Week 13 GI Flashcards
3 tests indicated for liver function
Bilirubin
Albumin
PT (extrinsic and common)
Chronic and acute liver injuiry investigations
Chronic liver disease:
US
Chronic viral hepatitis: HBV, HCV
Autoimmune:
Autoimmune hepatitis (AIH):
- ANA (anti nuclear antibody)
- SMA (anti smooth muscle antibody)
- LKA (anti liver kidney antibody)
AMA (anti mitochondrial antibody) - Primary biliary cirrhosis/cholangitis
Immunoglobulins - Increased IgG(AIH), Increased IgM (PBC)
Metabolic:
Ferritin (Haematochromotosis) - high
Caeruloplasmin (Wilsons) - low
Acute liver injury
US
Acute viral hepatitis: HAV, HBV, HCV, HEV, CMV
Autoimmune: ANA/SMA/LKM (AIH)
Immunoglobulins
Paracetamol levels
Fatty liver disease: Alcholic liver disease vs Non alcoholic liver disease
Presnts as asymptomatic abnormal LFTs or acute/chronic hepatitis - jaundic, fever, malaise, dark urine
Causes: alcohol, NAFLD: metabolic syndrome, drug e.g. methotrexate
Alcoholic
- Alcoholic steatosis (lipid vacuole filling heptocyte cytoplasm)
- Alcoholic hepatitis (neutrophils and lymphocytes filling hepatocytes with mallory bodies (damaged intermediate filaments)
- Alcoholic cirrhosis (periceullar fibrosis, bands of fibrous tracts between portal tracts)
Weight: variable
HbA1C: N
Alcohol intake: High
ALT: N/High
AST: High
AST/ALT ratio: High >1.5
GGT: very high
Triglycerides: variable
HDL: high
MCV: High
Non-alcoholic liver disease
- Steatosis
- Non alcoholic steatohepatitis
- Non alcoholic liver disease/Cirrhosis
Weight: high
HbA1C: high
Alcohol intake: normal
AST: N
ALT: N
GGT: N/high
AST:ALT: <0.8
Triglycerides: High
HDL: Low
MCV: N
Alcoholic hepatitis (characteristic clinical features, microscopy, assessment)
Form of alcoholic liver disease, inflammatory liver injury due to alcohol. Excess alcohol within 2 months
Jaundice
Increased bilirubin
AST:ALT ratio >1.5
Characterisitc features:
Hepatomeagly, fever, leucocytosis, hepatic bruit
Microscopy: Swelling of hepatocytes, mallory bodies (damgaged intermediate filaments in hepatocytes)
Assessment:
Glasgow alcohol hepatitis score
WBCC, Urea, Bilrubin, PT,
Chronic liver disease: clinical features
Clinical features: Spider naevi, foetor hepaticus (foul smelling breathe), encepalopathy, clubbing, palmar erythema
Prolonged PT time, decreaesed albumin
Assess severity: Childs Turcotte Pugh Score
- Encelopathy, ascites, bilirubin, albumin, PT
Portal hypetension (patho and clinical features)
Critical to manifestation of chronic liver disease:
- cirrhosis
- increased portal pressure (hypersplenism)
- porto-systemic shunting (oesophageal varices, encelopathy)
- vasodilation
- increased RAAS, catecholamines to compensate (leads to inreased Na+ and water rentention (ascites))
- renal vasoconstriction - leading to hepati-renal syndrome (renal failure)
Clinical features:
Caput madusae
Ascites
Splenomegaly (leads to thrombocytopenia)
Encelopathy
Hepatocellular carcinoma
Acute pancreatitis
Autodigestion of pancreas due to premature activation of pancreatic enzymes (commonly trypsin)
Causes:
Gallstones
Alcohol
Trauma
Infection - mumps
Clinical features: Epigastric pain radiates to back, nausea and vomiting, fever, increased WBCs
Diagnosis:
Requires 2 out of 3:
Pain
Increased serum amylase (3x ULN)
CT appearence
Severity
Mild - absence organ dysfunctin
Moderate - transient organ dysfunction
Severe - persistent organ dysfunction
Complications:
Pancreatic necrosis
Pancreatic abscess
Pancreatic psuedo cyst (no epithelial lining)
DIC
Investigations
US
MRCP (MRI cholangiopancreatography)
CT
Initial treatment:
ABCs, fluids, O2, Antibiotics? (Meropenem for pancreatitis with necrosis)
Management:
Early feeding
Treat cause
ERCP
Cholecystectomy (gallbladder removal)
Alcohol addictions service
Ascites (definition, investigations, treatment)
Build up of fluid in abdomen
Assessment:
Ascites tap (take fluid out) -
PMN (polymorphic nuclear) count
Increased WBC (>250 neutrophils) - indicates spontaneous bacterial peritonitis (infection of ascitic fluid)
- Increased lymphocytes indicates TB
Increased SAAG (serum albumin ascites gradient) - indicates portal hypertension
Management
Low salt diet
- Spironolactone (aldosterone antagonist)
SE: hyperkalaemia, hyponatraemia
- Frusemide (Na/CL-/K+ symporter anatagonists)
SE: hyponatraemia
- TIPSS (transjugular intrahepatic portosystemic shunt)
,Encepalopathy
Failure of cirrhotic liver to get rid of toxins which affects brain function
Due to GI bleeding, infection, electrolyte imbalance
Decreased hepatic/cerebral function, increased ammonia levels, inflammatory response
Assessed by Conns score (Grade 1-4)
Clinical sign: heptic flap
Treatment:
Lactulose
Most common cause of abnormal LFTs
Fatty liver (alcoholic, non-alcoholic)
Chronic hepatitis
Autoimmue - PBC, autoimmune hepatitis
Chronic pancreatitis
Repeated bouts of acute pancreatitis leading to fibrosis of parenchyma
Causes:
Alcohol, CF
Clinical features:
Epigastric pain radiating to back
Pancreatic insufficiency - malabsorption leading to stearrohea (fat in stool)
Secondary diabetes
Increased risk of pancreatic carcinoma
Differential acute pancreatisis
Ischaemic bowel disease
Peforated duodenum
Pancreatic cancer
Cholangitis
Pancreatic carcinoma
Adenocarcinoma arising from pancreatic ducts
Ductal adenocarcinoma - most common
Risk factors:
Smoking, chronic pancreatitis, BRCA gene
Clinical features:
Epigastric pain, weight loss, pancreatitis
Carcinoma in head of pancreas: painless obstructive jaundice, steatorrhea, palpable gallbladder (due to back up pressure of bile), new-onset diabetes, abdo pain (due to peri-neural invasion)
Premalignant stage: pancreatic intraepithelial neoplasia (PanIN)
Serum marker: CA 19-9
Treatment:
Whipple’s procedure: head of pancreas, duodenum, gallbladder, bile duct
Folforimox
Pancreatic tumours
Intraductal papillary mucious neoplasms
- Dysplastic linining secreting mucin
- Can become malignant
Mucinous cystic neoplasms
- mucinous lining, “ovarian stroma”
Serous cystadenoma
- benign
Gallstones
Gallstones can be made of cholesterol or bile. Due to increased cholesterol or decreased bile salts (solublises cholesterol in bile)
Risk factors:
Four Fs: Female, fat, fertile (oestrogen (due to increased HMG co-reductase, incresaased cholesterol synthesis)), forty’s
Also extravasuclar haemolysis (due to increased bilirubin so less soluble in bile), bilary tract infection e.g. E.coli
Complications:
Bilary colic:
Gallstone temporarily blocks cystic duct.
Acute cholecystitis:
Inflammation of gallbladder wall
Severe RUQ radiating to scapula, tenderness, fever
Increased WBCC, increased Alk phos
Can resolve by itself but also lead to empyema, gangrene, rupture
Chronic cholecystitis:
Chronic inflammation of gallbladder due to attacks of acute cholecystitis
- Vauge RUQ pain esp. after eating
Complication: porcelain gallbladder on XR (due to dystrophic Ca2+)
Treatment:
Cholecystectomy
Ascending cholangitis:
Bacterial infection of bile ducts, due to ascending infection of gram neg bacteria
Presents as sepsis, jaundice
Gallbladder carcinoma
Adenocarcinoma arising from epithelium that lines gallbladder wall
Risk factor: Gallstones
Presents in new onset cholecystitis in elderly women
Mucocoele
Colletion of mucus in gallbladder leading to distention
2 causes of asterixis (flapping tremor)
Liver failure
Drugs e.g. lithium, phenytoin
Type 2 resp failure (due to too much CO2)
Coeliac disease
Autoimmune disease due to gliadin found in gluten (rye, wheat, barley) leading to villus atrophy, intraepithelial lymphocytes, crypt hyperplasia. Assoc. with HLA DQ2/8
Differentials: lymphocytic colitis, IBS
Pathophys: Gliadin leads to inflammatory reaction - activation of T helper cells - lymphocytic repsonse - epithelial damage - villus flattening - loss of SA - malabsorption
Symptoms:
IDA (most common), Diarrhoea, Abdo pain, Dermatitis herpitformis
Complications:
- OP (due to decreased Ca+ absorption)
- Peripheral neuropathy (decreased B12)
- Enteropathy associated T cell lymphoma,
- Functional hyposplenism (due to folate deficiency. Shown by presence of Howell Jolly bodies)
Investigations
FBC, blood smear (microcytic and hypochromic RBCs)
-tissue transglutaminase (TTG)
Endomysial antibody (EMA) - more sensitive than TTG
Endoscopy
- atrophy and scalloping of mucosal folds, nodularity, mosiac pattern of mucosa
Duodenal biopsy (4 biopsies from distal duodenum as changes may be patchy (and must be on GFD))
Marsh Classification:
Stage 1: intraepithelail lymphocytes
Stage 2: crypt hyperplasia
Stage 3: villous atropy
Treatment:
Gluten free diet
TTG can be used to assess compliance (will be positive with ongoing exposure)
Chron’s (symptoms, complications, histology, investigations)
Chron’s : type of IBD characterised by transmural granulomatous inflammation of GI, affecting mouth to anus
Symptoms:
Episodic mild diarrhoea, pain, fever, may be precipitated by stress
Complications: Malabsorption, strictures, toxic megacolon, colonic carcinoma (less than UC)
Histology:
Transmural inflamamation
Skip lesions
fistulas
granulomas
Investigations
FBC, CRP, UEs, LFTs, stool cultures + C.diff. toxin, faecal calprotectin
Colonoscopy (1st line), sigmoidoscopy
Treatment: Surgery
UC (symptoms, complications)
Type of IBD characterised by diffuse inflammation, starting at rectum and up to colon, in a relapsing course
Symptoms:
Relapsing and remitting bloody diarrhoea, pain releived with bowel movement
Extra-intestinal symptoms: Erythema nodosum, uveitis, alk spondylitis, Primary sclerosing cholangitis
Histological hallmark: crypt abscess with neutrophils
Complications: Toxic megacolon, perforation, colonic carcinoma
Chron’s vs UC
Chron’s:
Transmural mucosa
Involves mouth to anus (usually terminal ileum)
Skip lesions
Granulomas
Lymphocyte infiltration
More common in women
Smoking can increase risk
UC:
Limited to rectum and colon
inflammation limited to mucosa
Continuous inflammation
More common in men
Smoking can reduce risk
Acute and Chronic histological changes in IBD
Acute changes during active disease:
Cryptitis
Loss of goblet cells
Crypt abcess
Ulceration
Chronic changes due to regeneration after ulceration
Crypt distortion
Loss of crypts
Submucosal fibrosis
Paneth cell metaplasia
Polyps of the colon
Hyerplastic polyps (most common, benign no malignant potential)
Harmatomtous (tumour comprimised of tissue normally present but disorganised) polyps
Inflammatory polyps
Majority of adenomas (benign glandular neoplasm) are polyps (has portential to be malignant via adenoma-carcinoma sequence
Adenoma-carcinoma sequence
Leads to adenocarcinoma
Risk factors:
Increased size of polyps (>2cm)
Increased no. polyps
IBD (UC higher risk)
Family history
Polyposis syndromes e.g. FAP (APC gene), Lynch syndrome (mismatch repair defects)
Duke’s staging
Bowel screening
50-70 for feocal occult blood (if +ve - colonoscopy)
Most common site of neuroendocrine tumour?
Appendix
Differential granulomas
TB
Sarcoidosis
Chron’s
Diverticular disease
Ischaemic damage
Superficial ulceration
Congestion of mucosal vessels - oedema - decreaed blood flow - necrosis
Diverticular disease
Pouch of mucosa that has herniated through a weak point in the musuclar propria
Due to increased luminal pressure assoc. with low fibre diets
Complications:
Perforation, Abscess
IBD treatments
IBD:
Corticosteroids - Budesonide, prednisolone
Side effects: OP, immunosuppresion, Cushingoid
Thiopurine - Purine anti-metabolite e.g. Aziothioprine
Side effects: N&V, leucopenia, pancreatitis
Biologics - Anti TNF: Inflixumab, Adalilumab, Golimumab
Anti adhesion: Vedolizimab
Side effects: Increased risk of infection e.g. TB, Hep B, lymphoma risk
UC:
Aminosalicylates: Anti-inflammatry e.g. Mesalazine
Side effects: renal impairment
Chron’s:
Methotrexate
Anti-folate
Side effects: GI upset, immunosuppresion, hepatotoxicity
Acute severe colitis
Pts who fail to repsonsd to optimal treatment 5-ASA/prednisolone
Investigations
Daily FBC, CRP, UEs
Stool cultures (inc C.diff)
Daily AXR
Treatment:
IV hydrocortisone
Prophylactic LMWH
Infliximab
Surgery
IBD - Which would NOT be an indication for starting azathioprine?
Acute severe colitis
What is highly sensitive in the detection of pneumoperitoneum?
Erect CXR
Classic presentation of head/neck cancer
Ulcer that will not heal
Colonic mucosa
Normal gastric body
SI
Duke’s stage criteria
A: Invasion into bowel wall, not through
B: Invasion through bowel wall but not lymph nodes
C: involves LNs
D: Widespread metastases
Candida albicans infection oesophagus
White plauqes in oesophagus
Histology:
Neutrophils infiltrated, congegrates at luminal aspect
PSA stain confirms the spores and hyphae of candida albicans
Barrett’s oeosphagus
Metaplasia from stratified squamous to non-ciliated columnar (glandular), normally intestinal, epithelium with goblet cells
Assoc. development of benign strictures
Can become dysplastic:
“Indefinite for dysplasia”, low grade, high grade
Low grade:
- Cells polarised
High grade:
- Nuclei lose polarity
- Mitotic figures
- Necrosis
Can lead to adenocarcinoma (p53)
Treatment: PPI
Endoscopy radiofrequncy abalation
LFTs and jaundice
Jaundice clinical features: Yellow sclera, skin, dark urine, pale stool, itching
Pre-hepatic: Haemolysis or increased bilirubin e.g. sickle cell, malaria
Hepatic: Hepatitis, Gilbert’s syndrome
- Dark urine
Post-hepatic: Obstruction in bile duct e..g gallstone
- Dark urine, pale stool
Lymphocytic colitis vs collagenous colitis
Lymphocytic colitis
Chronic watery diarrhoea, normal endoscopy
Assoc. with other autoimmune diseases e.g. myasthenia gravis, RA
Microscopy: colonic epithelial lymphocytosis
Increassed chronic inflammatory cells in lamina propria
Collagenous colitis (pic)
Chronic watery diarrhoea, with normal colonscopy
Mostly elderly women, smokers
May precede Crohn’s
Histology: patchy thickening of subepithelial basement membrane
