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
who gets gall stones?
v common
4Fs
forty, fat, fair females
what causes gallstones
imbalance in chemical composititon of bile - precipitation of stone
cholesterol stones = msot common pigmented stones (bilirubin and calcium)
mixed stones
risk factors for gallstones
obesity age female high triglycerides and low HDL DM OCP, HRT smoking crohns diseasee genetic and ethnic factors
presentation of gallstones
biliary colic is most common presentation - RUQ pain, N+V,
cholecystitis - RUQ pain, N+V, fever and tenderness
cholangitis - charcots triad= fever (rigors), jaundice and RUQ pain
investigations of gallstones
abdo ultrasound
LFTs (can be nromal)
treatment of gallstones
asymptomatic = leave alone unless in CBD
treat by surgery, pain releif and avoid food/drinks thattrigger symptoms
most common cause of liver injury
viral hepatitis
common and uncommon cuases of viral hepatitis
common: hep A, B, C, E
less common: EBV, HepD, arbovirus
acute viral hepatitis presentation
asymptomatic or symptomatic. with or without jaundice and itching
non specific flu like symptoms, gastroenteritis symtpoms.
fever, malaise, loss of apeitite, vomting, diarhrhoea, abdo pain, juandice, dark urine, light coloured stool
inidcates hepatocyte damage/ hepatitis
raised serum transaminases
diagnosis of acute hepatitis
liver function tests and serologic tests to identify the virus
treatment of acute hepatitis
hep A +B = no specific treamtent, just symptomatic
hep C = antiviral therpay
most common cause of acute abdomen
appendicitis
causes of appendicitis
infection secondayr to obsturction of lumen of appendix
- feaces, hyperplasia, bacterial overgrowth, necrosis
risk factors of appendicitis
M>F
10-20 yo
frequent antibiotic use
smokinbg
presetnation of appendicitis
abdo pain - preumbilical worsening 24hrs then migrates to right iliac fossa
pain worsened on movement
anorexia
nausea
constipation
vomiting
signs on examination of appendicitis
tenderness on percussion, guarding, rebound tenderness
investigations of appendicits
pregnancy test
urine dipstick - exclude UTI
FBC, CRP to rule out infection
treatment of appendicits
surgery to remove
causes of small bowel obstruction
adhesions (80%), hernias, crohns, intusseception, extrinsic involvement by cancer
causes of large bowel obstruciton
colonic carcinomas of colon, signmoid volvulus, diverticula disease
broad catagories of causes of bowel obstruction
mechanical - bowel above level of obstruction is dilated w increased secretion of fluid into lumen
functional - occurs with paralytic ileus - pseudoobstruction
presentation of bowel obstruction
mechanical: colicky abdo pain, assoicated with vomiting and absolute constipation
functional: pain not often present
signs of bowel obstruction
mechanical - tinkling sound and distension
functional - decreased bowel sounds
investigations of bowel obstruction
abdo XR - see gas throughout bowel
treatment of bowel obstruction
mechanical - small bowel obstruction may settle with conservative management (nasogastric suction and IV fluids to maintain hydration)
large bowel obstruction needs surgery
functional - conservative treamtnet
who gets femoral hernias
1 in 20 groin hernias are femoral (rest inguinal)
odler females
causes of femoral hernias
defect in surrounding msucle leading to fat or bowel poking into femoral canal
risk factors of femoral hernias
straining on the toilet if constipated
carrying and pushing heavy loads
obesity and persistent heavy coughs
presentation of femoral hernias
can appear suddenly due to strain and are normally a painful lump in inner upper part of thigh or groin
signs on examination of femoral hernia
lump can often be pushed back in or dissapears when lie down
treatment of femoral hernias
treatment is prompt due to risk of obstruction or strangulation
surgery
most ppl recover in 6 weeks, return to light activity in 2 weeks
who gets inguinal hernias?
M>W
occur as get older and muscle gets weaker
risk factors of inguinal hernias
straining on the toilet
carrying or psuhing heavy loads
persistent heavy cough
presentation of inguinal hernia
swelling or lump in groin
enlarged scrotum
may be painful
signs on examination of inguinal hernia
soft mass, may be reducible
treatment of inguinal hernia
treatment if painful, causes severe or persistent symptoms or if any serious complications develop
types of oesophgeal carcinoma and who gets it
adenocarcinoma = more in west, M»F
squamous caricnoma = less in west M»F
rhabdomysarcoma = very rare
Lipoma and GI stroma tumour = rare
causes of oesophageal adenocarcinoma
dietary nitrosamines (carcinogens)
GORD
barrets metaplasia
where does oesophgeal adenocarcinoma occur?
lower half of oesophagus
causes of oesophageal squamous carcinoma?
smoking alcohol low fresh fruit and veg diet chronic achalasia chronic caustic strictures
where do oesophageal squamous carcinomas occur?
anywhere in oesophagus
presentation of oesophageal carcinoma
dysphagia
haematemesis
incidental screening
symptoms of disseminated disease- lymphadenopathy, hepatomegaly (due to mets)
symptoms of local invasion - dysphonia, cough, haemoptysis, neck swelling, horners syndrome
investigations of oesophageal carcinoma
flexible oesophagoscopy and biopsy
barium swallow if fialed intubation or suspected post cricoid carcinoma
treatment of oesophageal carcinoma
squamous carcinoma - radical external radiotherapy + radical resection
adenocarcinoma (large) - neoadjuvant chemoradiotherapy + radical resection
adenocarcinoma (small) or high grade dysplasia in barrets - surgical resection
who gets gastric carcinomas?
over 50s
M»F
causes of gastric carcinoma
adenocarcinomas:
- nitrosamines (fresh fish, picked fruit)
- chronic atrophic gastritis
- blood group A
- chronic gastric ulceration related to H.Pylori
presentation of gastric carcinoma
dyspepsia weight loss, anorexia, lethargy anaemia occasionally upper GI bleeding dysphagia uncoomon unless proximal fundus and gastrooesophgeal junction involved
examination signs of gastric carcinom
weight loss
palpable epigastric mass
palpable supraclavicular lymph node (troisiers sign) = disseminated disease
investigations for gastric carcinoma
gastroscopy
barium swallow if gastroscopy contraindicated
staging by US and thoracoabdominal CT
treatment of gastric carcinoma
if early - surgical resection if patient well enough
advanced - surgery only in palliative, local ablation for symptom control, palliative chemo occasionally effective
who gets pancreatic carcinoma
60-70s
mostly ductal adenocarcinoma
risk factors for pancreatic caricinoma
cigarette smoking age high fat diet diabetes alcohol chronic pancreatitis
exposure to naphthalene and benzidine
hereditary factors + FH
presentation of pancreatic caricnoma
depends on location
- in head of pancreas:
obstructive jaundice + palpable gallbladder
pain - epigastric, LUQ, radiates to back
hepatomegaly due to mets
anorexia, N+V, fatigue malaise, dyspepsia, pruritis,
in body and tail: asymptomatic in early stages weight loss and back pain epigastric mass jaundice - spread to hilar lymph nodes or mets thrombophlebitis migrans diabetes mellitus
investigations of pancreatic carcinoma
FBC, LFTs, blood sugar elevated serum CA 19-9 transabdominal US doppler US of portal vein helical CT scan of pancreas FNA ERCP
treatment of pancreatic carcinoma
95% not suitable for surgery - even in resectable, 5yr survival is 12%
releive jaudice via ERCP
relief of duodenal obstruction (surgical gastric bypass)
relief of pain (morphine)
adjuvant chemo and resection can improve prognosis
who gets colorectal carcinoma
M»F
peak age - 45-64
more in younger
risk factors of colorectal cancer
polyposis syndromes (FAP, HNPCC, juvenile polyposis) strong FH previous history of polyps or CRCa chronic UC or chrons diet poor in fruit and veg
presentation of colorectal cancer
rectal location:
- PR bleeding
- change in bowel habit (diff defeacation, sense of incomplete, painful defecation (tenesmus))
descending sigmoid location:
- PR bleeding,
- change in bowel habit, increased fre, variable consistency, mucus PR bloating and flatulence
right sided location
- anaemia iron deficiency
emergency presentation:
- large bowel obstruction = colicky pain, bloating, bowels not open)
- perforation with peritonitis
- acute PR bleeding
investigations of colorectal cancer
PR examination or rigid sigmoidoscopy for rectal
flexible sigmoidoscopy
colonoscopy more reliable
tumour marker CEA not useful for diagnostic but used for monitoring
abdo CT
treatment of colorectal cancer
surgical resection only curative treatment
suitable if mets so long as you can also resect liver and lung
preop chemo
chemo in palliative
chronic liver failure is often the result of
cirrhosis
or alcohol related liver disease
types of alcohol related liver failure
alcoholic fatty liver disease (obese and alcoholic)
alcoholic hepatitis (alcoholics)
alcoholic cirrhosis (most advanced form)
symptoms of liver failure
nausea loss of apetite fatigue diarrhoea jaundice weight loss brusing or bleeding itching oedema ascites
causes of ascites
cirrhosis (commonest) liver cancer heart failure pancreatitis hypoalbuminaemia peritoneal tuberculosis
how does cirrhosis cause ascites
late stage liver disease
extensive liver fibrosis blocks blood flow from portal vein
blood backs up in portal vein = portal hypertension
fluid leaks out of portal vein into abdomen
signs of ascites
fullness in flanks
shifting dullness
tense ascites - uncomfortable and reduces respiratory distress
pleural effusion and peripheral oedema
investigations of ascites
diagnostic aspiration of 20ml ascetic fluid
albumin >11g/L suggests transudate, < = exudate
neutrophil count, gram stain and culture - ctyology for malignant cells and amylase to exclude pancreatic ascites
treatment of ascites
depends on cause
- diuretics , aim to lose 500g of body weight per day
- paracentesis if ascites is tense or resistant to standard medical therapy
causes of malnutrition
diseases complicated by malnutrition: anorexia nervosa, carcinoma of oesophagus or stomach, post op states, dementia,
protein energy malnutrition coexists wth infections frequently - infections may exacerbate this deficiency
presentation of malnutrition
children = kwashiorkor (swollen ankles, scaly skin, swollen abdo, depigmented hair) and marasmus (hair loss, wrinkled skin, severe wasting), cachexia
what is a perforated viscus
hollow organ with an abnormal opening
causes of perforated viscus
abdo trauma - stabbings, gunshots, RTA,
infections
complications of perforated viscus
spilling materials from GI organs into abdo
= toxic inside body cavity
bacteria can reach blood system and cause sepsis
= immediate medical attention needed
how does perforated viscus present
fever, low blood pressure, tachycardia, abdo pain, nausea, vomiting, abdo distention
signs on examination of perforated viscus
severe pain with abdo feeling rigid or board like when touched
treatment of perforated viscus
open surgery
who gets coeliac disease
bimodal peaks in infancy and adults (50s)
causes of coeliac disease
autoimmune inflammatory disease associated with LA DQ2 and DQ8
inflammatory cascade and release of mediators contribute to villous atrophy and crypt hyperplasia = typical histological features of coeliac disease
presentation of coeliac disease
tiredness and malaise
symptoms of small intestine disease
signs on examination of coeliac disease
few and non specific
anaemia and nutritional deficiency
dermatitis herpetiformis
investigations of coeliac disease
serum antibodies - IgA transglutaminase tTG antibodies
distal duodenal biopsies - for definitive diagnosis
blood count - mild anaemia
small bowel radiology or capsule endoscopy as well as bone densitometry
treatment of coeliac disease
gluten free diet and correct of any vitamin deficiences
