general Flashcards
Upper GI bleeds is proximal the ligament of
ligament of Trietz
lower GI bleeds is distal to the
ligament of Trietz
upper GI bleeds clinical features
haematemesis, melaena, elevated urea, dyspepsia, reflux, epigastric pain, NSAIDS use
lower GI bleed features
fresh, magenta stools, normal urea, painless, common in elderly
most common cause of an upper GI bleed?
peptic ulcer
Zollinger Ellison syndrome is
gastrin secreting pancreatic tumour that causes recurrent poor healing duodenal ulcers
Mallory Weiss tear is typically at the
oesophago-gastric junction
diuelafoy refers to
submucosal arteriolar vessel eroding through mucosa
lower GI haemorrhage Angiodysplasia treatment
Aargon phototherapy, tranexamic acid, thalidomide
acute GI bleeding Meckel’s diverticulum diagnostic investigation
nuclear scintigraphy
treatment of GI bleed in terms of circulation
wide bore access for fluids and blood
blood samples
catheter
tranexamic acid
haemorrhagic stroke features
high respiratory rate rapid pulse anxiety clammy, cool skin low urine output low blood pressure
bleeding uncontrolled at endoscopy treatment
sengstaken-blakemore tube trnasjugular intrahepatic porto-systemic shunt
recommended units of alcohol
6
FAST positive score to perform an AUDIT
> 3
AUDIT SCORE OF >20
possible dependence
AUDIT SCORE OF 16-19
higher risk
AUDIT SCORE OF 8-15
increasing risk
AAT to ALT ratio
> 2
causes of hepatic encephalopathy
Infection Drugs Constipation GI Bleed Electrolyte Disturbance
Glasgow hepatitis score criteria
Age WCC urea INR bilirubin
alcoholic hepatitis nutritional support requires
thiamine
small intestine is how long?
6m
small bowel is renewed every
4-6 days
large bowel turnover is every
3-8 days
intrinsic neuromuscular control of the small and large bowel
myenteric plexus via Meissener’s plexus
Auerbach Plexus
Meissener’s plexus location
base of submucosa
Auerbach plexus location
inner circular, and outer longitudinal layers of the muscularis propria
Crohn’s disease genetic association
NOD 2 gene
Ulcerative Colitis gene association
HLA
pANCA positive in which patients of IBD
75% in UC
11% in CD
ulcerative have granulomas?
no
Crohn’s disease granulomas
yes non-caseating granulomas
dysplasia in hindgut commonly
adenoma tubular
low grade adenoma dysplasia of the lower gut
increased nuclear number and size, reduced mucin
high grade dysplasia adenoma of the lower gut
carcinoma in situ, crowded, irregular, not yet invasive.
genetics of colorectal carcinoma
FAP
HNPCC
Peutz-Jeghers
congenital ano-rectal abnormalities
imperforate anus
uro-genital fistulae
hirschprung’s myenteric plexus deficiency
acquired ano-rectal abnormalities
haemorrhoids, fissure, abscesses, fistula in ano, ulceration, cancer, control of continence
procedure for prolapse and haemorrhoids
stapled anopexy
most likely site for a colo-rectal cancer site
left colon
anal squamous cancer treatment
radiotherapy
rectal adenocarcinoma treatment
neo adjuvant chemorad
laparoscopic resection
Dukes A 5yr survival
> 90% submucosa
drugs for acid suppression
antacids, H2 receptor antagonists, proton pump inhibitors
drugs affecting GI motility
anti-emetics, anti-muscarinics, anti motility
drugs affecting IBD
aminosalicylates, corticosteriods, immuno- suppressants, biologics
drugs affecting intestinal secretions
bile acid sequestrates and ursodeoxycholic acid
antacids contain what metals?
magnesium or aluminium
alginates mechanism for working
gel that floats on stomach
H2 receptors antagonists block which receptor
histamine
H2 receptor antagonists indicated for
GORD/peptic ulcer disease
side effects of PPI’s
GI upset, C.difficile infection hypomagnesaemia, B12 deficiency
mechanism of prokinetic agents on GI motility
parasympathetic control of smooth muscle and sphincter tone via Ach
vomiting centre is located
medulla
anti-motility drug mechanism for GI
opiate receptors to decrease ACh release
anti spasmodics mechanisms
- anti-cholinergic muscarinic antagonists
- direst smooth muscle relaxants
- Calcium CB’s
types of laxatives
bulk
osmotic
stimulant
softeners
contraindications and side effects of aminosalicylates in IBD
caution in renal impairment
may cause GI upset, blood dyscasias, renal impairment
IBD corticosteriods concerns
osteoporosis, weight gain, infection, addisonian crisis
IBD immunosuppressants mechanism
prevents formation of purines for Dna synthesis
adverse effects of immunosuppressants in IBD
bone marrow suppression, hypersensitivity, organ damage, drug interactions
biologics name
anti TNF alpha antibodies infliximab
cautions and effects of infliximab
TB, MS, pregnancy and infections.
effects are infection, reactions, anaemia, demyelination, malignancy, thrombocytopenia
drugs affecting biliary secretions
cholestyramine, ursodexycholic acid
mechanism of cholestyramine for biliary secretions
reduces bile salts, enables excretion as insoluble complex
cholestyramine side affects
reduces absorption of other drugs, affects fat soluble vitamin absorption and decrease vitamin K levels
ursodeoxycholic acid uses in what conditions
gallstones, Primary biliary cirrhosis
ursodeoxycholic acid mechanism for action
inhibits enzymes for cholesterol formation, slowly dissolves non-calcified stones
factors affecting absorption in the GI- drugs
pH, gut length, transit time
distribution GI affects - drugs
low albumin
metabolism GI affects -drugs
liver enzymes, increased gut bacteria, liver blood flow, gut wall metabolism
excretion affects in GI - drugs
biliary excretion
severity of liver disease classification
child-pugh classification
criteria for child Pugh classification
bilirubin, albumin, PT, encephalopathy, ascites
dangerous drugs to consider with liver disease
warfarin, aspirin, opiates
second leading cause of cancer death in the western world is
colorectal cancer
95% of colorectal cancers are what pathology?
adenocarcinomas
strongest risk factor for colorectal cancer
sporadic with no familial/genetic influence
2 histological types of colorectal adenoma polyps
tubular(75%) /villous
oncogenes involved in colorectal adenoma
k-ras, c-myc
loss of tumour suppressor genes in colorectal adenoma
APC, p53, DCC
Chemotherapy for treatment in colorectal cancer for
adjuvant, DUKES C +B, cleans up micrometastases
agent for chemotherapy in colorectal cancer
5-FU
radiotherapy in colorectal cancer is used only for
rectal cancer
Dukes stage A colorectal cancer 5yr survival percentage
83%
DUKES stage D colorectal cancer 5yr survival percentage
3%
age 50-74 receive a FOBT every how many years?
2 years
heritable conditions for colorectal cancer
FAP - familial adenomatous polyposis
HNPCC- hereditary non-polyposis colorectal cancer
FAP is a … condition (penetration)
autosomal dominant
FAP receives what medication as a form of prevention
NSAIDS chemoprevention
out of 2000 people in regards to bowel cancer how many people have cancer?
1
high risk features in rectal bleeding
persistent changes in bowel habit, with anal symptoms (>6 weeks), right sided abdominal mass, palpable rectal mass, unexplained iron deficiency
5 ethics
autonomy, equity, justice, beneficence, malfeasance
functional GI disorder’s examples
oesophageal spasm, non-ulcer dyspepsia, biliary dyskinesia, irritable bowel syndrome, slow transit constipation, drug related effects
causes of non-ulcer dyspepsia
reflux, low grade duodenal ulceration, delayed gastric emptying, irritable bowel syndrome
functional causes of vomiting
migraine, drugs, pregnancy, cyclical vomiting syndrome, alcohol.
alarming symptoms for functional bowel diseases and stools
age >50 short symptom history unintentional weight loss nocturnal symptoms male sex cancer history anaemia rectal bleeding recent antibiotics mass
investigations for functional bowel diseases
FBC, blood glucose, U+E, thyroid, coeliac, FIT, sigmoidoscopy, colonoscopy
functional causes of constipation
megacolon, idiopathic constipation, depression, psychosis, and institutionalised patients
organic causes of constipation
stricture, tumours, diverticular disease, proctitis and anal fissures
systemic causes of constipation
diabetes, hypothyroidism, hypercalcaemia
neurogenic causes of constipation
autonomic neuropathies, Parkinson’s disease, strokes, MS, spina bifida
clinical features of IBS
pain, altered habit, bloating, belching, wind, flatulence, mucus
NICE diagnostic criteria
mucus, abdominal bloating, symptoms made worse by eating, altered stool passage
calprotectin is released by
inflamed gut mucosa, differentiates by IBS and IBD
FODMAP
fermentable oligo, di, and mono saccharides and polyols
fructose, lactose, fructans, galactans and polyols
IBS drugs for pain
antispasmodics, linaclotide, antidepressants
IBS drugs for bloating
probiotics, linaclotide
IBS drugs for constipation
laxatives (bulking, softeners, stimulants, osmotic), linaclotide
diarrhoea IBS treatment
antimotility agents
FODMAP
psychological interventions for functional bowel disease
relaxation, hypnotherapy, CBT, psychodynamic
relaxation training for functional bowel disease uses
diarrhoea and psychological co-morbidity
hypnotherapy for functional bowel disease uses
pain, constipation, flatulence, anxiety
CBT for functional bowel disease uses
abdominal pain, bloating, flatulence
psychodynamic interpersonal therapy for functional bowel disease uses
history of abuse
IBS - D impact on intestinal motility
stronger frequent contractions
IBS -C impact on intestinal motility
contractions reduced
peristaltic rhythm is generated by pacemaker cells in the longitudinal muscles is every .. minutes
~3 minutes
function of somatostatin
controls secretion of insulin and glucagon
what is the name of the membrane bound enzyme that convers trypsinogen to trypsin
enterokinase
enzyme that cleaves peptide bonds
proteases
nucleases enzyme function
hydrolyses DNA/RNA
enzyme responsible for collagen digestion
elastases
phospholipids into fatty acids enzymes
phospholipases
starch to maltose + glucose enzyme
alpha amylase