GI Flashcards
F
Classify causes of dysphagia (3)
dysphagia - difficulty swallowing
- Obstruction (mechanical block) - luminal, mural, extra-mural
- Motility - local or systemic
- Inflammatory
Causes of dysphagia (2-3 each)
- obstructive
- motility
- inflammatory
Obstructive
- malignancy (oesoph/lung/mets)
- benign stricture (Plummer-Winsen/web)
- pharyngeal pouch (Zenker’s diverticulum)
- hiatus hernia
- Foreign body
Motility
- local - achalasia, MND (pseudobulbar palsy), stroke
- systemic - CREST syndrome, Sjorgren’s
Inflammatory
- oesophagitis (esniophilic, candida)
- tonsillitis
- IBD - apthous ulcers
Other
- globus hystericus (anxiety-related)
- oesophageal spasm
Dysphagia
Both solids and liquids means …
Just solids means…
Motility problem
Obstructive problem
Achalasia - definition, presentation
- A local motility disorder of the oesophagus, rare & often idiopathic.
- Presents with dysphagia, regurgitation, retrosternal pressure
Achalasia - findings from investigation (3) and mngmnt
medical, interventional andn surgical
- Inv - barium swallow (tapering of oesophagus - bird’s beak) OGD (rule out malignancy), manometry (shows reduced peristalsis)
- Mngmnt - CCB/nitrates prior to meal
- or Heller’s cardiomyotomy or BOTOX.
2WW referral guidelines for Upper GI cancer
- Any age with recent onset dysphagia or abdominal mass
- Or >55 with ALARMS symptoms
req 2WW for direct access upper GI endoscopy w/biopsy
ALARMS sx
Anaemia - iron deficiency (check Hb)
Loss of weight
Anorexia
Recent onset of progressive sx
Malaena/haematemesis (chronic GI blood loss)
Swallowing difficulty (dysphagia)
Medication classes causing dyspepsia (5)
- NSAIDs
- CCBs
- Nitrates
- Bisphosphonates
- Oral steroids (e.g. Pred)
Most common causes of dyspepsia (5)
- GORD
- Peptic ulcer disease
- Upper GI malignancy
- Funcitonal dyspepsia
- Gastritis
Gord - initial investigations & further inv (if necessary)
2WW if ALARMS/>55 with dysphagia/mass
Otherwise:
- H.pylori test (stool/urea breath/CLO rapid urease test)
- PPI trial (4 weeks)
Consider
- OGD w/biopsy
- Manometry
- Ambulatory ph monitoring
GORD - management
Conservative, medical, surgical
Conservative - lifestyle advice
Medical - PPI (Omeprazole) 8 weeks
Surgical - laporoscopic fundoplication
Peptic ulcer disease -
What sx are common to both gastric and duodenal uclers?
Distinguishing sx between the 2.
Sx - epigastric pain, nausea/vomiting, bloating.
Gastric (50-70yrs) - pain worsened by eating, associated with weight loss.
Duodenal (30-50 yrs, more common) - pain relieved by eating, associated with weight gain.
Complications of PUD (4) & signs
- Perforation (causes peritonitis –>guarding and referred pain to shoulder)
- Bleeding (malaena, haematemesis or iron def anaemia)
- Gastric outflow obstruction (if ulcer in pylorus) - nausea and vomiting
- Malignancy (H pylori associated)
most common artery for bleeding due to peptic ulcer
gastroduodenal
Medications that increase risk of PUD (4)
- NSAIDs
- SSRIs
- Oral corticosteroids
- Bisphosphonates
Medical management for proven PUD (no active bleeding)
- Full dose PPI for 1-2 mo OD
- Then long term low dose PPI PRN
other management - lifetsyle advice
How long should PPIs be stopped before doing OGD?
2 weeks
Ruptured peptic ulcer
Px: epigastric pain –> generalised
Ix and finding
Erect chest xray - pneumoperitoneum
and CT Abdo
What is Zollinger-Ellison syndrome?
Which test would be helpful?
A MEN-1 related condition caused by a gastrinoma, causing recurrent gastroduodenal ulcers, diarrhoea and malabsoprtion.
Bloods - fasting gastrin levels
Upper GI bleed: classification (3 categories)
upperGI = proximal from the ligament of Treitz (suspends the duodenojeju
Variceal
- oesophageal/gastric varices (CLD)
- Mallory-Weiss tear
Non-variceal
- Oesophagitis
- PUD
- Diverticular disease
Other
- Meds
- Bleeding disorder
- Aortic-enteric fistula
Upper GI bleed - acute managment
ABATED:
A-E
Bloods: FBC, U&E, LFT, coags, cross-match
Access: 2 x wide bore cannula
Transfuse: keep Hb >80. Or crystalloids.
Endoscopy (OGD): 4hr/24hr. Endoscopic intervention.
Drugs: stop NSAIDs and anticougulants.
What does the Glasgow-Blatchford score indicate, using what 3 parameters (+ other)?
Endoscopy within 4hr or 24hr.
Or if 0, consider discharge.
Takes into account urea, Hb, systolic BP and other signs (shock, cardiac/hepatic failure, pulse rate)
What does the Rockall score show?
What does >=3 initial and >=6 final indicate?
Mortality/riskof rebleed for patients after endoscopy - used for patients before endoscopy and after to determine suitability for surgery
>=3initial/>=6 = low risk for surgery
sort the blotch (G-B score) and then rock on (Rockall score)
What factors does the Rockall score take into account?
CASEE
- Comorbidities
- Age
- Signs of Shock
- Endoscopic findings (final score)
- AEtiology/cause of bleed
mortality following OGD for Upper GI bleed
Variceal management during OGD before UGIB?
For gastric/oesophageal varices?
Before - Terlipressin & IV Abx
During OGD:
* Oesophageal - band ligation
* Gastric - injection N-butyl-2-cyanoacrylate
Other options:
* balloon tamponande - Sengstaken Blakemore tube
* TIPSS - transjugular intrahepatic portosystemic shunt
Indications for surgery following UGIB (3)
- Rockall score >=3 initial or >=6 final
- Re-bleed
- Bleeding requiring >6 units or excessive perioperative bleeding
Coeliac disease is an autoimmune condition whereby antibodies are produced in response to gliadin. Malabsorption of the following results in which symptoms/complications:
- Carbs
- Proteins
- Fats
- Vitamin B2 (riboflavin)
- Vitamin B1 and B6
- Folate and iron
- Ca2+ and Vitamin D
- Vitamin K
- Diarrhoea, bloating, abdominal pain, weight loss
- Protein losing enteropathy (if severe)
- Steatorrhoea
- Angular stomatitis
- peripheral neuropathy
- anaemia
- osteoporosis
- ptechiae and reduced INR
Which 2 cancers are associated with Coeliac disease?
And what 3 autoimmune conditions?
EATL (Enteropathy associated T-cell lymphoma)
NHL (non Hodgkin-lymphoma)
DM
Primary bilary cholangitis
IgA deficiency
What blood tests are diagnostic for Coeliac disease?
anti TTG (95%)
anti-EMA
+ IgA in most but may have IgA deficiency
Typical endoscopic findings for coeliac (3)
- Villous atrophy
- Crypt hypertrophy
- Intra-epithelial lymphocytes
Why are coeliacs offered a pneumococcal vaccine?
Functional hyposplenism
Dermatological condition found in 15% of coeliac patients (pruritic, vesicular rash found on extensor surfaces)
Dermatitis herpetiformis - treat with dapsone or gluten-free diet
IBD - bimodal distribution for Crohn’s and UC
UC: 15-25, 55-65.
Crohn’s: 20-30, 60-70.
Macroscopic findings in UC/Crohns
- depth of inflamation
- type of ulceration
- continual/segmental
- thickening/non-thickening
- additional features
UC
* mucosal inflammation
* “denuded”, shallow
* continual
* non-thickening
* psuedopolyps
Crohn’s
* transmural inflammation
* cobblestone appearance
* segmental “skip lesions”
* thickening
* fistulae, “rose-thorn ulcers”
Microscopic changes in UC vs Crohns (3)
UC:
non-granulomatous
goblet cell depletion
crypt abscess formation
**Crohns: **
non-caseating granulomatous (in 50%), goblet cell hypertrophy
lymphocytic infiltration
basically everything is more intense/deep/dramatic in Crohn’s at micro/macroscopic level except for crypt abscesses - they are more common in UC
Complications of UC vs Crohn’s (2-3 each)
UC
1. Toxic megacolon
2. CRC
3. Primary sclerosing cholangitis
Crohn’s
1. Fistulae
2. Strictures
3. Bowel obstruction
4. Small bowel cancer (and CRC but less than for UC)
5. Osteoporosis
lower risk of GI malignancy in crohn’s than UC
Dermatological manifestations in IBD (2)
Erythema nodosum
Pyoderma gangrenosum
Inv - IBD
- Bloods - FBC, LFT, CRP, Haematinics, Blood cultures
- Stool - MC&S and faecal calprotectin
- Colonoscopy
- Barium enema (UC) or small-bowel follow-through (Crohn’s)
if non-diagnostic - further imaging e.g. U/S or MRI small bowel
Imaging modality for TMC or bowel obstruction
X-ray Abdo
Medical management of Crohn’s - first line for:
* Inducing remission
* Maintaining remission
- Glucocorticoids - oral/topical/IV (Prednisolone/Budesonide)
- Immunomodulators (Azathioprine/Mercaptopurine)
2nd line to induce remission is 5-ASA, and for maintenance is Methotrexate.
Medical management of UC - first line for:
* Inducing remission
* Maintaining remission
- Aminosalicylates (5-ASA) - Sulfasalazine/Mesalazine, rectal and/ororal
- same
Mx Flare-ups UC
Severity guaged by Truelove and Witt criteria
* Severe, aka >=6 bloody stools per day
* Mild-moderate (proctitis, proctosigmoid, L sided)
* Mild-moderate (extensive)
* Post severe relapse or >2 exac. in yr
- Severe: Admission; IV steroids (+/- IV Clicosporin if no improv in 72hr)
- Topical ASA –> oral ASA (4 weeks) if remission not acheived
- Topical ASA and oral ASA - e.g. Mesalazine x2
- Same but keep on low maintenance dose of Mesalazine
- Oral immunosuppressants: Azathioprine/Mercaptopurine
Surgical options for Crohn’s patients (3)
- Ileocecal resection / other segmental small bowel resections
- Stricturoplasty
- Temorary loop ileostomy
What should be assessed before offering Azathioprine or Mercap?
TPMT activity
Surgical options for UC?
Removal of colon and rectum (panproctocolectomy) - permanent iloestomy/J pouch
What is terminal ileitis and what can it result in?
A complication of Crohn’s.
Malabsorption of bile salts (normally absorbed form terminal ileum) –> Gall stones.
Liver Function Tests
Which LFTs suggest hepatocellular picture, a cholestatic picture, and which are indicators of hepatic synthetic function?
*** Hepatocellular: **aminotransferases (ALT and AST)
* Cholestatic: yGT and ALP
* Synthetic: Albumin, Prothrombin Time and Bilirubin
Liver Function Tests
Ratio indicatiing hepatocellular picture and cholestatic picture
Hepatocellular: ALT/ALP >5
Cholestatic: ALT/ALP <2
Note a “rise” in ALT is 10x and a rise in ALP is 3x.
ALT = Liver Trouble.
ALP= Liver Plus.
Liver Function Tests
Comparing the 2 aminotransferases (ALT and AST) what can be deduced?
AST>ALT: Alcoholic hepatitis or cirrhosis
Liver Function Tests
ALP gives an indicator of dysfunction in which areas?
Liver Plus:
biliary system and bones
- vitamin D deficiency, bony mets, bone tumours, #s, renal osteodystrophy
Pre-hepatic causes of jaundice (3)
and example for each
Increased production of bilirubin - UCB
- Haemolysis (G6PD deficiency, Hereditary sphero, Rhesus)
- Haemorrhage (ruptured AAA)
- Ineffective erythropoesis (thalassemia)
Hepatic causes of jaundice (unconjugated and conjugated)
reduced uptake, conjugation, excretion & hepatocellular dysfunction - mixed picture UCB/CB
Unconjugated
- Crigler-Najar
- Gilbert’s
- Hypothyroid
- Physiological jaundice of newborn
(drugs)
Conjugated
- Dubin Johnson
- Rotor
- liver disease (hep A/B/C, AIH, Wilson’s, Haemochromatosis, Budd-Chairi, Alpha-1 antitrypsin deficiency)
- Ca
- drugs
Post-hepatic causes of jaundice (infectious/mechanical)
obstructive jaundice - CB
Infectious
- Cholecystitis
- Cholangitis
Mechanical
- cholangiocarcinoma
- pancreatic cancer (painless jaundice)
- stricture
- gall stones
- PBC/PSC
Distinguish Primary bilary cholangitis (PBC) from primary sclerosing cholangitis (PSC).
Difference in autoantibodies?
PBC - fibrosis affects intrahepatic ducts, AMA
PSC - stricture formation affecting both intra & extra-hepatic ducts (bead on string appearance), pANCA
psc affects ALL (pan) over liver and extrahepatic ducts
What is acute liver failure?
Characteristic smell of breath?
Rapid onset of liver dysfunction, characterised by
1. Coagulopathy - raised PT
2. Encephalopathy - confusion
3. Abnormal LFTs - hepatocellular picture
4. Jaundice
-“sweet faecal smell”
Causes of ALF and acute-on-chronic LF
- Drugs - DILI (most common cause)
- Viral - hep A, B, E, CMV, EBV
- Vascular- Budd-Chairi, ischemic hepatitis
- Pregnancy - acute fatty liver of pregnancy, HELLP
- Other - autoimmune, other liver diseases
Investigations for ALF (4)
- Urgent Bloods - e.g. FBC, U&E, LFT, coags - INR and PT
- ABG? - metabolic acidosis
- Non-invasive Liver Screen (NILS) - paracetamol, auto-immune markers, caeruloplasmin, copper, viral)
- Imaging - abdo U/S (doppler for vascular causes)
Other - e.g. liver biopsy, ascitic tap, urine toxicity screen
hepatotoxic drugs (9)
VAMPPPIRES
Valproate
Amiodarone
Methotrexate
Pyrazinamide
Paraceatmol
Phenytoin
Isoniazid
Rifampicin
Ethanol
Simvastatin, Salicylates
How does acute liver injury differ from acute liver* failure*?
And acute-on-chronic liver failure?
ALI: liver damage and impaired liver function but without hepatice encaphalopathy.
ACLF: acute decompensation of liver disease associated with organ failure
Managing Acute Liver Failure - stop hepatotoxics, and treat underlying cause:
- Encephalopathy?
- Coagulopathy?
- Hypoglycaemia?
- Paracetamol overdose (DILI)?
- Autoimmune hepatitis?
- Opioid overdose (DILI)?
- Hepatorenal syndrome?
- Lactulose & Rifamixin
- IV Vit K, Plt, FFP (or blood transfusion)
- IV Glucose
- N-AC
- Immunosuppression - Azathioprine
- Naloxone
- Terlipressin (?TIPSS/haemodialysis), ICU
Severe flare-ups of UC - grading for mild, moderate and severe
Mild = 4 stools per day (with small amount of blood)
Moderate = 4-6 (varying amounts of blood)
Severe = >=6 bloody stools & systemically unwell
What are the treatment options for Barrett’s oesophagus (finding of gastric or intestinal epithelium within the oeophagus) - if metaplasia or dysplasia are found?
- Metaplasia - endoscopic surveillance w/biopsy (3-5yrly)
- Dysplasia - endoscopic intervention (mucosal resection or radiotherapy abalation)
- PPIs may help (?) at early stage
Alcoholic hepatitis - what blood results would you expect?
FBC
LFT
FBC - raised MCV (macrocytic anaemia)
LFT - AST/ALT >2
What can be used short term to manage acute episodes of alcholic hepatitis?
Hint - Maddrey’s discriminant function can help determine if patients would benefit this or not.
Prednisolone.
There are 3 types of autoimmune hepatitis, mainly affecting women. What antibody is associated with each?
Type 1 (Adult) - SMA+ and ANA
Type 2 (Child/Teen) - LKM+
Type 2 (Adult) - SLA+
Presentation of autoimmune hepatitis and distinguishing sx for type 1 and type 2
Jaundice, fatigue, general stigmata of liver disease.
Type 1 - gradual onset.
Type 2 - acute onset and amenorrhoea
Management of autoimmune hepatitis (2 options)
Prednisolone.
Azathioprine.
End stage - liver transplant.
What is NAFLD associated with, and what mechanism is behind this?
List the 4 stages.
NAFLD is thought of as the hepatic manifestation of metabolic syndrome (DM, HTN and obesity) - with insulin resistance being the key mechanism leading to steatosis.
1. NAFLD
2. NASH (non-alcoholic steatohepatitis)
3. Fibrosis
4. Cirrhosis
How is NAFLD diagnosed?
What is the first line investigation to assess degree of fibrosis?
What can be used to rule out fibrosis?
What other investigation could be done?
- On U/S scan - often incidental finding as “echogenicity” as NAFLD normally asx (or vague RUQ pain).
- 1st line - ELF (ENHANCED LIVER FIBROSIS) blood test
- the NAFLD fibrosis score
- FibroScan- measures elasticity of liver
Hep A: genome, acute/chronic, transmission, vaccine?, other.
- +ss RNA
- acute
- faecal-oral (shellfish)
- yes (e.g. travellers)
- most common worldwide & self-limiting.
Hep B: genome, acute/chronic, transmission, vaccine?, other.
- ds DNA (both strands)
- Both acute and chronic (in 10%)
- Blood and bodily fluids - e.g. IVDU, MSM, perinatal
- yes - routine (part of 6 in 1)
- supportive care + monitoring for complications ?antivirals.
Hep C: genome, acute/chronic, transmission, vaccine?, other.
- ss RNA
- Chronic (in 80%)
- Blood (mainly); IVDU, perinatal
- X
- risk of ** cirrhosis** in 1/3 and hepatocellular **carcinoma ** - monitoring (Fibroscan), direct acting antivirals. Most common in UK.
Hep D: genome, acute/chronic, transmission, vaccine?, other
- ss RNA
- Acute & Chronic
- Blood & bodily fluids
- x but hep B vaccine protective
- satellite virus - only survives in pts with Hep B (co/super-infection)
Hep E: genome, acute/chronic, transmission, vaccine?, other
- ss RNA
- Acute (chronic in immunosuppressed/pregnant)
- Faecal-oral (pork)
- X (except china)
- self-limiting.
A-1 ATD is an inherited cause of chronic liver disease. Mutant A1AT enzymes build up in the liver causing cirrhosis. What other organ is affected?
Lungs (COPD - emphysema, and bronchiecstasis).
*Due to faulty A1AT –> uninhibited neutrophil elastase enzyme –> breakdown of connective tissues
A1AT deficiency
Diagnostic markers (bloods & liver biopsy & CT thorax)
Management (2)
- Low serum A1AT
- Anti-Schiff + staining globule
- emphysema/bronchiecstasis
- smoking cessation, sx mngmnt, monitoring/transplant
What is hereditary haemochromatosis? (3)
- An inherited form of CLD (faulty HFE gene), autosomal recessive
- causes excessive iron deposition in tissues
- affects mainly heart, endocrine system, joints, liver and skin (IRON MEALS)
Myopathy (cardio)
Endocrine - hyp pituitarism
Arthritis
Liver - hepatomegaly, cirrhosis, carcinoma
Skin - slate grey
Endocrine manifestations of hereditary haemochromotosis (4)
- Thyroid - hypothyroid
- Parat- low Ca2+
- Gonads - amenh/infertility
- pancreas - t1dm
impairsfjunction of endocrine organs - reduced thyroid hormone, pth, gon
Bloods in HH - raised or reduced?
serum Fe
ferritin
transferrin
TIBC
- raised serum Fe
- raised ferritin
- raised transferrin
- reduced TIBC (not many free transferrin molecules available to bind to due to iron overload)
liver biopsy - perl’s stain
HH mngmnt (2)
Venesection
Deferrioxamine
monitoring vensection: transferrin<50% and ferritin <50 ug/l
What is Wilson’s disease?
What 3 systems does it mainly affect…
- Inherited cause of CLD
- Inability to remove copper from liver –> build-up in tissues
- Affects mainly CNS (psychosis, dementia, Parkinson’s - basal ganglia), eyes (corneal deposits - Kayser-Fleishcer rings), Liver (hepatitis, cirrhosis)
Also
- kidneys - Fanconi syndrome (RTA)
- bones - osteopenia
Inv for WIlson’s - bloods & 24hr urinary copper excretion, geentic analysis of ATP7B gene.
Blood findings - raised or reduced?
* Serum Careuloplasmin
* Total serum copper (aka careuloplasmin bound)
* Free serum copper
- Reduced careluoplasmin
- reduced total serum Cu
- increased free serum Cu
in wilson’s the copper reduced is “free”. total serum Cu refers to careulolasmin bound copper. because Cu isn’t bound to ceruloplasmin it builds up in organs.
Ferritin and careuloplasmin are both acute phase proteins - what conditions can they be raised in?
cancer
other causes of inflammation
Management - Wilson’s
Copper chalation (Pencillamine)
Primary bilary cholangitis:
affects which ducts?
antibodies?
Associations?
biopsy finding?
typical patient presentation?
_ rule…
LFTs?
- intrahepatic ducts
- AMA
- autoimmune conditions or no underlying pmhx (RA, Sjorgrens, coeliac)
- non-caseating granulomas
- middle aged female with jaundice and pruritus
- m rule: IgM, AMA, middle-aged “mum-type”
- raised yGT and ALP
- Risk of cirrhosis and hepatocellularcarcinoma
Primary sclerosing cholangitis
affects which ducts?
antibodies?
Associations?
biopsy finding? MRCP finding?
- both intra & extrahepatic ducts
- pANCA
- CRC, cholangiocarcinoma, UC (IBD)
- fibrotic cholangitis (liver biopsy) - onion skin appearance
- and beads on string appearance - stricture formation (on MRCP)
- jaundice, RUQ pain
sclerosing - more severe - risk of cancer (cholangiocarcinoma and crc)
General presentation of PBC and PSC
- often asx
- jaundice & pruritus
- RUQ in PSC
- more sx in PBC - e.g. xanthelasma,osteoporosis, steatorrhoea, and jaundice is late finding
Management for PBC and PSC (3)
- Immunosuppression - PBC
- Ca screening - PSC
- sx management - pruritius (colystyramine), cholesterol lowering (ursedeoxycholic acid)
- Liver transplant if bilirubin >100 in PBC
What is Budd-Chairi syndrome?
Typical triad of sx?
What would you expect the result of the serum:ascites albumin gradient to be?
- Hepatic vein thrombosis.
- Associated with hypercoaguable states (thrombophilia, pregnancy, COCP).
- Diagnosed by hepatic doppler.
- Sudden RUQ pain, ascites, hepatomegaly in context of a procoagulant state
- Raised; SAAG greater than 11 - shows that ascites is due to portal vein hypertension
Signs of liver cirrhosis include spider naevi, ascites, straiae, leuconychia, palmar erythema, clubbing, pallor & xanthelasma.
What are the main complications (5)?
- Hepatic encephalopathy
- Portal HTN - oesophageal varices (risk of bleeding out)
- Hepatocellular carcinoma
- Hepato-renal syndrome
- Ascites (–> SBP in 10%) - causative organism of staph epidermidis
What causes portal htn?
Liver cirrhosis causes increased resistance to blood flow entering the liver via the portal vein (from the gut). This results in a backflow pressure–> veins at anastomosis between the portal and the systemic venous system become swollen & torturous (varices).
Types of Ascites:
Transexudative (low protein content in ascites, more in blood SAAG >10) - causes
Exudative (high protein content in ascites, less in blood, SAAG <10)
Transexudative: portal hypertension
- Liver disease (cirrhosis, alcoholic liver disease, acute liver failure, mests)
- Cardiac disease (heart failure, constrctive pericarditis)
- Budd-Chairi syndrome (hepatic vein thrombosis), portal vein thrombosis, veno-occlusive disease, myxoedma
Exudative:
- Hypoalbuminaemia (nephrotic syndrome)
- Infection
- Malignancy
- Pancreatitis
- Bowel obstruction
- Bilary ascities
4 sites of varices (result of portal HTN)
- Gastro-oesophageal junction
- Rectum
- Ileocecal junction
- Anterior abdo wall (caput medusae)
Describe the fluid in ascites from liver cirrhosis, and 4 aspects of management - conservative, medical, interventional, prophylactic
Transudative (low protein content).
1. Low Na2+ diet
2. Paracentesis (ascitic tap or drain)
3. Rx - Spironalactone (diuretic)
4. Abx prophlyaxis for SBP (Ciprofloxacin)
SBP causative organism and rx
E Coli or Klebsiella
Aspiration –> Culture –> then abx e.g. Cefotaxime
What happens to kidneys in hepatorenal syndrome?
- Portal vein HTN causes pooling of blood
- Hypoperfusion to kidneys
- Rapidly deterioating kidney function
- Fatal without liver transplant within 1 week
How do laxatives help in Hepatic Encephalopathy?
How do ABx (Rifamixin) help?
- H.E is due to build up of toxins in brain, namely ammonia
- Ammonia conc increased dued to impaired hepatocellular function and because it bypasses liver due to portal htn
- Lactulose helps clear ammonia from gut before it is absobred into blood stream (so cannot reach brain)
- Abx reduce number of ammonia producing bacteria in gut
What do the Child-Pugh Score & MELD score indicate in regards to cirrhosis?
- Child-Pugh: severity
- MELD: for decompensated cirrhosis: 3 month mortality, dialysis/transplant requirement
Causes of acute pancreatitis
I- idiopathic
G- gall stones
E - ethanol
T - trauma
S - scorpion bite
M - mumps + infection
A - autoimmune
S - steroids
H - hypercalcaemia, hyperlipidemia
E - ERCP
D - drugs
Mesalazine
Azathioprine
Diuretics
Didanosine
Sodium Valproate
Mechanism behind acute pancreatitis
- Early activation of zymogens
- Auto-digestion of pancreatic cells
Acute pancreatitis - severe epigastric pain radiating to back + vomiting, guarding, absent bowel sounds.
Name 2 rare signs shwing periumbilical discolouration and flank discolouration
Cullen’s
Grey-Turner’s
Acute pancreatitis: main investigations
Serum amylase (raised in 75%)
and other routine bloods (LFTs - cholestasis, FBC - raised WCC, CRP - raised)
ABG- O2 and lactate (assess severity with Glasgow score)
+/- Imaging
- can diagnose with presentation and raised amylase x3
- u/s abdo if other cause e.g. gall stones, ct if abscess
lipase is more sensitive and specific but not routinely used
What scoring system is used for severity of acute pancreatitis?
Glasgow (>=3 severe) - using PANCREAS criteria
Management - acute pancreatitis
- HDU/IDU, analgesia, iv fluids
- Treat underying cause - gallstones (ERCP/cholecystectomy), inf (abx) etc
Clinical presentation of chronic pancreatitis
- Chronic epigastric pain –> back
- Steatorrhoea
- Weight loss
- Diabetes
steatorrhoea due to reduced lipase production (unable to break down fats). weight loss due to pancreatic insufficiency. diabetes due to loss of endocrine function.
Pancreatic cancer presents (late) with
- painless jaundice and
- painless _______
or new onset/worsening ____
On MRCP the swelling of both the common bile duct and the pancreatic duct is known as what?
- painless palpable gall bladder (Courvoisier’s sign)
- diabetes mellitus
- cholestatic picture on LFTs
Double duct sign.
gall bladder palpable due to cancer in head of the pancreas - blocks the CBD.
PANCREATIC CANCER REFERRAL GUIDELINES FOR CT ABDO
>40 with jaundice
>60 with weight loss + additional symptom (change in bowel habit/back pain/new onset diabetes etc)
The radical pancreaticoduodenectomy is known as what?
Whipple’s procedure
for pancratic cancer - resect tumour in head of pancreas
pancreatic cancer has a poor survival rate
Main pathologies of the gallbladder (3) and of the bilary tree (3-4)
GB
1. Bilary colic
2. Acute cholecystitis
3. Gallstones
BT
1. Acute cholangitis
2. Cholangiocarcinoma
3. PBC and PSC
Distinguish acute cholecystitis from ascending cholangitis
- presenting symptoms
- management
Cholecystitis =
RUQ pain - may radiate to right shoulder
fever
Murphy’s sign positive (arrested inspiration on palpation of RUQ).
IV Abx & Lap chole (within 1wk).
Cholangitis =
Charcot’s triad: RUQ pain, fever, jaundice (fluctuating).
IV Abx & ERCP.
what is Mirizzi’s syndrome?
gall stone within cystic duct - puts pressure on the common hepatic duct, ccausing obstruction of bile. Gall stone presentation but with jaundice/ deranged LFTs.
2 week referral guidelines CRC (>40, >50, >60, other)
When to refer without a FIT test
Give FIT test to:
* >40 with weight loss & abdo pain
* >50 with unexplained rectal bleeding
* >60 with anaemia (even if not IDA)
Any age with abdominal mass, change in bowel habit or iron deficiency anaemia *
* If FIT positive –> refer 2ww
If negative –> safetynetting or refer if ongoing concern
Direct 2WW referral w/o FIT if rectal, anal mass or U/E anal ulceration
FIT screening
- 60-74
- every 2 years
- or for pt with new sx but not on 2WW
- +ve –> colonoscopy
Genetic causes of CRC (adenoma x2 hamartoma x2)
Other risk factors
- HNPCC (most common, also endometrial/ovarian/stomach ca )
- FAP (rare, but 100% get CRC)
- Peutz-Jegher (rare, polyps, multiple cancers, melanotic lip pigmentation)
- Juvenile polyposis syndrome (mostly benign “juvenile” polyps)
Risk factors
- IBD
- Diet (red/processed meat, low fibre)
- Obesity, sedentary lifestyle
- Smoking
- Alcohol
Investigations (CRC)
* Gold-standard
* Other alternatives
* Once cancer diagnosed
* Tests for predicting relapse in patients previously treated for CRC
- Colonoscopy
- Sigmoidoscopy; CT colonography (if less fit for colonoscopy)
- CT TAP - staging, mets
- CEA - tumour marker and CT Tap
CRC operations: removal of
* Right hemicolectomy
* Left hemicolectomy
* High anterior resection
* Low anterior resection
* Abdomino-perineal resection
* Hartmann’s procedure
- caecum, ascending colon, hepatic flexure, proximal transverse colon,
- distal transverse, descending colon
- sigmoid colon (also called sigmoidectomy)
- sigmoid colon + upper rectum
- rectum+ anus (permanent colostomy as anus sutured)
- emergency procedure for acute obstruction (CRC, volvulus, diverticular disease) - sigmoid colectomy + end colostomy formation; temporary colostomy bag before reversal once pt optimised)
What is Low Anterior Resection syndrome?
- Increased bowel urgency, frequency,l incontinence
- difficulty controlling flatulence
Diverticulitis - acute abdominal pain (LIF) & systemic features. Gold standard test? Rx for uncomplicated diverticulitis?
CT Abdo
Co-amoxiclav
Hinchey Staging
Ischemic bowel disease can be split into acute mesenteric ischemia, chronic mesenteric ischemia and ischemic colitis.
All present with abdominal pain. How can they be distinguished?
- Acute mesenteric: embolusof artery supplying small bowelcausing sudden abdo pain and lactic acidosis (req surgery)
- Chronic mesenteric: “intestinal angina” - colicky, rare condition
- Ischemic colitis: compromise to blood supply of large bowel, non-embolic. Affects watershed areas most (e.g. splenic flexure). Thumb-printing on Abdo XR (conserv mngmnt).
Bowel obstruction: mechanical/functional obstruction resulting in proximal dilatation & increased peristalsis & vomiting (from backflow of pressure).
1. Distinguish closed loop and open loop.
2. Presentation of small vs large bowel obstruction.
3. 3 main causes.
- Closed loop - obstruction at both ends e.g. volvulus, adhesions, or large bowel with competent ileocecal valve. Req emergency surgery. Open loop -
- Vomiting (green, bilious), tinkling bowel sounds- small bowel. Vomiting less likely, and absent bowel sounds - large bowel. Both present with abdominal pain, distension, absolute constipation and reduced flatus
- Adhesions, hernias, cancer
also volvulus, diverticular disease, strictures, intussusception (children 6mo-2yrs)
Abdo x-ray findings (large vs small bowel )
Haustra (large bowel) do not extend full width.
Valvulae conninentes extend full width (small bowel)
What is “third spacing”?
What does it result in?
- Abnormal loss of fluid from the small bowel into the blood stream. E.g. in small bowel obstruction the fluid is unable to pass into colon where it would be reabsorbed.
- Hypotension & shock.
Blood findings, abdo x-ray, and mngmnt of bowel obstruction
- e- imbalance
- metabolic alkalosis
- raised lactate
- bowel loop dilatation
- drip & suck (iv fluids & NG tube)
- usually surgical intervention (e.g. stent, hernia repair etc)
What is paralytic ileus?
Presenting symptoms?
Finding on examination?
investigations?
mx?
- functional obstruction - temporary halt of peristalsis after surgery/inflammation/e- imbalance
- abdo pain, distension, N&V, consitpation, inability to pass flatus
- “sluggish” bowel sounds
- bloods - notably U&E (K+, Mg, PO4)
- Initially NBM +/- NG tube, drip and suck
Cholangiocarcinoma
cancer within the intrahepatic or extrahepatic bile ducts, most commonly the perihilar region
* Risk factors (2)
* Presentation - obstructive jaundice (3) and generalised signs (3)
* Couvoiser’s law states a palpable gallbladder + jaundice is most likely to be -
* Ix
* patients are managed with MDT and most aren’t curative (radio and chemo). What does pallaitive treatment involve?
- Primary sclerosing cholangitis (UC)
- Liver flukes (parasite)
- Pale stools/dark urine, pruritus
- weight loss, RUQ pain, palpable gallbladder, hepatomegaly
- Cholangiocarcinoma or pancreatic ca (typical cause of painless jaundice)
- Bloods - CA-19.9 (raised in cholangio and pancreatic ca and others)
- CT, CTTAP, ERCP(biopsy) / MRCP
- Relieve obstruction (stent insertion/surgical bypass), pallaitive chemo/radio/EOL care
Pancreatic ca
* Risk factors
* Average survival with advanced disease
* Presentation - obstructive jaundice (3) and general signs (3)
* Named signs - Courvoiser’s and *Troussea’s *
* Referral guidelines (>40 and >60) for direct access CT Abdo
* Investigations
* Surgery (only possible in 10-20% of patients; considered in small tumours isolated to head of pancreas) - names
- Painless obstructive jaundice + pale stools, dark urine, pruritus
- abdominal/back pain, weight loss, palpable epigastric mass, change in bowel habit, N&V, new onset diabetes or worsening of T2DM
- palpable gallbladder and jaundice = cholangiocarcinoma and pancreatic ca most likely
- migratory thrombophlebitis - inflamed blood vessels in different locations over time
- > 40 with jaundice
- > 60 with weight loss + additional symptom (change in BH, backpain, N&V, new onset diabetes)
- CA 19-9
- CT, CTTAP, biopsy (percutaneous or endoscopic) ERCP/MRCP
- Pancreatectomy (total/distal); Whipple’s (radical pancreaticoduodenectomy) Modified Whipple’s (pylorus preserving)
C.diff treatments
* First episode (1st, 2nd line, 3rd line)
* Recurrent episode: within 12 weeks sx resolution
* Recurrent: after 12 weeks
* Life-threatening
*
- Oral Vancomycin, 10 days
- Oral Fidaxomicin, 10 days
- Oral Vanco + IV Metro
* Oral Fidaxomicin
* Oral Vanco/Fidax
* Oral Vanco + IV Metro +/- surgery
Constipation
Initial - dietary modificiations
1st-3rd line therapy (class and examples)
Choice for faceal impaction from chronic constipation?
- Bulk-forming (Isphagula husk)
- Osmotic with stimulant effect (Macrogol)
- Stimulant laxative - soft stools but difficult to evacuate (Senna)
Chronic constipation
1. - Bisacodyl suppository / glycerol suppositiory (small plug)
2. - enema (liquid in bottle)
