common GI pathologies Flashcards
BIDI
Blockadge
Inflammation/infection
Damage/dysfunction
Ischaemia
Hep A
Hep B
Hep C
Hep D
hep A- faecal oral/ shell fish
hep B= blood products/IVDU/sexual/direct contact (*Far East, Mediterranean)
hep C: blood and sexual contact
D: needs B
E:
liver cirrhosis
- what is it
- causes
- signs and symptoms
- LFT’s
- investigations
- management
healthy liver
fatty liver
liver fibrosis
cirrhosis
chronic alcohol abuse
HBV
clubbing, hepatomegaly, spider naevi,l leukonychia
ascites, spon baterial peritonitis, oesophageal varices
LFT= raised ALT, low bilirubin ( portosystemic shunting as well as splenomegaly results in an increase in hemolysis and production of bilirubin), low alumin (liver not producing)
liver US, liver biopsy, ascitic tap, MRI
mx: fluid restriction,
? give albumin
drain, SBP give piperacillin, tazobactm (tazocin) liver transplant
Spontaneous Bacterial Peritonitis
infection of ascitic fluid
very dangerous
asitic tap for culture
treat: piperacillin, tazobactam
biliary colic
analgesia
rehydrate
NMB
elective cholectysectomy
acute cholcystitis
NMB analgesia IV abx co amoxiclav
acute cholcystitis
NMB analgesia IV abx co amoxiclav
peptic ulcer
breach of epithelium mucosa
H pylori infection- urea > amonia, co2 = acid
NSAIDs/aspirin
alcohol
H pylori erradication
clarithromycin
amoxicillin
for 7 days
breath test for c13 urea
peptic ulcer mx
PPI
test for H pylori
endoscopy if needed
acute bleeding peptic ulcer
endoscopy
adrenaline injection, cauterisation, clips
acute pancreatitis
epigastric pain which radiates to the back (referred pain - retroperitoneal)
AAA
pulsatile mass
hypotension
abdo pain radiates to back
bruising on flank
contrast enhanced CT scan
surgical emergnecy
AAA
pulsatile mass
hypotension
abdo pain radiates to back
bruising on flank
contrast enhanced CT scan *but not if burst
surgical emergency
splenic rupture
investigation
trauma (motorcycle)
intraperitoneal haemorrhage
fatal haemorrhage shock
haemodynamically unstable:
immediate laparotomy if haemo dynamically unstable with peritonism
haemodynamically stable:
urgent CT chest-abdo-pelvis with IV contrast
splenic infarction
- causes
- investigation
occlusion of splenic artery
haematological disease
thromboembolism
- lymphoma, sickle cell, CML
- embolic endocarditis, atrial fibrillation
CT abdo scan with IV contrast
renal stones
- symptoms
- investigation
- management
loin to groin pain
sudden onset
severe
flank to pelvis
n+v
haematuria
CT KUB non-contrast *
not with contrast because of nephrotoxic (AKI)
mx:
analgesia and fluid - NSAIDS
abx if infection
lithotripsy
location of ureteric stones
PUJ- renal pelvis becomes ureter
crossin the pelic bri- iliac vessel travel across ureter in the pelvis
VUJ- vesicoureteric junction . ureter enters the bladder
small bowel obstructions
causes- adhesions (prev surgery) hernia
colicky pain
reduced abdo sounds
DRIP and SUCK- IV fluids and NG tube
closed loop bowel obstruction* (emergency)
! strangulation
! ischaemic
volvulus
- sigmoid
- caecum
- midgut
twisting of loop of intestine around mesenteric attachement
closed-loop bowel obstruction
ischaemia due to compromised blood supply = bowel necrosis = perforation
sigmoid *older, pregnant, adhesions
symptoms: GI, vomiting, colicky, abdo distention, absoloute constipation
caecum *young peolpe congenital
*midgut- babies
clinical features of bowel obstruction
tympanic to percussion
sigmoid volvulus- conservative with decompression by sigmoidoscope and insertion of the flatus tube
ectopic pregnancy
b-HCG
surgical
methotrexate to stop pregnancy
urinary retention
inability to pass urine
pain and discomfort
palpable distended bladder
post void bedside bladder scan showing retained urine
BPH
immediate catheterise
check renal function for any high pressure urinary retention
ulcerative colitis (IBD)
inflammation limited to mucosa***
from rectum up to colon
25-35 y/o
bloody diarrhoea
mucus discharge
limited to large bowel
sigmoidoscopy
colonoscopy
chron’s (IBD)
transmural (all layers of the gut), skip lesions, mouth to anus.
no mucus
weight loss
red rash on shins
15-30 y/o
diarrhoea, abdo pain, weight loss
fbc (anaemia, malabsorption)
colonoscopy
fissure ano is common with chron’s , not UC
what is haemachromatosis?
an iron storage disorder
excess total body iron and deposition of iron in tissues
HFE gene on chromosome 6
autosomal recessive
haemachromatosis symptoms
Chronic tiredness
Joint pain
Pigmentation (bronze / slate-grey discolouration)
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms (memory and mood disturbance)
*usually after age of 40 when overload becomes symptomatic
*female- menstruation used to act as a regular elimination of iron frmo the body
diagnosis of haemochromatosis
- serum ferritin levels (acute phase reactant- increases in inflammation)
- genetic testing
- Liver biopsy with Perl’s stain to establish iron conc in the parenchymal cells
CT abdomen for increase attenuation of the liver
MRI deposits of iron in liver and heart.
haemochromatosis complications:
Type 1 Diabetes (iron affects the functioning of the pancreas)
Liver Cirrhosis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
Cardiomyopathy (iron deposits in the heart)
Hepatocellular Carcinoma
Hypothyroidism (iron deposits in the thyroid)
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
haemachromatosis management
venesection (a weekly protocol of removing blood to decrease total iron)
Monitoring serum ferritin
Avoid alcohol
Genetic counselling
Monitoring and treatment of complications
Wilson’s disease
excessive accumulation of copper in body and tissues caused by a mutation in ‘wilson disease protein’ chromosome 13.
responsible for removal of excess copper in the liver
autosomal recessive
Wilson disease features
Hepatic problems (40%)
Neurological problems (50%)
Psychiatric problems (10%)
chronic hepatitis- cirrhosis
CNS- neurological
*dysarthria
*dystonia
*if in basal ganglia= Parkinsonism (Tremor, bradykinesia, rigidity) assymetrical in Wilsons
CNS psychiatrical
*depression
*psychosis
Kayser-Fleischer rings in cornea
brownish circles surrounding the iris can be seen on naked eye
visualised on slit lamp exam
Haemolytic anaemia
Renal tubular damage leading to renal tubular acidosis
Osteopenia (loss of bone mineral density)
Wilson’s disease diagnosis
- serum caeruloplasmin
low =Wilsons (this is the protein which carries copper in the blood)
can be falsely normal or elevated in cancer or inflammatory conditions - liver biopsy. gold standard.
- 24 hour urine copper assay is sufficiently elevated
- scoring system which takes into account features and lab tests:
Low serum copper
Kayser-Fleischer rings
MRI brain shows nonspecific changes
Wilson’s disease management
copper chelation, using Penicillamine
Trientene
Peptic ulcer
ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum
- break down of protective layer of stomach/duodenum
- increase in stomach acid
protective layer of stomach = mucus and bicarbonate but this can be broken down by meds (NSAIDs, steroids) and H Pylori.
increased acid: stress, alcohol, caffine, smoking, spicy foods
gastric ulcers presentation
Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding causing haematemesis, “coffee ground” vomiting and melaena
Iron deficiency anaemia (due to constant bleeding)
gastric= worse with eating
duodenal= better with eating (pain comes on 2-3 hrs later)
management of peptic ulcer
endoscopy
rapid urease test CLO test for H Pylori
biopsy during endoscopy considered if exclude malignancy
PPI
peptic ulcer complications
Bleeding from the ulcer is a common and potentially life threatening complication.
Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).
Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.
Chron’s (NESTS)
No blood or mucus
Entire GI tract
Skip lesions- can be anywhere from mouth to anus
Terminal Ileum / Transmural Inflammation
Smoking is a risk factor
weight loss, strictures, fistulas
Ulcerative Colitis (CU= CLOSE UP)
Continuous Inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective +
Excrete blood and mcus
Use aminosalicylates
Primary sclerosing cholangitis
COLitis= COLONS and CONTINUOUS
presentation of IBD
Diarrhoea
Abdominal pain
Passing blood
Weight loss
Testing for IBD
Routine bloods for anaemia, infection, thyroid, kidney and liver function
CRP indicates inflammation and active disease
Faecal calprotectin (released by the intestines when inflamed) is a useful screening test (> 90% sensitive and specific to IBD in adults)
Endoscopy (OGD and colonoscopy) with biopsy is diagnostic
Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures.
Chron’s mx
Inducing remission:
1st line: steroids (oral prednisolone / IV hydrocortisone)
if does not work alone, consider adding:
azathioprine
mercaptopurine
methotrexate
infliximab
adalimumab
maintaining remission:
azathioprine, mercaptopurine
alternative:
methotrexate
infliximab
adalimumab
surgery if isease effects distal ileum
treat strictures and fistulas
UC management
mild-moderate:
1st: aminosalicylate (masalazine oral /rectal)
2nd: corticosteroids (prednisolone)
severe:
1st line: IV corticosterods (hydrocortisone)
2nd line: IV ciclosproin
maintain remission
aminosalicylate (mesalazine)
azathioprine
mercaptopurine
surgery:
typically UC only affects colon and rectum
can remove coln and recutm (panproctocolectomy)
leave a permanent ileostomy (ileo-anal anastomosis J pouch)
IBS (functional bowel disorder)
Diarrhoea
Constipation
Fluctuating bowel habit
Abdominal pain
Bloating
Worse after eating
Improved by opening bowels
Abdominal pain / discomfort:
Relieved on opening bowels, or
Associated with a change in bowel habit
AND 2 of:
Abnormal stool passage
Bloating
Worse symptoms after eating
PR mucus
IBS diagnosis (for exclusion of other pathologies)
Normal FBC, ESR and CRP blood tests
Faecal calprotectin negative to exclude inflammatory bowel disease
Negative coeliac disease serology (anti-TTG antibodies)
Cancer is not suspected or excluded if suspected
IBS management
General healthy diet and exercise advice:
Adequate fluid intake
Regular small meals
Reduced processed foods
Limit caffeine and alcohol
Low “FODMAP” diet (ideally with dietician guidance)
Trial of probiotic supplements for 4 weeks
IBS mx
1st line:
loperamide (diarrhoea)
laxatives (consiptation) *avoid lactulose as this can cause bloating
*linclotide is a specialist laxative if not responding to 1st line
antispasmodic (hyoscine butylbromide (buscopan)
2nd line:
TCA’s amitryptiline
3rd line:
SSRI
CBT
Coeliac disease
autoimmune condition, inflammation of the small bowel caused by auto antibodies in response to exposure to gluten targeting the epithelial cells of the intestine
early childhood but can start at any age
2 antibodies:
1. anti tissue transglutaminase (anti TTG)
2. anti endomysial (anti EMA)
*related to disease activity
affects any part of the small bowel in paticular jejunum
coeliac clinical features
atrophy of the intestinal villi (this usually absorbs nutrients from food which passes through the intestine)
- asymptomatic
- failure to thrive
- Diarrhoea
- Fatigue
- Weight loss
- Mouth ulcers
- Anaemia secondary to iron, B12 or folate deficiency
- Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
(rare) neurological symptoms
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
coeliac disease genetic and auto antibodies
HLA-DQ2 gene (90%)
HLA-DQ8 gene
Tissue transglutaminase antibodies (anti-TTG)
Endomysial antibodies (EMAs)
Deaminated gliadin peptides antibodies (anti-DGPs)
anti TTG and anti EMA are IgA. some pt have IgA deficiency so test total IgA as well*
Coeliac disease diagnosis
carry investigations out whilst pt on a diet containing gluten (to detect antibodies/inflamamtion)
- check total IgA
- check coeliac disease specific antibodies (anti TTG antibodies, anti endomysial antibodies)
- crypt hypertrophy, villous atrophy on endoscopy and intestinal biopsy.
coeliac associations and complications
association:
Type 1 Diabetes
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
complications
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)
coeliac treatment
Lifelong gluten-free diet is essentially curative. Relapse will occur on consuming gluten again. Checking coeliac antibodies can be helpful in monitoring the disease.
upper GI bleed causes
Oesophageal varices
Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum
upper GI bleed presentation
Haematemesis (vomiting blood)
“Coffee ground” vomit. This is caused by vomiting digested blood that looks like coffee grounds.
Melaena, which is tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability occurs in large blood loss, causing a low blood pressure, tachycardia and other signs of shock. Bear in mind that young, fit patients may compensate well until they have lost a lot of blood.
underlying pathology
Epigastric pain and dyspepsia in peptic ulcers
Jaundice for ascites in liver disease with oesophageal varices
Glasgow Blatchford Score
establishes risk of having an upper GI bleed or not
>0 indicated high risk
Drop in Hb
Rise in urea
Blood pressure
Heart rate
Melaena
Syncopy
Rockall score
used for patients that have had an endoscopy to calculate their risk of re- bleeding / overall mortality.
online calculator
Age
Features of shock (e.g. tachycardia or hypotension)
Co-morbidities
Cause of bleeding (e.g. Mallory-Weiss tear or malignancy)
Endoscopic stigmata of recent haemorrhage such as clots or visible bleeding vessels
management of upper GI bleed
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
Send bloods for:
Haemoglobin (FBC)
Urea (U&Es)
Coagulation (INR, FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood
Transfusion of GI bleed
Transfuse blood, platelets and clotting factors (fresh frozen plasma) to patients with massive haemorrhage
Transfusing more blood than necessary can be harmful
Platelets should be given in active bleeding and thrombocytopenia (platelets < 50)
Prothrombin complex concentrate can be given to patients taking warfarin that are actively bleeding
additional mx for oesophageal varcies
erlipressin
Prophylactic broad spectrum antibiotics
The definitive treatment is oesophagogastroduodenoscopy (OGD) to provide interventions that stop the bleeding, for example banding of varices or cauterisation of the bleeding vessel.
NICE recommend against using a proton pump inhibitor prior to endoscopy, however you may find senior doctors that do this.
C Diff infection
opportunistic, blood diarrhoea usually after amoxicillin
1st Metronidazole
2nd Vancomycin
AAA investigation
pulsatile mass with pain radiating to the back
Contrast enhanced CT gold standard for diagnosis
