gastroenterology Flashcards

1
Q

key questions in hx of dysphagia

A
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?
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2
Q

what would cause oropharyngeal dsphagia

A

salivary - sjorgrens
tongue - amyloid, hypothyroidism, MND
palatal/epiglottal/ upper oesophageal disorder - CVD, MND, Parkinsons

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3
Q

what would cause oesophageal dysphasia

A

benign mucosal disease - benign peptic stricture, oesophageal web (plummer vinson syndrome), candidial oesophagitis

malignant mucosal disease - carcinoma

motility disorders - oesophageal spasm, achalasia, oesophageal pouch

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4
Q
pharyngeal pouch
what is it 
pres 
ix
mx
A

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

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5
Q

mx of dysphagia

A

treat underlying cause

pro-kinetic - domperidone + metoclopramide - arrhythmias + long QT syndrome

nutrition? oral supplements, nasogastric feeding, PEG feeding

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6
Q

upper GI bleed differentials

A
oesophagitis
peptic ulcer
no diagnosis
varices/portal hypertensive gastropathy
erosive duodenitis or gastritis
mallory-weiss tear
malignancy
vascular malformations
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7
Q

RF - upper GI bleed

A
NSAIDS
apsirin
anticoag
h pylori
alcohol
corticosteroids
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8
Q

assessing GI bleeds scoring systems

A

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

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9
Q

endoscopic treatments for GI bleed

A
should be provided within 24 hours
adrenaline injection
ablative techniques - heat
mechanical - clips
banding techniques - for variceals
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10
Q

post endoscopy care in upper GI bleed

A

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

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11
Q

evidence of iron deficient anaemia in ix

A

low hb
low ferritin
microcytosis
hypochromia

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12
Q

test to assess the colon - in order of preference

A
colonoscopy(1 in 1000 risk of tear)/flexible sigmoidoscopy (invasive)
virtual colonoscopy (CT pneumocolon)
CT with long oral prep (older/frail pts)
colon capsule
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13
Q

what is definition of diarrhoea

A

the passage of 3+ loose or liquid in stools in 24 hrs

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14
Q

dysentry definition

A

+ mucus + blood in stools

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15
Q

classifying diarrhoea - four mechanisms

A

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

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16
Q

ix of IBD

A
bloods - FBC, CRP + U&E, LFTS
stool culture and micro
abdo xray
ileo-colonoscoy
small bowel ix - MRI small bowel/CT enterography/ capsule endoscopy
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17
Q

UC criteria

A

truelove + witts
staging severity
mild, mod, severe

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18
Q

mx IBD

A

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

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19
Q

coeliac dx

A
  1. immunoglobulins (look for IgA deficiency - can cause false negative antibody results) + TTG antibodies
  2. endomysial antibodies where about indeterminate
  3. OGD + duodenal biopsys (villous atrophy at histology)
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20
Q

when to transfuse in GI bleeds

A

shouldnt be transfusing unless haem drops below 70g/l unless have cardiovascular symps (aim for above 80g/l)

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21
Q

very poor looking ulcers that are squirting what do you prescribe in post endoscopy care?

A

IV PPI

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22
Q

ix chronic diarrhoea

A
RBC
CRP
TFT
Coeliac serology
stool sample 

if have cancer or inflam red flags then add on endoscopy and CT

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23
Q

compare crohns/UC

A
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
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24
Q

symptoms of coeliac:
typical
atypical
silent

A
TYPICAL
diarrhoea
steatorrhoea
weight loss
dermatitis
herpatiformis
ATYPICAL
ataxia
peripheral neuropathy
ammenorhoea
infertility
chronic fatigue
SILENT
IDA
osteoporosis
hyposplenism
abnormal LFTs
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25
Q
upper GI bleed 
pres
causes + classic features
ix
mx
A
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

  1. cancer - frank haematemesis, prodromal dyspepsia, b symps, variable amounts of bloof
  2. diffuse erosive gastritis - haematemesis and epigastric discomfort, usually underlying causes eg NSAIDs, haemodynamic comp
  3. 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

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26
Q
acute diarrhoea
definition
causes
red flags
ix
mx
comps
prognosis
A

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

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27
Q

cause of diarrhoea in traveller

A

ETEC e.coli - enterotoxinogenic

watery stools
abdo cramps
nausea

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28
Q

cause of diarrhoea in abx use

A

c.diff - vancomycin

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29
Q

cause of diarrhoea in HIV

A

CMV

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30
Q

cause of diarrhoea in small children

A

rotavirus

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31
Q

cause of diarrhoea in well water

A

giardiasis

prolonged
non-bloody

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32
Q

cause of diarrhoea in puppies

A

camplyobacter

flu-like prodrome -> crampy abdo pains fever, diarrhoea that may be bloody,
may mimic appendicitis
comps = Guillain-Barre Syndrome

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33
Q

cause of diarrhoea in cruise ships

A

norovirus

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34
Q

cause of diarrhoea in dystentry/bloody + mucuous

A

shigella

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35
Q

cause of diarrhoea in profuse vomiting within 6 hours of food

A

s.aureus (food handlers), bacillus cereus (rice)

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36
Q

cause of diarrhoea in ab cramp and profuse watery

A

v.cholera - rice water stools

severe dehydration resulting in weight loss
profuse, watery

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37
Q

cause of diarrhoea in Fever + ab cramp + bloody + milk/meat

A

campylobacter jejuni

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38
Q

cause of diarrhoea in Fever + ab cramp + bloody + salad

A

shigella

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39
Q

cause of diarrhoea Fever + ab cramp + bloody + poultry/shellf

A

salmonella

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40
Q

antidiarrhoeal agents

A

loperamide
diphenoxylate

opioid agonists so also reduce gut motility

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41
Q

cause of gradual onset diarrhoea, abdo pain, tenderness which may last for several weeks

A

amoebiasis

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42
Q
UC
what is it
types
pres + extra-intest
ix
mx
comps
A

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

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43
Q

UC flares classification

A

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

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44
Q

what is an aminosalicylate

A

mesalazine

5-aminosalicylic acid

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45
Q
crohns
what is it 
cause
pres + extraintestinal
ix
mx
comps
A
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

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46
Q

what must you assess before prescribing azathioprine or mercaptopurine?

A

thiopurine methyltransferase (TPMT) activity

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47
Q
coeliac
what is it 
associated disorders
who should be screened?
pres
ix
mx
comps
A

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
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48
Q

whats criteria called to grade severity of coeliac

A

marsh criteria

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49
Q

chronic diarrhoea
define
causes

A

Diarrhoea: > 3 loose or watery stool per day >14 days

causes
IBS
UC
Crohns
colorectal cancer
coeliac
thyrotoxicosis
laxative abuse
appendicitis
radiation enteritis
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50
Q

normal gut flora

functions

A

> 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
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51
Q

intestinal obstruction

causes

A

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
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52
Q

what does ileus mean

A

non-mechanical obstruction

paralytic ileus = bowel inactivity

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53
Q

what is the most common intestinal obstruction

and what does it increase the risk of

A

small bowel obstruction or colorectal malignancy

increases risk of:
volvulus
impaction
constipation
megacolon if dementia
alzheimers 
parkinsons
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54
Q
intestinal obstruction
causes
pres 
specific pres for:
- sigmoid volvulus
- paralytic ileus
ix
mx
A

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

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55
Q

who are calciums two ugly sisters

A

magnesium + phosphate

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56
Q

explain how the body works to increase serum calcium if its low

A
  1. pituitary gland tells parathyroid glad to release PTH
  2. this works on bone to release calcium (99% of calcium is stored in bone) and phosphate
  3. 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
  4. 1,25 dihydroxy vit d3 also works on gut to absorb more calcium and phosphate + proximal convuluted tubules in kidney to absorb more calcium
  5. in the
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57
Q

how your body works to decrease serum calcium

A

high serum calcium stimulates the thyroid gland to produce calcitonin (this has opposite effect to PTH)

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58
Q

what percent of phosphate, mg, ca is located in the bone

A

phosphate - 85% (rest is intracellular)
magnesium - 60%
calcium - 99%

calcium phosphate makes up hard matrix of bone
magnesium helps strengthen it

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59
Q

phosphate homeostasis - if its low

A

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

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60
Q

whats more dangerous hypo or hyper magnesium/phophate?

A

hypo

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61
Q
magnesium
amount in body
functions
RDA and where to get it
absorption/excretion in body
A

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

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62
Q
hypomagnesium
classification
causes
clinical effects
ix
mx
A

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!!!

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63
Q

hypermagnesaemia

A

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

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64
Q
phosphate intake 
where from
RDA
where absorbed
regulated by
exretion
plasma levels affected by:
A

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
65
Q

FGF 23
what is it
its affect
increased by?

A

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
66
Q

hypophosphataemia
classify
commonly seen in
mechanism

A

<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

67
Q

refeeding syndrome

what is it

A

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)

68
Q

hyperphosphataemia
causes
clinical effects

A
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
69
Q

how your body works to increase low magnesium

A

parathyroid creates PTH which acts on kidney to absorb more magnesium

70
Q
hypocalcaemia
classification
causes
pres
ix
mx
A

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

71
Q
dyspepsia
what is it 
causes
rf
red flags 
criteria
ix
mx
A

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

72
Q

stomachs attackers + defenders

A

attackers
Acid, pepsin, h.pylori, bile salts, smoking (impairs mucosal repair

defenders
Mucin secretion, cellular mucus, bicarbonate secretion, mucosal blood flow

73
Q

how does PPI work?

A

PPI decreases expression of H+/K+ antiporter on luminal membrane of parietal cells

74
Q

how do you test for h pylori

A

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

75
Q
gastric physiology 
areas of stomach
cell types 
what stimulates acid
what stops acid 
acid production
A

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:

  1. co2 and cl diffuse to cell from blood
  2. co2 + H20 (carbonic anhydrase) -> H2CO3 ->h+ +HCO3-
  3. H+ combines with cl, ATP pump to pump to duct (as HCl more conc)
  4. cAMP increased by gastrin, histamine, ACh to pump more acid
76
Q
H.pylori infection
what is it 
associations
symps 
pathophys
tests
complication
management
A

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:

  1. PPI + amoxicillin + clary
  2. PPI + metronidazole + clary
77
Q

laxatives

types, how they work, examples, indications, s/e, CI

A
  1. 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
  2. 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
  3. 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.
78
Q

antiemetics

types, how they work, examples, indications, s/e, CI

A
  1. 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.
  2. 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)
  3. 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

79
Q

where is the vomiting centre how does it receive inputs

A

medulla

receives inputs from chemoreceptor trigger zone, the solitary tract nucleus (innervated by vagus nerve), the vestibular system and higher neurological centres.

80
Q

physiology of vomiting

A
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

81
Q

what antiemetic would you prescribe for opioid sickness

A

dopamine D2 antagonist - metoclopramide and domperidone or antipsychotic haloperidol

82
Q

what antiemetic would you prescribe for diabetic gastroparesis sickness

A

dopamine D2 antagonist - metoclopramide and domperidone

83
Q

what antiemetic would you prescribe for n+v

from gut infection, radiotherapy, chemo, post surg

A

serotonin 5HT antagonists - ondansetron, granisetron

84
Q

what antiemetic would you prescribe for vertigo/motion sickness and morning sickness

A

cyclizine, cinnarizine, promethazine

vertigo - prochlorperazine, chlorpromazine

85
Q

what would you prescribe for chemo, radio sickness

A

prochlorperazine, chlorpromazine

radio - ondansetron, granisetron

86
Q

what would you prescribe for sickness due to gut infection

A

ondansetron, granisetron

87
Q

how does the vomiting reflex work to cause you to vomit

A

relaxation of lower oesphagus sphincter
epiglottis closure
contraction of diaphragm and abdominal muscles
increase intrabdominal pressure

88
Q

what would you prescribe for patients with sickness from reflux or hepatobiliary disorders

A

metoclopromide

89
Q

cyclizine dosage

A

50mg up to TDS

take 1/2 hours before departure

90
Q

higher neurological input to vomiting

A

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

91
Q

what factors can affect the chemoreceptor trigger zone to stimulate vomiting (general groups)

A

drugs - opiates

hormones - pregnancy

toxins - alcohol

metabolic imbalance - hypercalcaemia, uraemia, DKA

92
Q

gastric physiology phases

A
  1. cephalic - 20% - via vagus PSNS
  2. gastric 70% - vagal reflex, gastrin-histamine stimulation
  3. intestinal phase 10% - nervous mechanisms, hormonal mechanisms
93
Q
hypercalcaemia
def
causes
features 
ix - as you would in practise (full)
management
A
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

94
Q
peptic ulcer disease
types
causes/rf
pres - DU and PU sep
differentials
ix
mgmt
comps
A

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
95
Q
gastritis
def
types
symptoms
rf
rx
A
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

96
Q
GORD 
def 
epi
rf 
if prolonged =
pres
atypical pres
ix
ddx
urgent referral
mx
A
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

97
Q
hernia 
types 
def 
comps
anatomy of inguinal canal
why are they important
A
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

98
Q
inguinal hernia
rf
epi
types
pres
where is DIR + SIR
ix
mx
comps
A
rf
obesity 
constipation
chronic cough 
heavy lifting
male 

epi
75% of abdo wall hernias
95% male

types

  1. direct 20% - peritoneal sac through weakness in posterior wall of inguinal canal medially to inferior epigastric vessels - easily reduced
  2. 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
99
Q
femoral hernia
anatomy of fem canal + contents
epi
pres
differentials
comps
mx
A
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

100
Q
hiatus hernia
def
rf
causes
types
pres
ix
rx
A
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

101
Q

oesophagus blood supply, muscles and epithelium in upper, mid and lower third

A

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

102
Q
oesophagitis
eosinophilic
causes
grading
rx
A

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

103
Q
barrett's oesophagus 
def 
types 
causes
protective/rf
hx
ix
mgmt
comps
A
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

104
Q
oesophageal cancer
types 
rf
classic patient
pres 
ix
staging
spread to
mgmt
A

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

  1. FBC, UE, LFT, glucose, CRP
  2. FIRST LINE - endoscopy with brushing and biopsy of lesion
  3. ?CXR - mets
  4. CT/MRI - chest + abdo + pelvis for staging -> if shows no mets then local stage found by endoscopic USS
  5. double contrast barium swallow for dysphagia if benign motility diagnosis
  6. 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%
105
Q

differentials of dysphagia

A

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

106
Q
achalasia
def 
mech
pres
ix
mgmt
A

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

107
Q

systemic sclerosis
what is it
types

A

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!!

  1. diffuse cutaneous systemic sclerosis - trunk + proximal limbs, scl-70 antibodies, resp involement in 80% - ILD, pulm arterial HTN, comps = renal disease + HTN, poor prog
  2. scleroderma - without internal organ involvement
    - tightening + fibrosis of skin
    - plaques or linear
108
Q
scleroderma
what is it 
pathophys of GI features
features
autoantibodies
mx
A

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
109
Q

CREST

A

Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia

subtype of limited cutaneous systemic sclerosis

110
Q

rockall risk score

A

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)

111
Q
mallory-weiss tear
def 
causes
pres
rf
ix + mx
comp
A

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

112
Q
oesophageal varices
def 
location
rf
pres
ix
A

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

113
Q
volvulus
types
rf
pres
ix
mgmt
comps
A

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

114
Q
hirschsprungs
def
pres
ix
mx
A

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

115
Q

classic triad of gastro-oesophageal obstruction

A

wretching
pain
failed attempt to pass NG tube

116
Q
peritonitis/intra-abdo sepsis
def/types
abdo defence
pres
ix
mgmt
A

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
117
Q

differentials based on location of abdo pain

A

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

118
Q
anal fissure
what is it
pres
cause
mgmt
A

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

119
Q
fistulas
what is it 
types
causes
ix
mx
A

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

120
Q
anorectal abscess
what is it
cause
bacteria
rf
pres
ix
mx
A

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

121
Q

pilonidal sinus
what is it
mgmt

A

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

122
Q
perianal haematoma
what is it 
appearance
pres
histology
innervation
mgmt
A

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

123
Q

what is the dentate line

A

aka pectinate line

splits the upper 2/3 and lower 1/3 of anal canal

sits just above sphincter bit really

124
Q
haemorrhoids
what are they 
grading 
pain 
rf
pres
ix
mgmt
comp
A

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

125
Q
appendicitis
def
red flag
epi
pres
location
ddx
ix
mgmt
A

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
126
Q
diverticular disease
def + types
common location
epi
rf
pres
ddx
ix
severity classification
mgmt
comps
A

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
127
Q

meckles diverticulum
what is it
pres

A

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

128
Q

bowel ischaemia

types and differentiating

A

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

129
Q
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
A

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
130
Q
tropical sprue
def
pres
who
location
ix
mgmt
A
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

131
Q
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
A

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

132
Q
GIST (gastrointestinal stromal tumour)
type
patho
where
pres
ix
spread to 
mgmt
A

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

133
Q
MALT lymphoma
(mucosa-associated lymphoid tissue)
def
why diff
types
pres
aet
who 
course
gastric ix
mgmt
A
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
134
Q
GI carcinoid tumour
def
types/where
associated
mets 
secretions + effects
pres
O/E
carcinoid syndrome
ix
mgmt
comp
A
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

135
Q
colorectal cancer
where
type
mets
why imp
who 
rf
pres
criteria for HNPCC
ix
referral criteria
staging
screen
mgmt
mutation path
polyp types
A
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
136
Q
IBS
def
why import
who 
aet
types
criteria
course
extra-intestinal 
ddx
ix
mgmt
A

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
137
Q
acute mesenteric ischaemia
cause
patho
rf
pres
ix
ddx
mgmt
A

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%!!!

138
Q
chronic mesenteric ischaemia
aka
rf
pres
ix
mgmt
A

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

139
Q
ischaemic colitis
def
predisposing
pres
ix
mgmt
A
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

140
Q

TNM staging for gastric cancer

A

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

141
Q

colorectal cancer screening

A

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
142
Q

what would and anterior resection of the bowel remove

A

lower sigmoid

higher rectum

143
Q

what would an abdominoperineal resection remove?

A

for tumours of lower rectum
removes rectum and anus +/- sigmoid colon and suturing over anus
leaves patient with permanent colostomy

144
Q

what would a r hemicolectomy remove

A

caecum
ascending
proximal transverse colon

145
Q

what would a left hemicolectomy remove

A

distal transverse and descending colon

146
Q

glasgow-blatchford bleeding score

A

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
147
Q

colonoscopy vs CT pneumocolon vs CT abdo with long oral prep

A

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?

148
Q

c.diff spread
prevention
abx causes of it
at risk groups

A

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

149
Q

managment of peritonitis

A
correct fluid loss 
catheterise +/- GI decompression
abx therapy
analgesia
treat cause
150
Q
ascites 
def 
classification
causes
ix
mgmt
A

def
An accumulation of excess serous fluid within the peritoneal cavity.
Healthy men – no fluid
Women up to 20 ml

classification

  1. Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
  2. Stage 2 easily detectable but of relatively small volume.
  3. Stage 3 obvious, not tense ascites. (moderate)
  4. 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
151
Q

when does duodenum become jejunum

A

ligament of treitz

152
Q

whats included in the foregut, midgut, hindgut and their blood supply

A

foregut - oesophagus to ampula of vater, coeliac trunk

midgut - to 2/3 along transverse colon, superior mesenteric artery

hindgut - rest, inferior mesenteric artery

153
Q

rosvig sign

A

tender RIF when left palps

appecndicitis

154
Q

psoas stretch

A

sharp RIF pain when right kept straight and lifted, suggests appendicitis - with retrocaecal appendix

155
Q

rebound tenderness

A

when hand suddenly removed

suggests abdo wall inflamation +/- peritonitis

156
Q

tinkling bowel sounds

A

bowel obstruction

157
Q

how to approach laxative in a patient with constipation

A

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)

158
Q
vitamin c deficiency
aka
functions
consequences
features
A

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
159
Q

treatment for cdiff

A

If C. difficile does not respond to first line metronidazole, oral vancomycin should be used next,