting from intrahepatic or extra hepatic portal venous compression or occlusion
What are the causes of portal hypertension?
Obstruction of portal vein: congenital, thrombosis, extrinsic compression
Obstruction of flow within liver: cirrhosis, hepatoportal sclerosis, schistomiasis, sarcoidosis
List 5 porto-systemic anastomoses.
Oesophagea branch of left gastric vein (portal) and oesophageal tributaries of azygous system
Superior rectal branch of IMV (portal) and inferior rectal veins (systemic)
Portal tributaries of mesentery and retroperitoneal veins (systemic
Portal veins in liver and veins of anterior abdominal wall (systemic)
Portal branches in liver and diaphragm (bare area of liver)
What are the clinical manifestations of portal hypertension?
Splenomegaly Ascites Spider naevi Caput medusae Oesophageal/rectal varices - venous dilation, protrude into lumen, rupture/ulceration -> haemorrhage
Describe fulminant hepatic failure.
An acute and/or severe decompensation of hepatic function, defined as ‘… onset of hepatic encephalopathy within 2 months after diagnosis of liver disease’, which may be liked to brain oedema.
Decompensation due to increased metabolic demand
What are the causes of fulminant hepatic failure?
Hepatitis A, D, E Drugs Wilson's disease Pregnancy Reye's syndrome Alcohol
What are the features of fulminant hepatic failure?
Jaundice Encephalopathy decrease LOC Hypoglycaemia Decreased K+/Ca2+ Haemorrhage
What is the management of fulminant hepatic failure?
Specialist liver unit
Supportive therapy
Liver transplant
What is hepatic encephalopathy?
Reversible neurosychiatric deficit
Inability of liver to remove toxic substances (ammonia)
What might cause hepatic encephalopathy?
Sepsis/infection Constipation Diuretics GI bleeding Alcohol withdrawal
What are the clinical features of hepatic encephalopathy?
Flapping tremor
Decreased LOC
Personality changes
Intellectual deterioration - constructional apraxia, slow, slurred speech
Name some benign hepatic tumours.
Haemangioma Focal nodular hyperplasia Liver cell adenoma Liver cysts Polycystic liver disease Cystadenoma
What is a malignant primary hepatic tumour called?
Hepatocellular carcinoma (HCC)
Where are secondary/metastases in the liver generally from?
Colorectal (50%) Neuroendocrine Pancreas Breast Stomach Lung Ovary Kidney
20 cases of liver metastases per 1 HCC
Majority of mets are due to portal venous drainage
What pathological processes might cause diseases of the gallbladder and biliary tree?
Obstruction
Infection
Inflammation
Neoplasia
What % of the population has cholelithiasis (gallstones)?
10-20%
What are the risk factors for gallstones?
Female Increasing age Obesity (rapid weight loss) Multiparity Diet Developed countries Drugs (OCP) Ileal disease/resection Haemolytic disease
What types of stones might cause cholelithiasis?
Pigment stones - calcium bilirubinate, multiple, small, black
Pure cholesterol - usually solitary, up to 5cm (10%)
Mixed - cholesterol with calcium and bile pigment (80%)
What can cholelithiasis cause?
Biliary colic - impaction of stones, gallbladder conract, intermittent pain (post prandial)
Cholecystitis - Stones (maybe acalculus (ischaemia/infection). Oedema -> mucosa, ulceration -> fibropurulent exudate, pain, SIRS, pyrexia, sepsis
What are the potential complications of cholelithiasis?
Mucocoele Empyema Obstructive jaundice Ascending cholangitis Acute pancreatitis Biliary-enteric fistula/gallstone ileus Gallbladder carcinoma - 2% of all cancers, associated with gallstones Gallbladder perforation
How is mucocoele caused?
Impaction of stones, No superadded infection Mucus secretion Painful distension (Empyema also caused like this, with pus)
Describe ascending cholangitis.
Life threatening Charcot's triad: -RUQ pain -Jaundice -Fever
What is the function of the pancreas?
Endocrine - Insulin, glucagon, somatostatin
Exocrine - Fluid (HCO3-), Enzymes (proteolytic, amylase, lipolytic
What are the close anatomical relations of the pancreas?
Duodenum
Common bile duct
Portal vein
Coeliac trunk
What is pancreatitis?
Inflamatory process caused by effects of enzymes released from pancreatic acini
What are the different types of pancreatitis?
Acute - oedema, haemorrhage, necrosis
Chronic - fibrosis, calcification
What are the potential causes of acute pancreatitis?
GET SMASHED
Gallstones
Ethanol
Trauma
Steroids Mumps Autoimmune Scorpian bite Hyperlipidaemia ERCP/Iatrogenic Drugs
What is the pathogenesis of acute pancreatitis?
Duct obstruction - juice and bile reflux Acinar damage - from reflux or drugs Protease - tissue damage Lipase - fat necrosis Elastase - blood vessel destruction
What are the biochemical changes seen in acute pancreatitis?
Increased amylase, glycaemia and ALP/bilirubin
Decreased Ca2+
WHat are the clinical manifestations of acute pancreatitis?
Severe pain Vomiting Dehydration Shock/SIRS Ecchymosis Ileus
What is the prognostic classification of acute pancreatitis?
Clasgow/Ranson - Mild/severe
What is the treatment of acute pancreatitis?
Supportive
What is the mortality of acute pancreatitis?
Overall 10%
Severe = 30%
Haemorrhage = 50%
What happens to the pancreas in chronic pancreatitis?
Parenchymal destruction, fibrosis, loss of acini and duct stenosis
What causes chronic pancreatitis?
Chronic alcoholism
CF, inherited, biliary disease
What are the clinical manifestations of chronic pancreatitis?
Pain
Malabsorption - steatorrhea, decreased albumin, weight loss
DM
Jaundice
What % of pancreatic carcinomas are ductal?
90%
What are the risk factors for pancreatic carcinoma?
Smoking
Beta napthylamine
Benzidine
Familial pancreatitis
What are the clinical features of pancreatic carcinoma?
Initially symptomless Obstructive jaundice - palpable gallbladder Pain Vomiting Carcinomatosis Malabsorption Diabetes
What is the prognosis for pancreatic carcinoma?
5th of cancer death in UK (5%)
REsective surgery best current treatment but only 5-15% suitable, risks considerable morbidity and mortality, 15-35% 5 year survival rate
Overall, 1-year survival rate approx 12%
