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Y3 Charis > Gastro - ix do not use this > Flashcards

Gastro - ix do not use this Flashcards

1
Q

Extrinsic pathway of the clotting cascadeHow is it measuredNormal valueAffected by

A

PT14sWarfarin, Liver disease

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2
Q

Intrinsic pathway of the clotting cascadeHow is it measuredNormal valueAffected by

A

APTT34sHeparin, Haemophilias, von Willebrand disease

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3
Q

What is the Rockall score used for?

A

Used in upper GI bleedsDetermines risk of rebleeding + death

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4
Q

What does the Rockall score include? (5)

A

Broken into an initial (pre-endoscopy) and a final (post-endoscopy) scoreLook at haematemesis + malaena for tableInitialAge <60 0 60-79 1 >80 2Shock (BP + HR) HR >100 1 SBP <100 2Co-morbidities HF, IHD 2 Renal failure, Liver failure, disseminated malignancy 3 FinalStigmata of recent haemorrhage 2Diagnosis Mallory Weiss tear 0 Other Dx 1 Malignancy of the upper GIT 2

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5
Q

What is the Glasgow-Blatchford score (GBS) ?

A

Screening tool to assess the likelihood that a person with an acute UGIB will need to have medical intervention such as a blood transfusion or endoscopic intervention

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6
Q

What does the Glasgow-Blatchford score (GBS) include? (8)

A

Blood urea nitrogenHb SBPHRMelaenaSyncopeHepatic diseaseCardiac disease

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7
Q

Achalasia investigations

A
  • Barium swallow Bird’s beak appearance- CXR Dilated oesophagus behind the heart May show aspiration pneumonia- Manometry - gold standard for dx of achlasia To distinguish achalasia from other motility disorders a) high resting pressure in the lower oesophagus/cardiac sphincter, b)incomplete relaxation, c) absent peristalsis
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8
Q

Barret’s oesophagus ix

A
  • Endoscopy - velvety epithelium- Histology - visible columnisation (normal: squamous epithelial lining, abnormal: metaplastic columnar epithelium can become invasive adenocarcinoma of the oesophagus)
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9
Q

Oesophageal cancer ix

A
  • OGD + biopsy any lesion seen- Barium swallow Rat’s tail appearance of the oesophagus - Urgent endoscopy - biopsy any lesion seenGrade tumour histopathologicallyStage tumour by CXR, CT, PETEndoscopic US used less commonly Standard pre-treatment test Can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy Can identify abnormal or enlarged mediastinal and coeliac axis lymph nodes, and enable cytological examination by fine needle aspiration (FNA) This is often crucial in planning treatment, particularly prior to surgery Most accurate modality for local regional staging If there is no evidence of metastatic disease on PET-CT + pt is candidate for surgery Provides useful info about intramural vs transmural disease + local lymph node involvement
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10
Q

Gastritis ix

A

First line Ix- H. pylori testing –> 13C urea breath test/stool antigen test- FBC - ?iron deficiency anaemiaIx to consider- Endoscopy- Biopsy - gastric mucosal histology- Serum vitamin B12 N/Low in AI gastritis

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11
Q

Peptic ulcer disease ix

A
  • H. pylori testing –> 13C urea breath test/stool antigen test- FBC - ?iron deficiency anaemia- OGD If pt presents for the first time 55 + there are warning signs or bleeding ulcer or ALARMSWarning signs - >55 +- Chronic blood loss- Persistent vomiting- Epigastric mass- Unexplained, persistent, recent onset diarrhoea- Previous peptic ulcer disease- Previous gastric surgery- Pernicious anaemia- NSAID use- FHx of gastric carcinoma ALARMSAnorexiaLoss of weightAnaemia (Fe deficiency)Rectal bleedingMelaena/HaematemesisSwallowing difficulty (progressive dysphagia)Suspicious barium meal
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12
Q

ALARMS symptoms

A

AnorexiaLoss of weightAnaemia (Fe deficiency)Rectal bleedingMelaena/HaematemesisSwallowing difficulty (progressive dysphagia)Suspicious barium meal

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13
Q

GORD ix

A

1st line- 8 week trial PPI- OGD if symptoms do not improve after 8 week trial if pt >55 if patient has ALARMS symptoms Annual endoscopic surveillance for Barrett’s oesophagus Ambulatory pH monitorung - can demonstrate exposure to oesophageal acidCombined impedence pH testing - can quantify exposure to oesophageal acidGORD first line ix is upper GI endoscopyIn pt <55 or withour red flag symptoms - trial of PPIs before proceeding with investigations

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14
Q

GLASGOW scale

A

Scoring mechanism used clinically for assessing severity + prognosis of pancreatitis Based on results within 48h of admissionMnemonic: PANCREASPaO2 <8kPa or <60mmHgAge >55 yearsNeutrophlia >15x10^9 WBC/LCalcium <2.0mMRenal function: Urea >16mMEnzymes LDH >600 U/L or AST >200 U/LAlbumin <32 g/LSugar >10mM (in non-diabetics)if score >3 (incl 3) - severe pancreatitis likely, consider admission to ICU

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15
Q

Oesophageal spasm ix

A

Corckscew appearance on barium swallow

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16
Q

Anal fissures ix

A
  • Do not attempt DRE- Dx is clinical + further Ix only required if there are features of underlying pathology
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17
Q

Rectal prolapse ix

A

Imaging- Barium enema +/- colonoscopy - evaluate whole colon before rectal surgery + exclude other colonic lesions- Rigid proctosigmoidoscopy - assess rectum for additional lesionsAnal physiology tests- Distinguish between mucosa + full thickness prolapse- Anal sphincter manometry, electromyography of the anal sphincter, defecography, continence tests, pelvic floor, nerve stimulation tests (Pudendal nerve studies)Assess underlying conditionsSweat Cl- test –> CFStool microscopy + cultures –> GI infection

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18
Q

Haemorrhoids ix

A
  • Proctoscopy Pink mucosal swellings- Rigid/flexible sigmoidoscopy/Colonoscopy To exclude other pathology Defintive test is colonoscopy Flexible sigmoidoscopy combined with barium enema to assess proximal colon in high risk patients- FBC If concerned that pt has experienced significant bleeding –> Anaemia or infection - DRE
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19
Q

Appendicitis ix

A

1st line- FBC Increased WCC- Increased CRP- CT AP Abnormal appendix (>6mm diameter) / calcified appendicolith in assosciation with peri-appendiceal inflammation / appendiceal wall thickening / peri-appendiceal fat stranding / appendiceal wall enhancement - Urinalysis - exclude UTI- Pregnancy test - exclude ectopic pregnancy2nd line- US abdo- Urinalysis - Alverdo scoring system CT - 4-6 Appendectomy - >7

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20
Q

Alverdo scoring system for appendicitis SymptomsSignsLaboratory findingsResults

A

Symptoms - MAN- Migratory RIF pain - Anorexia- N+VSigns - TRF- Tenderness in RIF (2)- Rebound tenderness in RIF- Fever >38Laboratory findings - LS- Increased WCC (2) >10- Shift to the left of the neutrophils 5-6 possible7-8 probable>9 very probable CT - 4-6 Appendectomy - >7

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21
Q

Ix to confirm obstruction

A

AXRSmall bowel >3cmLarge bowel >6cmIf large bowel >9cm -risk of imminent perforation + need for urgent surgery

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22
Q

Colon cancer investigations

A

Bloods- FBC Anaemia- LFT Liver first site of metastasis of colon cancer (enterohepatic circulation)- U+Es- CEA (not used for dx but to monitor response to treatment, relapse, reucrrence of disease)- FOBT (used for screening)Imaging- Colonoscopy Gold standard for Dx of colon cancer- CT CAP Staging - Liver US Staging- Barium enema Apple core stricture

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23
Q

Volvulus Ix

A

Bloods- FBC -low Hb, high WCC if sepsis, gangrene- U+E Dehydration Sepsis (high lactate) Acidosis Hyponatraemia, hyperkalamia, hypochloaraemia, metabolic acidosis, lactcic acidosis, increased U + CrImaging- Upper GI contrast studies (diagnostic test)- AXR (ordered in ED) Sigmoid volvulus 65% - coffee bean shape in RUQ, assosciated with large bowel dilation Caecal volvulus 30% - caecal embryonic sign in LUQ, assosciated with small bowel dilation - Erect CXR if perforation is suspected

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24
Q

Choledocholithiasis investigations

A

EUS/MRCP

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25
Q

Gallstones/biliary colic ix

A
  • US abdo Shows gallstones + sludge in the gallbladder Allows measurement of the CBD diameterBloods- FBC - increased WCC due to inflammation from a complication of cholelithiasis (acute cholecystitis, colangitis, pancreatits)- LFTs - increased ALP due to obstruction of the cystic or bile duct- Serum lipase + amylase - pancreatitis is a complication of cholelithiasis
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26
Q

Cholecystitis ix

A
  • RUQ US Thickened gallbladder wall (>3mm) Distended gallbladder Pericholecystic fluid/air Gallstones +ve sonographic Murphy’s sign- HIDA (hepatobiliary iminodiacetic acid) scanning + MRI – helpful in cases where the US dx is unclear HIDA directly shows cystic duct obstruction Bloods- FBC - increased WCC- Increased CRP- LFTs Cholestatic picture Increased ALP, GGT, bilirubin
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27
Q

Acute cholangitis ix

A
  • ERCP First line Direct observaition of bile duct stone or other obstruciton Therapeutic - can be used for biliary stone extraction - Contrast CT 2nd line- MRCP - 3rd lineBloods- FBC - high WCC- LFTs - increased conjugated bil, increased ALP- Increased amylase indicated involvement of the lower part of the CBD- Blood cultures - bacteria are usually gram -ve
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28
Q

Mallory Weiss tear ix

A
  • OGD Dx test Needs to be performed within 24h- Angiography If OGD is unavailable/contra-indicated Bloods- FBC- Coagulation studies- Cross match/blood group if pt anaemic or ongoing bleeding - U+Es - Urea - high in pt w ongoing bleeding, part of Glasgow-Blatchford score- LFTs - to rule out liver disease (+ hence oesophageal/gastric varices) - ECG + cardiac enzymes - if myocardial ischaemia suspected as a result of blood loss
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29
Q

Toxic megacolon ix

A

AXR>6 cm

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30
Q

When should flexible sigmoidoscopy instead of colonoscopy be carried out to investigate UC?

A

When there is a risk of perforation

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31
Q

UC ix

A

Bloods- FBC (low Hb, high WCC)- High ESR/CRP- Low albumin- B12/folate deficiency (malabsorption)- Fe deficiency (bleeding, malabsorption) Stool- Stool culutre To exclude infective colitis/diarrhoea C. Diff higher prevelance in people with UC CMV considered in severe/refractory colitis - commonly reactivated in IBD pt due to immunosuppresants- Fecal calprotectin Distinguishes bn inflammatory + non-inflammatory causes of diarrhoea Conc in faeces correlates well with severity of intestinal perforationAXR To exclude toxic megacolonColonoscopy - not to be performed on an cute setting sue to risk of perforation Determines severity Histological confirmation Detection of dysplasia (UC pt at higher risk of colonic adenocarcinoma) Gross, uniform inflammation with a clear cut off point between normal and abnormal bowel Indicated in UC pt who are not responding well to treatmentsBiopsy Inflammed crypts filled with fibrin and polymorphonuclear leuckocytesDCBE Mucosal inflammation w granular appearance + filling defects (due to pseudopolyps) Narrowed colon Loss of haustral pattern - leadpipe appearance

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32
Q

Crohn’s disease Ix

A

Bloods- FBC (low Hb, high WCC, high plt)- High ESR/CRP- Low albumin- B12/folate deficiency (malabsorption)- Fe deficiency (bleeding, malabsorption) Stool- Stool culutre To exclude infective colitis/diarrhoea C. diff if recent abx use Yersinia enterocolitica if RIF pain- Fecal calprotectin Distinguishes bn inflammatory + non-inflammatory causes of diarrhoea Conc in faeces correlates well with severity of intestinal inflammationAXR To exclude toxic megacolon To assess CD severityColonoscopy - not to be performed on an acute setting sue to risk of perforation Differentiates bn UC + CD Defines presence + severity of morphological recurrence + predicts clinical course Useful for monitoring malignancy + disease progression Histological confirmationBiopsy Non-caseating granulomas in the bowel wall mucosa Transmural chronic inflammation with infiltration of macrophages, lymphocytes, plasma cells DCBE String sign of Kantor Rose thorn ulcers Cobblestone mucosa

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33
Q

What is Truelove’s and Witt’s severity index and what does it include (6)?

A

It classifies the severity of UCIncludes - Number of stools- Blood in stools- Anaemia- Pulse rate (>90bpm)- Fever (>37.8)- ESR/CRP (mm/h)

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34
Q

Mild UC according to Truelove’s and Witt’s severity index

A

<4 stools per day no more than small amount of blood in stoolsno anaemiapulse rate <90no feverN ESR/CRP (<30)

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35
Q

Moderate UC according to Truelove’s and Witt’s severity index

A

4-6 stools per day more blood than for mildno anaemiapulse rate <90no feverN ESR/CRP (<30)

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36
Q

Severe UC according to Truelove’s and Witt’s severity index

A

> 6 stools per day Visible blood in stools + 1 or more systemic upsets:anaemiapulse rate >90fever >37.8 ESR >30

37
Q

Cirrhosis ix

A

Bloods- FBC Low hb - bleeding Macrocytosis - alcohol abuse Thrombocytopenia (<150) - most sensitive + specific laboratory finding for dx of cirrhosis in the setting of chronic liver disease- LFTs Increased transaminases AST>ALT - alcoholic hepatitis ALT>AST - viral hepatitis Bil N at start, serum levels rise as cirrhosis progresses- Low sodium- Low albumin- Prolonged PTTTests to consider- Abdo US/CT/MRI Can detect signs of advanced cirrhosis + complications of cirrhosis (e.g. portal HTN)- CXR might show elevated diaphragm + pleural effusion- Upper GI endoscopy Presence of oesophageal-varices- Transient elastography/acoustic radiation force impulse imaging Used to diagnose cirrhosis for people with NAFDL + advanced liver fibrosis - Liver biopsy Most specific + sensitive test for x of cirrhosis If liver elastography is not suitable Not necessary in pt with advanced liver disease + atypical clinical/laboratory/radiological findings of cirrhosis - ascites, coagulopathy, shrunken nodular-appearing liver

38
Q

Signs of portal HTN on abdo US/CT/MRI

A

AscitesSplenomegalyIncreased diameter of the portal vein (>13mm)Collateral vesselsHepatocellular carcinoma

39
Q

What is the child-pugh-turcotte classification?

A

It estimates the prognosis in those with cirrhosis

40
Q

What does the child-pugh-turcote classification include? (5)

A
  • Serum albumin- Serum bilirubin- INR- Ascites- Encephalopathy
41
Q

Tumour markers- Breast cancer- Ovarian cancer- Pancreatic cancer- Biliary cancer (cholangiocarcinoma)- Prostate cancer- Colorectal cancer- Hepatocellular carcinoma- Non seminomatous germ cell tumourshttps://patient.info/doctor/tumour-markers

A
  • Breast cancer - CA 15-3, CA 27-29 Ca 27-29 (more sensitive + specific) but lacks predictive value in the earliest stages of breast cancer and thus has no role in screening for or diagnosing the malignancy- Ovarian cancer CA 125- Pancreatic cancer CA 19-9- Biliary cancer (cholangiocarcinoma) CA 19-9- Prostate cancer PSA- Colorectal cancer CEA- Hepatocellular carcinoma AFP- Non seminomatous germ cell tumours AFP, bHCG
42
Q

Cholangiocarcinoma investigations

A
  • Abdo US Identifies malignant vs benign lesions Mass lesion Dilated intrahepatic ducts- Contrast MRI Optimal imaging for dx of cholangiocarcinoma - MRCP, ERCP, PCT To visuallise site of obstruction ERCP/PCT to obtain samples for biopsy or cytological analysis - Tumour markersCA19-9CA125CEASerumBil raisedALP raisedGGT raisedALT mildly raisedPTT prolonged obstruction of CBD/ cystic duct - subsequent reduction in fat-soluble vitamins (ADEK)
43
Q

Liver abscess investigations

A
  • Liver US Variably echoic lesion Biliary tree examination Guides aspiration + drainage- Contrast CT abdo Gas within lesion - bacterial abscess Guides aspiration + drainageGram stain + culture of aspirated abscess fluid- FBC, ESR, CRP - inflammatory pic- LFT - increased ALP, mildly elevated AST, hypoalbiminaemia - Blood cultures- PTT, APTT - aspiration contra-indicated in the presence of abnormal clotting
44
Q

Liver abscess - ix if amoebiasis is suspected

A
  • Serum ab test- Stool ag detection test (may contain cysts or trophozoites)- Ag testing/PCR of aspirated abscess fluidfor Entamoaeba histolytica
45
Q

Liver failure ix

A

Blood• FBCLeucocytosis - ?infection Iron deficiency anaemiaThrombocytopenia – chronic liver diseaseRaised INR (>1.5) • LFTsRaised transaminasesNormal ALPRaised bilirubin • U+EsRaised U + CrMetabolic derangements in potassium, phosphate, magnesium• ABG – metabolic acidosis in paracetamol overdose• Arterial blood lactate – important prognostic indicator in paracetamol-associated ALF• LowPseudocholinesteraseGlucose • High Ammonia levelsLactateCreatinine • Blood cultures – pt very susceptible to infection• Viral serology Antihepatitis A IgM, antihepatitis B core IgM, hep B surface antigen, antihepatitis C IgG, antihepatitis E IgM May indicate infection that ppt hepatic failure• Autoimmune hepatitis markersAntinuclear antibody (ANA), anti-smooth-muscle antibody, quantitative immunoglobulins (IgG)• Test for specific conditions – Wilson’s disease, paracetamol levels (urine toxicology screen)Imaging • Doppler USBudd-Chiari syndrome – ?hepatic vein thrombosisHepatic surface nodularity - ?cirrhosis • CT/MRIDemonstrates hepatic anatomyExcludes other pathology (particularly patients with massive ascites, obesity, under consideration for transplantation) • Head imaging – cerebral oedema • EEG – level of encephalopathy• Liver biopsy

46
Q

Wernicke’s encephalopathy ix

A
  • Diagnosis is clinical- Therapeutic trial of parenteral thiamine - treat Wernicke’s as an emergency- Blood thiamine + its metabolites- Blood Mg - Mg serves as a co-factor in enzymes that need thiamine pyrophosphate - deficiency may impair the therapeutic benefit of thiamine Exclude causes:- BM glucose- FBC - ?infection- Serum ammonia - exclude hyperammonaemia that causes hepatic encephalopathy (Wernicke’s is due to B1 deficiency)- Blood alcohol level- Urinary + serum drug screen – to exclude concomitant intake by the patient Ix to consider- LP – to exclude meningitis, encephalitis- SAH – may present with similar findingsMonitor complications- U+E - if condition goes unnoticed - hypotension + lactic acidosis - renal dysfunction + electrolyte abnormalities
47
Q

What does “thumb printing” on XR, CT mean?

A

Submucosal oedema or haemorrhage

48
Q

First line investigation for acute mesenteric ischaemia + findings

A
  • CT angiogramo Shows arterial blockage due to emboli or thrombus o Evidence for extent of bowel compromise from ischaemia o Stratification of patients to identify those who would benefit from mesenteric angiography from those who require primary surgery o If findings are non-specific and non-diagnostic for colonic ischaemia – colonoscopy may be required Bowel wall thickening, dilation Thumb-printing sign suggestive of submucosal oedema or haemorrhage Gas in ectopic places – Pneumatosis intestinalis, Portal venous gas Occlusion of the mesenteric vasculature Streaking mesentery Solid organ infarction
49
Q

Intestinal ischaemia ix + findings

A
  • FBC Leucocytosis Anaemia bc of melaena exacerbates ischaemia- ABG/lactate level Acidosis + increased serum amylase Degree of acidosis determines severity of illness- CT angio- Sigmoidoscopy/colonoscopy Mucosal sloughing Mucosal petechiae Submucosal haemorrhagic nodules, errosions, ulcerations Luminal narrowing Necrosis Gangrene
50
Q

Investigations to investigate causes of intestinal ischaemia

A
  • ECG, Echo - AF, arrhythmias, MI (predispose to acute mesenteric ischaemia)- Coagulation panel - underlying coagulopathy- AXR
51
Q

Chronic mesenteric ischaemia investigations

A

• FBC, LFT, U+Es - malnutrition, dehydration• Mesenteric duplex US - first line ix, non-invasive method of demonstrating arterial blood flow, affected by obesity, respiratory movements• Arteriography - gold standard to show site of arterial blockage or stenosis

52
Q

Ischaemic colitis ix

A

• Colonoscopy - blue, swollen mucosa sparring the rectum• Abdo XR - abnormal segment outlined with gas• Barium enema - thumb printing in early phaseo Mucosa may then return to normal or progress with similar appearance to Crohn’so May then resolve spontaneously or progress to narrowing of the intestine +/- sacculation of the antimesenteric border• CT, MRI, angiography

53
Q

SBO investigations

A

• Upright + supine AXRo Help determine whether patient has a partial or complete SBO + whether the obstruction is simple or complicatedo Partial SBO: gas throughout the abdomen and into the rectumo Complete SBO: no distal gas, staggered air-fluid levelso Complicated SBO: free air under the diaphragm (perforation), thumb-printing (ischaemia)o Poor sensitivity so might need a CT scan when AXR is inconclusive (determine underlying cause, extent + location of obstruction)• U+Eo Dehydration: increased urea + electrolyte imbalance

54
Q

LBO investigations

A

Bloods• FBC o Increased WCC – infective or inflammatory cause, complication e.g. perforationo Microcytic anaemia – malignancy • U&Eso Elevated urea or creatinine o Deranged from dehydration, fluid shifts, sepsis o Colon normally absorbs NaCl + H2O and secretes K + HCO3 - this is disrupted in the obstructed colon  may produce hypokalaemia • Serum amylase/lipase – can be elevated with any significant intra-abdominal event• Coagulation studies – coagulopathy may be present in sepsis from perforation Imaging• Erect CXR – indicates perforation• Plain AXRo Dx confirmed by colonic dilationo 3/6/9 ruleo Small bowel <3cmo Large bowel <6cmo Sigmoid colon <9cm Ix to consider• Contrast enemao Performed after initial assessment to confirm dxo Bird’s beak in colonic volvuluso Contra-indicated if perforation or peritonitis are suspected

55
Q

PSC ix - Bloods

A

• ALP – N or Increased• GGT – Increasedo Indication of bile duct injury +/or obstructiono Supports liver origin of elevated ALP rather than bone• AST, ALT – mildly elevated• Bilirubin – N or increased, predominantly conjugated• Albumin – N in early-stage disease, low in advanced liver disease/pt w active IBD• FBCo Indication of liver dysfunction due to advanced liver disease + suggestive of portal HTNo N or thrombocytopenia +/- anaemia, leukopenia• PTT – N or prolongedo Indication of liver synthetic functiono Vitamin K deficiency due to malabsorption from cholestasis• No auto-antibodies specific to/diagnostic of PSC• But there may be – hypergammaglobulinaemia, raised IgM levels, perinuclear antineutrophil cytoplasmic ab (p-ANCA), anticardiolipin (aCL) ab, antinuclear ab

56
Q

PSC ix - Imaging

A

• Abdo USo Non-invasive initial test to ix for bile duct abnormality o May also provide evidence of more advanced liver diseaseo Can’t diagnose/exclude PSC – no adequate evaluation of the biliary treeo Abnormal (dilated) bile ducts (+/- cirrhotic liver, ascites, splenomegaly)• MRCPo Standard procedure to visualise the intrahepatic + extrahepatic bile ductso Preferred to ERCPo Normal/multi-focal intrahepatic +/or extrahepatic strictures and dilatations +/- dominant biliary stricture (bead like appearance as a result of stricture formation)• ERCPo When MRCP is non-diagnostic or when therapeutic intervention is anticipated (e.g. brush cytology to evaluate for co-existing malignancy, extraction of bile duct stones, dilation of prominent bile duct strictures)o Risk of procedure-related complications – pancreatitis, bacterial cholangitis, bleeding, liver abscess, perforation o During interventional procedures accessing the biliary tract, brush cytology should be performed to rule out cholangiocarcinoma • MRI – to exclude other disease + evaluate the biliary system • Liver biopsy – rarely diagnostic + may be useful for staging PSCo Polymorph infiltration of bile ducts

57
Q

best single test for screening household contacts of HBV-infected individuals to determine need for vaccination

A

Anti-HBc

58
Q

What is transient elastography?

A

Non-invasive test that has a high diagnostic accuracy for the detection of cirrhosis

59
Q

HAV ix

A

• IgM anti-hepatitis A virus serology (HAV) – detected 5-10 days before symptom onset + remains elevated for 4-6 months• IgG anti-hepatitis A virus serology (HAV) – levels begin to rise soon after IgM levels + stay elevated throughout the person’s lifetimeo +ve result – prior infection or recent disease - should be interpreted along with results of IgM anti-HAV + clinical featureso In the absence of IgM it indicates past infection or vaccination rather than acute infection• Raised ALT + AST but ALT>AST (about 4 weeks after exposure)• Raised Bil (rises soon after ALT + AST)• Raised blood U + Cr in fulminant hepatitis

60
Q

HBV ix

A

• LFTs - raised ALT, AST, ALP, Bilirubin, low albumin• FBC – microcytic anaemia, thrombocytopenia – portal HTN resulting from HBV related cirrhosis• HBsAg (HB surface antigen)o Establishes dx + indicates active infection o 4 weeks after exposure to the virus – mean time from exposure to detection is 30 dayso Presence for >6m implies chronic HBV infection• Anti-HBs (antibody to HBsAg)o Appears several weeks after HBsAg has disappearedo Detectable in those immunised with HB vaccineo Provides life-long immunity, suggestive of resolved infection o Alone imply vaccination • IgM + IgG Anti-HBc (antibody to HB core antigen)o IgM anti-HBc - appears within weeks, remains detectable for 4-8 months (acute infection)o IgM anti-HBc - During the window between disappearance of HBsAg + appearance of Anti-HBs –> IgM Anti-HBc is the only way to make dx of acute HBV infection o Not very reliable marker for acute infection as it can become positive in acute flares or acute reactivationo Does not provide immunity o IgG anti-HbC - chronic infection o Best single test for screening household contacts of HBV infected individuals to determine need for vaccinationo Imply past infectionChronic hepatitis can be divided into HBeAg+ve or HBeAg-ve disease• HBeAgo Found in the serum in the early part of acute HBV infectiono Usually disappears at or soon after the peak in ALT o Its presence >3 months after onset of illness indicates a high likelihood of development of chronic HBV infection• Ab to HBeAgo Seroconversion from HBeAg to ab to HBeAg - useful indication of clearance of virus, suggestive of treatment-related clearance of HBVo Seroconversion can be a temporary phenomenon – should be analysed in association with the serum HBV DNA level• HBV DNAo Measured by PCRo Assesses candidacy for antiviral therapy + monitors response to therapy• Patients with chronic hepatitis B are positive HBsAg for at least six months or positive HBsAg and negative IgM to HBcAg.

61
Q

HCV ix

A

• Hep C antibodies• Enzyme immunoassay (EIA)• Nuclei acid amplification tests (NAATs) – used to confirm early infection/viremia in a patient with positive EIA/assess the effectiveness of anti-viral therapy • Serum aminotransferases – ALT may be elevated + used to measure disease activity • Viral genotyping – every patient in order to determine the dose + duration of therapy + to estimate the most appropriate regimen• Liver biopsy – not used to diagnose HCV, useful in staging fibrosis + degree of hepatic inflammation

62
Q

HDV ix

A

Anti-HDV ab

63
Q

HBsAg -veanti-HBc -veanti-HBs -ve

A

Susceptible

64
Q

HBsAg -veAnti-HBc +veAnti-HBs +ve

A

Immune due to natural infectioon

65
Q

HBsAg -veAnti-HBc -veAnti-HBs +ve

A

Immune due to hepatitis B vaccination

66
Q

HBsAg +veAnti-HBc +veIgM anti-Hbc +veAnti-HBs -ve

A

Acutely infected

67
Q

HBsAg +veAnti-HBc +veIgM anti-Hbc -veAnti-HBs -ve

A

Chronically infected

68
Q

HBsAg -veAnti-HBc +veAnti-HBs -ve

A

four possibilities1. resolved infection (most common)2. false-positive anti-HBc thus susceptible3. Low level chronic infection4. Resolving acute infection

69
Q

Presence of HBsAg(Hep B surface antigen)

A
  • Indicates that the person is infectious- Can be detected in the serum in high levels during are cute or chronic hepatitis B infection- Ag used to make HBV vaccine
70
Q

Presence of anti-HBs(Hep B surface antibody)

A
  • Recovery + immunity from HBV- Also develop in people who have been successfully vaccinated against HBV
71
Q

Anti-HBc total hepatitis B core antibody

A
  • Indicates previous or ongoing infection with HBV in an undefined time frame- Appears at the onset of symptoms in acute HB and persists for life
72
Q

IgM anti-HBcIgM antibody to hepatits B core antigen (IgM anti-HBc)

A
  • Presence indicates acute infection - Positivity indicates recent infection with hepatitis B virus (<6m)
73
Q

Autoimmune hepatitis ix

A

• Biopsy - most important diagnostic procedure, essential to establish dx, evaluate disease severity + determine the need for treatment –> Interface hepatitis with portal mononuclear and plasma cell infiltrate• Inflammatory changes (histology) • Very raised aminotransferases• Mildly to moderately increased bilirubin, GGT, ALP• Prolonged PTT, decreased albumin• IgG predominant polyclonal hypergammaglobulinemia • Exclusion of viral/drug-induced/metabolic liver disease• Presence of circulating auto-antibodies (9)o Antinuclear ab (ANA)o Smooth muscle ab (SMA)o Perinuclear antineutrophil cytoplasmic auto-antibody (pANCA)o Anti-liver-kidney microsomal-1 ab (anti-LKM-1)o Anti-soluble liver antigen or liver/pancreas (anti-SLA/LP)o Anti-liver cytosol 1 (anti-LC1)o Antiphospholipid antibodieso Anti-single-stranded DNA (anti-ssDNA antibodies)o Anti-double-stranded DNA (anti-dsDNA antibodies)

74
Q

Auto-antibodies in Autoimmune hepatitis

A

o Antinuclear ab (ANA)o Smooth muscle ab (SMA)o Perinuclear antineutrophil cytoplasmic auto-antibody (pANCA)o Anti-liver-kidney microsomal-1 ab (anti-LKM-1)o Anti-soluble liver antigen or liver/pancreas (anti-SLA/LP)o Anti-liver cytosol 1 (anti-LC1)o Antiphospholipid antibodieso Anti-single-stranded DNA (anti-ssDNA antibodies)o Anti-double-stranded DNA (anti-dsDNA antibodies)

75
Q

PBC ix

A

Bloods• N FBC• Raised IgM• Raised ESR• LFTso Raised ALP + GGT – suggests presence of cholestasis o Bilirubin – N at first, rises as disease progresseso PTT + Albumin – N until a late stageo Prolonged PTT – suggestive of impaired liver synthetic function compatible with the presence of advanced liver disease or can reflect vitamin K malabsorption in the context of cholelithiasis • Raised cholesterol, lipid, HDL (therefore no raised risk of CHD)• Autoantibodies- immunofluorescence + ELISAo Antimitochondrial antibody (95%) – diffuse staining throughout the cytoplasm [FIRST LINE IX]o Antinuclear antibody (35%)  PBC – staining of multiple dots within the nucleus + nuclear rim staining  Autoimmune hepatitis + SLE – diffuse nuclear staining o Other antibodies, esp related to thyroidImaging• Liver US - to exclude obstruction as a result of cholestasis e.g. stones – always should be done before a dx of PBC is made• Cholangiography - to exclude PSC• Transient elastography - to evaluate degree of liver fibrosis• Liver biopsy o To show cholestatic picture when autoantibodies are not diagnostic o To differentiate PBC from autoimmune hepatitis o PBC– chronic nonsuppurative cholangitis of the interlobular + septal bile ducts, bile duct lesions (biliary ductular cell disruption with inflamed portal tracts), granulomata formation, ductopenia (bile duct loss) w/ progressive biliary fibrosis o Autoimmune hepatitis – interface hepatitis

76
Q

Alcoholic hepatitis biopsy result

A

Necrosis of liver cells with infiltration of leukocytes and the presence of Mallory bodies within the hepatocytes

77
Q

Slight increase in amylase (200-600 U/L) (13)vsVery large increase in amylase (>1000U/L) // increase in lipase levels (above 300 U/L)vs Low levels of amylase

A

Slight increase in amylase- Pancreatitis- Perforated peptic ulcer- Acute appendicitis- Acute cholecystitis - Leaking AAA- Bowel obstruction- Mesenteric ischaemia- Mumps- Pancreatic carcinoma- Opioids- Renal failure- DKA- Head injuryVery large increase in amylase - diagnostic of acute pancreatitisLow levels of amylase- Alcoholics - unable to produce amylase- Severe/necrotic pancreatitis - In chronic pancreatitis amylase will be normal - Hypertriglyceridemia - triglycerides can interfere with the amylase assay + produce falsely low result

78
Q

Interpret the following LFTs1. High AST+ALT2. High ALP, GGT, bilirubin3. High ALP, Normal GGT4. Isolated high GGT

A
  1. Hepatocyte damage, liver pathology2. Pathology in the biliary tree/extrinsic compression of the biliary tree3. Other source producing ALP rather than the liver (e.g. bone, placenta)4. Alcohol excess (not necessarily alcoholism)
79
Q

Biliary dilation diagnosis

A

US>6mm CBD diameter

80
Q

Acute pancreatitis investigations

A

-Serum amylase/lipase (first line) If lipase:amylase >5 - favours alcoholic pancreatitis - AST/ALT if >3x the upper limit –> gallstone disease as the aetiology- US abdo Can reveal gallstones may show pancreatic inflammation, calcification, fluid collections- ABG Hypoxaemia Disturbances in acid/base balance- FBC Increased WCC Decresed Hct (haemorrhage) // increased Hct (dehydration)- Increased CRP

81
Q

Chronic pancreatitis investigations

A

First line investigations to order- CT abdo Pancreatic calcifications Focal/diffuse enlargement of the pancreas Ductal dilation Vascular complications - Abdo US - done if CT is unavailable - Blood glucose may be increasedInvestigations to consider- Faecal elastase - good marker of endocrine pancreatic function Only synthesised + exreted by the pancreas Direct correlation bn elastase in stool + in pancretic fluid Low stool elastase - hgh sensitivity for pancreatic compromise Low sensitivity for diagnosing exocrine pancreatic insufficiency Specificity of stool elastase levels compromised in patients with disease of the small bowel (e.g. coeliac disease, Crohn’s- Amylase will be normal- MRCP + ERCP - beading of the pancreatic duct (alternating dilation + stenosis)

82
Q

PeritonitisFBCU+EsABG results

A

FBC - increased WCCU+Es - Increased Na, Decreased KABG - acidosis

83
Q

To diagnose peritonitis in people with ascites the ascitic fluid should contain ______

A

> 250 polymorphonuclear cells/μLpolymorphonuclear = having a nucleus with several lobes and a cytoplasm that contains granules, as in an eosinophil or basophil

84
Q

Why do we need to co-administer Mg with thimamine?

A

Mg serves as a co-factor in enzymes that need thiamine pyrophosphate Therefore deficiency may impair the therapeutic benefit of thiamine

85
Q

What does elevated urea and normal creatinine indicate?

A

They indicate active gastrointestinal bleeding

86
Q

Alcoholic hepatitis ix

A

LIVER• Elevated AST, ALT , AST>ALT + AST:ALT >2o N: 30 units/L (men), 19 units/L (women)• Elevated GGT - up• Elevated bilirubin (both conjugated + unconjugated) o Reflects impaired metabolic function of the liver in the absence of biliary obstruction + Has prognostic utility in ALD • Elevated serum PTT/INR - Used to evaluate synthetic function of the liverElevated in advanced liver cirrhosis, liver failure• Low albumin BLOOD• FBCLow Hb – iron deficiency, GI bleeding, folate deficiency, haemolysis, hypersplenism High WCC – infection, alcoholic hepatitis-related leukaemoid reactionLow platelets – may be secondary to alcohol induced BM suppression, folate deficiency, hypersplenism • U+Es, Mg, PO43-o Low Na – advanced liver cirrhosiso Low K, Low PO43- - cause of muscle weakness in ALDo Low Mg – can cause persistent hypokalaemia, may predispose patients to seizures during alcohol withdrawal o HIgh U + N Cr - active GI bleeding o High U + High Cr - hepatorenal syndrome • Low folateo Increased requirements for folate in hepatic disease + decreased intake IMAGING• Liver US (screen for HCC every 6-12 months in ADL w cirrhosis)• Liver biopsyo Necrosis of the liver cells and infiltration of leucocytes with the presence of Mallory bodies within the hepatocyteso In the context of a history of alcohol abuse is diagnostic but is not absolutely indicated in all patients

87
Q

Gastric cancer ix

A

• Upper gastrointestinal endoscopy + biopsy required to confirm dx (multiple ulcer edge biopsies)o If gastric lesion is suspicious and biopsy is negative, a repeat biopsy is necessaryo PPIs should be withheld after endoscopy to avoid misdiagnosis (prescribed because early disease has features of dyspepsia without weight loss,o anaemia, dysphagia)• To determine stageo CT CAP – determines presence/absence of metastatic diseaseo EUS – staging, FNA of regional nodes, used to asses operability in the absence of metastatic disaseo CXRo PET scan more sensitive than CT for distant metastases

88
Q

NASH/NAFLD ix

A

• Liver biopsy + histopathological analysis o Definitive diagnosis Bloods• FBCo Hypersplenism - anaemia, thrombocytopenia • LFTso AST, ALT - increased, ALT>ASTo ALP – increasedo GGT – increasedo Total bilirubin – begins to increase with decompensated disease• Lipid panel - high cholesterol, LDL, triglycerides, low HDL• PPT + INR - increased indicates impaired/decompensated liver synthetic function• Serum albumin - decrease indicates impaired liver synthetic function• Iron studies – many will have increased transferrin saturation, increased ferritinImaging To define extent + course of diseaseSteatosis - focal or diffuseSteatohepatitis - diffuse• USo Hyper-echogenic, bright image • CT/MRI to monitor course + extend of disease

Y3 Charis (35 decks)

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