gastroenterology Flashcards
key questions in hx of dysphagia
duration solids/liquids pain weight loss - red flag (malignancy) previous med history - HIV? (oral candidida) systemic sclerosis? (affects motility) medications - anticholinergics/opioids cigarettes + alcohol where the problem is - oropharyngeal/oesophageal/gastric?
what would cause oropharyngeal dsphagia
salivary - sjorgrens
tongue - amyloid, hypothyroidism, MND
palatal/epiglottal/ upper oesophageal disorder - CVD, MND, Parkinsons
what would cause oesophageal dysphasia
benign mucosal disease - benign peptic stricture, oesophageal web (plummer vinson syndrome), candidial oesophagitis
malignant mucosal disease - carcinoma
motility disorders - oesophageal spasm, achalasia, oesophageal pouch
pharyngeal pouch what is it pres ix mx
defect between constrictor and transverse cricopharyngeal muscle
through killian’s dehiscence
pres foul taste struggle to swallow 5 x more common in men regurg aspiration neck swelling which gurgles on palpation
ix
barium swallow with fluroscopy
mx
surgery
mx of dysphagia
treat underlying cause
pro-kinetic - domperidone + metoclopramide - arrhythmias + long QT syndrome
nutrition? oral supplements, nasogastric feeding, PEG feeding
upper GI bleed differentials
oesophagitis peptic ulcer no diagnosis varices/portal hypertensive gastropathy erosive duodenitis or gastritis mallory-weiss tear malignancy vascular malformations
RF - upper GI bleed
NSAIDS apsirin anticoag h pylori alcohol corticosteroids
assessing GI bleeds scoring systems
rockall - determines mortality - use when have undergone endoscopy
glasgow blatchford scoring - tool that help discriminate whether they need inpatient or outpatient (discharge score) - stratifies patients on their risk and hence whether they need to stay in or not
endoscopic treatments for GI bleed
should be provided within 24 hours adrenaline injection ablative techniques - heat mechanical - clips banding techniques - for variceals
post endoscopy care in upper GI bleed
PPI or H2RA
H.pylori - ensure eradicated
varices secondary prevention - beta blockers
gastric ulcer - rescope in 6-8 weeks as may be malignant (if not healed biopsy it)
rebleed - rescope
evidence of iron deficient anaemia in ix
low hb
low ferritin
microcytosis
hypochromia
test to assess the colon - in order of preference
colonoscopy(1 in 1000 risk of tear)/flexible sigmoidoscopy (invasive) virtual colonoscopy (CT pneumocolon) CT with long oral prep (older/frail pts) colon capsule
what is definition of diarrhoea
the passage of 3+ loose or liquid in stools in 24 hrs
dysentry definition
+ mucus + blood in stools
classifying diarrhoea - four mechanisms
osmotic
- osmotic laxatives - lactulose
- lactulose/fructose intolerance
secretory
- defects of ion absorption, stimulant laxatives, gut hormone (VIPpmas/gastrinomas), enterotoxins (eg vibrio cholera)
malabsorption
- pancreatic insufficiency
- crohn’s disease
- celiac disease
abnormal motility
- post vagotomy
- IBS
- carcinoid
MOST IS MUTLIFACTORIAL
ix of IBD
bloods - FBC, CRP + U&E, LFTS stool culture and micro abdo xray ileo-colonoscoy small bowel ix - MRI small bowel/CT enterography/ capsule endoscopy
UC criteria
truelove + witts
staging severity
mild, mod, severe
mx IBD
steroids
truelove and witt (UC classification)
anticoag - Dalteparin
review for extra-intestinal manifestations
escalation review at day 3 - stool freq/CRP/albumin
-> surgery/infliximab/ciclosporin
coeliac dx
- immunoglobulins (look for IgA deficiency - can cause false negative antibody results) + TTG antibodies
- endomysial antibodies where about indeterminate
- OGD + duodenal biopsys (villous atrophy at histology)
when to transfuse in GI bleeds
shouldnt be transfusing unless haem drops below 70g/l unless have cardiovascular symps (aim for above 80g/l)
very poor looking ulcers that are squirting what do you prescribe in post endoscopy care?
IV PPI
ix chronic diarrhoea
RBC CRP TFT Coeliac serology stool sample
if have cancer or inflam red flags then add on endoscopy and CT
compare crohns/UC
crohns: terminal ileum skip lesions, mucus cobblestoning transmural - granulomas, focal crypt abscesses, increased goblet cells crampy abdo pain comps: fistulas, abscess, obstruction string sign + rose thorn ulcers on barium x-ray slight increased risk for colon cancer surgery for comps such as stricture
UC: rectum proximally continguous submucosa or mucosa - focal crypt abscess, goblet cells depletion ulcers, polyps bloody diarrhoea comps: haemorrhagic, toxic, megacolon lead pipe colon (narrow + short), loss of haustrations on barium xray marked increase in colon cancer curative surgery
symptoms of coeliac:
typical
atypical
silent
TYPICAL diarrhoea steatorrhoea weight loss dermatitis herpatiformis
ATYPICAL ataxia peripheral neuropathy ammenorhoea infertility chronic fatigue
SILENT IDA osteoporosis hyposplenism abnormal LFTs
upper GI bleed pres causes + classic features ix mx
pres haematemesis (bright red = above stomach/active haemorrhage, coffee ground = stomach or below) +/or malaena (bleeding in small bowel) epigastric discomfort sudden collapse haemodynamic instability -> initiate glasgow blatchford score
causes
OESOPHAGEAL
1. oesophagitis - small fresh blood streaking vomit. malaena rare. ceases spont. hx of GORD.
2. cancer - usually small volume of blood, unless erosion of major vessels. dysphagia, b symps
3. mallory weiss - brisk small to mod volume of bright red blood following bout of repeated vom. malaena rare. ceases spont. alc or hyperemesis gravidarum
4. varices - large fresh blood. swallowed blood may cause malaena. haemodynamic comp. may stop spont but re-bleeds are common.
5. oesophageal rupture (boerhaave syndrome) - triad of vomiting, chest pain and subcut emphysema
GASTRIC
- cancer - frank haematemesis, prodromal dyspepsia, b symps, variable amounts of bloof
- diffuse erosive gastritis - haematemesis and epigastric discomfort, usually underlying causes eg NSAIDs, haemodynamic comp
- gastric ulcer - small low volume bleeds, iron deficiency anaemia, erosion into vessel = signifcant bleed + haematemesis
DUODENUM
1. posteriorly sited duodenal ulcer = maj haemorrhage
pain of duo ulcer occurs several hours after eating
ix
glasgow blatchford score - assess need for intervention eg bloof prod/surgery/inpatient
rockall - morbidity and mortality in upper gi bleeds
raised urea
mx
ABCDE
massive haem protocol if systemic comp - only reg can do this
2 large bore cannulas
2 x units blood (o D-), xmatch, FBC, U+E + ur/cr, LFTs, coag, fluids (441 RBC, FFP, platelets)
TXA
CXR, ECG, ABG, catheter, reg monitoring
ODG - find cause + mx (patients with suspected varices should receive terlipressin + proph broad spec abx) within 24 hours - sclerotherpy/banding
balloon - sengstaken blakemore tube (minnesota tube)
oesophagitis/gastritis? PPI
All who have received intervention should receive a continuous infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
ALL gastric ulcers need endoscopic follow up - NO duodenal do
acute diarrhoea definition causes red flags ix mx comps prognosis
Diarrhoea: > 3 loose or watery stool per day
Acute diarrhoea < 14 days
causes
gastroenteritis - +abdo pain or n+v
diverticulitis - classically causes left LQ pain and diarrhoea/fever
antibiotics - some broad spec, cytotoxic, PPI, NSAID, metformin, thyroxine, SSRI, statin, c.diff is also seen with abx use
constipation causing overflow - hx of alternating diarrhoea + constipation, may lead to faecal incontinence in elderly
red flags Blood (CMV, shigella, salmonella, c.jej, e.histolytica), recent ABX (c.diff), vomiting, weight loss, watery + high volume (dehydration)
ix
assess for dehydration
stool sample for culture and sensitivity
mx supportive: fluid intake and nutrition only use drugs when clear cause when to admit: - vomiting and cant keep down - features of shock/dehydration - bloody diarrhoea
comps
reactive arthritis
lactose intolerance
IBS
prognosis
most improve 2-4 days
cause of diarrhoea in traveller
ETEC e.coli - enterotoxinogenic
watery stools
abdo cramps
nausea
cause of diarrhoea in abx use
c.diff - vancomycin
cause of diarrhoea in HIV
CMV
cause of diarrhoea in small children
rotavirus
cause of diarrhoea in well water
giardiasis
prolonged
non-bloody
cause of diarrhoea in puppies
camplyobacter
flu-like prodrome -> crampy abdo pains fever, diarrhoea that may be bloody,
may mimic appendicitis
comps = Guillain-Barre Syndrome
cause of diarrhoea in cruise ships
norovirus
cause of diarrhoea in dystentry/bloody + mucuous
shigella
cause of diarrhoea in profuse vomiting within 6 hours of food
s.aureus (food handlers), bacillus cereus (rice)
cause of diarrhoea in ab cramp and profuse watery
v.cholera - rice water stools
severe dehydration resulting in weight loss
profuse, watery
cause of diarrhoea in Fever + ab cramp + bloody + milk/meat
campylobacter jejuni
cause of diarrhoea in Fever + ab cramp + bloody + salad
shigella
cause of diarrhoea Fever + ab cramp + bloody + poultry/shellf
salmonella
antidiarrhoeal agents
loperamide
diphenoxylate
opioid agonists so also reduce gut motility
cause of gradual onset diarrhoea, abdo pain, tenderness which may last for several weeks
amoebiasis
UC what is it types pres + extra-intest ix mx comps
form of IBD
always starts at rectum and works it way back but never beyond ileoceacal valve
types
40% proctitis - rectosigmoid
30% left sided colitis (to splenic flexure)
20% pancolitis
SMOKING DECREASES RISK
pres 15-25 + 55-65 bloody diarrhoea urgency tenesmus abdo pain - LLQ extra intestinal: - primary sclerosing cholangitis - uveitis - episcleritis - colorectal cancer -arthritis - erythema nodosum - pyoderma gangrenosum - clubbing -osteoporosis - ankylosing spondilitis
ix 1. FBC - all decreased U+E, LFT ESR/CRP - high in active 2. faecal calprotectin - IBS vs IBD 3. stool culture and micro incl CMV + c.diff 4. p-ANCA 5. barium enema - loss of haustrations - superficial ulceration - pseudopolyps - long standing disease: colon is narrow and short - 'drainpipe colon' 6. FIRST LINE: flexible sigmoidoscopy with rectum biopsy (x2 from 5 sites including distal ileum and rectum): - red, raw mucosa that bleeds easily - up to submucosa - widespread ulceration - pseudopolyps - inflam cells in lamina propria - neutrophils migrate through walls of glands to form crypt abscesses - depletion of goblet cells + mucin - infrequent granulomas 7. AXR - toxic megacolon
mx
aim: inducing and maintaining remission
INDUCING
mild/mod -
- rectal? = topical aminosalicylate - no remission in 4 weeks + oral, then still no? + topical or oral corticosteroid
- rectum/sigmoid/ left colon? = topical aminosalicylate, if remission not achieved <4 weeks ->+ high-dose oral amino OR switch to high-dose oral amino + topical corticosteroid -> still no? then both oral
- extensive? = topical amino + high-dose oral amino -> no in 4 weeks? stop topical + both oral
severe colitis
-> admit, IV steroids (ciclosporin given if steroid CI), if no improvement after 72 hours consider + IV ciclo or surg.
MAINTAINING
mild/mod - topical or oral aminosalicylate
severe or >/= 2 exacerbations/year -> oral azathioprine or oral mercaptopurine
comps
x2 risk of colorectal cancer
toxic megacolon by opiates
osteoporosis if steroids
UC flares classification
technically this is truelove and witts criteria
mild
- fewer than 4 stools a day with or without blood
- no systemic
- normal ESR and CRP
moderate
- 4-6 stools/day
- minimal systemic
severe
- >6 stools/day containing blood
- evidence of systemic disturbance eg
fever, tachycardic, abdo tenderness, distension or reduced bowel sounds, anaemia, hypoalbuminaemia
if severe should be admitted
what is an aminosalicylate
mesalazine
5-aminosalicylic acid
crohns what is it cause pres + extraintestinal ix mx comps
type of IBD commonly affects terminal ileum + colon but anyway from mouth to anus occurs in all layers hence why common to have strictures, fistulas, adhesions chronic relapsing/remitting
cause
unknown but strong genetic
pres late adolescence or early adulthood non-specific eg weight loss/lethargy diarrhoea abdo pain perianal disease - skin tags/ulcers extra-intestinal: - primary sclerosing cholangitis - uveitis - episcleritis, conjunctivitis - fatty liver - colorectal cancer -arthritis - sacrolitis - erythema nodosum - pyoderma gangrenosum - clubbing -osteoporosis - ankylosing spondilitis
ix FBC (all low), U+E, LFT CRP/ESR -raised faecael calprotectin - raised vit b12/D low stool culutre + micro ileocolonoscopy + biopsy - deep ulcers, skip lesions - inflam in all layers -> serosa - goblet cells - granulomas small bowel enema - strictures (kantors string sign), proximal bowel dilation, rose thorn ulcers, fistulae
mx
stop smoking
NSAIDs/pill avoid
INDUCING REMISSION
glucocorticoids (oral pred/IV hydro) - oral/topical/IV or budesonide
enteral feeding
mesalazine (aminosalicytes 5-ASA) are used second line
azathioprine or mercaptopurine or methotrexate used as an add on
metronidazole used for isolated peri-anal disease
MAINTAINING stopping smoking azathioprine/mercaptopurine = FIRST LINE methotrexate = SECOND LINE 5-ASA if had prev surg surgery - 80% of patients eventually have surgery
complication
small bowel cancer
colorectal cancer
osteoporosis
what must you assess before prescribing azathioprine or mercaptopurine?
thiopurine methyltransferase (TPMT) activity
coeliac what is it associated disorders who should be screened? pres ix mx comps
what is it
autoimmune condition caused by sensitivity to protein gluten
repeated exposure -> villous atrophy -> malabsorption
conditions associated
- dermatitis herpetiformis (vesicular, pruritic skin eruption)
- autoimmune - T1DM, autoimmune hepatitis
- HLA-DQ2/8
who should be screened? Autoimmune thyroid disease Dermatitis herpetiformis Irritable bowel syndrome Type 1 diabetes First-degree relatives (parents, siblings or children) with coeliac disease
pres chronic/intermittent diarrhoea FTT in kids persistent or unexplained GI symps - n+v prolonged fatigue bloating abdo pain cramping iron-deficiency anaemia steatorrhoea
ix
diagnosis = immunology and jejunal biopsy
should have been exposed to gluten for at least 6 weeks prior to testing
immunology -> tissue transglutaminase antibodies (IgA), endomyseal antibody (IgA), anti-gliadin antibody (IgA or IgG) not recommended by NICE
biopsy (x4 from D2 onwards) - villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
complications - anaemia: iron, folate + b12 deficient hyposplenism osteoporosis osteomalacia lactose intolerance enteropathy-associated T-cell lymphoma of small intestine subfertile, unfavourable preg outcomes oesophageal cancer small bowel adenocarcinoma dental probs buttock wasting in children
mx GLUTEN FREE DIET fucking obviously things that include gluten: - wheat (bread, pasta, pastry) - barley - beer (whisky is fine) - rye - oats foods that are gluten free - rice, pots, corn IMMUNISATION - pnemoococcal + booster every 5 years
whats criteria called to grade severity of coeliac
marsh criteria
chronic diarrhoea
define
causes
Diarrhoea: > 3 loose or watery stool per day >14 days
causes IBS UC Crohns colorectal cancer coeliac thyrotoxicosis laxative abuse appendicitis radiation enteritis
normal gut flora
functions
> 400 species of bacteria
mainly anaerobes
functions:
- bacterial enzymes aiding reabsorption back across the intestinal wall (bilirubin, bile acids, cholesterol, drugs)
- digestion of fibre
- metabolism of certain vitamins - vit k
- synthesis of B12, folic acid, thiamine
- interfere and compete with exogenous pathogens preventing infection
intestinal obstruction
causes
intraluminal
- tumour
- diaphragm disease (fibrose)
- meconium ileum
- gallstone ileus
bowel wall - intramural
- inflammatory - crohns, diverticulitis
- tumours
- neural - hirschsprungs disease
outside the bowel pressing on it - extraluminal
- adhesions
- volvulus
- tumour - peritoneal deposits
what does ileus mean
non-mechanical obstruction
paralytic ileus = bowel inactivity
what is the most common intestinal obstruction
and what does it increase the risk of
small bowel obstruction or colorectal malignancy
increases risk of: volvulus impaction constipation megacolon if dementia alzheimers parkinsons
intestinal obstruction causes pres specific pres for: - sigmoid volvulus - paralytic ileus ix mx
CAUSES
adhesions, hernias, malignancy!!
small = adhesions (75% - from prior operations), strangulated hernia, malignancy or volvulus, crohns, paralytic ileus, intussusception
large = colorectal malignancy (>70),
increased risk further down bowel as faeces more solid, diverticulum, sigmoid volvulus, crohns
volvulus = Rotation of gut on mesenteric axis - sigmoid (= 5% all obs) or caecal
paralytic ileus = Bowel ceases to function and no peristalsis. *Intestinal pseudo-obstruction or Ogilvie’s
From massive dilatation of colon: associated with chest infection, MI, stroke, AKI
post-operative ileus - from handling of the bowel
congenital - neonatal obstruction eg CF
other - hirshprungs - aganglionic section of the bowel
PRES
Nausea, vomiting (early in high-level, faeculent in low level),
abdominal pain (diffuse, central, abdominal, colicky),
failure to pass bowel movements, constipation (early in low level, late in high-level)
Abdominal distension (larger the lower the blockage),
high pitched bowel sounds (tinkling) - more in small bowel,
tympany due to air filled stomach or hyperresonant bowel,
silent bowel = ileus
SPECIFIC PRES
sigmoid volvulus = like large bowel with pain, constipation, late vomiting, marked distension + previous episode
paralytic ileus = often in the elderly with autonomic imbalance resulting in sympathetic over-activity in colon
*Severe pain, tenderness, pyrexia in ischaemia and perforation (acute abdomen with peritonism)
FIRST - drip + suck
- NBM
- IV fluids
- NG tube on free drainage
ix
fluid balance
plain AXR - supine and erect:
- distended loops of proximal bowel (>3cm small, >6cm colon, >9cm caecum)
- loss of haustra
- fluid levels and distended small bowel throughout = paralytic ileus
- gas under diaphragm + riglers sign = perf (pneumoperitoneum)
- laddering small bowel in SBO
CT - confirm
mx
FBC, UE, Cr, G+S
uncomplicated-> fluid resus + correct electrolytes, intestinal decompression eg endoscopy, NG tube (drip+suck)
no clear diagnosis? laparotomy + consent for stoma
early surg if peritonitis or evidence of perf
baso rx cause
who are calciums two ugly sisters
magnesium + phosphate
explain how the body works to increase serum calcium if its low
- pituitary gland tells parathyroid glad to release PTH
- this works on bone to release calcium (99% of calcium is stored in bone) and phosphate
- PTH also works on kidneys as it stimulates 1a-hydroxylase to activate vit D (produces 1,25 dihydroxy vit D3 - active version of vit d) - this active vit d also stimulates bone to release calcium and phosphate. it also works as negative feedback on PTH to stop this process overdoing it. PTH also acts on distal convuluted tubule to absorb calcium
- 1,25 dihydroxy vit d3 also works on gut to absorb more calcium and phosphate + proximal convuluted tubules in kidney to absorb more calcium
- in the
how your body works to decrease serum calcium
high serum calcium stimulates the thyroid gland to produce calcitonin (this has opposite effect to PTH)
what percent of phosphate, mg, ca is located in the bone
phosphate - 85% (rest is intracellular)
magnesium - 60%
calcium - 99%
calcium phosphate makes up hard matrix of bone
magnesium helps strengthen it
phosphate homeostasis - if its low
stimulates 1a-hydroxylase in the kidneys to create 1,25 OHD (calcitriol) which acts on the gut to stimulate phosphate, vit d and calcium absorption
also the PTH on the calcium cards - works for this too
whats more dangerous hypo or hyper magnesium/phophate?
hypo
magnesium amount in body functions RDA and where to get it absorption/excretion in body
after potassium its the most abundant intracellular cation
only 1% of the bodys amount in extracellular space
functions
- co-factor in dna + protein synth, oxidative phosphorylation
- enzyme cofactor
- neuromuscular excitability - ca channel antagonist
- pth secretion and function
RDA - 300mg/d
found in cereals, green veg, beans, nuts
absorbed in small intestine
80% filtered in glomeruli (rest is probs bound to protein) - nearly all reabsorbed in loop of henle
hypomagnesium classification causes clinical effects ix mx
low - get symps if <0.5mmol/L
severe if <0.4mmol/L
causes of hypomag
- decreased intake (alcoholism, IV fluids or Total Parenteral Nutrition)
- increased losses (diarrhoea, malabsorption, fistula, renal tubular disorders, diuretics, aminoglycosides, cisplatin, PPIs, hypercalcaemia)
- redistribution (acute panc, ‘hungry bones’ syndrome)
clin effects
similar to hypocalcaemia
NEUROMUSCULAR
weakness, parasthesia, tetany
chvostek and trousseaus signs - independant of low ca (increased neuromuscular excitability)
seizures, confusion, coma
CARDIO
ECG - arrythmias/arrest (similar to hypokalaemia)
METABOLIC
hypokalaemia due to renal loss of K+ (as magnesium is required for retention and absorption of K in the kidney)
hypocalcaemia - due to low PTH and resistance
exacerbates digocin toxicity
ix
lab will usually add on magnesium test if they see low k or calc
mx
magnesium must be replaced before K+ and Ca supplements will work
severe or mod with symps - IV Mg then oral (40mmol/day)
mild/mod - oral - magnaspartate (10mmol/sachet)/day
- this can cause diarrhoea (oral mag salts)
identify and rx cause!!!
hypermagnesaemia
uncommon as requires very high intake and renal impairment
or IV mg (eg in pre-eclampsia + eclamptic fits)
no effects until >2mmol/L, usually higher
clinical effects
loss of deep tendon reflexes, flaccid paralysis, mental changes
cardio - brady + hypotensive
phosphate intake where from RDA where absorbed regulated by exretion plasma levels affected by:
abundant in foods esp diary and meat
RDA - 50 mmol
small intestine + large 60-70%
regulated by active vit d
90% filtered in glomeruls - reabsorbed by prox tubule: energy dependent
regulated by: PTH, active vit D, FGF23
plasma levels affected by
- insulin
- growth hormone
- glucocorticoids
FGF 23
what is it
its affect
increased by?
glycoprotein produced by bone cells - clasts + blasts
its affect
reduces renal absorption: lowers serum phosphate
inhibits activation of vit D - neg feedback
can be increased by
- genetic disorders
- tumour secretion
- drugs
hypophosphataemia
classify
commonly seen in
mechanism
<0.8mmol/l
severe if <0.3-0.35 - lab will phone in results
commonly seen in critical care burns alcoholism malnutrition sepsis
mechanism
1. inadequate intake - chronic over months
2. transcellular shift: acute - insulin (pushes phosphate into cells), resp alk
if both combines - severe acute hypophos
refeeding syndrome
what is it
metabolic disturbance as a result of reinstitution of nutrition to patients who are starved or malnourished
causes
malnourishment - cancer, cachexia, eating disorders, alcoholism, post surg
drugs - insulin, glucose, salicylates, b-adrenergics (salbs, theophylline), paracetamol OD, iron infusions, blood stimulants eg EPO
+ vit B12
renal loss - proximal tubule damage
FGF23 secretion - oncogenic
avoid it by: anticipating it checking and replacing k, mg, po4 before starting Total parental nutrition nutrition MDT local trust guidelines
clinical effects reduced ATP and oxygen binding capacity to haemoglobin MULTISYSTEM: - all blood cells - muscles - weakness, rhado, resp failure - CNS - confusion, seizures, coma CVS - cardiomyopathy - bones- pain, osteomalacia (chronic)
rx
IV PO4 for severe or mod with symps
caution giving too much too quick as comes with k+ so can cause hyperkalaemia
oral - phosphate sandoz (16mmol/tablet) - s/e diarrhoea (patients dont like)
skimmed milk (30mmol/L)
hyperphosphataemia
causes
clinical effects
causes INCREASED INTAKE phosphate enemas cows milk to infants RELEASE FROM CELLS - tumour lysis syndrome (ALL treatment) - rhabdomylsis REDUCED EXCRETION - chronic kidney disease is commonest cause OTHERS DKA alc excess acute liver failure refeeding syndrome primary hyperparathyroidism osteomalacia
clinical effects
- binds to calcium -> hypocalcaemia: tetany (calcium phosphate precipitates in soft tissues: myocardium, lungs, kidneys)
- chronic in CKD causes vascular calcification and managed with phosphate binders and low phosphate diet
consequences red blood cell haemolysis white blood cell and platelet dysfunction muscle weakness and rhabdomyolysis central nervous system dysfunction
how your body works to increase low magnesium
parathyroid creates PTH which acts on kidney to absorb more magnesium
hypocalcaemia classification causes pres ix mx
classification
<2mmol/l
causes
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
features
As extracellular calcium concentrations are important for muscle and nerve function many of the features seen in hypocalcaemia seen a result of neuromuscular excitability:
tetany - muscle twitching, cramping and spasm
perioral paraesthesia
?chronic - depression, cataracts
ECG - QT prolongation, mainly from a delayed ST segment.
seizures
Trousseau’s sign - twitching italian (carpal spasm if brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic, wrist flexion and fingers drawn together)
chvosteks sign - tapping over parotid causes facial muscles to twitch
ix Adjusted Ca Exclude CKD (U+E), acute panc (amylase), rhabdo (check CK) Serum Mg, PO4, PTH Evaluate vit D metabolism ECG
mx
acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause
if hypomag - correct first otherwise ca will never increase
dyspepsia what is it causes rf red flags criteria ix mx
what is it
Pain or discomfort in upper epigastric region may be heartburn or acid reflux
causes PUD - do H.pylori oesophagitis achalasia GORD oesophaeal/gastric cancer functional (70%) -> ROME criteria: 6M of post-prandial fullness, early satiety, epigastric pain/burning + no structural probs meds: - NSAIDS - decrease mucus and bicarb secretion FYIII - steroids - SSRIs - bisphosphonates - nitrates
rf
Smoking, alcohol, H.pylori, NSAIDs
red flags - ALARMS (wt loss, recurrent vom, dysphagia, chronic bleeding) A - anaemia L - loss of wt A - anorexia R - recent onset (if>55) M - melaena S - swallowing difficulty
ix FBC for alarm e.g. IDA Test for h.pylori Endoscopy (upper GI - ODG) if ALARMS or >55 (2 week wait) Barium swallow may be useful
mx
split into URGENT, NON-URGENT, OTHER
1. urgent - anyone who has dysphagia, upper abdo mass, >55 + weight loss + (1 x epigastric pain, reflux or dyspepsia) = urgent referral to endoscopy 2WW)
2. non-urgent- haematemesis, >55 with treatment resistant dyspepsia or epigastric pain with low haem or raised platelet count with (nausea, vom, weight loss, reflux, dyspepsia, epigastric pain), n+v with (wt loss, reflux, dyspepsia, epigastric pain) - for endoscopy
3. OTHER - step-wise
1. review meds
2. Lifestyle - stop offending drugs, decrease tobacco, avoid aggravating foods, lose weight
+ over the counter antacids
3. trial PPI 4/52 - if no response H2 receptor antagonist (ranitidine) or long term OR ‘test and treat’ approach Test for h.pylori, triple therapy 1 week
stomachs attackers + defenders
attackers
Acid, pepsin, h.pylori, bile salts, smoking (impairs mucosal repair
defenders
Mucin secretion, cellular mucus, bicarbonate secretion, mucosal blood flow
how does PPI work?
PPI decreases expression of H+/K+ antiporter on luminal membrane of parietal cells
how do you test for h pylori
carbon-13 urea test or stool antigen test or lab based serology
test of cure - no need to check for h pylori eradication if symps have resolved
however if repeat testing is required then a carbon-13 urea breath test should be used
gastric physiology areas of stomach cell types what stimulates acid what stops acid acid production
areas of stomach
Cardia, fundus, body, antrum, pylorus
cell types
Chief cells - pepsinogen (to pepsin by HCl)
G-cells - gastrin (antrum)
Parietal cells - intrinsic factor and HCl (fundus + body)
D-cells - somatostatin (antrum)
Goblet cells - mucus + bicarbonate
stimulate acid
Gastrin (CCK-2), histamine (H2), ACh (M3)
stop acid
somatostatin
acid production:
- co2 and cl diffuse to cell from blood
- co2 + H20 (carbonic anhydrase) -> H2CO3 ->h+ +HCO3-
- H+ combines with cl, ATP pump to pump to duct (as HCl more conc)
- cAMP increased by gastrin, histamine, ACh to pump more acid
H.pylori infection what is it associations symps pathophys tests complication management
Helicobacter pylori is a Gram negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease
curved bacillus
associations
PUD - 95% of duodenal and 75% gastric ulcers have h.pylori
increases risk of gastric carcinoma by 6 x
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis
symps
Fullness, bloating, early satiety, epigastric pain/burning
pathophys
H.pylori through mucus layer
Urease secretor - urea + water -> ammonia + CO2 -> neutralise acid (for survival) + mucosal cell death, chronic inflammation -> ulceration
tests
C13 urea breath test - can be done by GP
stool antigen test + CLO test (rapid urease test - pink with h.pylori)
- must stop PPI for 2 weeks before or abx for 4 weeks
complication anaemia IDA - uses iron for growth - decreases vit c - micro-erosions and chronic bleeding
management - triple therapy of eradication over 7 days, either:
- PPI + amoxicillin + clary
- PPI + metronidazole + clary
laxatives
types, how they work, examples, indications, s/e, CI
- bulk-forming
how? contain hydrophilic substance eg polysaccharide or cellulose which is not absorbed or broken down in the gut - like dietry fibre this attracts water into the stool - increasing its mass. therefore must have adequate water intake with these laxatives. this stimulates peristalsis, relieving constipation. also helps in chronic diarrhoea - therefore can also be used in diverticular disease, IBS, managing stoma output.
examples - ispaghula husk, methylcellulose, sterculia.
indications - constipation + faecal impaction, mild chronic diarrhoea
s/e - mild distension, flatuence
CI - intestinal obstruction, ileus - osmotic
how? osmotically active and remain in gut lumen. they hold water in the stool, maintaining its volume and stimulating peristalsis. lactulose also stimulates ammonia absorption, which inhibits the proliferation of ammonia producing bacteria - NOTE this is helpful in liver failure patients as ammonia is important in the pathogenesis of hepatic encephalopathy.
examples - lactulose, macrogol, phosphate enema
indications - constipations + faecal impaction, bowel prep, hepatic encaphalopathy.
s/e - flatulence, abdo cramps, nausea. phosphate enema can cause local irritation and electrolyte disturbances.
CI - intestinal obstruction, phosp enemas causes significant fluid shift so be careful in heart failure, ascites, electrolyte disturbance - stimulant
how? increase water and electrolyte secretion from colonic mucosa which increases volume of colonic content and stimulating peristalsis
examples - senna, glycerol suppositories, docusate sodium
indications - constipation, faecal impaction.
s/e - cramps, diarrhoea, prolonged use = melanosis coli (reversible pigmentation of intestinal wall)
CI - intestinal obstruction, rectal preps avoided in fissures, haemorrhoids.
antiemetics
types, how they work, examples, indications, s/e, CI
- dopamine D2 receptor antagonists
- how? D2 is the main receptor in the chemoreceptor trigger zone in medulla (vom centre). dopamine is also an important neurotransmitter in gut where it relaxes stomach and lower oesophagus sphincter and inhibits gastroduodenal coordination. thus those that block d2 receptors have a prokinetic effect- promoting gastric emptying, which contributes to antiemetic action.
- examples - metoclopramide, domperidone
- indications - n+v and reduced gut motility (hence for opioid n or diabetic gastroparesis)
- s/e - diarrhoea. metoclopramide = extrapyramidal (most commonly acute dystonic reaction eg oculogyric crisis.) domperidone doesnt do this as it doesnt cross the blood brain barrier. (vom centre is outside BBB).
- CI - children, young adults, GI obstruction, perf, parkinsons, antipsychotics. - histamine H1 receptor antagonists
- how? histamine and acetylcholine (muscarinic) receptors are in vom centre and in its communication with vestibular system. cyclizine block both these receptors. so good for nausea when with vertigo/motion.
- examples - cyclizine, cinnarizine, promethazine
- indications - n +v particularly in reduced gut motility
- s/e - drowsiness, cyclizine least sedating, anticholinergic s/e eg dry mouth, throat. post IV can cause transient tachycardia causing palps. can be unpleasant.
- CI - hepatic encephalopathy, prostatic hypertrophy (as they are susceptible to anticholinergic effects eg urinary retention) - phenothiazines
- how? blockade of various receptors incl D2 in CTZ and gut and to a lesser extent H1 and acetylcholine (muscarinic) receptors in the vom centre and vestibular system
- examples - prochlorperazine, chlorpromazine
- indications - chemo, radio, vertigo sickness, psychotic disorders (first gen for schizo)
- s/e - drowsiness + postural hypotension, extrapyramidal syndromes, QT prolongation
- CI - severe liver disease (hepatotoxic) and those susceptible to anticholinergic effects
serotonin 5HT receptor antagonists
- how? high density of 5HT receptors in the CTZ and key neurotransmitter in the gut in response to emetic stimuli. acting on 5HT receptors stimulates vagus nerve which in turn stimulates vom centre through solitary tract nucleus. serotonin is not a part of communicating between vestibular system and vom centre.
- examples - ondansetron, granisetron
- indications - n+v from CTZ stimulation eg drugs and visceral stimuli (gut infection, radiotherapy), hyperemesis gravidarum but NOT in motion sickness
- s/e - rare but constipation, headaches, diarrhoea
- CI - prolonged QT interval
muscarinic receptor antagonists - ayoscine
where is the vomiting centre how does it receive inputs
medulla
receives inputs from chemoreceptor trigger zone, the solitary tract nucleus (innervated by vagus nerve), the vestibular system and higher neurological centres.
physiology of vomiting
defence mechanism motion sickness chemo morning sickness certain drugs cause it.
vomiting centre in medulla has mainly muscarinic receptors and its use is to send signals to stimulate vomiting reflux.
vom centre is stimulated by CTZ (which contains dopamine D2 and 5HT receptors and also located in medulla but outside BBB) and so CTZ is the area to be stimulated by circulating emetic toxins eg chemo/drugs
vestibular nuclei in pons of brain stem that is stimulated by inner ear labyrinth through CNVIII has muscarinic and H1 receptors - which stimulates CTZ which in turn stimulates vom centre.
higher centres are stimulated to create a vom reflex from pain, repulsive smell or sight directly to the vom centre
the stomach/gut can activate vom centre + CTZ through vagus nerve - this can happen through some foods/infection/drugs aggravating lining
what antiemetic would you prescribe for opioid sickness
dopamine D2 antagonist - metoclopramide and domperidone or antipsychotic haloperidol
what antiemetic would you prescribe for diabetic gastroparesis sickness
dopamine D2 antagonist - metoclopramide and domperidone
what antiemetic would you prescribe for n+v
from gut infection, radiotherapy, chemo, post surg
serotonin 5HT antagonists - ondansetron, granisetron
what antiemetic would you prescribe for vertigo/motion sickness and morning sickness
cyclizine, cinnarizine, promethazine
vertigo - prochlorperazine, chlorpromazine
what would you prescribe for chemo, radio sickness
prochlorperazine, chlorpromazine
radio - ondansetron, granisetron
what would you prescribe for sickness due to gut infection
ondansetron, granisetron
how does the vomiting reflex work to cause you to vomit
relaxation of lower oesphagus sphincter
epiglottis closure
contraction of diaphragm and abdominal muscles
increase intrabdominal pressure
what would you prescribe for patients with sickness from reflux or hepatobiliary disorders
metoclopromide
cyclizine dosage
50mg up to TDS
take 1/2 hours before departure
higher neurological input to vomiting
physical - raised ICP / infection
smell - CN 1
psychological - fear, anticipation, pain
vestibular apparatus - VIII
taste - VII anterior 2/3 and IX posterior 1/3
gag - IX
what factors can affect the chemoreceptor trigger zone to stimulate vomiting (general groups)
drugs - opiates
hormones - pregnancy
toxins - alcohol
metabolic imbalance - hypercalcaemia, uraemia, DKA
gastric physiology phases
- cephalic - 20% - via vagus PSNS
- gastric 70% - vagal reflex, gastrin-histamine stimulation
- intestinal phase 10% - nervous mechanisms, hormonal mechanisms
hypercalcaemia def causes features ix - as you would in practise (full) management
definition >2.6 mmol/L < 3 asymp 3-3.5 prompt treatment >3.5 dysrhythmia + coma only unbound ca is physiologically important so adjust for albumin (+ 0.1 for every 4g/L albumin is below 40g/L and -0.1 for every 4g/L albumin is above 40g/L)
causes MAIN - 90% of cases 1. primary hyperparathyroidism- commonest in non-hospitalised patients 2. malignancy - commonest in hospitalised due to eg bone mets, myeloma, PTHrP from squamous cell lung cancer OTHERS granuloma forming diseases - sarcoidosis, TB, histoplasmosis vit d intoxication acromegaly thyrotoxicosis thiazides, antacids dehydration addisons disease pagets disease of the bone
features - bones, stones, groans, psychic moans, thrones, tones
bones - pain
stones - kidney or biliary
groans - abdo discomfort, nausea, Peptic UD, anorexia, polydipsia, pancreatitis
psychic moans - depression, anxiety, cog dysfunction, confusion, coma
thrones - constipation + frequent urination
muscle tone - weakness, decreased reflexes
corneal calcification
shortened QT interval on ECG
hypertension
cardiomyopathy
ix HISTORY thirst, renal colic bony symps mood weight loss/anorexia GI - pain, dyspep, consti, panc skin - granulomatous red flags for malig - bowel habit change MEN 1 - FHH thyrotoxicosis or hypoadrenalism diet diet/meds - lithium EXAM: neck, LN, GI cardio/resp status - sarcoid/TB/malig breasts - malig urinalysis - renal disease or haematuria thyroid status signs of addisons disease TO REQUEST: FBC, ESR, U/E, bone, TSH, Ft4, prolactin, vit d, PTH, alk phos, calcitonin calcium to creat clearance ratio albumin FEC + SEC, 24hr urinary calc, serum and urine plasma electrophoresis ECG, CXR, AXR, USS renal tract, DEX calcium sensing receptor gene seq skeletal survey serum ACE OGD
management
rehydration with normal saline - 3-4L/day
following rehydration IV bisphosphonates may be used
takes 2-3 days to work with max effect at 7 days
if fluid overloaded - seek help from senior and add loop diuretics
check vit D status
SECOND LINE - glucocorticoids
peptic ulcer disease types causes/rf pres - DU and PU sep differentials ix mgmt comps
types
80% duodenal ulcer - common at duodenal cap, may erode gastroduodenal art
20% gastric ulcer - common on lesser curve, may erode L gastric artery
causes/rf h.pylori NSAIDS, SSRI, corticosteroids, bisphosphonates alc, smoking - unclear stress bile acids pepsin
pres
Epigastric pain point to pain with one finger
DU - post prandially (1-3 hours), when hungry which is relieved by eating
GU - on eating
Pain radiation to back if posterior duodenal ulcer as related pancreas
nausea
oral flatuence
bloating
distention
ddx AAA GORD gastric cancer gallstones panc canc IBS drug-induced zollinger-ellison syndrome - if h.pylori if neg and ulceration is refactory - gastrin secreting tumours in duodenum
ix
FBC - IDA
h.pylori testimg
endoscopy - ONLY IF first pres >55 or ALARMS
biopsy if NSAID and Hpylori -ve as ?zollinger-ellison
mgmt stop cause or make sure taken after food smoking cessation h.pylori triple therapy PPI (omeprazole) or H2RA (ranitidine) for 8 weeks
comps haematemesis melaena acute abdo and peritonism with perf perf - pneumoperitoneum so get an erect CXR urgently
gastritis def types symptoms rf rx
def - broad term covering inflammation to the lining of the stomach
types
- pangastritis and antral gastritis
- may be erosive or non-erosive
symptoms
Symptoms of dyspepsia: Post-prandial fullness, early satiety, epigastric pain/burning, nausea/vomiting, belching
rf alcohol NSAIDS h.pylori reflux
rx
as for dyspepsia but basically consider need for endoscopy - urgent or non urgent and in mean time change lifestyle, PPI or ranitidine and hpylori eradication
GORD def epi rf if prolonged = pres atypical pres ix ddx urgent referral mx
def reflux of acid contents
epi
2 x men
rf
obesity, preg - hgih intra-abdominal pressure
large meals - raised gastric pressure
lifestyle factors - smoking, alc, fat (delays gastric emptying), coffee
systemic sclerosis - decreased oesophageal peristalsis
hiatus hernia - loss of LOS
drugs - TCA, anticholinergics, nitrates, CCB relax tone of LOS/ cardiac sphincter
if prolonged = oesophagitis ulceration stricture formation barrett's oesophagus
pres
Heartburn: burning feeling rising stomach to neck relieved by antacid. Related to meals, posture (lying down), straining
Water brash: excessive salivation
Acid brash: retrosternal discomfort - regurgitation of acid or bile
Odynophagia - painful swallowing related oesophagitis or stricture
Belching
atypical pres
non-cardiac chest pain
resp - chronic hoarseness, chronic cough, noctural asthma, chronic aspiration causing pneumonia
ix endoscopy - gold standard - if not been investigated with this then treat as dyspepsia FBC - ?anaemia barium swallow for hiatus hernia oesophageal pH monitoring \+/- CXR
DDx oesophagitis from drugs - NSAIDs, doxy, bisphos infection - CMV, candida peptic ulcer oesophageal spasm
urgent referral for ?cancer ALARMS (obvs!!) A - anaemia L - loss of wt A = anorexia R = recent onset if >55 M = melaena A = swallowing difficulty \+ vomiting, barrett's oesophagitis, lump
mx
lifestyle:
- reduce weight
- stop smoking
- reduce alcohol
- raise bed at night
- reg small meals
- avoid drugs like nitrates, anticholinergics, TCA or damage mucosa like NSAID, bsphos
aluminium or magnesium salts - antacids
alginates - protective floating raft - gaviscon
NICE 1ST LINE FOR ENDO PROVEN GORD = PP1 4or8/52 or H2RA
step-down PPI for long-term suppression if works but if doesnt then double dose for further 4/52
IF ENDO NEG = full dose PPI for 4/52, if response then offer low dose treatment PRN with limited repeat prescriptions, if no response then H2RA or prokinetic for one month
surgery - laprascopic fundoplication
hernia types def comps anatomy of inguinal canal why are they important
types inguinal femoral incisional epigastric umbilical hiatus
def protrusion of a viscus through a defect in the wall through its containing cavity
comps
irreducible, obstruction (bowel contents cant pass through), incarcerated (contents of hernial sack stuck), strangulated (ischaemia + obstruction)
anatomy of inguinal canal
borders - MALT
M - roof - 2 x muscles - internal oblique, transverse abdominis
A - anterior - 2 x aponeurosis - of external oblique + inferior oblique
L - floor - 2 x ligaments - inguinal + lacunar
T - posterior - Transversalis fascia (lateral) + cojoint Tendon (medially)
contents - men spermatic cord, women round ligament
why imp
7% of all surgical visits
inguinal hernia rf epi types pres where is DIR + SIR ix mx comps
rf obesity constipation chronic cough heavy lifting male
epi
75% of abdo wall hernias
95% male
types
- direct 20% - peritoneal sac through weakness in posterior wall of inguinal canal medially to inferior epigastric vessels - easily reduced
- indirect - 80% peritoneal sac through deep inguinal ring +/- superficial associated with patent inguinal canal - more likely to strangulate and more common (due to processus vaginalis to regress)
pres
lump - disappears on pressure or lying down
+/- pain (?incarceration/strangulation)
indirect = pain in scrotum + dragging
cough impulse - finger through top of scrotum into external ring and palpate for lump when coughing
where is:
DIR - halfway across inguinal ligament
SIR - split in external oblique aponeurosis superior and lateral to pubic tubercle
ix
USS
if perf - erect CXR, FBC (leukocytosis), ABG (raised lactate)
MX
advise stop smoking, weight loss, diet
treat even if asymp - surgical reduction or excision of hernial sac + closure of defect with minimal tension eg mesh - open do not do manual work for 2-3 weeks, lapro 1-2 weeks
comps recurrence within 5 years - 1% wound infection intestinal injury chronic pain
femoral hernia anatomy of fem canal + contents epi pres differentials comps mx
anatomy Anterior - inguinal ligament Posterior - pectineal ligament Medial - lacunar ligament Lateral - femoral vein contains cloquets node
epi
w>m
pres
lump in groin - inferior and lateral to pubic tubercle
if strangulated = red, tender, tense, irreducible +/- colic, vomit, distention (obstruction = surg emergency)
ddx
hydrocele
comps
20% strangulate @ 3m
mx
all repaired
hiatus hernia def rf causes types pres ix rx
def herniation of abdo viscera through oesophageal aperture of diaphragm - mainly gastric cardia
rf obesity preg ascites age
causes
widening diaphragm hiatus
shortening oesophagus eg chronic GORD
pushing up of stomach by intra abdo pressure
types sliding (90%) - gastro-oesophageal junction slides into thoracic cavity rolling (10%) - gastro-oesophago junction stays in place but stomach herniates
pres
reflux more common in sliding
ix
CXR
barium study
endoscopy
mx
lifestyle
PPI long term
surgery - gastropexy if refractory
oesophagus blood supply, muscles and epithelium in upper, mid and lower third
upper
blood - inferior thyroid
muscle - voluntary striated
epithelium - stratified squamous
mid
blood - aortic oesophageal
muscle - mixed
epi - squamocolumnar junction
lower
blood - left gastric
muscle - smooth muscle
epi - columnar
oesophagitis eosinophilic causes grading rx
eosinophilic - when unresponsive to PPI due to infiltration of eosinophils, topical steroids
causes
similar to GORD but more so drugs taken with inapprop water NSAIDS, doxy, bisphos
grading
endoscopy - Los Angeles:
A - one or more mucosal breaks < 5mm none extending between tops of mucosal folds
B - same but > 5mm
C - mucosal breaks extending between tops of two or more mucosal folds involving < 75% of mucosal circumference
D - mucosal breaks involve > 75% of mucosal circumference
mx
2/12 PPI
barrett's oesophagus def types causes protective/rf hx ix mgmt comps
def Any portion of normal distal squamous epithelium is replaced by metaplastic columnar epithelium clearly visible (>1cm) above gastro-oesophageal junction on endoscopy and confirmed on biopsy Proximal displacement of squamo-columnar junction via mucosal inflammation and erosion
types
short - <3cm
long - >3cm
causes
chronic GORD +/- HH
protective - NSAID, h.pylori
rf GORD male smoking obesity
hx
50 y.o white man with chronic reflux +/- dysphagia
ix
endoscope + biopsy (transoesophageal)
mgmt
low grade - lifestyle + long term PPI +/- ablation
endoscopic surveillance every 3-5 yrs
high grade - oesophagectomy
comps
5% progress to adenocarcinoma of oesophagus in 10-20 years
oesophageal cancer types rf classic patient pres ix staging spread to mgmt
types
80% SCC upper 2/3
rest adenocarcinoma lower 1/3 - both are common and aggressive
apaz now adeno more common in developed world
squam most in third world
RF smoking alc SCC - chronic inflam and stasis - achalasia AC - barrett's, obesity, GORD shit
classic pt
old man from middle east
pres
RED FLAGS:
- Dysphagia (solids>liquids)
- Vomiting
- Anorexia and weight loss
- Symptoms of GI related blood loss e.g. melaena
- Symptoms of infiltration - intractable hiccups and persistent retrosternal pain
- Upper ⅓ specific - hoarseness and cough - less common
- Lymphadenopathy
ix
- FBC, UE, LFT, glucose, CRP
- FIRST LINE - endoscopy with brushing and biopsy of lesion
- ?CXR - mets
- CT/MRI - chest + abdo + pelvis for staging -> if shows no mets then local stage found by endoscopic USS
- double contrast barium swallow for dysphagia if benign motility diagnosis
- bronchoscopy if hoarseness
staging Tis T1 - invasion of lamina propria/submucosa T2 - invasion of muscularis propria T3 - invasion of adventitia T4 - invasion of adjacent structures
spreads to liver lung stomach LNs
mgmt surg +/- chemo/radio abx and antithrombotic prophyl endoscopic mucosal resection - early - standard procedure Ivor-lewis oesophagectomy total oesophagectomy - mckeown 5 yr survival 20%
differentials of dysphagia
normally pharyngeal or oesophagus disease
oesophageal = GORD, oesophagitis, oesophageal cancer (food sticking), pharyngeal cancer
neurological - CVA, achalasia, diffuse oesophageal spasm , MS, MND
others - pharyngeal pouch, external compression (mediastinal tumour), CREST or scleroderma
achalasia def mech pres ix mgmt
def
Disorder of motility of lower oesophageal sphincter
Smooth muscle layer has impaired peristalsis and sphincter fails to relax
mech
Often an aganglionic segment in auerbachs plexus (sim Hirschsprung’s) this is acquired and so presents in adults
Possible effect of interstitial cells of Cajal (pacemaker cells)
pres Dysphagia of BOTH solids + liquids Regurgitation (90%) Chest pain in 50% - retrosternal and after eating ?Inhalation pneumonias
DDx: GORD/ stricture
ix
CXR - inhalation, vastly dilated oesophagus behind heart
Barium swallow - characteristic bird’s beak dilated oesophagus with distal narrowing, fluid level
oesophageal Manometry - gold standard high resting pressure and incomplete relaxation on swallowing
mgmt
CCB/nitrates - reduce pressure in LOS may lead to GORD
Surgery - endoscopic dilatation first-line - may lead to perforation
heller cardiomyotomy
botox injection intra-sphincteric if high surg risk
systemic sclerosis
what is it
types
Systemic sclerosis is a condition of unknown aetiology characterised by hardened, sclerotic skin and other connective tissues. It is four times more common in females.
types
1. limited cutaneous systemic sclerosis - raynaud’s, face and distal limbs predom,, anti-centromere antibodies. subtype is CREST!!
- diffuse cutaneous systemic sclerosis - trunk + proximal limbs, scl-70 antibodies, resp involement in 80% - ILD, pulm arterial HTN, comps = renal disease + HTN, poor prog
- scleroderma - without internal organ involvement
- tightening + fibrosis of skin
- plaques or linear
scleroderma what is it pathophys of GI features features autoantibodies mx
type of systemic sclerosis that has tightening and involvement of skin
pathophys
GI very common as it causes dysmotility due to collagen deposition and loss of smooth muscle dysfunction
features
reflux oesophagitis
delayed gastric emptying
watermelon stomach - can cause GI bleeding + anaemia
autoantibodies
Anti-topoisomerase 1
Anti-centromere antibody (ACA)
Anti-RNA polymerase III
mx lifestyle as for GORD high dose PPI pro-motility agents - metoclop or domperidone dilation of oesophageal strictures
CREST
Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
subtype of limited cutaneous systemic sclerosis
rockall risk score
Pre-endoscopy - for mortality (/7)
Age: 60-80 = 1, 80+ = 2
Shock: tachycardia PR > 100 = 1, hypotension = 2
Co-morbidity: heart (IHD, HF) = 2, renal/liver/malignancy = 3
Post endoscopy - for rebleed (/11) *<3 is low risk
Dx: MW/no bleeding (0), all other (1), malig (2)
Blood visible: no blood or dark spot (0), clot, or bleed (2)
mallory-weiss tear def causes pres rf ix + mx comp
def
linear muscosal tear at oesophago-gastric junction
boerhaave - oesophageal tear
caused
persistent vom/wretching - sudden increase in intra abdo pressure
pres haematemesis melana light headed dizzy etc
rf excessive alc bulimia raised ICP gastroenteritis
ix + mx
endoscopy
as upper GI bleed
usually ceases spont
comps
pneumomediastinum
surgical emphysema
oesophageal varices def location rf pres ix
def
dilated veins at junction between portal and systemic venous circ
10% of UGI bleeds
location
distal oesophagus
proximal stomach
main rf
chronic liver disease
portal HTN
pres haematemesis melaena abdo pain features of liver disease
ix endoscopy FBC clotting U+E LFT
mx
can cease spont but as upper GI bleed
volvulus types rf pres ix mgmt comps
types
sigmoid - counterclockwise twisting - becomes overloaded with faeces causing it to sink downwards + twist
caecal - clockwise
rf Psychiatric disorders Neurological disorders Nursing home residents Chronic constipation Pelvic masses (including pregnancy) Adhesions previous
pres intestinal obstruction sudden onset colicky lower abdo pain gross distention + palpable mass no flatus/stool empty rectum
ix
Abdominal xray – coffee bean sign (dilated, twisted sigmoid colon that looks like a giant coffee bean)
CT scan to confirm diagnosis and identify other pathology (bowel wall ischaemia)
mx
endoscopic (sigmoidoscope) decompression - for no peritonitis only + flatus tube alongside for 24 horus
laparotomy - hartmanns - sigmoid
right hemicolectomy - caecal
comps
obstruction
ischaemia
perf - peritonitis
hirschsprungs def pres ix mx
Absence of parasympathetic ganglion cells in myenteric and submucosal plexus of rectum
pres
Mainly diagnosed in childhood abdominal distension and failure to pass meconium within 48 hrs
ix
AXR - dilated lower bowel
anal manometry
rectal biopsy - gold standard
mx
rectal washout/bowel irrigation
surg
classic triad of gastro-oesophageal obstruction
wretching
pain
failed attempt to pass NG tube
peritonitis/intra-abdo sepsis def/types abdo defence pres ix mgmt
def/types
def = Inflammation of the peritoneum (the lining of the abdomen)
types =
1. Localised peritonitis is caused by underlying organ inflammation (e.g. appendicitis or cholecystitis)
2. Generalised peritonitis is caused by perforation of an abdominal organ (e.g. perforated duodenal ulcer or ruptured appendix)
3. Spontaneous bacterial peritonitis is associated with spontaneous infection of ascites in cirrhotic liver disease, is treated with antibiotics and carries a poor prognosis
abdo defence
omentum attempts to confine infection by wrapping around
pres
Abscess: fever + pain (psoas = flank to groin)
Signs: swinging pyrexia + palpable mass
Peritonitis: pain + anorexia + nausea + vomiting
Signs: high fever, tachycardia, tenderness on palpation, guarding, rebound tenderness
ix FBC U+E LFT CRP blood culture culture peritoneal fluid Amylase/lipase INR abg - o2 + calcium for scoring pancreatitis + lactate g + s AXR erect CXR - pneumoperitoneum for perf USS abdo CT
mx ABCDE NBM IV access IV fluids + abx (abscess metronidazole + 3rd gen ceph, other - met + cefotaxime) analgesia + antiemetic NG tube if vom + ?obstruction catheterise for fluid balance escalate may need lapro or open surg
differentials based on location of abdo pain
Right Upper Quadrant
- Biliary Colic
- Acute Cholecystitis
- Acute Cholangitis
Right Iliac Fossa
- Acute Appendicitis
- Ectopic Pregnancy
- Ovarian Cyst
- Meckel’s Diverticulitis
Epigastric
- Pancreatitis
- Peptic Ulcer Disease
- Abdominal Aortic Aneurysm
Central / Generalised
Abdominal Aortic Aneurysm
Intestinal Obstruction
Ischaemic Colitis
Left Iliac Fossa
Diverticulitis
Ectopic Pregnancy
Ovarian Cyst
Suprapubic
Acute Urinary Retention
Pelvic Inflammatory Disease
Loin to Groin
Renal Colic (kidney stones)
Abdominal Aortic Aneurysm
Pyelonephritis
anal fissure what is it pres cause mgmt
what is it
tear in mucosa of anal canal
pres
pain on defacation
‘shards of glass’
bright red blood on paper or stool
cause
constipation
IBD
HIV, sphilis, herpes
mgmt acute (<6 w) dietry fibre lots of fluids warm bath laxative (adult = bulk forming eg ispaghula husk, child = osmotic eg lactulose) analgesia topical anaesthetic lubricant
chronic >6w
as above plus
topical ointment -GTN relaxes smooth muscle BD 8/52
surgery - lateral internal sphincterotomy
fistulas what is it types causes ix mx
Track communicates between (two epithelial surfaces) skin and anorectal canal due to discharging abscess from blockage of intramuscular glands
types enterocutaneous - intestine to skin enterocolic - large or small bowel (anal would be this one) enterovaginal enterovesicular
causes
abscess
crohns
rectal carcinoma
ix
MRI
mx
if no IBD or obstruction should heal by themselves
surgical - fistulotomy and excision
anorectal abscess what is it cause bacteria rf pres ix mx
what is it
collection of pus in anorectal region
cause infection of fissure STI blocked anal gland perianal abscess 60% from direct extension of sepsis in intersphincteric plane
bacteria
gut - e.coli
rf diabetes immunocomp IBD anal sex
pres
discharging rectum
fever
perianal pain - throbs and worse on sitting
perianal abscess - tender inflamed localised swelling
ix
DRE +/- MRI for fistula
mgmt
drain then pack - heal in 3-4 w
analgesia
abx if immunocomp
pilonidal sinus
what is it
mgmt
what is it
Small hole or tunnel at skin caused by obstruction of hair follicles at natal cleft which may lead to abscess formation and sinus
mgmt
Excision of sinus tract and primary closure
Advise: hygiene and hair removal
perianal haematoma what is it appearance pres histology innervation mgmt
aka external haemorrhoids
dilated vascular plexuses, below the dentate line
appearance
2-4mm dark blueberry under skin
pres
painful
doesnt really bleed
hist
stratified squam epithelium
innervation
below dentate = somatic nerve
very sensitive to pain = inferior rectal nerve
mgmt
excise
what is the dentate line
aka pectinate line
splits the upper 2/3 and lower 1/3 of anal canal
sits just above sphincter bit really
haemorrhoids what are they grading pain rf pres ix mgmt comp
aka internal haemorrhoids
abnormally enlarged vascular mucosal cushions in anal canal
grading
Grade 1: no prolapse
Grade 2: prolapse on strain, reduce spontaneously
Grade 3: prolapse on strain, reduce manually
Grade 4: permanent prolapse
pain
painless above dentate line therefore visceral innervation
rf
Constipation, prolonged straining, increased abdo P (ascites, pregnancy, chronic cough)
pres
pres Bright red painless rectal bleeding on defecation (on paper or dripping, not mixed in stool) Anal itch from chronic mucus discharge feeling of lump around anus constipation
ix
DRE
inspect and ask patient to bear down
proctoscopy
mgmt
consider ddx eg fissure, cancer, IBD
refer on 2ww if suspect anal cancer
prevent constipation - fibre, fluid, bulk form, topical anaesthetic eg instillagel, anusol cream, topical steroids
rubber band ligation (grade 2)
haemorrhoidectomy if large - very painful
comp
strangulation
thrombose - extremely painful purple, PR exam impossible due to pain
appendicitis def red flag epi pres location ddx ix mgmt
def
The appendix is a small, thin tube of bowel sprouting from the caecum
Appendicitis is inflammation of the appendix
Results from obstruction of the appendix and subsequent infection and inflammation by gut flora
red flag
rupture -> lifethreatening peritonitis, perf 20%
epi
Peak incidence in ages 10-20
pres
early periumbilical pain T10 moves to RIF as peritoneum is involved (Mcburneys point 1/3 of distance from umbilicus to ASIS
pain aggravated by movement so shallow breathing + no coughing
nausea + v
anorexia
low grade fever
peritonitis - localised tenderness, guarding, rebound tenderness
rovsing’s sign +ve - palpation of LLQ increases pain in RLQ (stretches peritoneal lining)
ddx GI obstruction constipation perf ulcer meckles diverticulitis crohns uro - torsion, calculi, UTI gynae - extopic, ovarian cyst, PID DKA
ix clinical CT urinalysis - UTI preg test FBC CRP USS - in women to exclude gynae stuff
mgmt admit all laproscopic appendicectomy IV fluids + opiate analgesia IV metronidazole and third gen cephalosporin
diverticular disease def + types common location epi rf pres ddx ix severity classification mgmt comps
def + types
A herniation of mucosa through thickened colonic muscle
diverticulosis - asymptomatic
diverticulitis - diverticular inflammation
often described as ‘wear and tear of the bowel’
common loc
sigmoid and descending colon
epi
50% have diverticular by 50
75% asymp
25% symp
rf age obesity low dietry fibre smoking NSAIDs
pres
diverticular - found incidentally or left abdo pain worse on eating relieved in flatus/defecation +/- bloating, bleeding, constipation/diarrhoea
diverticulitis - LLQ pain (asians RLQ) + bleeding, intermittent pain with bowel habits, fever and tachy, anorexia, nausea, vomiting, localised tenderness and abdo mass, reduced bowel sounds unless obstruction
ddx
sympt IBS
diveriticulitis: appendicitis, crohns, colorectal cancer
ix colonoscopy - rule out cancer flexisig @ bleed FBC barium enema - in uncomp CXR - pneumo AXR - large/small bowel dilatation, ileus, obstruction CT cologram CT abdo scan with contrast
severity classification - hinchey I - para-colonic abscess II - pelvic abscess III - purulent peritonitis IV - faecal peritonitis
mgmt
asymp - high fibre diet avoid NSAIDs and opiates
diverticular disease - admit if signif blood loss, fluids + fibre, bulk form lax (ispaghula), paracetamol
diverticulitis - ?admit, broad spec abx (co-amox) for 7d, paracetamol, clear liquids 2-3 days
30% require surg: sepsis, fistula, obstruction, perf = resection + colostomy
comps 1/3 pts develop comps POFASH Perf Obstruction Fistula Abscess Stricture Haemorrhage- abrupt painless bleeding or cramps with urge followed by large blood - ceases spont
meckles diverticulum
what is it
pres
what is it
Vestigial remnant of vitellointestinal duct @ distal ileum (within 100cm of ileocaecal valve)
pres
Asymptomatic or haemorrhage (50% of complications) more common at children <2 or intestinal obstruction
*Always consider in DDx of rectal bleed or intestinal obstruction
bowel ischaemia
types and differentiating
types
acute mesenteric ischaemia - typically small bowel, embolus, sudden, severe, poorly localised pain, urgent surg, high mortality
chronic mesenteric ischaemia
aka intestinal angina
ishaemic colitis - large bowel, multifactorial, transient less severe symps, bloody diarrhoea, ‘thumbprinting’, conservative managememt
malabsorption general clinical features most important to find causes blinding testing common pres of: - steatorrhoea - iron/folate/B12 defi - vit a def - vit d/ca def - vit k def
general clinical features:
change in weight/growth
GI symps - chronic diarrhoea, steatorrhoea
fh - coeliac, crohns, CF
signs of deficiency - iron, folate, B12, bleeding (vit k), oedema (protein/calorie)
most imp to find - coeliac, CD, chronic panc
aet
mucosal, intraluminal, structural, extra GI
MUCOSAL
coeliac, infection, HIV enteropathy, lymphatic obstruction (lymphoma, TB, cardiac disease)
INTRALUMINAL
pancreatic insufficiency - lack of enzymes, cholestatic jaundice, terminal ileum disease
STRUCTURAL
intestinal hurry: post-gastrectomy, crohns, amyloidosis, short bowel synd
EXTRA GI
hyper/pothyroid/parathyroid, DM, carcinoid, eating disorder
blind testing FBC, LFT, ESR, CRP iron - ferritin, folate, B12 albumin + corrected calcium clotting screen + INR (vit k) anti-endomysial, anti-reticulin, alpha-gliadin stool - faecal elastase (A1AT), microscopy and culture AUSS gallbladder, liver, panc barium studies- structural ileocolonoscopy + biopsy
common pres of: steatorrhoea - foul, floating, pale iron/fol/b12 - pallor/glossitis vit a - hyperkeratosis/scaliness vit d/ca - bones/stones/mones/groans/thrones vit k - haemorrhage
tropical sprue def pres who location ix mgmt
def Malabsorptive disease of small bowel characterised by inflammation and villous flattening
pres
Very similar presentation to coeliac disease: begins with acute diarrhoea, fever and malaise -> chronic steatorrhoea, malabsorption, malaise, weight loss, vitamin deficiencies (iron, folate, B12, A, D, K), ankle oedema (albumin)
who
tropical areas: se asia, caribbean
where
small bowel
ix
FBC - macrocytic anaemia B12/folate at 60%
K+, iron. albumin - low as of malab, diarrhoea
ur - raised due to volume depletion
vit d, ca, phosp abnormal
faecal fat >15g/day
check stools for cysts, ova, parasites
jejunal biopsy - incomplete villous atrophy (coeliac = complete)
mgmt
fluid replacement
abx - tetracycline 6-12 months
nutritional support - folate, B12, iron (not with tetra as of chelation
gastric cancer why import where most common in stomach and world rf types pres signs of incurable referral criteria ix spread to staging mgmt palliation prognosis
why import
4th most common cancer in world
2nd most common cancer death
17th most common cancer in UK
where most common
50% pylorus
japan, china, finland, colombia
rf 95% over 55 m:w 2:1 h.pylori x2 poor diet - high salt/pickles/nitrates/spice smoking atrophic gastritis blood group A nitrosamines exposure E-cadherin gene mutation polyps pernicious anaemia
types cardia/GO junction - adenocarcinoma - 90%: - type 1 = true oesophagel cancers, related to barretts - type 2 = carcinoma of cardia, arising from cardiac type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction - type 3 = sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer. adenocarcinoma split into intestinal (most common, gland-forming) or diffuse (signet cells, aggressive and met) - based on Lauren criteria distal carcinoma (>5cm from OG junction)
pres vague - dyspepsia, wt loss, vom, dysphagia, anaemia RED FLAGS FOR DYSPEPSIA - ALARMS A - anaemia L - loss of wt A - anorexia R - recent onset >55 M - malaena S - swallowing difficulty MOST PRESENT LATE
signs of incurable:
epigastric mass, liver (hepatomeg, jaun), troisiers sign - virchows node
referral criteria
immediate = signif acute GI bleed
2ww = dyspepsia + dysphagia/wt loss/vom/IDA/mass
2ww = >55 + new onset dyspep
2ww = worsening dyspep + barretts/atrophic gastritis (pernicious anaemia)
ix
FBC, LFT, U+E, clotting etc
**flexible gastroscopy + biopsy (should biopsy all ulcers)
signet ring cells seen in biopsy = cancer - large vacuole of mucin, with displaced nucleus to one side, higher the number the worse the prognosis
HER2 testing
spread to
ovary = krukenburg’s tumour
to lung + liver
via local, lymphatic, blood-borne, transcoelmic (across peritoneal cavity)
staging method = spiral CT abdo, thorax, pelvis for metastatic disease - gastric wall thickening, lymphadenopathy, lung/liver or endoscopic USS PET CT for junctional tumours TAUSS for spread diagnostic lapro TNM
mgmt
nutritional support/deficiency screen + symptom control
surgery = distal tumour - subtotal gastrectomy, proximal - total gastrectomy if <5cm OG junction, type 2 OG tumour oesophagogastrectomy
+ lymphadenectomy
perioperative chemo - 5-FU fluorouracil comb
palliation
epirubicin, cisplatin, 5-FU
blood trans for symp anaemia
prog
15% survive
GIST (gastrointestinal stromal tumour) type patho where pres ix spread to mgmt
type
Soft tissue sarcoma and most common mesenchymal tumour
patho
Oncogenic kinase mutation. 80% have KIT receptor tyrosine kinase mutation
where
50% stomach
pres early satiety bloating fever wt loss night time sweating GI bleed
ix
CT chest abdo pelvis
MRI if needed
DONT biopsy if resectable
spread
liver
mgmt
complete surgical resection with careful handling to avoid rupture and disemination
imatinib - tyrosine kinase inhibitor -adjuvant
MALT lymphoma (mucosa-associated lymphoid tissue) def why diff types pres aet who course gastric ix mgmt
def subtype of non-hodgkins lymphoma - extranodal marginal site lymphoma b- cell lymphoma indolent - calmer, stays mostly confined to stomach
why diff
Lymphoid proliferation is in MALT not LNs, follow a different course to nodal B-cell lymphomas
types
gastric - assoc with hpylori
pres
dyspepsia +/- fever, nausea, constipation, wt loss, pain + ulcer
anaemia
aetiology chronic infection or autoimmune hpylori @ 90% gastric MALT c.jejuni @ small bowel MALT Hep c - splenic MALT
who
60 f
ix
gastroscopy + gastric biopsy - prominent follicles surrounded by lymphocytes
FBC, UE, LFT
phenotyping circulating lymphocytes +/- BM biopsy
mgmt early = erad hpylori - can cause complete remission in 70% \+ OGD followup if advanced - rituxumab + chemo + radio surgery
GI carcinoid tumour def types/where associated mets secretions + effects pres O/E carcinoid syndrome ix mgmt comp
def rare slow growing neuroendocrine tumour arising from embryonic gut, often asymp accounts for 2/3 of gastroenteropancreatic tumours
types/where
foregut, midgut (most common), hindgut
70% are in R bronchi
associated
30% with carcinoid syndrome
mets
liver 50%
secretions + effetcs
vasoactive serotonin + bradykinin
causes = Bronchospasm, diarrhoea, skin flushing, R sided valvular lesions
pres pain wt loss palpable mass vague r sided abdo discomfort bronchospasm - wheeze
O/E R mass hepatomeg telangiectasia tricuspid regurg pellagra (niacin deficiency - dermatitis and diarrhoea) hypotension
carcinoid syndrome
due to release of serotonin, bradykinin, substance P, gastrin, somatostatin
Flushing (post coffee, alcohol, food), diarrhoea, abdo pain, palpitations, hypotension, wheezing
can cause cushings
ix
Plasma chromogranin A (sensitive but not specific)
24 hr urinary 5-HIAA (>25mg = strong evidence)
Endoscopy or endoscopic ultrasound
CT/MRI
FBC, renal, UE, LFT, TFT, PTH, calcium, calcitonin, prolactin, aFP, CEA, b-HCG
mgmt
surg resection
non-resectable - somatostatin analogue eg ocretide (blocks 5HT release), radio, chemo
comp
obstruction
carcinoid crisis - ocreotide + plasma infusion
colorectal cancer where type mets why imp who rf pres criteria for HNPCC ix referral criteria staging screen mgmt mutation path polyp types
where 2/3 colon 1/3 rectum 40% rectum 30% sigmoid
type adenocarcinoma (adenoma is precurser), GIST, carcinoid
mets
LIVER
why imp
3rd most common cancer UK
2nd most common death
who
75% in over 65
rf
age
fam hx
ibd
FAP - familial adenomatous polyposis - AD - mutation at APC gene 100% penetrance
HNPCC - hereditary non-polyposis colorectal cancer (Lynch syndome), AD, 80% lifetime risk, defective DNA mismatch repair: colon, endometrial, ovary, stomach
Obesity, smoking, high alcohol, sedentary, DM
pres change in bowels rectal bleeding anaemia jaundice hepatomeg R sided cancer = weight loss, naemia, occult bleed, mass in RIF L cancer = colicky pain, rectal bleed, obstruction, tenesmus, less advanced at pres
criteria for HNPCC- AMSTERDAM 3-2-1 3 or more relatives wuth assoc cancers (1 must be 1st degree, colorectal, endometrium, small intestine, ureter 2 or more successive generations 1 before 50 FAP excluded
ix
PR exam + colonoscopy + biopsy of lesion
if tumour below peritoneal reflection - should have mesorectum evaluated with MRI
FBC, LFT (anaemia, liver mets)
flexible sigmoidoscopy
CEA - carcinoembryonic antigen
FOB - faecal occult blood
CT colonography if colonoscopy fails - CT with bowel prep and contrast
CT for mets A/T/P + liver USS (this is for staging)
once staged - discuss at MDT
referral criteria
2ww -
1. patients >= 40 years with unexplained weight loss AND abdominal pain
2. patients >= 50 years with unexplained rectal bleeding
3. patients >= 60 years with iron deficiency anaemia OR change in bowel habit
4. tests show occult blood in their faeces (see below)
2ww considered in:
there is a rectal or abdominal mass
there is an unexplained anal mass or anal ulceration
patients < 50 years with rectal bleeding AND any of the following unexplained symptoms/findings:
-→ abdominal pain
-→ change in bowel habit
-→ weight loss
-→ iron deficiency anaemia
staging - DUKES CRITERIA - 5 year survival
A - mucosa - 90%
B - into muscularis propria through serosa 70%
C - regional LN 30%
D - distant mets/liver 5%
screening
60-75 2 yearly with FOB then +ve for colonoscopy
mgmt surgery - R or L hemicolectomy + LN clearance chemo - if advanced/mets - FOLFOX - folinic acid plus fluorouracil plus oxaliplatin follow up: - 2x CT scan TAP yearly - 6monthly CEA in first 3 yrs - colonoscopy at 1 and 5 years may need stoma eg covering loop ileostomy - temp to protect distal anastomosis, left for 6-8 weeks and then reversed, lower right abdo chemo dont really work on HNPCC
mutation path Normal cell - APC mut Early adenoma - K-ras Intermediate adenoma - SMAD 2-4 Late adenoma - P53 Adenocarcinoma
polyp types inflam - IBD hyperplastic polyp - low risk HNPCC tubular adenoma/adenomatous polyp - most common tubulovillous adenoma - highest risk
complications Bleeding / infection / pain Damage to nerves, bladder, ureter or bowel Post op ileus Anaesthetic risks Conversion to open Anastomotic leak / failure Requirement for a stoma Failure to remove the tumour DVT/PE Hernias Adhesions
IBS def why import who aet types criteria course extra-intestinal ddx ix mgmt
Functional disorder where abdo pain is associated with defecation or change in bowel habit
why import
Significant negative impact on QoL and social functioning
who
woman 20-30
aet
Increased psychological distress associated with abnormal smooth muscle activity
types
IBS-C (constipation) <25% loose >75% constipated
IBS-D opposite
IBS-M mixed both >25%
criteria
6 month history of ABC (abdominal pain, bloating, change of bowel habit)
Relieved by defecation or altered bowel frequency + 2 or more of:
- Mucus, worse on eating, abdominal bloating, altered passage (Straining, urgency)
course
chronic - remissions/relapses
extra-intestinal
Migraine, backache, lethargy, urinary frequency/urgency, dyspareunia, depression
ddx
coeliac
IBD
gynaecological (ovarian cancer, endometriosis, PID)
ix FBC, ESR, CRP coeliac screen - EMA/TTG ca-125 ovarian cancer faecal calprotectin - IBD \+/- TFT, faecal occult blood test, colonoscopy
mgmt
lifestyle + diet - Decrease stress, relaxation, active physical activity, less caffeine, regular meals, fluids, decrease alcohol, high-fibre foods
meds - placebo effect Diarrhoea - loperamide Bloating - peppermint oil Constipation - laxatives e.g. ispaghula Abdo pain - antispasmodics - buscopan (hyoscine butylbromide) Psychological therapy second-line - amitriptyline 5-10mg
acute mesenteric ischaemia cause patho rf pres ix ddx mgmt
cause
Mesenteric artery embolic, thrombus, mesenteric venous thrombus, non-occlusive (NOMI)
patho
Impaired blood to intestine, bacterial translocation (passage int bact to sterile tissue) and systemic inflammatory response
rf vascular impairment previous CVE HTN/hypo hypercoag tumour infection
pres
mod-severe colicky pain poorly localised
pain out of proportion to symps and no tenderness/peritonitis
ix
gold standard - angiography
AXR for obstruction, ileus, thickened bowel, thumbprinting (odema and inflam)
ddx AAA biliary disease ectopic diverticulitis
mgmt ABCDE IV fluid papaverine - relieve spasm heparin for mesenteric venous thrombosis surgical angioplasty
mortality 90%!!!
chronic mesenteric ischaemia aka rf pres ix mgmt
aka
intestinal angina - chronic atherosclerotic
rf smoking HTN DM hyperlipidaemia
pres
weight loss
prostprandial pain
fear of eating
ix arteriography gold standard FBC LFT U+E for malnutrition and dehydration
mx
nitrate therapy
anticoag
operate - bypass surg
ischaemic colitis def predisposing pres ix mgmt
def Compromised blood circulation to colon SMA to middle colic to transverse (⅔), IMA to left colic to descending
predisposing Thrombosis (IMA), emboli (MA, cholesterol), decreased cardiac output, shock, trauma, coag disorders (protein C/S deficienct, antithrombin III deficiency), contraceptive pill, cocaine
pres
acute pain LIF
ix
ABG - met acidosis
colonoscopy: blue swollen mucosa
barium enema: thumbprinting in early phase - oedema
mgmt
relieve hypoperfusion: bowel rest and supportive care
TNM staging for gastric cancer
Tumour
TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
Tis: Carcinoma in situ: intraepithelial tumour without invasion of the lamina propria
T1: Tumour invades lamina propria or submucosa
T1a: Tumour invades the lamina propria or the muscularis mucosae
T1b: Tumour invades the submucosa
T2: Tumour invades the muscularis propria
T3: Tumour penetrates the subserosal connective tissue without invasion of the visceral peritoneum or adjacent structures
T4: Tumour invades the serosa or adjacent structures
T4a: Tumour invades the serosa
T4b: Tumour invades adjacent structures
Node
NX: Regional lymph node(s) cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis in 1–2 regional lymph nodes
N2: Metastasis in 3–6 regional lymph nodes
N3: Metastasis in 7 or more regional lymph nodes
Metastasis
MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis or positive peritoneal cytology
colorectal cancer screening
Screening for colorectal cancer has been shown to reduce mortality by 16%
the NHS offers home-based, Faecal Immunochemical Test (FIT) screening to older adults
another type of screening is also being rolled out - a one-off flexible sigmoidoscopy
FIT every 2 years between 60-74 sent through post a type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb) if abnormal then -> colonoscopy
At colonoscopy, approximately:
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer
flexi sigmoidoscopy: new used to detect polyps that are premalignant >55 can self-refer up to age of 60
what would and anterior resection of the bowel remove
lower sigmoid
higher rectum
what would an abdominoperineal resection remove?
for tumours of lower rectum
removes rectum and anus +/- sigmoid colon and suturing over anus
leaves patient with permanent colostomy
what would a r hemicolectomy remove
caecum
ascending
proximal transverse colon
what would a left hemicolectomy remove
distal transverse and descending colon
glasgow-blatchford bleeding score
stratifies upper GI bleeds who are low risk and candidates for outpatient management
haemoglobin BUN sex heart rate >100 maelena present recent syncope hepatic hx disease cardiac failure present
colonoscopy vs CT pneumocolon vs CT abdo with long oral prep
colonoscopy - good for cancer, polyps, take samples there and then, but need prep of bowel, ?sedation, cant see small stuff that well, patients dont like
CT pneumocolon - aka CT virtual colonoscopy, used as screening, used when unsuccessful colonoscopy, assess strictires, if view blocked by tumour in colonoscopy, cant be used in acute inflam, recent surg or colostomy, but quicker, view whole colon what ever is in there, but ionising radiation
CT abdo - obvs of whole abdo?
c.diff spread
prevention
abx causes of it
at risk groups
spread - faecal-oral route
prevention - spores highly resistant to chemicals, alcohol hand rub doesnt kil it, hand washing using soap does
abx causes - ampicillin, amoxicillin, cephalosporins
at risk groups - poor hygiene, childreen in nursary, prepping unwrapped or uncooked food, HCW/social care staff working with vulnerable people
managment of peritonitis
correct fluid loss catheterise +/- GI decompression abx therapy analgesia treat cause
ascites def classification causes ix mgmt
def
An accumulation of excess serous fluid within the peritoneal cavity.
Healthy men – no fluid
Women up to 20 ml
classification
- Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
- Stage 2 easily detectable but of relatively small volume.
- Stage 3 obvious, not tense ascites. (moderate)
- Stage 4 tense ascites. (Large)
causes
Transudates (protein <25 g/L)
Low plasma protein concentrations: Malnutrition Nephrotic syndrome Protein-losing
enteropathy
High central venous pressure: Congestive cardiac failure
Portal hypertension: Portal vein thrombosis /Cirrhosis
Exudates (protein >25 g/L)
Peritoneal malignancy
Tuberculous peritonitis
Budd–Chiari syndrome (hepatic vein occlusion or thrombosis)
Pancreatic ascites
Others: Chylous ascites , Meigs’ syndrome
ix clinically - abdo distention 1.5-2l - puddle sign - 150ml - shifting dullness - 500ml - flanks fullness 1500+ml - fluid thrill LFT cardiac function -echo AXR, USS, CT abdo ascitic aspiration fluid for micro, cytology, culture including mycobacteria, analysis of protein content and amylase
mgmt treat cause sodium restriction diuretics paracentesis (up to 4-6l/day with colloid replacement) indwelling drain peritoneovenous shunting
when does duodenum become jejunum
ligament of treitz
whats included in the foregut, midgut, hindgut and their blood supply
foregut - oesophagus to ampula of vater, coeliac trunk
midgut - to 2/3 along transverse colon, superior mesenteric artery
hindgut - rest, inferior mesenteric artery
rosvig sign
tender RIF when left palps
appecndicitis
psoas stretch
sharp RIF pain when right kept straight and lifted, suggests appendicitis - with retrocaecal appendix
rebound tenderness
when hand suddenly removed
suggests abdo wall inflamation +/- peritonitis
tinkling bowel sounds
bowel obstruction
how to approach laxative in a patient with constipation
PR exam - stool in rectum? phosphate enema
no? look for bowel obstruction
if no -> go for one of osmotic (hosp fave), softener, stimulant (palliative), bulk-forming (elderly)
vitamin c deficiency aka functions consequences features
aka
scurvy
functions
- antioxidant
- collagen synthesis: acts as a cofactor for enzymes that are required for the hydroxylation proline and lysine in the synthesis of collagen
- facilitates iron absorption
- cofactor for norepinephrine synthesis
leads to:
- defective synthesis of collagen -> cap fragility (bleeding tendency) and poor wound healing
features gingivits, loose teeth poor wound healing bleeding from gums, haematuria, epistaxis general malaise
treatment for cdiff
If C. difficile does not respond to first line metronidazole, oral vancomycin should be used next,
