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
``` 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 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
26
``` 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
27
cause of diarrhoea in traveller
ETEC e.coli - enterotoxinogenic watery stools abdo cramps nausea
28
cause of diarrhoea in abx use
c.diff - vancomycin
29
cause of diarrhoea in HIV
CMV
30
cause of diarrhoea in small children
rotavirus
31
cause of diarrhoea in well water
giardiasis prolonged non-bloody
32
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
33
cause of diarrhoea in cruise ships
norovirus
34
cause of diarrhoea in dystentry/bloody + mucuous
shigella
35
cause of diarrhoea in profuse vomiting within 6 hours of food
s.aureus (food handlers), bacillus cereus (rice)
36
cause of diarrhoea in ab cramp and profuse watery
v.cholera - rice water stools severe dehydration resulting in weight loss profuse, watery
37
cause of diarrhoea in Fever + ab cramp + bloody + milk/meat
campylobacter jejuni
38
cause of diarrhoea in Fever + ab cramp + bloody + salad
shigella
39
cause of diarrhoea Fever + ab cramp + bloody + poultry/shellf
salmonella
40
antidiarrhoeal agents
loperamide diphenoxylate opioid agonists so also reduce gut motility
41
cause of gradual onset diarrhoea, abdo pain, tenderness which may last for several weeks
amoebiasis
42
``` 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
43
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
44
what is an aminosalicylate
mesalazine | 5-aminosalicylic acid
45
``` 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
46
what must you assess before prescribing azathioprine or mercaptopurine?
thiopurine methyltransferase (TPMT) activity
47
``` 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 ```
48
whats criteria called to grade severity of coeliac
marsh criteria
49
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 ```
50
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
51
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
52
what does ileus mean
non-mechanical obstruction paralytic ileus = bowel inactivity
53
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 ```
54
``` 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
55
who are calciums two ugly sisters
magnesium + phosphate
56
explain how the body works to increase serum calcium if its low
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
57
how your body works to decrease serum calcium
high serum calcium stimulates the thyroid gland to produce calcitonin (this has opposite effect to PTH)
58
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
59
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
60
whats more dangerous hypo or hyper magnesium/phophate?
hypo
61
``` 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
62
``` 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!!!
63
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
64
``` 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
65
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
66
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
67
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)
68
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 ```
69
how your body works to increase low magnesium
parathyroid creates PTH which acts on kidney to absorb more magnesium
70
``` 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
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``` 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
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stomachs attackers + defenders
attackers Acid, pepsin, h.pylori, bile salts, smoking (impairs mucosal repair defenders Mucin secretion, cellular mucus, bicarbonate secretion, mucosal blood flow
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how does PPI work?
PPI decreases expression of H+/K+ antiporter on luminal membrane of parietal cells
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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
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``` 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: 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
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``` 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: 1. PPI + amoxicillin + clary 2. PPI + metronidazole + clary
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laxatives | types, how they work, examples, indications, s/e, CI
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.
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antiemetics | types, how they work, examples, indications, s/e, CI
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
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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.
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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
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what antiemetic would you prescribe for opioid sickness
dopamine D2 antagonist - metoclopramide and domperidone or antipsychotic haloperidol
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what antiemetic would you prescribe for diabetic gastroparesis sickness
dopamine D2 antagonist - metoclopramide and domperidone
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what antiemetic would you prescribe for n+v | from gut infection, radiotherapy, chemo, post surg
serotonin 5HT antagonists - ondansetron, granisetron
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what antiemetic would you prescribe for vertigo/motion sickness and morning sickness
cyclizine, cinnarizine, promethazine | vertigo - prochlorperazine, chlorpromazine
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what would you prescribe for chemo, radio sickness
prochlorperazine, chlorpromazine | radio - ondansetron, granisetron
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what would you prescribe for sickness due to gut infection
ondansetron, granisetron
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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
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what would you prescribe for patients with sickness from reflux or hepatobiliary disorders
metoclopromide
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cyclizine dosage
50mg up to TDS | take 1/2 hours before departure
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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
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what factors can affect the chemoreceptor trigger zone to stimulate vomiting (general groups)
drugs - opiates hormones - pregnancy toxins - alcohol metabolic imbalance - hypercalcaemia, uraemia, DKA
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gastric physiology phases
1. cephalic - 20% - via vagus PSNS 2. gastric 70% - vagal reflex, gastrin-histamine stimulation 3. intestinal phase 10% - nervous mechanisms, hormonal mechanisms
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``` 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
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``` 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 ```
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``` 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
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``` 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
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``` 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
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``` 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 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 ```
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``` 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
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``` 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
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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
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``` 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
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``` 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
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``` 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 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% ```
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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
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``` 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
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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!! 2. diffuse cutaneous systemic sclerosis - trunk + proximal limbs, scl-70 antibodies, resp involement in 80% - ILD, pulm arterial HTN, comps = renal disease + HTN, poor prog 3. scleroderma - without internal organ involvement - tightening + fibrosis of skin - plaques or linear
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``` 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 ```
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CREST
Calcinosis, Raynaud's phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia subtype of limited cutaneous systemic sclerosis
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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)
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``` 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
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``` 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
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``` 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
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``` 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
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classic triad of gastro-oesophageal obstruction
wretching pain failed attempt to pass NG tube
116
``` 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 ```
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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
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``` 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
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``` 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
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``` 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
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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
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``` 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
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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
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``` 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
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``` 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 ```
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``` 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 ```
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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
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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
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``` 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 ```
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``` 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
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``` 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
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``` 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
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``` 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 ```
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``` 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
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``` 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 ```
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``` 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 ```
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``` 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%!!!
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``` 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
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``` 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
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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
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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 ```
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what would and anterior resection of the bowel remove
lower sigmoid | higher rectum
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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
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what would a r hemicolectomy remove
caecum ascending proximal transverse colon
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what would a left hemicolectomy remove
distal transverse and descending colon
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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 ```
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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?
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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
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managment of peritonitis
``` correct fluid loss catheterise +/- GI decompression abx therapy analgesia treat cause ```
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``` 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 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 ```
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when does duodenum become jejunum
ligament of treitz
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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
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rosvig sign
tender RIF when left palps | appecndicitis
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psoas stretch
sharp RIF pain when right kept straight and lifted, suggests appendicitis - with retrocaecal appendix
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rebound tenderness
when hand suddenly removed | suggests abdo wall inflamation +/- peritonitis
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tinkling bowel sounds
bowel obstruction
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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)
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``` 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 ```
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treatment for cdiff
If C. difficile does not respond to first line metronidazole, oral vancomycin should be used next,