Gastro Flashcards
Pancreatic secretions - exocrine
Trypsinogen
Chymotrypsinogen
Pancreatic amylase
Lipase
Pancreatic secretions - endocrine
Glucagon - from alpha cells
Insuln from beta cells
Somatostatin from delta cells
Pancreatic polypeptide by PP cells
Gastrin source
G cells in antrum
Gastrin stimulated by
Gastric distension and amino acid in antrum
Gastrin action
Secretion of pepsin, gastric acid and intrinsic factor
Cholecystokinin-pancreozymin (CCK-PK) source
duodenum and jejunum
Cholecystokinin-pancreozymin (CCK-PK) stimulated by
fats, and amino acids in SI
Cholecystokinin-pancreozymin (CCK-PK) action
Pancreatic secretion
gallbladder contraction
delayed gastric emptying
Secretin source
Duodenum and jejunum
Secretin stimulated by
ACID in the small bowel
Secretin action
pancreatic bicarbonate secretion
delays gastric emptying
Motilin source
Duodenum and jejunum
Motilin stimulated by
acid in the small bowerl
Motilin action
increased motility
Vasoactive intestinal peptide (VIP) source
SI
Vasoactive intestinal peptide (VIP) stimulated by
neural stimulation
Vasoactive intestinal peptide (VIP) action
inhibits gastric acid/peptin secretion - stimulates secretion by intestine and pancreas
Gastric Inhibitory peptide (GIP) source
duodenum and jejunum
Gastric Inhibitory peptide (GIP) stimulated by
glucose ,fats and amino acids
Gastric Inhibitory peptide (GIP) action
inbihits gastric secretion
stimulates insulin secretion
Somatostatin source
D cells in pancreas
Somatostatin stimulated by
Vagal and adrenergic stimulation
Somatostatin action
Inhibits gastric and pancreatic secretion
Pancreatic POlypeptide source
PP cells
Pancreatic Polypeptide PP stimulated by
Protein rich meal
Pancreatic Polypeptide action
inhibition of pancreatic and billiary secretion
factors increasing Fe absorption
increased erethropoesis (ie pregnancy)
GI blood loss
Vitamin C/Gastric acid
Factors decreasing Fe absorption
Gasrtrectomy
Achlorydria
SI disease
Drugs such as desferrioxamine
Folate deficiency caused by
body demand increase such as prengnacy and haemolysis
methotrexate
B12 defiecincy caused by
Dietary deficiency post-gastrectomy (lack of IF) Atrophic gastritis (pernicious anaemia) terminal ileal disease blind loops
Causes of mouth ulcers
IBD HIV Drugs Ca Nutritional deficiency Bechets celiac sweet syndrome
Achalasia
- -lack of peristalsis and lack of relaxation of lower oesophageal sphincter
- -1/100,000 per year
- -any age but rarely children
- -CXR may show air/fluid behind the heart
GORD/GERD predisposing factors
Hiatus hernia Obesity Smoking Etoh Caffiene Large meals late at night Drugs - theophyllines, nitrates, antibholinergics
Causes of oesophagitis
Candidal - immunosuppressed - on abx on steroids particularly inhaled
Chemical - nsaids
eosinophillic
HSV
two types of hiatus hernia
sliding - 80% may cause aspiration./acid reflux
rolling - 20% may obstruct or strangulate
Oesophogeal Ca risk factors
Smoking Etoh Plummer-Vinson syndrome Achalasia Barrets Chinese/Russian ethnicity Obesity Tylosis
Osophogeal Ca clinical features
Pain and dyspepsia
Progressive dysphagia for liquids then solids
Weight loss
Vomiting
Clinical symptoms of peptic ulcer disease
Epigastric pain (can radiate to back if posterior duodenal ) vomiting relapsing and remitting course weight loss fe deficiency acute haemorrage
causes of upper GI bleeds
Common Duodenal - 35% Gasrtic 20% Gastric erosions 18% Mallory Weiss tear - 10%
5% or less
Duo or osophagitis
upper GI ca
varices
Rare 1% or less Angiodysplasia Hereditary Talengiectasia POrtal hypertension Aorto-duodenal fistula
Risk assessment tool for upper Gi bleed
Glasgow-Blatchford
Clinical signs of Zollinger-Ellinson
pain and dyspepsia from multiple ulcers
steatorrhoea/diarrhoea
diagnosis - high serum fasting gastrin levels - CT/MR scanning
Treatment of zollinger ellinson
HIgh dose PPI (80-120mg od)
Surgery
Chemotherapy
Somatostatin analogues
Gastric Ca risk factors
Japanese Hypo/achlorhydria (ie pernicious anemmia partial gastrectomy) male high salt/nitrates gastric polyps
Gastric Ca clinical presentation
Dyspepsia weight loss Epigastric pain anorexia early satiety Fe deficiency anemia maelena
Scoring systems for acute pancreatitis
APCHE
Ransom
Glasgow criteria
most unreliable in first 48 hours
Causes of acute pancreatitis
Gallstones Etoh Viral (mumps) Trauma Drugs (azothioprine, coocp furusomide, steroids) Hypercalcemia Hypertriglyceridemia Post surgery/ERCP
Early complications of pancreatitis
ARDS
renal failure
DIC
pleaural effusions
Late complications of pancreatitis
splennic/portal vein thrombosis
pseudocyst
abscess
Pancreatitis clnical features
secere epigastric pain - radiating to the back - vomiting.
Amylase raised above circa 300
Plain Xray may show sentinal loop
Chronic pancreatitis features
Malaborption and steatorrhea
Abdo pain
T2DM
Coeliac Disease clinical features
Diarrhoea mouth ulcers Weight loss Malaise weakness - ataxia abdo pain amenorrhoea
Coeliac complications
Nutriotional deficiency increased Gi malargnany but this returns to normal with treatment dermatitis herpetiformis osteomalacia abnormal LFTs
Refeeding syndrome pathophysiology
Overenthusiastic feeding
surge in insulin
intracellulur shift in potassum phosphate and magnesium
Can cause cardiac problems, seizures, delerium, parasthesia
refeeding monitoring and treatment
U&E daily including Mg Ca and Po4
Thiamine
Transmural inflamation (Chrohns or UC)?
Chrohns
Mucosa and submcusoa only (Chrohns or UC)?
UC
Crypt abcesses (Chrohns or UC)?
UC
smoking? (Chrohns or UC)?
Smokers more prone to Chrohns but less likely in UC
Primary SCLEROSING cholangitis (Chrohns or UC)?
C
Primary BILIARY cirrhosis (Chrohns or UC)?
UC
Cobblestone mucosa (Chrohns or UC)?
C
Rose thorn ulcers (Chrohns or UC)?
C
Skip lesions (Chrohns or UC)?
C
Fistulae? (Chrohns or UC)?
C
Definition of acute severe colitis
True-love and witts criteria
> 6 bloody stools
plus any signs of systemic shock
Psuudomembrinous colitis otherwise known as
Cdiff
Campylobactor features
Gram negative rods
fecal oral
headache and malaise prior to diarrhoea
abdo pain may be severe
Cholera features
Vibrio Cholerae - gram negative rods
spread is fecal oral
rice water stools
Giardiasis features
flagellate protozoa
fecal oral spread
bloading and non bloody diarrhoea
Salmonella features
Gram negative bacillus divided into enteric (tyhic/paratyhic) and those causing gastro-enteritis
GI TB features
mimicks chrohns disease
occasionally spontaneous peritonitis
clinical features are non-specific
Diagnosis by biopsy
Causes of jaundice types
Pre-hepatic
Hepatic
Post Hepatic
Prehepatic causes of jaundice
Haemolysis
Gilberts syndrome etc
hepatic causes of jaundice
Etoh hepatitis Viral hepatitis Drugs - augmentin etc Wilsons disease Chirrosis Hepatic Metastases Hepatic congestion in cardiac failure
Post-Hepatic causes of jaundice
Gallstones carcinom of pancreas lymphadenopathy PBC PSC Biliary artresia
Synthetic measurs of liver function
Albumin and PT
Obstructive jaundice
ALP raised
hepatocellular jaundice
ALT raised
Chronic livery disease LFTs
May be “normal” but poor synthetic function
Investigations for Jaundice
LFT
Viral serology
autoantibodies
Liver USS - single most useful test
CT scan
MRCP
Congenital Hyperbilirubinaemia types
Gilbert
Crigler Najjar
Dubin-Johnson
Rotor
Congenital Hyperbilirubinaemia benign except
Crigler Najjar
Congenital Hyperbilirubinaemia fatal no treatment
Crigler Najjar type 1
Congenital Hyperbilirubinaemia survive to adulthood
Crigler Najjar type 2
Gilbert syndrome genetics
Autosomal dominant
Crigler Najarr genetics
Type 1 autosomal recesive
Type 2 autosomal dominant
Dumin Johnson/Rotor genetics
Autosomal recessive
Gilbert Syndrome clinical features
increased unconjigated bilirubin
asymptomatic jaundice
increases with fasting
Dubin-Johnson clinical features
jaundice, right upper quadrant pain and malaise
Rotor clinical features
increase in CONJUGATED bilirubin
Ascitis types
Transudates and exudative
Causes of transudative ascities
portal hypertension
nephrotic syndrome
malnutrition
myxoedema
Causes of exudative ascititis
Ca
Intra-abdominal TB
Pancreatitis
Hepato-renal syndrome
Acute kidney injury can complicate chronic liver disease
Type 1 rapidly progressive renal failure - high mortality rate
Type 2 mortality again high but onset and progression slower
Hep A features
Spread: fecal oral Virus: RNA Clinical: anorexia/jaundice/nausea/joint pain/fever Treatment: supportive Chronicity: none Vaccine: Yes
Hep B features
Spread: blood born Virus: DNA Clinical: acute fever, arteritis, glomerulonephritis, arthorpathy Treatment: supportive and ?antivirals Chronicity: 5% chronic carriage Vaccine: Yes
Hep C features
Spread: blood born/sti Virus: RNA Clinical: acute hepatitis Treatment: peg interferon alpha Chronicity: 60-80% Vaccine: No
Hep D features
Spread: blood born but depends on Hep B infection
Virus: incomplete
Clinical: exacerbates Hep B infection
Treatment: Interferon of limited benefit
Chronicity: increased incidence of chirosis
Vaccine: No
Hep E features
Spread: Blood born Virus: RNA Clinical: acute self limiting but 25% mortality in pregnancy Treatment: supportive Chronicity: none Vaccine: No
Hep B serology HBsAg
Acute infection -SiCK NOW
Hep B sereology HBeAg
High infectivety - spreading it EVRYWHERE
Hep B sereology Anti-HBs
immune from getting SICK
Hep B sereology Anti-HBe
Declining infectivity - stopped spreading it EVERYWHERE
Hep B serology anti-HBe IgM
recent infection <6 MONTHS
Hep B sereology anti Hbc IgG
Lifelong marker of post infection - not immunity
GOT it - might GET it again.
Drug induced hepatitis Cholestatis examples
cause bile duct inflammation
flucloxaccilin
anabolic steroids
oral contraceptives
Drug induced hepatitis
direct hepatocellular damage from statins anti-TB drugs, ketoconoazole.Fulminant liver failure possible.
Hepatic necrosis
where ability of liver to metabolise toxins fails - gluthathione levels fal and toxic metabolites accumulate = ie paracetamol OD
Four stages of chirossis
liver cell necrosiss
inflammation
fibrosis
nodular regeneration
chirosis definition
irreversible destruction and fibrosis of liver architecture with some nodular regeneration
Causes of chirrhosis
Etoh Haemochromatosis PBC Wilsons NASH Auto-immune hepatitis
Clinical features of Chirrhosis
Confusion/encephalopathy bruiding/bleeding oedema (hypo-abuminaemia) ascites jaundice palmar erethema/dupetrons contacture/caput medusa/splenomegaly) GI haemorrage.
Portal Hypertension - Budd Chiari
thrombosis or obstruction of hepatic vein
Portal hypertension - thrombotic causes
Portal thrombosis or Budd Chiari
Primary Billiary Chirrosis features
Cholestatic jaundice
xanthelasma
hepatosplenomegaly
high ALP/IgM
Diagnosis is AM2 antibodies
Pyogenic absesses
Hepatic absess following intra-abdominal sepsis or spontaneously - ecoli - proteus/ staph A
Patients have swingin pyrexia - weight loss - right upper quadrant pain and anorexia
Acute Abdomen causes
Appendicitis Perforated viscus IBD Diverticular diseases Obstruction Ischaemia Incaraterd hernia
torsion
PID
endometriosis
Pancreatitis
Cholycystitis/Cholangitis
Peritonitis
renal calculi
spenic infarcts
Ix for Acute Abdomen
Bloods - inc amylase and Ca, and VBG CXR AXR ECG CT abdo