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Take 2: Electric Boogaloo > Phase 2 - GI > Flashcards

Phase 2 - GI Flashcards

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)

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2
Q

Non-infective causes of diarrhoea

A

CancerRadiationChemicals- Poisoning- sweeteners- medications Inflammatory bowel diseaseIBS / malabsorptionEndocrine/hormonal eg ThyrotoxicosisAnatomical e.g. post colesectomy

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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
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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?)
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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
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6
Q

Which mirobes are associated with fresh water/swimming

A

CryptosporidiumGiardiaAeromonas

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7
Q

Which animals are particularly associated with diarrhoea causing pathogens

A

Reptiles - salmonellaPuppies - campy

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8
Q

Characteristic symptoms of small bowel diarrhoea (esp proximally)

A

watery, large volume- cramping, bloating, flatulence

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9
Q

Characteristic signs/symptoms colonic diarrhoea

A

frequent, small volume, painfulMay contain blood, mucusOft associated feverCan see RBCs + inflammatory cells in stool microscopy

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10
Q

Function of action of cholera toxin

A

Exports chloride into lumen - water follows-> v. watery rice water stools

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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

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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

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13
Q

Site of pain in yersinia spp diarrhoea and Complications.

A

RLQ painYersinia septicaemia - in IMPAIRED IMMUNITY or IRON-OVERLOAD states

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14
Q

Which antibiotics in particular can predispose to C. difficile

A

CLINDAMYCINCo-amoxiclav (penicillins)Ciprofloxacin (quinolones)Cephalosporins:- CEFUROXIME- CEFTRIAXONE- CEFALEXINAny BROAD SPECTRUM antibiotics

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15
Q

Virulence factors of C. diff

A

SPORE-formingToxinGram +veAnaerobic

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16
Q

When does C. diff infection typically start

A

During/up to 1 MONTH after antibiotics course

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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

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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
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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

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20
Q

Indications for testing for diarrhoea

A

Severe illnessBloody diarrhoea/mucusHigh risk (>70, immunocomp, IBD, pregnant)Prolonged (>1 week)Public health concerns

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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

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22
Q

What is Zollinger Ellison syndrome

A

GASTRIN SECRETING TUMOUR - causes a triad- pancreatic tumour- gastric acid hypersecretion- Widespread Peptic ulcers

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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

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24
Q

What causes enteric fever

A

Salmonella Enterica subtypes Typhi and Paratyphi

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25
Q

Presentation of enteric fever

A

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

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26
Q

Diagnosis of enteric fever

A

2 large volumes of blood culture - before antibioticsGOld standard - bone marrow aspirate

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27
Q

Complications of enteric fever

A

GI bleedPerforation/peritonitisAbscessesMyocarditisOft need emergency surgery(typically in week 2-3)2-3% -> chronic carriers (asymp) - resides in gallbladder

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28
Q

Medical treatment for enteric fever

A
  • azithromycin- ciprofloxacin (quinolone)- cephalosporins- meropenem
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29
Q

What is the CLO test

A

Campylobacter-Like Organism testit is a RAPID UREASE TEST - used for H. pylori detection

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30
Q

What is a Mallory Weiss tear

A

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

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31
Q

Pathophysiology of Crohn’s

A

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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32
Q

Risk factors for Crohn’s

A

Family history(Jewish ethnicity)SMOKING (2x risk)NSAIDsCHRONIC STRESS/DEPRESSION

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33
Q

Symptoms of Crohn’s

A

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

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34
Q

Diagnosis of Crohn’s

A

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

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35
Q

Treatment for Crohn’s

A

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

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36
Q

Complications of Crohn’s

A
  • PERFORATION- Perianal ABSCESSES- FISTULAS- ADHESIONS- Strictures- Small bowel obstruction
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37
Q

Pathophys of Ulcerativ colitis

A

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

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38
Q

Risk factors for UC

A

Family history(Jewish)- NSAIDs- CHRONIC STRESS/DEPRESSIONSMOKING IS PROTECTIVE

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39
Q

Symptoms of UC

A

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

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40
Q

Diagnosis of UC

A

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

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41
Q

Treatment for UC

A

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

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42
Q

Complication of UC

A

TOXIC MEGACOLONalso INCREASED risk of COLON CANCER

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43
Q

UC vs Crohn’s

A

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

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44
Q

What is tropical sprue

A

CHRONIC bowel inflammation, acquired from TROPICS (SE asia, india, caribbean) - unknown cause

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45
Q

Signs/Symptoms of Tropical sprue

A
  • DIARRHOEA, steatorrhoea- ABDO PAIN- WEIGHT LOSS (malabs)- Dehydration- Vit/folate/iron Anaemias - FATIGUE
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46
Q

Investigation for tropical sprue

A

JEJUNAL TISSUE BIOPSY (gold)- shows INCOMPLETE VILLOUS ATROPHY (* coeliac has COMPLETE villous atrophy)

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47
Q

Treatment for tropical sprue

A

Drink TREATED WATERTETRACYCLINE for 6mths

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48
Q

Define Coeliac disease

A

Autoimmune condition where exposure to gluten (wheat, barley, rye) causes MUCOSAL INFLAMMATION of SMALL BOWEL and MALABSORPTION

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49
Q

Pathophys of Coeliac disease

A

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

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50
Q

Risk factors for COELIAC

A
  • GENETIC - HLA-DQ2 (or HLA-DQ8) * FAMILIAL LINK (10% in 1st degree relatives)- other AUTOIMMUNE conditions e.g. T1DM- IgA Deficiency
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51
Q

Signs/symptoms of Coeliac disease

A
  • 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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52
Q

Diagnosis of Coeliac

A

Blood tests:- RAISED ANTI-tTG (1st LINE)- Raised anti-EMA (2nd)ENDOSCOPY + DUODENAL biopsy (gold)

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53
Q

Management of Coeliac

A

LIFELONG GLUTEN-FREE diet

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54
Q

Define IBS

A

A chronic FUNCTIONAL bowel disorder characterised by ADBO PAIN + change in BOWEL HABITSNO ORGANIC CAUSE

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55
Q

Aetiology of IBS

A

NO ORGANIC CAUSE- Food hypersensitivity (to short chain carbs esp)- Visceral hypersensitivity- Gut MICROBIONE alteration (bacteria metabolise sugars -> gas + bloating)

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56
Q

Risk factors for IBS

A

FEMALEYOUNGER (peak 20-30 y/o)ANXIETY/DEPRESSION/STRESS- eating disordersPrevious GI infection

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57
Q

Signs and symptoms of IBS

A

Think ABC- ABDOMINAL PAIN (improves with defecation)- BLOATING- CHANGE in BOWEL HABITSSymptoms worse after eating

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58
Q

Types of IBS

A
  • IBS-C (constipation)- IBS-D (diarrhoea)- IBS- M (mixed - alternte constipation/diarrhoea)- IBS unclassified (other)
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59
Q

Differentials for IBS

A

IBDCoeliac diseaseLactose intolerenceFood allergiesGI infections

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60
Q

DIagnosis of IBS

A

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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61
Q

Management of IBS

A

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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62
Q

What are FODMAPs

A

FermentableOligosaccharidesDisaccharidesMonosaccharidesAndPolyolsjust remember they are short-chain carbs - poorly absorbed

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63
Q

Define Gastritis

A

Inflammation of stomach mucosal lining

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64
Q

Causes of gastritis

A

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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65
Q

Pathophys of NSAIDs causing gastritis

A

Inhibits COX-1 enzyme (cyclooxygenase)-> INHIBITS PROSTAGLANDIN SYNTHESIS -> REDUCED MUCUS secretionmucosa -> inflamed by gastric acid

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66
Q

Pathophys of Autoimmune gastritis

A

PARIETAL cell and INTRINSIC FACTOR ANTIBODIES-> REDUCED VIT B12 absorption in terminal ileum-> PERNICIOUS ANAEMIA

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67
Q

Signs/symptoms of Gastritis

A
  • DYSPEPSIA (indigestion)- EPIGASTRIC PAIN- anorexia (loss of appetite)- nausea/vomiting (too acidic)
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68
Q

Diagnosis of gastritis

A
  • 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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69
Q

Differentials for gastritis

A
  • peptic ulcer disease- GORD- gastric CARCINOMA
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70
Q

Management of gastritis

A

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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71
Q

Complications of gastritis

A

PEPTIC ULCERS- bleeding/anaemiaMALT lymphoma (mucosa-associated lymphoid tissue)GASTRIC CANCER

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72
Q

Types of peptic ulcers

A

GastricDuodenal (more common)

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73
Q

Causes of peptic ulcer disease (PUD)

A
  • 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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74
Q

Pathophys of H. pylori infection

A

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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75
Q

Signs/symptoms of PUD

A

DYSPEPSIAEPIGASTRIC PAIN- Duodenal: BETTER after eating (for 1-5hrs)- Gastric: WORSE after eatingHAEMATEMESIS/MELENA (perforation of artery)

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76
Q

Diagnosis of PUD

A

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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77
Q

Treatment of PUD

A

Treat underlying:- stop NSAIDs- H. pylori triple therapy (CAP/ClaMP)Reduce smokng/alcohol/stress

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78
Q

Description of Dyspepsia

A

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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79
Q

Define GORD

A

Gastro-oesophageal reflux disorderReflux of gastric contents into the oesophagus due to LOWER oesophageal SPHINCTER (LOS) RELAXATION

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80
Q

Risk factors for GORD

A
  • OBESITY- Pregnancy- HIATUS HERNIAS- Smoking- NSAIDs, alcohol, caffine (increased acid)MALE (2x)
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81
Q

Signs/symptoms of GORD

A
  • HEARTBURN- REGURGITATION (worse when lying down)- Epigastric pain- Dysphagia- DYSPEPSIA- Bloating/belching- Extra-GI: * cough, asthma, DENTAL EROSION * hoarse voice
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82
Q

DIagnosis of GORD

A

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)

83
Q

GORD management

A

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)

84
Q

Function of action of PPIs

A

Inhibit gastric secretion by blocking H+/K+ ATPase in parietal cells

85
Q

What is Barrett’s oesophagus

A

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
Q

Epidemiology of Barrett’s oesophagus

A

Common in middle-aged Caucasian male

87
Q

Diagnosis of Barrett’s oesophagus

A

Upper GI ENDOSCOPY + BIOPSY (required)- diagnosed as Barrett’s if METAPLASTIC COLUMNAR EPITHELIUM found 1/MORE CM ABOVE gastro-oesophagel junction

88
Q

Management of Barrett’s oesophagus

A

PPIENDOSCOPIC SURVAILLANCE

89
Q

Differentials for Barrett’s oesophagus

A

GORDOesophagitisOesophageal carcinoma

90
Q

Pathophys of Barrett’s

A

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)

91
Q

Diverticulitis vs diverticulosis vs Diverticular disease

A

-itis = inflammation- osis = diverticula are present but not inflamedDiverticular disease = Diverticula are SYMPTOMATIC (5%) but not necessarily inflamed

92
Q

What is a diverticulum

A

OUTPOUCHING of colon wall, most frequently in the SIGMOID colon

93
Q

Pathophys of Diverticulitis

A

High PRESSURES in colon/WEAK WALL -> diverticulaFaecal matter/bacteria gather inside -> inflammation + VESSEL RUPTURE (bleeding)

94
Q

Risk factors for diverticular disease

A

HIGHER PRESSURES:- CONSTIPATION- Obesity- NSAIDs (enhanced permeability to toxins/bacteria due to mucosal impairment)- Smoking + COPD/chroic cough- Age

95
Q

Sign/symptoms of Diverticular disease

A

think BBL:- BOWEL HABITS change- BLOATING/flatulence- LLQ PAIN- Nausea/vomitingDiverticulitis:- all of above+ FEVER+ Blood in stool

96
Q

Complications of Diverticular disease

A

Infection -> ABSCESS- BOWEL PERFORATION or FISTULAE (bladder, vagina)- PERITONITIS- Haemorrhage- ObstructionRisk increases with recurrence

97
Q

Diagnosis of Diverticular disease

A

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
Q

Treatment of diverticular disease

A

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

99
Q

Treatment for diverticulitis

A

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
Q

Where is McBurney’s point

A

2/3 from umbilicus to ant sup ileac crest

101
Q

Pathophysiology of Acute appendicitis

A

OBSTRUCTION in lumen of appendix -> STASIS -> bacterial OVERGROWTH -> InflammationCan rupture or form an appendix mass

102
Q

Causes of acute appendicitis

A

FAECOLITH (faces stone) - most commonForeign bodiesIntestinal WORMS/PINWORMLYMPHOID HYPERPLASIA

103
Q

Epidemiology of appendicitis

A

PEAK in 10-30 y/o- v. common surgicalemergancy

104
Q

Signs/symptoms of Acute appendicitis

A
  • 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)
105
Q

Diagnosis of Acute appendicitis

A

Bloods:- WCC (very high - suggests uti), ESR/CRPABDO US (kids + preggo)ABDO CT WITH CONTRASTUrinalysis (exclude UTI)Pregnancy test (exclude ectopic preg)

106
Q

DIff diagnosis for appendicitis

A

Gynae:- ECTOPIC PREGNANCY- ovarian TORSION- RUPTURED ovarian CYSTGI: IBD, diverticulitis, Meckel’s diverticulumGU: kidney stones, UTITesticular TORSION

107
Q

Management of appendicitis

A

APPENDICECTOMY(usually laproscopic - severe may require open surgery)

108
Q

Define bowel obstruction + types of bowel obstruction

A

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

109
Q

Causes of intestinal obstruction

A

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)

110
Q

Define adhesion and how does it cause obstruction

A

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
Q

Investigations for abdo obs

A

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)

112
Q

Signs/symptoms of small bowel obs

A
  • COLICKY abdo pain (higher up)- DISTENSION (but less severe than if large bowel)- BILIOUS VOMITING FIRST- theeen CONSTIPATION’TINKLING’ bowel SOUNDS
113
Q

Causes of Small bowel obs

A
  • 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
Q

What is the coiled-spring appearance on X-rays caused by

A

The mucosal folds of the SMALL bowel

115
Q

Management of small/large bowel obstruction

A

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

116
Q

Causes of large bowel obs

A
  • MALIGNANCY (90%)- SIGMOID VOLVULUS (5%) - coffee bean shape on XR- DIVERTICULITIS
117
Q

Signs/symptoms of large bowel obs

A
  • CONTINUOUS abdo pain- SEVERE DISTENSION- CONSTIPATION FIRST- theeen VOMITING (BILIOUS then FAECAL)- ABSENT bowel SOUNDS
118
Q

What often initially contraindicates surgery in intestinal obs patients

A

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)

119
Q

Findings of examination of intestinal obs patient

A

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

120
Q

What is Taxis

A

Analgesia + pushing hernia back through hole (if patient too high risk for hernia repair surgery)

121
Q

Complications of small bowel obs

A

Kidney failure (most common)Arrhythmia (from electrolyte imbalance)Lung issueDelerium

122
Q

What is intestinal pseudo-obstruction

A

AKA Ogilvie syndromeColonic dilation in ABSCENCE of MECHANICAL OBSTRUCTION

123
Q

Pathophys of pseudo-obs

A

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)

124
Q

Investigations for intestinal pseudo-obs

A

1st line: Abdo XRay (megacolon → dilation >10cm )Gold standard: CT of the abdomen and pelvis with contrast (no transition zone)

125
Q

Causes of intestinal pseudo-obs

A
  • Post-operative (paralytic ileus)/recent trauma* Neurological (Parkinson’s, multiple sclerosis, Hirschsprung’s)* Medications (opioid, calcium channel blockers, antidepressants)* Electrolyte imbalance
126
Q

Management of intestinal pseudo-obs

A

‘Drip and suck’ management IV NEOSTIGMINE - Acetylcholinesterase inhib (same as in myesthenia gravis)Surgical decompression for unstable patients (caecostomy, ileostomy)

127
Q

Types of Oseophageal cancer

A

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)

128
Q

Risk factors for oesophageal adenocarcinoma

A

GORD (and BARRETT’S)ObesityHerniasSmokingOLDER ageMALECAUCASIAN

129
Q

Risk factors for oesophageal squamous cell carcinoma

A

SMOKINGALCOHOLOlder ageMALEBAMEAchalasiaPlummer-Vinson syndromeHOT FOOD/BEVERAGE

130
Q

What is Plummar-Vinson syndrome? What classical triad does it present with.

A

Causes Oesophageal websTRIAD: - DYSPHAGIA- IRON-DEF ANAEMIA- OESOPHAGEAL WEBS

131
Q

Signs/symptoms of oesphageal cancer

A

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)

132
Q

When is a 2-week endoscopy (i.e urgent management) indicated

A

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

133
Q

Investigation for upper GI cancer

A

UPPER GI ENDOSCOPY + BIOPSYCT/MRI of chest/abdo (staging/metastases)(bloods?)

134
Q

Differentials for oesophageal cancer

A

AchalasiaStricturesBarrett’s oesophagous

135
Q

Management of Oesophageal cancer

A

surgical RESECTION- ADJUVENT RADIO/CHEMOtherapyPALLIATIVE care (5yr prognosis = 25%)

136
Q

Types of gastric cancer

A

Type 1 (intestinal) - better prognosis- affects ANTRUM + LESSER CURVATUREType 2 (diffuse) - (5-year survival of 3-10%)- Can affect anywhere in stomach - esp CARDIA

137
Q

Pathophys of Type 1 gastric cancer

A

End result of inflammatory process:- CHRONIC GASTRITIS -> ATROPHIC GASTRITIS -> intestinal METAPLASIA/DYSPLASIAThe cells are WELL-DIFFERENTIATED and TUBULAR

138
Q

Pathophys of Type 2 gastric cancer

A

Highly metastatic neoplasm, rapid progression.Development of LINITIS PLASTICA (leather bottle stomach)Cells are POORLY DIFFERENTIATED and SIGNET RING CELLS are present

139
Q

Risk factors for Type 1 Gastric cancer

A

MALEOLDERChronic/atrophic gastritis:- H. PYLORI- High salt diet- Smoking/ALCOHOL- Obesity

140
Q

Risk factors for Type 2 gastric cancer

A

FEMALEYOUNGER (<50 y/o)BLOOD TYPE AGENETIC - subtype = Hereditary Diffuse Gastric CancerH. PYLORI

141
Q

Signs/symptoms of gastric cancer

A
  • VIRCHOW’S NODE ENLARGEMENT (lump in LEFT SUPRACLAVICULAR area) = Troisier’s sign- WEIGHT LOSS- Nausea/vomiting- Haematemesis/melaena- Dysphagia- Anorexia- Epigastric pain(think ALARMS)
142
Q

Investigations for gastric cancer

A

Upper GI ENDOSCOPY (GASTROSCOPY) + BIOPSYEndoscopic Ultrasound (assess depth of tumour invasion + detecting nodal involvement before surgery)CT/MRI (chest/abdo) - staging + metastases

143
Q

Management of gastric cancer

A

Surgical RESECTION (sub/total gastrectomy) + ADJUVANT RADIO/CHEMOTHERAPYPalliative careSupportive care

144
Q

Risk factors for bowel cancer

A

FAMILY HISTORY- esp HEREDITARY (autosomal dominant) conditions * Familial adenomatous polyposis * Lynch syndrome/Hereditary nonpolyposis colorectal cancer (HNPCC)IBDObesityDMSmokingAlcohol

145
Q

Pathophys of familial adenomatous polyposis

A

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

146
Q

Pathophys of HNPCC

A

Born without MLH DNA REPAIR PROTEIN- if other one later becomes non-functional -> no DNA repair proteinHigh cancer AND TRANSMISSIBLE genetic risk.

147
Q

Why is it particularly important to identify that a bowel cancer is HNPCC/Lynch syndrome

A

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

148
Q

SIgns/symptoms of bowel cancer

A

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

149
Q

Investigation for bowel cancer

A
  • 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
150
Q

What indicates that individual should be referred for suspected colorectal cancer

A
  • OVER 40 with ABDO PAIN AND unexplained WEIGHT LOSS- OVER 50 - UNEXPLAINED RECTAL BLEEDING- OVER 60 - CHANGE in BOWEL HABIT or IRON dif ANAEMIA
151
Q

Management of bowel cancer

A

Surgical RESECTION (for ADENOCARCINOMAS)- (pre-malignant polyps can be removed during colonoscopy)Radio/Cehmotherapy (if METASTATIC)

152
Q

Which drugs are incidentally protective against colorectal cancer

A

NSAIDs (not recommended to take just for thisreason tho)

153
Q

Bowel cancer screening - which ages, frequency and what test

A

60-74 y/oevery 2 YEARSFAECAL IMMUNOCHEMICAL TEST (FIT)

154
Q

What is the gastrografin challange

A

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

155
Q

Signs/symptoms of oesophagel variceal rupture

A

HAEMATEMESIS - more like coughing it outABDO PAINSHOCK, HYPOTENSION, PALLOR

156
Q

Treatment for acute bleed from oesophageal varices

A

Emergancy!- ABCDETERLIPRESSIN (vasopressin analogue) for vasoconstriction- if bleeding ABNORMALITY -> VIT KSURGERY within 24HR- ENDOSCOPIC VARICEAL BAND LIGATION

157
Q

Treatment for non-ruptured oesophageal varices

A

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)

158
Q

Diagnosis of oesophageal varices

A

Upper endoscopyGraded - SIZE + RISK of BLEEDING

159
Q

Causes of oesophageal varices

A

PORTAL HYPERTENSION- CHIRRHOSIS- PORTAL VEIN THROMBOSIS- RIGHT HF- SCHISTOSOMIASIS (tropical fresh water worm)

160
Q

What is Zenker’s diverticulum

A

Outpouching from pharynx - food gets stuck

161
Q

Signs/symptoms of Zenker’s diverticulum

A
  • Pseudo-choking- BAD BREATH- Infection
162
Q

Oesophageal strictures

A

Scarring of oesophagus -> narrowingCaused by anything that causes inflammation/scarring (e.g. GORD)

163
Q

What is Achalasia

A

Degeneration of ganglions in Auerbach’s/myenteric plexus (muscularis propria/externa)NERVES in LOS DON’T WORK - LOS can’t relax -> OBStypically in elderly

164
Q

Signs’symptoms of achalasia

A

DYSPHAGIA - BOTH solids AND liquids (unlike more progressive dysphagia in cancer)Heart burnFOOD REGURGITATION -> ASPIRATION PNEUMONIA

165
Q

Investigations for Achalasia

A

ENDOSCOPYBarium SWALLOW - BIRD’S BEAK SIGNMANOMETRY (change in pressure) - gold

166
Q

Treatment for achalasia

A

LIFESTYLE - smaller, more frequent mealsNITRATES or CCB (nifedipine/verapamil) - relax LOSBotox - relax LOSSurgery - cardiomyotomy (surgery of cardia in oesophagus)- could lead to GORD

167
Q

What is the standard investigation for any GI bleeds/dysphagia

A

ENDOSCOPY

168
Q

What covers the stomach lining

A

MUCIN (protects from acid + where H. pylori live during infection)

169
Q

Stomach changes in chronic H. pylori infection

A

Can get INTESTINAL METAPLASIA- slight population predisposition for gastric cancer

170
Q

Complications of peptic ulcers

A

Severe haemorrhage - erosion into gastroduodenal artery (duodenal ulcer) AND into left gastric artery (gastric ulcer)-> perforation into peritoneum -> peritonitis- duodenal ulcers can cause pancreatitis

171
Q

Appearance of peptic ulcers

A

Typically look PUNCHED OUT with a clean border- raised inflam border may indicate cancer

172
Q

Treatment of haemodynamically stable non variceal GI bleed

A

Typically from ulcersTreated via endoscopy:- Inject adrenaline into base of ulcer (vasoconstriction)- Ligate with clips - can also use themal coagulation, fibrin or thrombin

173
Q

Important organisms associated with DIarrhoea

A
  • Salmonella enterica serotype Enteritidis- Salmonella enterica serotype Typhi- Shigella sonnei- Escherichia coli O157:H7 (EHEC)- Campylobacter jejuni- Helicobacter pylori- Cryptosporidium parvum- Rotavirus
174
Q

Salmonella enterica subsp enterica serotype Enteritidis

A
  • Poultry + eggs (widepread in nature)- Incubation period 12-36h -> fever- Antibiotics not usually required
175
Q

Salmonella enterica serotype Typhi (Paratyphi)

A
  • Usually travellers from TROPICS/developing- Usually waterborne (canned meat, shellfish)- Carriage in gall bladder- Incubation 12->14 days -> ENTERIC FEVER + SEPTICAEMIA- Treat with CIPROFLOXACIN
176
Q

Shigella sonnei

A
  • 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.
177
Q

Escherichia coli O157 (EHEC)

A
  • 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
178
Q

Campylobacter jejuni

A
  • 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
179
Q

Helicobacter pylori

A
  • G -ve SPIRAL- UREASE POSITIVE- Detected from normally sterile site- CHRONIC ACTIVE GASTRITIS, PUD, GASTRIC MALIGNANCIES- cagA gene- UREA BRETH TEST, ENDOSCOPY (CLO test), ELISA- Eradication can make gastric B-cell lymphma REGRESS- Treatment: CAP or ClaMP
180
Q

Cryptosporidium parvum

A
  • 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
181
Q

Rotavirus

A
  • 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
182
Q

Define gastroenteritis

A

A syndrome characterised by gastrointestinal symptoms including:- nausea- vomiting- diarrhoea - abdominal discomfort

183
Q

What is systemic sclerosis

A

Muscles not working - covered in MSK- a cause of SWALLOWING DIFFICULTIES

184
Q

Conditions linked to swallowing difficulties

A
  • Achalasia- Oesophageal cancer- Zeneker’s Diverticulum- Strictures- Systemic sclerosis
185
Q

Pathophys of chronic mesenteric ischaemia

A

Atherosclerotic narrowing of GI blood vessels (in mesentry) causing decreased supply to bowel

186
Q

Risk factors for Chronic mesenteric ischaemia

A

Same as cardio risks- Obesity, hypercholesteroaemia, sedentry lifestyle etc

187
Q

Signs/symptoms of chronic mesenteric ischaemia

A
  • Central colicky abdominal pain after eating (aka postprandial pain)- Weight loss (eating causes pain)- Abdominal bruit (due to turbulent blood flow)
188
Q

Main investigation for chronic mesenteric ischaemia

A

CT contrast/ANGIOGRAPHY

189
Q

Management of Chronic mesenteric ischaemia

A

lifestyle, secondary prevention, surgery

190
Q

Pathophys of Acute mesenteric ischaemia

A

Rapid blockage of mesenteric vessels leading to Ischaemia -> INFARCTION- necrosis + perforation- sepsis- peritonitisSuperiour mesenteric artery most commonly affectes - small bowel almost always affected

191
Q

Risk factors for Acute mesenteric ischaemia

A
  • ATRIAL FIBRILATION (blood clots)- Same as cardiac risk factors
192
Q

Causes of acute mesenteric ischaemia

A

ThromboembolismVasospasmHernia (strangulated)

193
Q

Signs/symps + Dx + Tx of acute mesenteric ischaemia

A
  • 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
194
Q

Ischaemic colitis

A

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 arterySame S&S, investigation + management as Acute mesenteric ischaemia except- PAIN in LEFT ABDO

195
Q

Define pseudomembranous colitis

A

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

196
Q

Risk factors for pseudomembranous colitis

A
  • Recent antibiotic use - Staying in a hospital/ nursing home- Older age (>65yo)- Use of PPI- IBD - Immunocompromised - CMV infection (OWL’S EYE bodies)
197
Q

Investigations for pseudomembranous colitis

A
  • 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)
198
Q

Management of pseudomembranous colitis

A
  • 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)
199
Q

Anal issues

A

HaemorrhoidsAnal fissureAnal fistulaPilonidal sinus/abscessPerianal/Anorectal AbscessLOOK AT PTS AND Haroon’s notes

200
Q

How long deos a typical case of gastritis from food last

A

around 48 hrs

201
Q

Define Meckel’s diverticulum + pathophys

A

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.

202
Q

Presentation of Mecklel’s diverticulum

A
  • 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
203
Q

Investigations for Meckel’s diverticulum

A
  • 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)
204
Q

Treatment of Meckel’s diverticulum

A

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

Take 2: Electric Boogaloo (20 decks)

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