Phase 2 - GI Flashcards
(204 cards)
1
Q
Infective causes of diarrhoea
A
Intraluminal infectionSystemic infectionTypically VIRAL:1. Rotavirus (main in kids)2. Norovirus (main in adults)Also TRAVELLER’S diarrhoea (can be caused by a variety of things esp EHEC)
2
Q
Non-infective causes of diarrhoea
A
CancerRadiationChemicals- Poisoning- sweeteners- medications Inflammatory bowel diseaseIBS / malabsorptionEndocrine/hormonal eg ThyrotoxicosisAnatomical e.g. post colesectomy
3
Q
Evaluation for acute diarrhoea is warranted in individuals with which symptoms?
A
- persistent FEVER, - BLOODY diarrhoea,- severe ABDO PAIN, - symptoms of VOLUME DEPLETION (eg, dark or scant urine, symptoms of orthostasis/postural hypotension), - HISTORY of IBD, - immunosuppression
4
Q
Relevant history for diarrhoea
A
- ONSET/duration- CHARACTERISTICS of stool- Food/drink- Travel- IMMUNE status (immunocompromised can be affected by stuff normal immune people aren’t affected by)- Unwell contacts- Hobbies + FRESH WATER- ANIMAL contact- MEDS (recent - C. DIFF?)
5
Q
What food is particularly related to which pathogen (+ inc. period + associated symptoms)
A
- Take-aways (lots of microbes/toxins)- Warm rice - BACILLUS CEREUS (1-6hr - toxin) - PROFUSE VOmiting- Meat/BBQ - campylobacter spp, (24-72hr) - PROFUSE DIARRHOEA + SEVERE abdo pain - clostridium perfringens (12-24hr) - Diarrhoea + COLICKY abdo pain- Poultry/eggs - Salmonella spp (16-48hr) - Diarrhoea + some abdo pain- SHELLFISH - NOROVIRUS, - V. parahaemolyticus - salmonella enterica serotype Typhi- FINGER FOODS - STAPH AUREUS (1-6hr - pre-formed toxin) - SEVERE vomiting + FEVER
6
Q
Which mirobes are associated with fresh water/swimming
A
CryptosporidiumGiardiaAeromonas
7
Q
Which animals are particularly associated with diarrhoea causing pathogens
A
Reptiles - salmonellaPuppies - campy
8
Q
Characteristic symptoms of small bowel diarrhoea (esp proximally)
A
watery, large volume- cramping, bloating, flatulence
9
Q
Characteristic signs/symptoms colonic diarrhoea
A
frequent, small volume, painfulMay contain blood, mucusOft associated feverCan see RBCs + inflammatory cells in stool microscopy
10
Q
Function of action of cholera toxin
A
Exports chloride into lumen - water follows-> v. watery rice water stools
11
Q
What does oral rehydration for diarrhoea consist of
A
1L water with 6 level teaspoons of sugar and 1/2 a level teaspoon of salt- need sugar to give energy for active transport
12
Q
Typical site of campy diarrhoea pain; what are it’s late onset complications
A
Periumbilical - mimics acute appendicitisComplications - Guillan Barre Syndrome and reactive arthritis
13
Q
Site of pain in yersinia spp diarrhoea and Complications.
A
RLQ painYersinia septicaemia - in IMPAIRED IMMUNITY or IRON-OVERLOAD states
14
Q
Which antibiotics in particular can predispose to C. difficile
A
CLINDAMYCINCo-amoxiclav (penicillins)Ciprofloxacin (quinolones)Cephalosporins:- CEFUROXIME- CEFTRIAXONE- CEFALEXINAny BROAD SPECTRUM antibiotics
15
Q
Virulence factors of C. diff
A
SPORE-formingToxinGram +veAnaerobic
16
Q
When does C. diff infection typically start
A
During/up to 1 MONTH after antibiotics course
17
Q
Natural history of C. diff infection
A
Asymptomatic carriage (or -> watery diarrhoea)-> fulminant disease with severe colitis -> toxic megacolon (potentially)toxin producing C. diff can cause psudomembranous colitis - layer of dead cells creating a membrane-esq
18
Q
Management of C. diff
A
- stop inciting antibiotic as soon as possibleContact precautions/hand hygiene (hand washing > alcohol - c. diff spores not killed by alcohol)Antibiotics:- METRONIDAZOLE- VANCOMYCINStool transplant
19
Q
Investigations for diarrhoea
A
STOOL TESTS:- microscopy (blood/pus)- CULTURE- Ova, cysts and parasites x3- Toxin detection (C difficile)PCR: Multi-pathogen molecular panels (use primers for specific pathogens - typically for viruses, C. diff, campy)Blood tests:- Culture- Raised Inflammatory markers (ESR/CRP) - possible infection * Alongside anaemia = IBD/cancer- EOSINOPHILIA = PARASITES * Alongside anaemia - think hookworm- may test vomit- Electrolytes + creatinine (won’t necessarily aid diagnosis but important)Endoscopy/biopsy if necessary
20
Q
Indications for testing for diarrhoea
A
Severe illnessBloody diarrhoea/mucusHigh risk (>70, immunocomp, IBD, pregnant)Prolonged (>1 week)Public health concerns
21
Q
Diarrhoea red flags (may become severe, complications etc.)
A
DehydrationElectrolyte imbalance- RENAL FAILUREImmunocompSevere abdo painCANCER RISK FACTORS:- >50 y/o- chronic diarrhoea- weight loss- blood in stool- family history
22
Q
What is Zollinger Ellison syndrome
A
GASTRIN SECRETING TUMOUR - causes a triad- pancreatic tumour- gastric acid hypersecretion- Widespread Peptic ulcers
23
Q
GI red flags
A
Think ALARMSAnaemiaLoss of weightAnorexia (loss of appetite)Recent onset of progressive symptoms (it’s always low-level been there but it recently got worse)MASSES/MELENA (or any other GI BLEEDING)Swallowing difficulties (DYSPHAGIA)and >55 y/o- points to GI cancer
24
Q
What causes enteric fever
A
Salmonella Enterica subtypes Typhi and Paratyphi
25
Presentation of enteric fever
Generalised RLQ pain, FEVER, CHILLSHeadache, myalgiaRelative bradycardiaCONSTIPATION/green diarrhoea(Rose spots (faint salmon-colored macules on the trunk and abdomen))more common in kids/younger ppl
26
Diagnosis of enteric fever
2 large volumes of blood culture - before antibioticsGOld standard - bone marrow aspirate
27
Complications of enteric fever
GI bleedPerforation/peritonitisAbscessesMyocarditisOft need emergency surgery(typically in week 2-3)2-3% -> chronic carriers (asymp) - resides in gallbladder
28
Medical treatment for enteric fever
- azithromycin- ciprofloxacin (quinolone)- cephalosporins- meropenem
29
What is the CLO test
Campylobacter-Like Organism testit is a RAPID UREASE TEST - used for H. pylori detection
30
What is a Mallory Weiss tear
Longitudinal TEAR in tissue of LOWER OESOPHAGUS (typically only sub-/mucosa) due to SUDDEN INCREASES in INTRA-ABDOMINAL PRESSURE -> blood loss- oft caused by violent COUGHING/VOMITING (alcoholism, bulimia); hiatus hernias; weight liftingCommon in 20-50 y/o malesTypically diagnosed and treated via ENDOSCOPY- mainly LIFESTYLE CHANGES (maybe CBT/therapy for alcohol/bulimia)Symptoms:- Haematemesis (blood in VOMIT)- Melena- systemic: postural hypotension/dizziness (from blood loss) *if severe - anaemia, fatigue, SOB, shock
31
Pathophysiology of Crohn's
NOD2 mutation -> faulty GI epithelumEnteric pathogens get into wall -> T cell mediated immune response (TNFa, IL1, IL6)-> Granulomas + destruction of GI tissueCauses TRANSMURAL ULCERS, in SKIP LESIONS through the whole gut but particularly in TERMINAL ILEUM AND PROXIMAL COLON. Also, FISSURES in lining.-> COBBLESTONE APPEARANCE
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Risk factors for Crohn's
Family history(Jewish ethnicity)SMOKING (2x risk)NSAIDsCHRONIC STRESS/DEPRESSION
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Symptoms of Crohn's
ABDO PAIN (usually) in RLQMALABSORPTION:- B12, FOLATE, IRON deficiency (FATIGUE)- Increased risk of kidney/gallstones (malabsorption of bile salts)- WEIGHT LOSS, ANOREXIA- CHANGES IN BOWEL HABIT * watery diarrhoea/steatorrhoea, (melena)Extra GI:- CLUBBING- APHTHOUS ULCERS - episcleritis/uvitis- erythema nodosum/ pyoderma gangernosum- Ankylosing Spondylitis
34
Diagnosis of Crohn's
pANCA -ve (perineuclear anti-neutrophil cytoplasmic antibodies); may be ASCA +ve (antibodies to do with yeast)increased FECAL CALPROTECTIN (non-specific - present in any type of IBD)BIOPSY - transmural inflammation with non(?)-caseating granulomas
35
Treatment for Crohn's
For FLARES:- STEROIDS * mild - PREDNISOLONE * severe - HYDROCORTISONE- and Mesalazine or Sulfasalazine (5-ASA - used for IBD in general) - (or methotrexate as 2nd line) For maintaining REMISSION - immunosuppression:- AZATHIOPRINE (5-ASA)- METHOTREXATEBiologics:- INFLIXIMAB (anti-TNFa)- ustekenumab (IL 12 +23 inhib)SURGERY NOT CURATIVE BUT VERY COMMON
36
Complications of Crohn's
- PERFORATION- Perianal ABSCESSES- FISTULAS- ADHESIONS- Strictures- Small bowel obstruction
37
Pathophys of Ulcerativ colitis
AUTOIMMUNE condition linked to HLA B27 GENE (also linked to other inflam diseases e.g. ARTHRITIS (esp ankylosing spondylitis))CIRCUMFERENTIAL, CONTINUOUS inflammation extending proximally from the RECTUM to CEACUM (doesn't affect ileum) .MUCOSAL/SUBMUCOSAL ULCERS (muscularis if severe). Formation of CRYPT ABSCESSES + CRYPTITIS, GOBLET CELL DEPLETION.Ulcerated areas become granulomatous - excess tissue can form PSEUDOPOLYPSDestruction of mucosa/epithelium -> bloodLarge intestine malabsorption -> diarrhoea
38
Risk factors for UC
Family history(Jewish)- NSAIDs- CHRONIC STRESS/DEPRESSIONSMOKING IS PROTECTIVE
39
Symptoms of UC
ABDO PAIN (usually LLQ) BLOODY, watery DIARRHOEA with MUCUSTENESMUS (rectal pain on defecation)Extra GI - A PIE SAC:- ANKYLOSING SPONDYLITIS (also linked to HLA B27)- Pyoderma gnagrenosum- Iritis (ANTERIOR UVEITIS or Episcleritis)- ERYTHEMA NODOSUM (nodules + arthralgia)- SCLEROSING CHOLANGITIS- Aphthous ulcers/amyloidosis- CLUBBING
40
Diagnosis of UC
Bloods:- CRP/ESR (inflam)- WCC- iron/vit B/folate ANAEMIAS (malabs)IBD markers:- pANCA +ve - RAISED FECAL CALPROTECTIN (non-specific)COLONOSCOPY + BIOPSY (if viable - risk of perforation - GOLD STANDARD): - CONTINUOUS MUCOSAL INFLAM - CRYPT ABSCESSES + distortion- REDUCED GOBLET CELLS'lead pipe sign' on x-ray
41
Treatment for UC
Flare:- Mild: * MESALAZINE or SULFASALAZINE (salysilic acid) * PREDNISOLONE (steroid)- Moderate/severe: * Fluid resus if needed * IV STEROID (HYDROCORTISONE) * INFLIXIMABRemission:AZATHIOPRINE(METHOTREXATE - 2nd line)Ciclosporin (calcineurin inhib - not as commonly used now)Biologic:INFLIXIMAB (TNFa inhib)SURGERY IS CURATIVE (but less common in UC) - COLECTOMY is GOLD STANDARD
42
Complication of UC
TOXIC MEGACOLONalso INCREASED risk of COLON CANCER
43
UC vs Crohn's
Crohn's: - entire GI - transmural- skip lesions- fissures common- granulomas present- COBBLESTONE- Strictures common (due to scarring)- Thickened wall, narrow lumen- ADHESIONS (inflammation/surgery)- creeping fat around intestine- raised cancer riskUC: - colon/rectum- MUCOSAL/submucosal - continuous- fissures uncommon- no granulomas- PSEUDOPOLYPS- Strictures uncommon- Thin wall, dilated lumen- No adhesions- normal fat- EVEN HIGHER CANCER RISK
44
What is tropical sprue
CHRONIC bowel inflammation, acquired from TROPICS (SE asia, india, caribbean) - unknown cause
45
Signs/Symptoms of Tropical sprue
- DIARRHOEA, steatorrhoea- ABDO PAIN- WEIGHT LOSS (malabs)- Dehydration- Vit/folate/iron Anaemias - FATIGUE
46
Investigation for tropical sprue
JEJUNAL TISSUE BIOPSY (gold)- shows INCOMPLETE VILLOUS ATROPHY (* coeliac has COMPLETE villous atrophy)
47
Treatment for tropical sprue
Drink TREATED WATERTETRACYCLINE for 6mths
48
Define Coeliac disease
Autoimmune condition where exposure to gluten (wheat, barley, rye) causes MUCOSAL INFLAMMATION of SMALL BOWEL and MALABSORPTION
49
Pathophys of Coeliac disease
TYPE 4 HYPERSENSITIVITY REACTION (T CELL MEDIATED - delayed)Gluten braks down to Gliadin -> binds to IgA- travels to lamina propria -> deaminated by tTG- macrophages present it via MHC -> activates CD4+-> inflammatory cytokines-> B cells make AUTOANTIBODIES * ANTI- TISSUE TRANSGLUTAMINASE (anti-tTG) * ANTI-ENDOMYSIAL antibody (anti-EMA)-> CD8 also activated(mainly gliadin triggers immune response)Targets EPITHELIAL cells of SMALL intestineCausing:-> COMPLETE VILLOUS ATROPHY-> CRYPT HYPERPLASIA-> INTRAEPITHELIAL LYMPHOCYTES
50
Risk factors for COELIAC
- GENETIC - **HLA-DQ2** (or HLA-DQ8) * FAMILIAL LINK (10% in 1st degree relatives)- other AUTOIMMUNE conditions e.g. T1DM- IgA Deficiency
51
Signs/symptoms of Coeliac disease
- DERMATITIS HERPETIFORMIS (papules on ELBOWS, KNEES, BUTTOCKS)- Angular stomatitis- Mouth ulcers- STEATORRHOEA (pale, floating stools - fatty)- DIARRHOEA- BLOATING- Weight loss- ANAEMIA (2ndry to iron/b12/folate deficiency)- Failure to thrive (children)
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Diagnosis of Coeliac
Blood tests:- RAISED ANTI-tTG (*1st LINE*)- Raised anti-EMA (2nd)ENDOSCOPY + DUODENAL biopsy (gold)
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Management of Coeliac
LIFELONG GLUTEN-FREE diet
54
Define IBS
A chronic FUNCTIONAL bowel disorder characterised by ADBO PAIN + change in BOWEL HABITSNO ORGANIC CAUSE
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Aetiology of IBS
NO ORGANIC CAUSE- Food hypersensitivity (to short chain carbs esp)- Visceral hypersensitivity- Gut MICROBIONE alteration (bacteria metabolise sugars -> gas + bloating)
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Risk factors for IBS
FEMALEYOUNGER (peak 20-30 y/o)ANXIETY/DEPRESSION/STRESS- eating disordersPrevious GI infection
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Signs and symptoms of IBS
Think ABC- ABDOMINAL PAIN (improves with defecation)- BLOATING- CHANGE in BOWEL HABITSSymptoms worse after eating
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Types of IBS
- IBS-C (constipation)- IBS-D (diarrhoea)- IBS- M (mixed - alternte constipation/diarrhoea)- IBS unclassified (other)
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Differentials for IBS
IBDCoeliac diseaseLactose intolerenceFood allergiesGI infections
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DIagnosis of IBS
Rule out diff:- anti-tTG/anti-EMA (coeliac)- faecal calprotectin (IBD)- FBC, ESR/CRP (inflammation - IBS is NOT INFLAMMATORY)- Colonoscopy (COLORECTAL CANCER)Roman IV criteria:- RECURRENT abdo pain at least 1 DAY/WEEK for the past 3 MONTHS- BEGAN at least 6 MONTHS AGO and has 2/more of following: * RELIEVED by DEFECATION * change in bowel APPEARANCE * change in bowel FREQUENCY
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Management of IBS
Conservative:- educate/reassure- LOW FODMAP (short chain carbs) DIET- AVOID CAFFINE/ALCOHOLIf constipated - increase fluid intake + avoid lactose (causes bloating)Medical:- LOPERAMIDE (antimotility - diarrhoea)- LAXTIVES (constipation)- Antispasmodics (BUSCOPAN - for cramps)- Tricyclic antidepressants- CBT
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What are FODMAPs
FermentableOligosaccharidesDisaccharidesMonosaccharidesAndPolyolsjust remember they are short-chain carbs - poorly absorbed
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Define Gastritis
Inflammation of stomach mucosal lining
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Causes of gastritis
Acute:- HELICOBACTER PYLORI- NSAIDs- ALCOHOL abuse- STRESS (critically ill, major surgery, life events)- Ischaemia (cells stop producing mucin)Chronic:- H. PYLORI- AUTOIMMUNE
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Pathophys of NSAIDs causing gastritis
Inhibits COX-1 enzyme (cyclooxygenase)-> INHIBITS PROSTAGLANDIN SYNTHESIS -> REDUCED MUCUS secretionmucosa -> inflamed by gastric acid
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Pathophys of Autoimmune gastritis
PARIETAL cell and INTRINSIC FACTOR ANTIBODIES-> REDUCED VIT B12 absorption in terminal ileum-> PERNICIOUS ANAEMIA
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Signs/symptoms of Gastritis
- DYSPEPSIA (indigestion)- EPIGASTRIC PAIN- anorexia (loss of appetite)- nausea/vomiting (too acidic)
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Diagnosis of gastritis
- H. pylori * UREA BREATH TEST * STOOL ANTIGEN TESTNOTE: need to stop PPI at least 2 WEEKS before, and ANTIIBIOTICS at least 4 WEEKS beforeENDOSCOPY (+ biopsy)- see INFLAMMATION/atrophy + MORE PROMINANT RUGAE- Autoimmune (low B12, parietal cell antibodies, intrinsic factor antibodies - via bloods)
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Differentials for gastritis
- peptic ulcer disease- GORD- gastric CARCINOMA
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Management of gastritis
H. pylori:- Triple therapy * 1st LINE: CAP - Clarithromycin (500mg), Amoxicillin (1g), PPI (typically omeprazole) * if penicillin allergy: ClaMP - Clarithromycin (500mg), Metronidazole (400mg), PPIStop ALCOHOL or NSAIDs if relevantAutoimmune: IM VIT B12 (cyanocobalamine)
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Complications of gastritis
PEPTIC ULCERS- bleeding/anaemiaMALT lymphoma (mucosa-associated lymphoid tissue)GASTRIC CANCER
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Types of peptic ulcers
GastricDuodenal (more common)
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Causes of peptic ulcer disease (PUD)
- Gastritis (-> peptic ulcer -> gastric adenocarcinoma)- H. pylori infection- NSAIDs (tho ENTERIC COATED NSAIDs don't dissolve in stomach, only duodenum)- Alcohol excess- BILE REFLUX into stomach (mucin not designed for alkali)
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Pathophys of H. pylori infection
Live in mucus layer overlying gastric mucosa (mucin)- SYNTHESISE + secrete UREASE-> converts urea to ammonia which reacts with H+ in lumen to form AMMONIUM (toxic to gastric mucosa)-> DECREASED MUCUS - Increased INFLAMMATION (H. pylori releases chemokines -> neutrophils)-> INCREASED ACID production (gastritis -> peptic ulcer)
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Signs/symptoms of PUD
DYSPEPSIAEPIGASTRIC PAIN- Duodenal: BETTER after eating (for 1-5hrs)- Gastric: WORSE after eatingHAEMATEMESIS/MELENA (perforation of artery)
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Diagnosis of PUD
H. pylori tests- urea breath test- stool antigen testENDOSCOPY + BIOPSY (gold) - usually only if red flags present- Histology + UREASE TEST to check for H. pylori
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Treatment of PUD
Treat underlying:- stop NSAIDs- H. pylori triple therapy (CAP/ClaMP)Reduce smokng/alcohol/stress
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Description of Dyspepsia
Early satiation- AnorexiaSevere epigastric painAcidic tasteExcessive bloating/belching after mealsNausea(these are the things to look for in questions about gastritis etc. i think)
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Define GORD
Gastro-oesophageal reflux disorderReflux of gastric contents into the oesophagus due to LOWER oesophageal SPHINCTER (LOS) RELAXATION
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Risk factors for GORD
- OBESITY- Pregnancy- HIATUS HERNIAS- Smoking- NSAIDs, alcohol, caffine (increased acid)MALE (2x)
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Signs/symptoms of GORD
- HEARTBURN- REGURGITATION (worse when lying down)- Epigastric pain- Dysphagia- DYSPEPSIA- Bloating/belching- Extra-GI: * cough, asthma, DENTAL EROSION * hoarse voice
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DIagnosis of GORD
FBC - anaemia24-HOUR pH MONITORING (pH <4 for >4% of the time is ABNORMAL)UPPER GI ENDOSCOPY (typically in more severe)Manometry (change in pressure through oesophagous - to check for motility disorder)IF RED FLAGS PRESENT - 2-WEEK ENDOSCOPY REFERAL (Dysphagia OR >55 y/o WITH weight loss AND Upper abdo pain OR reflux OR dyspepsia)
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GORD management
Conservative:- Smoking cessation - Reduce alcohol intake - Lose weight (if obese) - Eat smaller meals - Avoid eating 3-4 hours before sleepingMedical:- over-counter ALGINATES (Gavison)- PPI (omeprazole, lansoprazole)- If PPI not tolerated: H2 receptor antagonist (Ranitidine - an antihistamine)Surgical:- Nissen fundoplication (fundus wrapped around back of oesophagus - secure with sutures - keeps anchored below diaphragm)
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Function of action of PPIs
Inhibit gastric secretion by blocking H+/K+ ATPase in parietal cells
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What is Barrett's oesophagus
METAPLASIA of STRATIFIED SQUAMOUS to SIMPLE COLUMNAR EPITHELIUM.- complication of GORDA PRE-MALIGNANT condition - associated with 3-5% INCREASED RISK of OESOPHAGEAL ADENOCARCINOMA (determined by degree of dysplasia)
86
Epidemiology of Barrett's oesophagus
Common in middle-aged Caucasian male
87
Diagnosis of Barrett's oesophagus
Upper GI ENDOSCOPY + BIOPSY (required)- diagnosed as Barrett's if METAPLASTIC COLUMNAR EPITHELIUM found 1/MORE CM ABOVE gastro-oesophagel junction
88
Management of Barrett's oesophagus
PPIENDOSCOPIC SURVAILLANCE
89
Differentials for Barrett's oesophagus
GORDOesophagitisOesophageal carcinoma
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Pathophys of Barrett's
Acid kills squamous cells as they have NO protective MUCINAfter acid kills squamous cells and before columanr cells grow in - the there is effectively an ulcer there - PAINFULColumnar cells grow in (metaplastic -> dysplastic -> neoplastic progression leads to oesophageal adenocarcenoma)
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Diverticulitis vs diverticulosis vs Diverticular disease
-itis = inflammation- osis = diverticula are present but not inflamedDiverticular disease = Diverticula are SYMPTOMATIC (5%) but not necessarily inflamed
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What is a diverticulum
OUTPOUCHING of colon wall, most frequently in the SIGMOID colon
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Pathophys of Diverticulitis
High PRESSURES in colon/WEAK WALL -> diverticulaFaecal matter/bacteria gather inside -> inflammation + VESSEL RUPTURE (bleeding)
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Risk factors for diverticular disease
HIGHER PRESSURES:- CONSTIPATION- Obesity- NSAIDs (enhanced permeability to toxins/bacteria due to mucosal impairment)- Smoking + COPD/chroic cough- Age
95
Sign/symptoms of Diverticular disease
think BBL:- BOWEL HABITS change- BLOATING/flatulence- LLQ PAIN- Nausea/vomitingDiverticulitis:- all of above+ FEVER+ Blood in stool
96
Complications of Diverticular disease
Infection -> ABSCESS- BOWEL PERFORATION or FISTULAE (bladder, vagina)- PERITONITIS- Haemorrhage- ObstructionRisk increases with recurrence
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Diagnosis of Diverticular disease
External exam:- tenderness + guarding (peritoneum irritated)- Distended and tympanic to percussion (gas)- Bowel sounds diminished (colon not working well)Bloods - inflammatory (ESR/CRP, WCC)COLONOSCOPY (for acute bleeds)- CONTRAINDICATED if PROFUSE BLEEDING - avoid further perforationCONTRAST CT SCAN (gold) -> US, MRI
98
Treatment of diverticular disease
Conservative:- avoid NSAIDs/opioids (increased risk of perforation)- lifestyle advice * stop smoking, weight loss, exercise * high-fibre diet if toleratedMedical (only if needed):- bulk-forming laxatives- simple analgesia (paracetamol)- antispasmodic (mebeverine) if crampingNO ANTIBIOTICS
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Treatment for diverticulitis
ORAL ANTIBIOTIC (if systemically unwell)- CO-AMOXICALV- if penicillin allergy: Cefalexin/Trimethoprim + METRONIDAZOLEIf systemically well - do same as for diverticular disease (lifestyele advice + simple analgesia)If very severe/complicated or persistant with treatment:- URGENT SURGERY (esp resection)
100
Where is McBurney's point
2/3 from umbilicus to ant sup ileac crest
101
Pathophysiology of Acute appendicitis
OBSTRUCTION in lumen of appendix -> STASIS -> bacterial OVERGROWTH -> InflammationCan rupture or form an appendix mass
102
Causes of acute appendicitis
FAECOLITH (faces stone) - most commonForeign bodiesIntestinal WORMS/PINWORMLYMPHOID HYPERPLASIA
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Epidemiology of appendicitis
PEAK in 10-30 y/o- v. common surgicalemergancy
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Signs/symptoms of Acute appendicitis
- UMBILICAL PAIN -> R Ileac Fossa PAIN (migratory)- Nausea/vomiting- Anorexia- PyrexiaOn examination:- **ROSVING SIGN** (palpating LIF causes RIF pain)- Psoas sign (RIF pain on hip extension)- Obturator sign (RIP pain on R hip flexion + internal rotation)- GUARDING- REBOUND TENDERNESS (pain on releasing pressure)
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Diagnosis of Acute appendicitis
Bloods:- WCC (very high - suggests uti), ESR/CRPABDO US (kids + preggo)ABDO CT WITH CONTRASTUrinalysis (exclude UTI)Pregnancy test (exclude ectopic preg)
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DIff diagnosis for appendicitis
Gynae:- ECTOPIC PREGNANCY- ovarian TORSION- RUPTURED ovarian CYSTGI: IBD, diverticulitis, Meckel's diverticulumGU: kidney stones, UTITesticular TORSION
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Management of appendicitis
APPENDICECTOMY(usually laproscopic - severe may require open surgery)
108
Define bowel obstruction + types of bowel obstruction
The interruption of passage through the bowel (can be surgical emergancy)- form of intestinal failure where gut is unable to absorb necessary water/nutrients/electrolytes to sustain life -> requires IV supplementation/replacement- small bowel obstruction (most common)- large bowel obstruction- pseudo obstruction
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Causes of intestinal obstruction
Intraluminal obstruction:* DIAPHRAGM DISEASE (white membrane across lumen - linked to NSAIDs) - typically small bowel* GALLSTONE ILEUS - gib stone erodes from gallbladder into small bowel* TUMOURS - bigger issue in left colon (solid faeces)Intramural obstruction:* CROHN'S (esp in ileum) - thinkening wall = strictures* DIVERTICULAR DISEASE (esp in sigmoid)* INTRAMURAL TUMOURS* HIRSCHPRUNGER'S DISEASE (babies) - AGANGLIONIC area - NO CO-ORD movement (blocks)Extraluminal obstruction:* ADHESION* PERITONEAL TUMOUR (esp ovarian carcinoma)* VOLVULUS (esp in sigmoid)
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Define adhesion and how does it cause obstruction
Band of fibrous tissue that often form during the healing process after injury (e.g. after open surgery)Can obstruct in 2 ways:- kink the bowel- press against/over bowel (compressing lumen)more common in small bowel
111
Investigations for abdo obs
1ST LINE: ABDO X-RAY (RULE OF 3/6/9)- small bowel dilation > 3cm- large bowel > 6cm = dilation- ceacum > 9cmABDO/PELVIS CT with CONTRAST = gold!Bloods:- FBC: anaemia might indicate cancer; WCC - inflam- kidney function (increased vomiting -> kidney failure)- Potential High Lactate (lactic acidosis - associated with sepsis/severe inflam)
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Signs/symptoms of small bowel obs
- COLICKY abdo pain (higher up)- DISTENSION (but less severe than if large bowel)- BILIOUS VOMITING FIRST- theeen CONSTIPATION'TINKLING' bowel SOUNDS
113
Causes of Small bowel obs
- ADHESIONS (75%) - past abdo/gynae surgery- diaphragm diseaseHERNIAS (10%) - esp INGUINAL (in groin - esp in older)Crohn'sMALIGNANCY - esp ILEOCECAL VALVE- INTUSSUSCEPTION (bowel folds inside of itself - like fingers on gloves when you take them off) * more common in CHILDREN - softer bowels - Becomes ISCAHEMIC
114
What is the coiled-spring appearance on X-rays caused by
The mucosal folds of the SMALL bowel
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Management of small/large bowel obstruction
Same for both!A-e assessmentConservative (if stable):- 'DRIP AND SUCK' * insert IV CANNULA - fluid resus ('drip') * NIL BY MOUTH (NBM) * insert NASOGASTRIC TUBE - decompress stomach ('suck')- CATHETER - monitor urine output- ANALGESIA, ANTIEMETICS, ANTIBIOTICS (as necessary)Surgical (if unstable) - depends on cause:- Laparotomy (open surgery)- Adhesiolysis for adhesions - Hernia repair/Taxis (and RESECT if ISCHAEMIC)- Tumour resections- Bowel resection(avoid surgery where possible - may cause furter scarring + cancers can spread through blood in cut)- can sometimes untwist volvulus via coloonoscopy but oft ISCHAEMIC so need to RESECT
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Causes of large bowel obs
- MALIGNANCY (90%)- SIGMOID VOLVULUS (5%) - coffee bean shape on XR- DIVERTICULITIS
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Signs/symptoms of large bowel obs
- CONTINUOUS abdo pain- SEVERE DISTENSION- CONSTIPATION FIRST- theeen VOMITING (BILIOUS then FAECAL)- ABSENT bowel SOUNDS
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What often initially contraindicates surgery in intestinal obs patients
Being starvedMost people don't eat fro ~2 DAYS before going to hospital- need to IV resus firstComorbidities may also make surgery unsuitable (esp as obs oft occurs in OLD ppl - OVER 70s)
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Findings of examination of intestinal obs patient
DEHYDRATED- wight lossPotential Low pulse/BP (3rd place loss - blood stuck in parts of intestine e.g. hernia, volvulus)Potential low O2Potential scars (from prev surgery)Abdo DISTENSIONTendernessPotential hernia (always check)Do PR exam - IF YOU CAN FEEL ALL SIDES OF RECTUM it is DEFLATED so NO GAS getting through
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What is Taxis
Analgesia + pushing hernia back through hole (if patient too high risk for hernia repair surgery)
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Complications of small bowel obs
Kidney failure (most common)Arrhythmia (from electrolyte imbalance)Lung issueDelerium
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What is intestinal pseudo-obstruction
AKA Ogilvie syndromeColonic dilation in ABSCENCE of MECHANICAL OBSTRUCTION
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Pathophys of pseudo-obs
PARASYMP NERVE DYSFUNCTION-> ABSENT SMOOTH MUSCLE(can be caused by Hirschsprung's disease but that originates due to an issue with the migration of ganglionic cells to the Meissner's (submucosa) + Auerbach's (muscularis) plexuses in the intestine. The aganglionic area is continuously contracted and narrowed)
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Investigations for intestinal pseudo-obs
1st line: Abdo XRay (megacolon → dilation >10cm )Gold standard: CT of the abdomen and pelvis with contrast (no transition zone)
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Causes of intestinal pseudo-obs
* Post-operative (paralytic ileus)/recent trauma* Neurological (Parkinson’s, multiple sclerosis, Hirschsprung's)* Medications (opioid, calcium channel blockers, antidepressants)* Electrolyte imbalance
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Management of intestinal pseudo-obs
'Drip and suck’ management **IV NEOSTIGMINE** - Acetylcholinesterase inhib (same as in myesthenia gravis)Surgical decompression for unstable patients (caecostomy, ileostomy)
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Types of Oseophageal cancer
Adenocarcinoma (common in developed world - progresses from Barrett's oesophagus - lower 1/3)Squamous cell carcinoma (more common in developing countries - upper 1/3 typically)
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Risk factors for oesophageal adenocarcinoma
GORD (and BARRETT'S)ObesityHerniasSmokingOLDER ageMALECAUCASIAN
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Risk factors for oesophageal squamous cell carcinoma
SMOKINGALCOHOLOlder ageMALEBAMEAchalasiaPlummer-Vinson syndromeHOT FOOD/BEVERAGE
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What is Plummar-Vinson syndrome? What classical triad does it present with.
Causes Oesophageal websTRIAD: - DYSPHAGIA- IRON-DEF ANAEMIA- OESOPHAGEAL WEBS
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Signs/symptoms of oesphageal cancer
PROGRESSIVE DYSPHAGIA (solids THEN liquids - both at same time more likely to be achalasia)- Odynophagia (painful swallowing)WEIGHT LOSSANOREXIAHoarse voice (if pressing on recurrent laryngeal)the GI RED FLAGS (thing ALARMS)
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When is a 2-week endoscopy (i.e urgent management) indicated
In people with:- DYSPHAGIA OR- >55 y/o with WEIGHT LOSS AND 1 of the following: * UPPER ABDO PAIN * REFLUX /N+V * Treatment resistant DYSPEPSIA * Anaemia or raised platelets
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Investigation for upper GI cancer
UPPER GI ENDOSCOPY + BIOPSYCT/MRI of chest/abdo (staging/metastases)(bloods?)
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Differentials for oesophageal cancer
AchalasiaStricturesBarrett's oesophagous
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Management of Oesophageal cancer
surgical RESECTION- ADJUVENT RADIO/CHEMOtherapyPALLIATIVE care (5yr prognosis = 25%)
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Types of gastric cancer
Type 1 (intestinal) - better prognosis- affects ANTRUM + LESSER CURVATUREType 2 (diffuse) - (5-year survival of 3-10%)- Can affect anywhere in stomach - esp CARDIA
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Pathophys of Type 1 gastric cancer
End result of inflammatory process:- CHRONIC GASTRITIS -> ATROPHIC GASTRITIS -> intestinal METAPLASIA/DYSPLASIAThe cells are WELL-DIFFERENTIATED and TUBULAR
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Pathophys of Type 2 gastric cancer
Highly metastatic neoplasm, rapid progression.Development of LINITIS PLASTICA (leather bottle stomach)Cells are POORLY DIFFERENTIATED and SIGNET RING CELLS are present
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Risk factors for Type 1 Gastric cancer
MALEOLDERChronic/atrophic gastritis:- H. PYLORI- High salt diet- Smoking/ALCOHOL- Obesity
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Risk factors for Type 2 gastric cancer
FEMALEYOUNGER (<50 y/o)BLOOD TYPE AGENETIC - subtype = Hereditary Diffuse Gastric CancerH. PYLORI
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Signs/symptoms of gastric cancer
- VIRCHOW'S NODE ENLARGEMENT (lump in LEFT SUPRACLAVICULAR area) = Troisier's sign- WEIGHT LOSS- Nausea/vomiting- Haematemesis/melaena- Dysphagia- Anorexia- Epigastric pain(think ALARMS)
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Investigations for gastric cancer
Upper GI ENDOSCOPY (GASTROSCOPY) + BIOPSYEndoscopic Ultrasound (assess depth of tumour invasion + detecting nodal involvement before surgery)CT/MRI (chest/abdo) - staging + metastases
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Management of gastric cancer
Surgical RESECTION (sub/total gastrectomy) + ADJUVANT RADIO/CHEMOTHERAPYPalliative careSupportive care
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Risk factors for bowel cancer
FAMILY HISTORY- esp HEREDITARY (autosomal dominant) conditions * Familial adenomatous polyposis * Lynch syndrome/Hereditary nonpolyposis colorectal cancer (HNPCC)IBDObesityDMSmokingAlcohol
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Pathophys of familial adenomatous polyposis
Autosomal dominant mutation in APC GENE (adenomatous polyposis coli - tumour suppressor gene) prevents it from binding to/removing BETA CATENIN which BINDS to DNA and UPREGULATES genes for EPITHELIAL PROLIFERATIONcauses increased polyp formation (covers walls of gut) in TEENS/EARLY 20S, all of which are ADENOMAS- colorectal cancer is linked with the presence of polyps (esp adenomatous) so they inevitably get bowel cancer
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Pathophys of HNPCC
Born without MLH DNA REPAIR PROTEIN- if other one later becomes non-functional -> no DNA repair proteinHigh cancer AND TRANSMISSIBLE genetic risk.
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Why is it particularly important to identify that a bowel cancer is HNPCC/Lynch syndrome
High genetic transmissability so RISK OF FURTHER CANCER in RELATIVESImplications for therapy:- Certain chemo doesn't work in HNPCC (e.g. 5-FU)- Cells DON'T RECOGNISE DNA DAMAGE- apoptosis not activated
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SIgns/symptoms of bowel cancer
Think ALARMS:ANAEMIALOSS of WEIGHT(Anorexia)(Recent onset of progressive symptoms)Masses/BLEEDING (PR BLEED in this case)(Swallowing difficulties - not so much)CHANGE IN BOWEL HABIT- TENESMUS (repeadtedly needing to empty bowels)ABDO PAIN
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Investigation for bowel cancer
- rectal exam (38% can be found this way)COLONOSCOPY + BIOPSY - gold- sigmoidoscopyCT COLONOGRAPHY (if UNFIT for colonoscopy)- uses contrast (possibly gastrografin) + can construct 3D imageCT TAP (thorax, abdo, pelvis) - staging (Duke's/TNM)Carcinoembryonic antigen (CEA) test - found in babies but higher levels in adults could indicate cancer
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What indicates that individual should be referred for suspected colorectal cancer
- OVER 40 with ABDO PAIN AND unexplained WEIGHT LOSS- OVER 50 - UNEXPLAINED RECTAL BLEEDING- OVER 60 - CHANGE in BOWEL HABIT or IRON dif ANAEMIA
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Management of bowel cancer
Surgical RESECTION (for ADENOCARCINOMAS)- (pre-malignant polyps can be removed during colonoscopy)Radio/Cehmotherapy (if METASTATIC)
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Which drugs are incidentally protective against colorectal cancer
NSAIDs (not recommended to take just for thisreason tho)
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Bowel cancer screening - which ages, frequency and what test
60-74 y/oevery 2 YEARSFAECAL IMMUNOCHEMICAL TEST (FIT)
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What is the gastrografin challange
A test used for SMALL BOWEL OBSTake up gastric content first to clearDrink 2-3 cups of GASTROGRAFIN (contrast)X-RAYS taken at (usually) 30-60 min INTERVALS - follows passage through small bowel to identify obstruction
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Signs/symptoms of oesophagel variceal rupture
HAEMATEMESIS - more like coughing it outABDO PAINSHOCK, HYPOTENSION, PALLOR
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Treatment for acute bleed from oesophageal varices
Emergancy!- ABCDETERLIPRESSIN (vasopressin analogue) for vasoconstriction- if bleeding ABNORMALITY -> VIT KSURGERY within 24HR- ENDOSCOPIC VARICEAL BAND LIGATION
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Treatment for non-ruptured oesophageal varices
PROPANOLOL (or beta blocker in general)Not super urgent Endoscopic variceal band ligationTIPS - Transjugular intrahepatic portosystemic shunt - diverts blood to larger veins (can cause hepatic ENCEPHALOPATHY - blood bypassing liver)
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Diagnosis of oesophageal varices
Upper endoscopyGraded - SIZE + RISK of BLEEDING
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Causes of oesophageal varices
PORTAL HYPERTENSION- CHIRRHOSIS- PORTAL VEIN THROMBOSIS- RIGHT HF- SCHISTOSOMIASIS (tropical fresh water worm)
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What is Zenker's diverticulum
Outpouching from pharynx - food gets stuck
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Signs/symptoms of Zenker's diverticulum
- Pseudo-choking- BAD BREATH- Infection
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Oesophageal strictures
Scarring of oesophagus -> narrowingCaused by anything that causes inflammation/scarring (e.g. GORD)
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What is Achalasia
Degeneration of ganglions in Auerbach's/myenteric plexus (muscularis propria/externa)NERVES in LOS DON'T WORK - LOS can't relax -> OBStypically in elderly
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Signs'symptoms of achalasia
DYSPHAGIA - BOTH solids AND liquids (unlike more progressive dysphagia in cancer)Heart burnFOOD REGURGITATION -> ASPIRATION PNEUMONIA
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Investigations for Achalasia
ENDOSCOPYBarium SWALLOW - BIRD'S BEAK SIGNMANOMETRY (change in pressure) - gold
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Treatment for achalasia
LIFESTYLE - smaller, more frequent mealsNITRATES or CCB (nifedipine/verapamil) - relax LOSBotox - relax LOSSurgery - cardiomyotomy (surgery of cardia in oesophagus)- could lead to GORD
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What is the standard investigation for any GI bleeds/dysphagia
ENDOSCOPY
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What covers the stomach lining
MUCIN (protects from acid + where H. pylori live during infection)
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Stomach changes in chronic H. pylori infection
Can get INTESTINAL METAPLASIA- slight population predisposition for gastric cancer
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Complications of peptic ulcers
Severe haemorrhage - erosion into gastroduodenal artery (duodenal ulcer) AND into left gastric artery (gastric ulcer)-> perforation into peritoneum -> peritonitis- duodenal ulcers can cause pancreatitis
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Appearance of peptic ulcers
Typically look PUNCHED OUT with a clean border- raised inflam border may indicate cancer
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Treatment of haemodynamically stable non variceal GI bleed
Typically from ulcersTreated via endoscopy:- Inject adrenaline into base of ulcer (vasoconstriction)- Ligate with clips - can also use themal coagulation, fibrin or thrombin
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Important organisms associated with DIarrhoea
- *Salmonella enterica* serotype Enteritidis- *Salmonella enterica* serotype Typhi- Shigella sonnei- Escherichia coli O157:H7 (EHEC)- Campylobacter jejuni- Helicobacter pylori- Cryptosporidium parvum- Rotavirus
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Salmonella enterica subsp enterica serotype Enteritidis
- Poultry + eggs (widepread in nature)- Incubation period 12-36h -> fever- Antibiotics not usually required
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Salmonella enterica serotype Typhi (Paratyphi)
- Usually travellers from TROPICS/developing- Usually waterborne (canned meat, shellfish)- Carriage in gall bladder- Incubation 12->14 days -> ENTERIC FEVER + SEPTICAEMIA- Treat with CIPROFLOXACIN
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Shigella sonnei
- Non-motile + anaerogenic- Inc. period 1-7d (usually <4)- Usually mild, can lead to dysentry- Usually self-limiting- Treatment rarely antibiotics, ocassionally rehydration- FAECO-ORAL SPREAD- YOUNG CHILDREN, NURSERY SCHOOLS etc.
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Escherichia coli O157 (EHEC)
- lactose fermenting (red on MacConkey)- Vero cells make verocytotoxins- Inc. period 2-10d- HAEMORRHAGIC COLITIS - less common serious HAEMOLYTIC URAEMIC SYNDROME - ACUTE RENAL FAILURE, THROMBOCYTOPAENIA, Microacgiopathic HAEMOLYTIC ANAEMIA- Usually self-limiting- More common in US- FARM ANIMALS (cattle) -> RAW/partially cooked GROUND BEEF- LOW INFECTIVE DOSE
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Campylobacter jejuni
- Gram -ve + SPIRAL- 42C optimal, needs selective medium- Inc. period 3-5d- Sometimes SEVERE ABDO PAIN and/or BLOODY STOOLS, FEVER - Acute is self-limiting- CHRONIC: - CIPROFLOXACIN - ERYTHROMYCIN- common in UK- ANIMAL carriage esp BIRDS-> UNDERCOOKED CHICKEN- LOW INFECTIVE DOSE
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Helicobacter pylori
- G -ve SPIRAL- UREASE POSITIVE- Detected from normally sterile site- CHRONIC ACTIVE GASTRITIS, PUD, GASTRIC MALIGNANCIES- *cag*A gene- UREA BRETH TEST, ENDOSCOPY (CLO test), ELISA- Eradication can make gastric B-cell lymphma REGRESS- Treatment: CAP or ClaMP
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Cryptosporidium parvum
- Detect OOCYSTS (resistant to cholrine)- modified ZIEHL-NEELSEN satin- Inc. period 4-14d- Sometimes flu-like (malaise, fever etc)- More common in DEVELOPING countries- CHILDREN+ IMMUNOCOMPROMISED- WATERBORNE, ZOONOTIC, PERSON-PERSON- LOW INFECTIVE dose- Possible treatment - CHEMO: spiramycin, paramomycin
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Rotavirus
- INFANTS (high mortality in developing)- Inc. period 1-7d- FAECO-ORAL, WATER, ?Food- VOMITING (sometimes projectile) - may have associated upper resp infection- adults oft asymp or wide variety of symps- Usually SELF-LIMITING after 2-3D- ocassional death from dehydration- AUTUMN + EARLY WINTER- INSTITUTIONAL- RESISTANT TO MANY DISINFECTANT- LOW INFECTIVE DOSE- STOOL ANTIGEN TESTING- Isolation + barrier nursing
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Define gastroenteritis
A syndrome characterised by gastrointestinal symptoms including:- nausea- vomiting- diarrhoea - abdominal discomfort
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What is systemic sclerosis
Muscles not working - covered in MSK- a cause of SWALLOWING DIFFICULTIES
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Conditions linked to swallowing difficulties
- Achalasia- Oesophageal cancer- Zeneker's Diverticulum- Strictures- Systemic sclerosis
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Pathophys of chronic mesenteric ischaemia
Atherosclerotic narrowing of GI blood vessels (in mesentry) causing decreased supply to bowel
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Risk factors for Chronic mesenteric ischaemia
Same as cardio risks- Obesity, hypercholesteroaemia, sedentry lifestyle etc
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Signs/symptoms of chronic mesenteric ischaemia
- **Central colicky abdominal pain after eating** (aka postprandial pain)- Weight loss (eating causes pain)- Abdominal bruit (due to turbulent blood flow)
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Main investigation for chronic mesenteric ischaemia
CT contrast/ANGIOGRAPHY
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Management of Chronic mesenteric ischaemia
lifestyle, secondary prevention, surgery
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Pathophys of Acute mesenteric ischaemia
Rapid blockage of mesenteric vessels leading to Ischaemia -> INFARCTION- necrosis + perforation- sepsis- peritonitisSuperiour mesenteric artery most commonly affectes - small bowel almost always affected
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Risk factors for Acute mesenteric ischaemia
- ATRIAL FIBRILATION (blood clots)- Same as cardiac risk factors
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Causes of acute mesenteric ischaemia
ThromboembolismVasospasmHernia (strangulated)
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Signs/symps + Dx + Tx of acute mesenteric ischaemia
- Classical triad: - Severe central colicky abdominal pain - worse postprandial - Abdominal bruit / cardiac issues (AF/aneurysm) - Rapid hypovolemia → shock (pallor, weak rapid pulse etc) (blood trapped in vessels)- Nausea and vomiting- Melena/ haematochezia- Increasing abdominal distensionAmylase is often raised so check- 1st line = bloods + ABG- CT with IV contrastTx = Surgery (resection or revascularisation) + fluid resus, catheter- Prophylactic Abx if confirmed
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Ischaemic colitis
Most common ischaemic bowel disease- **Splenic flexure** most commonly affected, despite dual supply from SMA and IMA, as it is the most **distal**- **Rectum is resistant** to ischaemia due to dual supply from **IMA and internal iliac artery**Same S&S, investigation + management as Acute mesenteric ischaemia except- PAIN in LEFT ABDO
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Define pseudomembranous colitis
Inflammation of the colon due to overgrowth of Clostridium difficile and a recent history of antibiotic use.Creates a membranous appearance due to layer of dead cells. Caused by certain types of C. diff with toxins
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Risk factors for pseudomembranous colitis
- Recent antibiotic use - Staying in a hospital/ nursing home- Older age (>65yo)- Use of PPI- IBD - Immunocompromised - CMV infection (OWL'S EYE bodies)
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Investigations for pseudomembranous colitis
- Blood test (raised WCC = leukocytosis) - Stool sample (C.difficile infection) - Abdominal XRay or CT abdomen (colonic dilatation) - Colonoscopy (raised yellow plaques)- Histology (owl eyes inclusion body for CMV)
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Management of pseudomembranous colitis
- Stop causative agent - Start another antibiotic that is effective against C.difficile - Oral fidaxomicin, **vancomycin, metronidazole**- **Hydration and electrolyte** replacement Infection control:- Hand hygiene - Private rooms Faecal microbiota transplant (if recurrence)
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Anal issues
HaemorrhoidsAnal fissureAnal fistulaPilonidal sinus/abscessPerianal/Anorectal AbscessLOOK AT PTS AND Haroon's notes
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How long deos a typical case of gastritis from food last
around 48 hrs
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Define Meckel's diverticulum + pathophys
Commonest CONGENITAL MALFORMATION of the small bowel.A true diverticulum caused by the failure of the vitelline duct (communication between yolk sac + midgut) to obliterate during 5th week of fetal development.
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Presentation of Mecklel's diverticulum
- Age <2 years - more common in males- Haematochezia - bleeding could -> hypotension/tachycardia- Small bowel obs common - Intractable constipation (complete/severe) - indicative - N+V - abdo cramps- Periumbilical pain radiating to RLQ (like apendicitis) = Meckel's diverticulitis - more common in older- Diffuse tenderness if perforation -> peritonitis- Uncommonly can feel abdo mass - could indicate intussusception at diverticulum
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Investigations for Meckel's diverticulum
- FBC (low Hb/Hct if bleeding; leukocytosis with left shift - inflam)- **Technetium-99m prertechnetate (Meckel's) scan - enhancement of diverticulum**- CT abdo/pelvis- Abdo US - may show intussuseption, diverticulitis or bowel obs - if intussuseption suspected -> contrast enema- Mesenteric angiography if bleeding - can localise but less useful than Meckel's scan- **ENDOSCOPIC EXPLORATION (diagnostic)**- surgical exploration (if necessary)
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Treatment of Meckel's diverticulum
Asymp = no treatment (but if detected during surgery for something else - may excise)Symptomatic:- EXCISION OF DIVERTICULUM (+ oposing region of ileum if bleeding) - may resect segment of small bowel if perforation + peritonitis- lysis of any adhesions present- consider blood transfusion if necessary
