Gastroenterology Flashcards
Definition of Crohn’s Disease
IBD which affects entire GIT mouth to anus, transmural inflammation
Risk factors for Crohn’s
GxE Genetic predisposition Family history Smoking Western lifestyle
Signs & Symptoms of Crohn’s
Potential differentials
Diarrhoea +/- mucus Weight loss FTT Fatigue Maliase Crampy abdo pain Skin manifestations: pyoderma grangrenosum, erythema nodosum Complications e.g. bowel obstruction
Differentials: IBS, IBD e.g. UC, gastroenteritis, C diff infection, malignancy, coeliac, acute appendicitis
Investigations into potential IBD
• Bloods: ○ FBC; anaemia (Hb), infection (WCC) ○ U&Es ○ LFTS; low albumin ○ CRP/ESR; inflammation ○ Fe studies; anaemia, B12 & folate; nutritional status
• Stool: ○ Culture; r/o infective process ○ Calprotectin • Colonoscopy ○ Biopsies to confirm Crohn's vs UC ○ R/O malignancy Surveillance as well for CrCa risk
Management of Crohn’s
Management: - aim to induce & maintain remission
Medical
• Steroids - used in acute exacerbations +/- 5-ASA analogues to reduce inflammation
• 5-ASA e.g. sulfasalazine, mesalazine - reduce relapses, anti-inflammatory agents
• Immunosuppressives e.g. azathioprine, methotrexate - reduce relapses, steroid sparing agents
• Anti-TNF agents e.g. infliximab - very affective in achieving & maintaining remission, usually reserved for refractory cases
Surgical
• Local resection of disease
• Stoma formation
• Treatment of complications
Complications of Crohn’s
GI complications • Haemorrhage e.g. PR bleeding • Bowel strictures • Bowel obstructions • Fistula formation • Malabsorption Colorectal carcinoma
Other complications
• Kidney stones
• Gallstones
Uveitis
Pathology of Ulcerative Colitis
‘‘CLOSE UP’’
Continuous submucosal inflammation of large intestine
Continuous inflammation Limited to colon & rectum Only submuscoal Smoking - protective Excrete blood/mucus Use aminosalicytes Primary sclerosing cholangitits
Risk factors for UC
Genetic predispositon
Ex-/non-smokers
S&S of UC
Diarrhoea Constipation - when rectum becomes inflamed Mucus PR bleeding Weight loss Fever Skin manifestations
Management of UC
Medical - induce & maintain remission
• Mesalazine (topical anti-inflammatory) +/- steroids in acute flare ups
• Thiopurines (azathioprine and mercaptopurine): work through purine synthesis inhibition in lymphocytes leading to immunosuppression.
○ Must check TPMT enzyme activity before use.
○ Homozygous mutations in TPMT can lead to dangerous bone marrow suppression.
○ Major side-effects include pancreatitis and hepatotoxicity.
• Biologics: infliximab/adalimumab
○ tumour necrosis factor alpha inhibitors
Surgical
Panproctocolectomy; technically curative
Complications of UC
• Hemorrhage • Toxic megacolon • Colorectal carcinoma • Fatty liver Primary sclerosing cholangitis
Pathology of colorectal carcinoma
Mostly adenocarcinoma
Tend to arise from adenoma-carcinoma sequence - due to damage & repair cycles
Common mutations inc APC - Kras - p53
Risk factors/aetiology - colorectal carcinoma
Environmental factors - diet, red meat, alcohol
Chronic inflammation or IBD
Hereditary syndromes - Lynch (MLH1 & MSH2), FAP (APC)
Signs & Symptoms of Colorectal carcinoma (L vs R)
Left sided & rectum; CIBH, rectal bleeding, blood/mucus, tenesmus
Right sided (later presentation); IDA, signs of anaemia, weight loss, lower abdominal pain (rarer)
2WW Criteria for CrCa
Aged 40 or over with unexplained weight loss AND abdominal pain
Aged 50 or over with unexplained rectal bleeding
Aged 60 or over with IDA or CIBH
Any +ve FIT tests
Investigations into CrCa
Examination - PR & abdominal
Bloods - FBC (anaemia), Fe studies (anaemia), LFTs, CEA
Stool - culture, calprotectin, FIT or FOB test
Imaging - sigmoid/colonoscopy + biopsies, CT/MRI for staging
Treatment for CrCA
Surgery - resection, stoma formation +/- chemotherapy
Palliative options inc stenting/bypass
Complications of CrCa
Bowel Obstruction
Perforations
Pathology of oesophageal ca
Upper - squamous cell, arises from mutational damage/repair cycles
Lower - adenocarcinoma, due to GORD/Barrett’s oesophagus
Risk factors for oesophageal ca
SCC - diet, smoking, HPV-16, HPV-18, alcohol
Aden - GORD, Barrett’s, reflux, obesity, ZE syndrome
S&S of oesophageal ca - potential differentials
- Progressive dysphagia
- Weight loss
- Cachexia
- Fever
- Anaemia
- Retrosternal pain
- Hoarse voice
Differentials: any condition which may cause/contribute to dysphagia e.g. strictures, achalasia, myasthenia gravis
Investigation - Oesophageal Ca
OGD + biopsy
CXR
Barium swallow
CT/PET for staging
2WW Criteria for Oesophageal Ca
Any patient with dysphasia
Any patient >55yrs with w/l + upper abdominal pain/reflux/dyspepsia
Treatment options for oesophageal ca
surgery - oesophagectomy
chemo
RT
palliative options - stenting
Definition of lower GI bleeds
bleeding distal to ligament of Treitz (suspensory ligament of the duodenum)
Causes of lower GI bleeds
Anatomical - anal fissures, fistulas, haemorrhoids, diverticulosis
Inflammation - IBD (UC, CD), infection
Vascular - ischaemic colitis, angiodysplasia
Neoplasia - colorectal carcinoma, polyps
Other - upper GI bleeds, trauma
Investigations for lower GI bleeding
History + PR examination
Bedside - obs, ECG, blood glucose, lying/standing BP
Bloods - FBC, U&Es, LFTs, Clotting, X-match
Stool - culture, calprotectin
Imaging - erect CXR, CTAP, colonoscopy/OGD
Management of lower GI bleeds
Initial A to E assessment & quantify state of shock
• Minor bleeds – conservative management
• Major – colonoscopy & treat lesion, interventional radiology options
Oakland Scoring - predicts readmission
https://www.mdcalc.com/oakland-score-safe-discharge-lower-gi-bleed
Oakland score - parameters & what’s it used for
Use in patients presenting with lower GI bleed (urgent, emergent, or primary care setting) to help determine if outpatient management is feasible.
Age, sex, previous GI bleed, HR, BP, Hb, DRE examination
Definition of UGIB & common sources
Bleeding proximal to ligament of Treitz
Oesophagus, stomach, duodenum
Causes of UGIB
Oesophagus - varices, oesophagitis, MW tear, malignancy
Stomach - varices, gastric ulcer, MW tear, malignancy
Duodenum - peptic ulcer, duodenitis, diverticulum, aortoduodenal fistula
Risk factors for UGIB
Medication - NSAIDs, Steroids, anticoagulants Advancing age Alcoholism/excess CLD CKD PUD/prev PUD Prev h.pylori infection
Investigations for UGIB
Bedside - observations, BP, BM’s, ECG, monitor UO
Bloods - FBC, U&Es, LFTs, clotting, ABG/VBG, G&S, X-match
Imaging - erect CXR, endoscopy
Management of UGIB
Initial resuscitation & A to E - consider blood products
Non-variceal - PPI, adrenaline + clips/thermal coag
Variceal; terilpressin, prophylactic abx, adrenaline + bands/TIPs
Scoring system for UGIB
Blatchford - primary assessment, - when to scope
0-2 – low risk
>2 – admit
Rockall - post endoscopy, ABCDE (age, BP & HR, co-morbidity, diagnosis, endoscopic findings)
Re-bleeding risk
Pathophysiology of Coeliac Disease
Autoimmune reaction to prolamin peptides in gluten, barley & rye
Immunological response leads to mucosal damage & villous atrophy in small intestine
Leads to malabsorption
S&S of Coeliac Disease
V varied, can be asymptomatic
Diarrhoea Bloating Steatorrhoea Abdo pain Weight loss FTT Primary amenorrhea Fatigue Malaise
Investigations for Coeliac Disease
Examination - signs of anaemia, malnutrition, dermatitis herpetiformis
Bloods - FBC, Fe studies, B12, folate, Ca, Anti-TTG & anti EMA
Stool - culture, ?calprotectin
Endoscopy - visualisation & biopsy
Management of Coeliac Disease
Gluten free diet
Education & dietary support
Vit & mineral supplements if needed
Pathophysiology of pancreatitis
Pancreatitis is caused by the abnormal release and activation of enzymes, which cause autodigestion of pancreatic tissue
Aetiology of pancreatitis - I GET SMASHED
Idiopathic GALLSTONES - women & older patients ETHANOL - men & younger patients Trauma Steroids Mumps/EBV/CMV Autoimmune Scorpions Hyperlipidemia ERCP, emboli Drugs e.g. furosemide, thiazide diuretics, azathioprine
S&S of Pancreatitis
Can be quite vague
Abdominal/epigastric pain - radiating to back, relieved by leaning forwards, worse on movement, a/w nausea & vomiting
Anorexia/LOA
Steatorrhoea
Abdominal tenderness/distension
Cullen’s (umbilical) & Turner’s (flank) signs - haemorrhagic
Investigations into pancreatitis
Bloods - FBC (WCC), U&Es (urea), LFTs (LDH, AST, albumin), Amylase, Lipase, ABG
Imaging - CXR (r/o GI perf), USS (gallstones & biliary dilatation), CT/MRI (assess for complications)
Glasgow Score - Pancreatitis
Severity Score; 0-1 mild, 2 moderate, 3 or more severe
‘‘PANCREAS’’
paO2 <8 age >55 neutrophils >15 calcium <2 renal function, urea >16 enzymes (LDH, AST) albumin <32 sugar >10
Management of Pancreatitis
Resuscitation & A-E assessment IV fluids Analgesia NBM & NG tube ERCP & cholecystectomy - gallstones (if needed)
Complications of Pancreatitis
- Chronic pancreatitis
- Malnutrition
- QOL
- Pseudocysts
- Necrosis
Pathophysiology of Cirrhosis
Chronic damage to liver leading to loss of hepatocytes
Hepatocytes replaced by fibrosis & nodules
Leads to portal HTN & liver failure
Aetiology of Cirrhosis
Alcoholism NAFLD Viral hepatitis - B&C Autoimmune hepatitis Hereditary - haemochromatosis, Wilson's Vascular - Budd Chiari syndrome Drugs - MTX, amiodarone
S&S of Cirrhosis
Early non-specific signs - anorexia, weight loss, fatigue, weakness, nausea
Loss of synthetic function - easy bruising, abdominal swelling, ankle oedema
Loss of detoxification - altered sleep, jaundice, personality changes, amenorrhea
PR bleeding/melena
Haematemesis
Signs of examination of chronic liver disease
'’ABCDE’’ - ascites & asterixis, bruises, clubbing, dupuytren’s contracture, erythema (palmar)
jaundice
spider navei
caput medusa
organomegaly - liver/spleen
Investigations for cirrhosis
Bloods - FBC (Hb, MCV, Plts), LFTs, Clotting, AI/serology screen, albumin, AFP
Ascitic tap - micro, C&S, biochem, cytology
Liver USS+ biopsy - gold std
Endoscopy?
Child Pugh Score - Cirrhosis
Severity & prognosis
5 markers (3x max each)
Albumin, Ascites, Bilirubin, INR/PT, HE
Management of Cirrhosis
Treat/reverse cause
Prevent further damage - alcohol, diet, avoid hepatotoxic drugs
Dietary support - high protein, low na diet
Monitor & treat complications
Potential complications of Cirrhosis
Ascites - drain, diuretics
HE - laxatives
UGIB - ?TIPS
SBP - abs & prophylaxis
Definition & causes of acute liver failure
Acute dysfunction w/o underlying liver disease
Causes: trauma, drug OD (paracetamol), alcohol excess, infection (Hep A/B/E), pregnancy related, Budd-Chiari syndrome
Definition of autoimmune hepatitis
Chronic relapsing hepatitis with an unknown aetiology, characterised by the presence of autoimmune features, hyperglobulinaemia and autoantibodies
Pathogenesis & Aetiology of Autoimmune hepatitis
Commonly affects women of all ages (type 1) & younger women/girls (type 2)
Thought to be genetic predisposition & environmental trigger (e.g. drugs, infection)
Auto-immune reaction causes chronic inflammation & damage, can lead to cirrhosis & failure
Type 1 (Classic): anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (SMA), anti-actin antibodies, anti-liver soluble antigen
Type 2: anti-LKM (liver kidney microsomes), antibodies to liver cytosol antigen
‘Ways’ in which AIH can present
• Asymptomatic (25%) - persistently elevated LFTs
• Acute hepatitis (40%) - fever, RUQ pain, anorexia, hepatomegaly, N&V, diarrhoea, jaundice
• Chronic liver disease/cirrhosis
Acute liver failure (rare) - jaundice, confusion, coagulopathy
Investigations for AIH
Routine bloods • FBC - low Hb, Plts & WCC may be low in hypersplenism • U&Es • LFTs - deranged, AST/ALT esp in acute • Clotting Non invasive liver screen • Auto-antibodies; ANA, anti-SMA, anti-LKM • Immunoglobulins Imaging • USS etc to r/o other causes • Not diagnostic Biopsy
Management of AIH
Immunosuppression - mainstay of management
• Steroids i.e. prednisolone
• Azathioprine
Follow up & monitoring - remission = normal AST/ALT
Cholelithiasis vs Choledocholithiasis vs Cholecystitis
Cholelithiasis: refers to gallstones - solid deposits that develop in the gallbladder.
Choledocholithiasis: refers to gallstones within the biliary tree.
Cholecystitis - inflammation of gallbladder, commonly caused by gallstones
Types of gallstones & risk factors for developing them
Mixed, cholesterol or pigment
Female Age Diet - high fat Medication - high oestrogen Obesity Family hx/genetics Crohn's Haemolytic disorders
Causes of cholecystitis
Gallstones (calculous)
Non-calculous cholescystitis (significant systemic upset or following major surgery)
S&S of Gallstones
Asymptomatic
but can present with biliary colic (intermittent severe RUQ pain) or cholecystitis
S&S of cholecystitis
RUQ/epigastric severe pain, tenderness & guarding N&V Pyrexia Tachycardia can become hypotensive
Murphy’s sign - catching breath
Investigations for cholecystitis
Bedside - observations, BM, urine dip, preg test
Bloods - FBC, cultures, U&Es, CRP, LFT, amylase
Imaging - USS
Management of Cholecysitis
Medical - abx, fluids, analgesia
Surgical - cholecystectomy, ERCP or MRCP if CBD stones present
Management of Gallstones
Conservative - fluids, anti-emetics, analgesia
Lifestyle advice - dietary, weight loss
Monitor & treat complications
Definition & risk factors for cholangiocarcinoma
Cancer arising from bile ducts (can be intra or extrahepatic)
RFs: primary sclerosing cholangitis (UC pts), liver flukes (parasitic infections)
Clinical features of cholangiocarcinoma
Obstructive jaundice - pale stool, dark urine, generalised itching W/L RUQ pain Palpable GB Hepatomegaly
Investigation & Dx of Cholangiocarcinoma
Bloods - liver & jaundice screen, LFTs, bilirubin, albumin, serology, Ca19-9
Imaging (Dx) - CT or MRI + biopsy, ct staging
MRCP/ERCP can aid in dx or management
Treatment of cholangiocarcinoma
Surgery - can be curative in early stages, combined with chemo/RT
Palliative options in majority of cases e.g. stents, bypass obstruction, sx control with chemo/RT
Definition of Primary Sclerosing Cholangitis (PSC)
An autoimmune mediated disease characterised by cholestasis, bile duct strictures & hepatic fibrosis
Primary: refers to PSC. Absence of another identifiable cause.
Secondary: refers to any condition causing bile duct damage and biliary obstruction.
Pathology of PSC
Autoimmune ‘attacks’ causing progressive inflammation & hepatic fibrosis as well as destruction of intra & extrahepatic ducts. This leads to reduction in flow of bile (cholestasis), narrowing of bile ducts (stricturing) and cirrhosis of liver
Aetiology of PSC
Genetic predisposition x environmental trigger
Strong a/w IBD especially UC
Clinical features of PSC
Can remain asymptomatic especially in early stages, can be incidental finding or symptoms tend to develop from cholestasis
• Incidental finding - persistently raised ALP
• Intermittent jaundice, itching, fatigue, RUQ pain
• Hepatomegaly, splenomegaly & stigmata of CLD
Can also present with cholangitis (Charcot’s Triad)
• Fever
• RUQ pain
Jaundice
Diagnosis of PSC
PSC is characterised by a ‘cholestatic’ pattern on LFTs and absence of autoantibodies.
MRCP - gold std, visualise biliary strictures & dilatation
Treatment options of PSC
Medical - aimed at managing complications
• Cholangitis - IV abx & fluids
• Bone disease - at increased risk of osteoporosis & osteopenia, Vit D supplements
• Itching - cholestyramine
ERCP - balloon dilatation & stents
• Help to manage disease
Liver transplant
• Only option which alters survival, recurrence is a risk
Complications of PSC
Cholangiocarcinoma • COD in majority of patients with PSC • Low threshold for imaging if suspected Colorectal carcinoma • Due to a/w IBD, annual colonoscopies Hepatic malignancy Due to cirrhosis, 6mths USS +/- AFP
Definition & pathophysiology of hepatocellular carcinoma
Primary malignancy of hepatocytes
Damage & repair cycles promoting mutations
Risk factors/aetiology of HCC
Chronic liver disease - alcoholic liver disease, NAFLD, cirrhosis, hepatitis, AIH
Metabolic liver disease - haemochromatosis
Alfatoxins
Clinical presentation of HCC
Stigmata of chronic liver disease on examination Weight loss Fatigue Maliase Weakness LOA Ascites/abdominal distension Jaundice
Investigations for HCC
Bloods - full liver screen e.g. FBC, U&Es, LFTs, AI, serology, AFP
Imaging - CT or MRI +/- biopsy, CT staging
Treatment options for HCC
Surgical resection Local therapy e.g. ablation Transplant Chemo e.g. multikinase inhibitors (e.g. Sorafenib) RT or brachytherapy
Definition of gastric carcinoma
Malignancy of stomach - adenocarcinoma (90%)
Risk factors for gastric cancer
Smoking Alcohol Diet Obesity Atrophic gastritis H. pylori infection
S&S of gastric cancer
Constitutional symptoms: fevers, anorexia, lethargy, weight loss
Dysphagia: if involvement of gastric cardia
Indigestion
Dyspepsia
Nausea/vomiting
Haematemesis/melaena
Post-prandial fullness
Examination - suspected gastric cancer
Usually absent unless late presentation with distant spread
Pallor Cachexia Lymphadenopathy Virchow node: left supraclavicular node Metastatic lesions Hepatomegaly Sister Mary Joseph nodule: periumbilical metastasis
2WW Criteria - gastric cancer
• Upper abdominal mass consistent with gastric cancer, OR
• Dysphagia, OR
• > 55 years with weight loss and one of the following:
○ Upper abdominal pain
○ Reflux
o Dyspepsia
Dx of gastric cancer
- OGD +/- biopsy
- CT/MRI staging
- Bone scan - mets
- USS for lymph nodes
Management of gastric cancer
Medical • Chemo & radiotherapy - 5FU • Targeted monoclonal abs - HER2 Surgical Gastrectomy - full or partial
Pancreatitis cancer - most common type
Ductal adenocarcinoma (85%)
Risk factors for pancreatic cancer
Age, smoking, alcohol, chronic pancreatitis, diabetes, hereditary syndromes (BRCA, FAMMM), genetics
Clinical presentation of pancreatic cancer
Later presentation
Jaundice, abdo pain & unexplained weight loss
diarrhoea, steatorrhoea, dark urine, new onset diabetes, signs of metastasis
2WW criteria for pancreatic cancer
New onset jaundice >40yrs
>60yrs w/ unexplained weight loss +: diarrhoea, constipation, back pain, abdominal pain, nausea, vomiting or new onset diabetes
Investigations for pancreatic cancer
Bloods: FBC, U&Es, LFTs, clotting, Ca19-9. CEA
Imaging: USS, CT/MRI pancreas, CT-TAP, PET staging, ERCP
Biopsy
Treatment of pancreatic cancer
Medical - chemo (pal), pain control, nutritional support
surgical - <20% suitable, Whipple’s (possibly) for HOP tumours with no vascular involvement or mets
Definition of primary biliary cirrhosis
Typical patient?
Chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis and ultimately cirrhosis
Typical patient - female (9:1), around 50yrs old, may have a family hx
Pathophysiology of PBC
Autoimmune attack of small intrahepatic bile ducts. Damage & destruction of these ducts causes obstruction of the outflow of bile (cholestasis). This leads to a backpressure into the liver which causes irritation leading to fibrosis, cirrhosis & liver failure.
Bile acids, bilirubin & cholesterol are no longer being excreted through bile ducts into intestines & so they build up in the blood - cause itching, jaundice, increased risk of CVD.
Aetiology & Risk factors for PBC
unknown exact cause, most likely GxE
Possible environmental triggers
Infection, pollutants, bacteria
Female sex
Middle aged
Other AI conditions e.g. thyroid, coeliac
Rheumatoid conditions e.g. systemic sclerosis, Sjogren’s & RA
Clinical features of PBC
Can be incidental finding on blood tests - persistently raised ALP & cholesterol Fatigue Pruritis GI disturbances Abdominal pain Jaundice Pale stools Xanthoma/xanthelasma Signs of CLD - ABCDE
Investigations for PBC
Bloods
• FBC
• U&Es
• LFTS - raised ALP & GGT, bilirubin (can be normal or raised in later stages)
• Clotting - prolonged PTT
• Autoantibodies - anti-mitochondrial antibodies (most specific to PBC) & anti-nuclear antibodies
• ESR - raised
• Immunoglobulins - IgM raised
Imaging
• USS - excludes extrahepatic biliary obstruction e.g. gallstones, strictures
• Liver biopsy - diagnostic & used in staging
Management of PBCMedical
- Ursodeoxycholic acid - reduced intestinal absorption of cholesterol
- Colestyramine - bile acid sequestrate, can help with pruritis
- Immunosuppression is considered in some patients
Surgical
• Liver transplant - in end stage liver disease
Monitor & treat complications
Aetiology of Bowel Obstruction
Mechanical: small (adhesions, hernia, malignancy, intussuspection), large (colorectal cancer, volvulus, diverticular strictures)
Non-mechanical: pan-intestinal (paralytic ileus), colonic (acute colonic psuedo-obstruction)
Clinical features of bowel obstruction
Abdominal pain, distension, vomiting & obstipation
Anorexia
Small bowel diarrhoea
Complete constipation
Abdominal tenderness/peritonism
Rebound
Abdominal distension
Abdominal mass
Investigations - bowel obstruction
Bedside - observations, ECG, fluid balance, catheter, PR examination, pregnancy test
Bloods - VBG/ABG (lactate), FBC (WCC), U&Es (electrolytes, dehydration), LFTs, clotting, CRP (high),
amylase, group & save
Imaging - erect CXR (free air), abdominal XR (dilated bowel loops), CTAP
Bowel dilation limits on X-ray
Small - >3cm
Large - >6cm
Caecum - >9cm
Management of Bowel Obstruction
Conservative/supportive - NBM, Drip & Suck, analgesia, anti-emetics, abx if needed, correction of electrolytes
Endoscopic - decompression, stenting
Surgery - resection, laparotomy/laparoscopy
Pathophysiology behind appendicitis & aetiology
Obstruction of lumen of appendix
Stasis & bacterial overgrowth, increase in intraluminal pressure, venous congestion & ultimately arterial compromise leading to necrosis
Aetiology - faecoliths, lymphoid hyperplasia, carcinoid tumours, fibrous strictures
Clinical Features - Appendicitis
Colicky abdominal pain migrated to RIF & becomes constant
Symptoms: Abdominal pain, RIF pain, nausea, anorexia, constipation
Signs: RIF tenderness, percussion tenderness, localised guarding, tachycardia & pyrexia
Rovsing’s Sign - palpation in LIF causes pain in RIF
Investigations - Appendicitis
Bedside - examination, observations, urine dip & pregnancy test
Bloods - FBC, U&Es, LFTs, clotting, amylase, CRP, group & save
Imaging - USS (+ pelvic to r/o gynae) & CT can confirm dx in older patients
Management of appendicitis
Conservative - for acute uncomplicated appendicitis (antibiotics - co amoxiclav)
Surgical - laparoscopic appendectomy/open if needed, pre-op co-amox & post op 7days abx if pus or perforation
Definition & Pathophysiology of Acute/Ascending Cholangitis
Acute infection & inflammation of biliary tree
Usually occurs due to bacterial overgrowth after obstruction of biliary tree
Aetiology - Acute Cholangitis
• Choledolithasis - stones in biliary tree • Benign Strictures • Chronic pancreatitis • Iatrogenic injury (e.g. during cholecystectomy) • Radio / chemo-therapy • Idiopathic • Malignant Strictures • Pancreatic cancer • Gallbladder cancer Cholangiocarcinoma
Clinical Presentation - Acute Cholangitis
• Charcot’s Triad - RUQ pain, jaundice & fever
Nausea & vomiting
Investigations - Acute Cholangitis
Bedside
• Observations
• ECG
• Urine dip & cultures
• Pregnancy test - in female patients of child bearing age
Bloods
• FBC - WCC
• U&Es - dehydration
• CRP - inflammation
• LFTs
• Amylase
Imaging
• USS - useful in checking presence of stones
• CT - good visualisation of the biliary tree, evaluate for abnormal lesions/tumours or where other dx
MRCP - offers excellent visualisation of the biliary tree. Often used where CT/USS are inconclusive.
Management of acute cholangitis
Antibiotics
Fluids
Analgesia
Biliary Drainage - ERCP/Percutaneous transhepatic cholangiography
Definitions of diverticulosis, diverticular disease & diverticulitis
Diverticulosis - presence of diverticula (outpouching of colonic mucosa & submucosa through muscular wall of large bowel)
Diverticular disease - diverticulosis a/w complications e.g. haemorrhage
Diverticulitis - acute inflammation & infection of diverticula
Risk factors for diverticulitis
Diet - red meat, low fibre Smoking Obesity Family history Medications - NSAIDs increase risk of perforation
Clinical presentation of diverticulitis
Abdominal pain, fever & tenderness in LIF Anorexia Nausea Guarding Tachycardia
Investigations - Diverticulitis
CT abdomen pelvis is imaging modality of choice for diagnosis of diverticulitis
• Bedside: observations, urine dip & pregnancy test
• Bloods: FBC, U&Es, LFTs, CRP, amylase, clotting, G&S
• Imaging: CT abdo pelvis w/ contrast ideally
Management - Diverticulitis
Very dependent on severity & this can range significantly
• Consider inpatient vs outpatient management
○ Outpatient - fit & healthy, younger patients w/ mild disease
○ Inpatient - older, more frail patients w/ more severe disease
• Antibiotics; Co-amoxiclav or ciprofloxacin (if penicillin allergic)
○ OP - 7 day course
○ IP - IV abx regime
• Analgesia; paracetamol
○ Avoid NSAIDs & opioids due to increase risk of perforation
• Follow-up
○ Patients managed in the community should be reassessed at 48 hours and given appropriate safety-net advice.
○ Outpatient colorectal follow-up and colonoscopy (if appropriate) should be arranged.
Complications - Diverticulitis
Bowel strictures
Fistula
Diverticular Bleed
Types & Aetiology - Jaundice
TYPES & CAUSES
1) Pre-hepatic; increased hemolysis, livers ability to conjugate is overwhelmed hemolytic anaemia, Gilbert’s syndrome
2) Hepatic; dysfunction of liver, mixed picture HCC, cirrhosis, iatrogenic, drugs, AIH
3) Post-hepatic; obstruction intramural (gallstones), mural (cholangiocarcinoma), extramural (abdominal masses
Jaundice - INTERPRETATING LFTs & URINE
Pre-hepatic = normal LFTs, increased urobilinogen (urine), no bilirubin in urine Hepatic = all round bad LFTs, mixed picture on bilirubin in urine Post-hepatic = classic cholestatic LFTs (increased GGT, ALP), bilirubin+++ urine (dark), no sterco (pale stools)
‘Types’ - Ascites
Transudate (little/no protein)
Exudate (protein)
SAAG; >1.1 = transudate
Transudate fluid - ultrafiltration of plasma due to raised portal pressure
Exudate tends to be leakage of whole contents of plasma due to inflammatory causes (normal portal pressure)
Causes of Ascites
Transudate: Cirrhosis Congestive cardiac failure Acute liver failure (trauma, OD) Liver metastasis HVT or PVT
Exudate: Infection – bacterial, fungal, TB Malignancy Pancreatitis Nephrotic Syndrome Bowel Obstruction
