abdominal Flashcards
what is GORD?
gastro oesopahgeal reflux
inflammatory disease causing reflux of acidic gastric content through the lower oesophageal sphincter
mechanism of GORD
Combination of:
- transient relaxation of the lower oesophgeal sphincter
- increased lower abdo pressure
- reduced LOS tone
- delyaed gastric emptying
- impaired oesophgeal clearance
= all impair stomach emptying
risk factors of GORD
preg/obesity fatty foods smoking alcohol, chocolate, coffee stress anticholinergic drugs, calcium channel antagonists and nitrate drugs hiatus hernia
presentation of GORD
heart burn (dyspepsia) acid taste in back of mouth often related to eating and related to other symptoms - nausea, fullness in upper abdo or belching worse lying down chest pain
investigation of GORD
mostly clinical diagnosis
if more complicated needs gastroscopy
- oesphagitis = symotoms +mucosal breaks, endoscopy-negaive reflux disease = symptoms + normal endoscopy
barium swallow and oesophageal pH monitoring in extremes
red flags for urgent endoscopic investigation
red flags in GORD presentation
upper abdo mass dysphagia >55yo weight loss \+ upper abdo pain + reflux dyspepsia
treatment of GORD
lifestyle changes - try and denity and avoid precipitating dietary factors , lose weight, stop smoking, raise bed, stress reduction etc
medication - reduce acid with PPI an dH2-receptor antagonist
complications of GORD
BARRETS (basal cell hyperplasia and ulcers form if basal cell formation connot keep up)
= haemorrhage perforation, fibrosis, epithelial regeneration
what is H pyrlori
bacteria found in stomahc
produces urea = more stomach acid
treatment of H pylori
PPI + 2antibiotics (lansoprazole + clarithromycin + amoxicillin)
refer to endoscopy (if dysphagia, >55 and alarm symptoms)
alarm symptoms in peptic ulcer presentation
anaemia loss of weight anorexia recent onset/progressive symptoms meleana/haematemesis swallowing difficulties
risk factors for peptic ulcers
H.pylori smoking NSAIDs steorids reflux of duodenal contents delauyed gastric emptying stress
presentation of peptic ulcers
upper abdo discomfort - burning sensation, heaviness, ache
related to eating and accompanied by other symptoms - nasea, fullness in upper abod or belching
epigasgtric pain associated with hunger =
specific foods =
duodenal
stomach
diagnosis of peptic ulcers
upper GI endoscopy
test for Hpylori
measure gastrin concentrations when off PPIs if zollinger ellison syndrme suspected
biopsy to exclude maligancy
treatment of peptic ulcers
lifestyle - decrease alcohol and tobacco
Hpylori eradication
drugs to reduce acid - PPI, H2 blockers
stop drugs that may have caused - NSAIDS, antiplatelets
complications of peptic uclers
bleeding, perforation, malignancy, decreased gastric outflow
causes of acute upper GI bleed
50% = bleeding from peptic uclers
other cuases - oesophageal varcies, oesophagitis, gastric erosions
presentation of acute upper GI bleeds
haematemesis - severe = red with clots, less severe = coffee ground
meleana - high urea (digestion of blood)
known dyspepsia/ulcer, liver disease oesphgeal varice, dysphagia, weight loss
investigations of acute GI bleeds
signs of chronic liver disease PR to check for meelana peripherally cool and clammy - cap refil, low urine output low GCS or encephalopathy tachycardic
rockall risk assessment
treatment of upper GI bleed
pre endoscopy durg therapy
- stop Aspirin, NSAIDs and warfarin
PPIs to hgih risk patients
antibiotics to those with suspected variceal haemorrhgae
determine sight if bleeding
surgery fro thermal therpay if bleeding does not stop.
mallory weiss tear
A Mallory-Weiss tear is a tear of the tissue of your lower esophagus. It is most often caused by violent coughing or vomiting. A Mallory-Weiss tear can be diagnosed and treated during an endoscopic procedure. If the tear is not treated, it can lead to anemia, fatigue, shortness of breath, and even shock.
median age of onset of Crohns
30 yo
M=W
causes of crohns
3 essential co factors:
- genetic susceptibility
- environment (smoking increases risk in crohns, decreases in UC. stress precipitates relapses)
- host immune repsonse
risk factors of crohns
genes smoking stress depression appendectomy NSAIDs oral contraceptives Family history
presentation of crohns
depends on part of bowel involved:
- commonest = ileocaecal
- small bowel = pain and wt loss
- colonic disease = diarhhoea, bleeding and pain on defeacation
- perianal disease = anal tags, fissures fistulae and abscess foramtion
full thicknes of wall is inflamed
iritis, arthritis, erythema nodosum pyoderma gangrenosum
signs of crohsn
mouth uclers
signs of systemic illness (anorexia, fatigue, malaise, fever, clubbing)
anal or peri anal ski tag, fisutal or abscess
abdo pain and tenderness
tenderness or mass in RLQ
investigation of crohns
FBC (anaemia)
C-reactive protein and erythrocyte sedimentation rate
U+Es
LFTs
stool microscpy and culture
cobblestone appearance of bowel on colonscopy
transmural inflammation
treatment of crohns
smoking cessation colorectal cancer screening ensure risk of osteoprosis is managed managed pain - analgesics corticosteorids immunosuppressants - azathioprine and mercaptopurine and methotrexate or cytokine modulating drugs (infliximab and adalimumab)
nutrition
causes of UC
GENETIC SUSEPCTIBILITY
- genetic association is stronger for CD than UC,
ENVIRONMENT
- smoking halves the risk, depression and stress precicpate relapses, altered enteric microflora
HOST IMMUNE REPOSNE
risk factors for UC
family history
oral contraceptives
not smoking
how does UC present
diarrhoea, containing blood and mucus course - perisstent diarrhoea, relapses, remissions, severe fulinant colitits extraintestinal manifestations faecal urgency nocturnal defeacation tenesmus abdo pain (LLQ) pre def. pain, releived on passage
tenesmus
persisent, painful urge to pass stool even when recutm is empt
signs on examination of UC
weight loss, faltering growth in children , anorexia, extraintesitnal manfedtations (uveitis, iritis, inflammatroy arthritis, erythema nodosum pyoderma gangrenosum)
investigations of UC
FBC, inc ferritin CRP and ESR U+Es LFTs tissue transgulatminase stool microscopy and culture - cdiff, campylobacter, escherichia coli faecal calprotectin
treatment of UC
manage pain (paracetamol)
manage constipation or diarrhoea
manage fatigue (exclude depression or anaemia)
surgery - colectomy with ileoanal anastamosis)
terminal ilium sued to form reservoir
panprocxtoclectomy with ileostomy
whole colon and rectum removed and the ileum bought out onto the abdo wall as astoma
infective gastroenteritis
inflammation of the intestines
who gets infective gastroenteritis
20% of UK pop per year
young, old, travellers and immunocompromised
what causes infective gastroenteritis?
enteric infection with viruses, bacteria and protozoa
how does gastroenteritis present?
sudden onset diarrhoea +/- vomiting
blood or mucus in stool
fever or malaise
investgiations for gastroenteritis
diagnosis made clinically - symptoms and signs
culture of stool sample may be necessary to determine cause
treatment of infective gastroenteritis
adequate hydration
antimotility agents such as loperamide
empirical antibiotics given o thse with severe symptoms or blood diarrhoea, pending the results of stool sample
acute pancreatitis causes
1 GALLSTONES #2 ALCOHOL
l GET SMASHED
idiopathic gallstones ethanol trauma steroids mumps autoimmune scorpian bites hyperlipidaemia/hypothermia ERCP drugs
presentation of acute pancreatitis
severe abdo pain of sudden onset
may radiate into the back
nausea and vomtiing
treatment of acute pancreatitits
aggressive IV water and electrolyte replacement + opiate analgesia (not morphine)
if hypoxic, give O2
surgery to remove gallstones - ERCP
chronic pancreatitis
ongoing inflammation of pancreas accompanied by irreversible architectural changes
causes of chronic pancreatitis
mostly alcohol consumption
high fat and protein diets amplify damage by alcohol
4 pathological features of chronic pacnreatitis
continuous chronic inflammation
fibrous scarring
loss of pancreatic tissue
duct strictures with formation of calculi
presentation of chronic pancreatitis
prolonged ill health
chronic epigastric pain radiating through to back
steatorrhoea
diagnosis of chronic pancreatitis
normal serum amylase
fiagnosis by CT scan + endoscopic ultrasound or MRI
plain abdo radiography - speckled calcification
diabetes mellitus needs excluding
treatment of chronic pancreatitis
lifestyle changes - smoking anbd drinking
pain releif
screen for DM and osteoporosis
pancreatic enzyme supplementation
corticosteorids for autoimmune
treatment of hyper triglyc. or hypercal.
treatment of DM
SIGNS of acute pancreatitis
abdo tenderness
abdo distension
bluish discoloration around umbilicus (cullens sign) or flank (grey-turners sign) if haemorrhagic
tachycardia and hypotension - shock
investigation of acute pancreatitis
lipase or amylase levels
CT, MRI or ultrasound
risk factors for chronic pancreatitis
smoking autoimmune disease genetic abnormalities drugs obstructive causes tropical causes