Gastroenterology_Medicine Flashcards
What are the markets of liver synthetic dysfunction?
Bilirubin
Albumin - slow to change so gives good idea of chronic disease
Coagulation screen (APTT, PT, INR)
Causes of hepatic decompensation in CLD? Key features of decompensation?
Dx & Mx of decompensated chronic liver disease?
Cause of hepatic decompensation in CLD:
- Hypokalaemia
- Constipation (given lactulose in hospital)
- Alcohol
- GI bleed (lots of protein (Hb) enters the bowel –>liver can’t cope)
- HCC
Decompensated CLD –> Ascites, jaundice & encephalopathy
- Severely scarred liver (cirrhosis) in CLD –> back pressure on portal vein –> PORTAL HTN = splenomegaly, ascites, varices - caput medusae, oesophageal & rectal
Ix:
-
Serum Ascites Albumin Gradient (SAAG) - serum albumin conc vs ascites conc - 11.1g/L
- <11.1g/L = exudative cause - peritonitis (infection), peritoneal malignancy OR n_ephrotic syndrome_ (pee out albumin so low serum albumin)
- Otherwise = transudative cause - cirrhosis, renal failure, HF
- >250 neutrophils = spontaneous bacterial peritonitis (SBP) –> Tazocin/3rd gen cephalosporin
- If protein conc <15g/L give prophylactic oral ciprofloxacin
Mx:
- Paracentesis (ascitic drain) –> post-paracentesis circulatory dysfunction (drops BP) SO if >5L drained give human albumin solution (HAS) 8g/L drained
- Spironolactone (2nd line - Furosemide) - to prevent fluid accumulation
- (Salt restrict)
- Hepatic encephalopathy (liver not dealing with toxins) - give Lactulose + Rifaximin to prevent
- Coagulopathy - OGD (check for varices) + vit K (needed for clotting)
Gallstone disease - spectrum? RFs? Types of gallstone?
Spectrum:
-
Biliary colic - obstruction of gallbladder/bile duct (usually by stones)
- Sx: RUQ pain (after fatty meal) ± scapular pain
-
Cholecystitis - inflammation of gallbladder
- Sx: RUQ pain + FEVER
-
Ascending cholangitis - infection ascending biliary tract + entering systemic circulation
- Sx: Charcot’s triad = RUQ pain, fever + JAUNDICE
- Severe Sx: Reynold’s pentad = above + CONFUSION + SEPSIS
RFs (5Fs): Fat, Female, Fertile, Forty, Fair
Types of gallstone: mixed (80%), cholesterol (10%, bigger & smaller in #), pigment (10%, smaller & more numerous)
Interpreting LFTs + causes
Liver - raised AST + ALT
- Causes: viral/alcoholic hepatitis, hepatotoxic drugs
- Most causes increase in ALT > increase in AST EXCEPT Alcoholic hepatitis - AST 2x > ALT
- AST also rises in muscle damage e.g. MI (normal ALT)
Biliary - raised GGT + ALP
- Causes: gallstones, cholecystitis, cholangitis, PSC/PBC
- NOTE: acute alcohol intake increases GGT
- NOTE: ALP can come from BONE (& placenta) - only biliary if GGT also raised
Chronic liver disease
- Functions of liver? Outcome of failure?
- Causes? Ix?
- Important complication?
- Scoring?
Functions of the liver –> failure:
- Albumin (plasma oncotic pressure) –> oedema
- Bilirubin metabolism –> jaundice
- Clotting factors –> coagulopathy
- Detoxification –> encephalopathy
Causes:
- Common - alcoholic liver disease, viral hepatitis, NASH (non-alcoholic steatohepatitis)
- Less common - AI hepatitis, PSC/PBC, HF, alpha1-antitrypsin def, haemochromatosis, Wilson’s disease
Ix:
- Alcohol history
- Hep B/C serology
- Ferritin, transferrin, A1AT, ceruloplasmin (Wilson’s)
- Ig, auto-abs (ANA in AI hep, AMA in PBC)
Important complication = VARICES
- Normal venous return: GI tract –hepatic portal vein –> liver –> hepatic vein –> systemic circulation
- Physiological hepatosystemic anastomoses (connection of portal vein to systemic circulation) sites - oesophagus, spleen, umbilicus, rectum
- MEMORY AID: BUTT, GUT, CAPUT
- Pathological process:
- In the case of cirrhosis - nodules impede flow of blood through the liver to the hepatic vein –> reducing blood flow to the systemic circulation
- Backflow of blood to the hepatic portal vein = increased –> backflow to hepatosystemic anastomoses:
- Oesophagus –> Oesophageal varices
- Spleen –> Splenomegaly
- Umbilicus –> Caput Medusae
- Only from portal HTN if running from below umbilicus up
- Rectum –> Rectal varices
Score for prognosis & need for liver transplant = Child-pugh score (A = 5-6; B = 7-9; C = 10-15 –> C is most severe)
Jaundice breakdown & causes by type & Ix to differentiate
Pre-hepatic - unconjugated bilirubin comes from breakdown of RBCs
- Haemolysis related-causes (excess prod) - AIHA, SCD, G6PD def, malaria
- Ix:
- Bloods: excess unconjugated bilirubin (exceeds capacity of liver to conjugate it)
- Urine: normal (unconjugated bilirubin is insoluble)
- Stool: normal as liver functioning normally
Hepatic - bilirubin absorbed into liver –> conjugated –> excreted via biliary tract into duodenum
- Liver disease related-causes - cirrhosis, hepatitis, Gilbert’s syndrome, drugs
- Ix:
- Bloods: high unconjugated (liver less able to conjugate quickly) & conjugated bilirubin (leakage of conjugated bilirubin into circulation)
- Urine: dark (leaked conjugated bilirubin is soluble)
- Stool: slightly pale (reduced conjugated bilirubin to GI tract)
Post-hepatic - conjugated bilirubin –> soluble urobilingogen (yellow): 1) Absorbed into circulation –> excreted via kidneys 2) Remaining –oxidised–> stercobilin (brown)
- Biliary disease related-causes (prevent bile outflow) - gallstones, head of pancreas tumour, cholangiocarcinoma, PSC/PBC
- Ix:
- Bloods: high conjugated bilirubin (backlog as obstruction at biliary tree so can’t reach duodenum and instead leaks into blood)
- Urine: dark (leaked conjugated bilirubin is soluble)
- Stool: very pale (no conjugated bilirubin reaches GI tract –> no stercobilin generated)
Chronic diarrhoea - ddx? Sx? Distribution? Histology? Ix? Mx?
IBD
- Truelove & Witts’ severity index = severity criteria for IBD
-
Crohn’s disease
- Sx: RIF pain (terminal ileum), failure to thrive (incl. between attacks)
- Distribution: mouth to anus (esp. terminal ileum), skip lesions
- Histology: transmural, non-caseating granuloma (also in sarcoidosis)
-
Ix:
- OGD/colonoscopy/capsule endoscopy
- Gastografin follow-through
-
Mx:
- Induction:
- Steroids (induce remission)
- 5-ASA (mesalazine)
- Maintenance:
- Steroid-sparing agents (methotrexate, azathioprine, mercaptopurine)
- Biologics e.g. Anti-TNF (infliximab)
- Induction:
-
Ulcerative colitis
- Sx: gen. abdo pain, PR blood & mucus
- Distribution: ONLY rectum & colon, continuous
- Histology: mucosa & submucosa, mucosal ulcers, crypt abscesses
-
Ix:
- Flexible sigmoidoscopy/colonoscopy
-
Mx:
- Induction:
- 5-ASA
- Steroids
- Maintenance:
- 5-ASA (mesalazine)
- Steroid-sparing agents (azathioprine)
- Biologics (infliximab)
- Surgery (proctocolectomy, IJ pouch)
- Induction:
Coeliac disease
-
Def: inflammatory response to gluten (immune reaction to gliadin)
- DQ2/8 (on HLA typing)
-
Sx: abdo Sx (steatorrhoea, diarrhoea, bloating), failure to thrive
- Exam: blistering rash on both knees. aphthous mouth ulcers
- Assoc: T1DM
- Distribution: duodenum
- Histology: subtotal villous atrophy with crypt hyperplasia
-
Ix: (maintain normal diet - eat gluten for 6wks before testing)
- Haematinics - macrocytic anaemia, low Fe, B12/folate
- Serological testing:
- Screening: Anti-TTG & total IgA (check for selective IgA def in case this caused false ‘-ve’ anti-tTg abs)
- If weakly +ve –> anti-endomysial abs (more sensitive & specific)
- OGD & duodenal biopsy
- Histology: sub-total villous atrophy with crypt hyperplasia
- Mx: gluten avoidance
Irritable bowel syndrome - Dx of exclusion
-
Sx: bloating, related to stress, diarrhoea/constipation, relieved by defecation
- “Pellet-like stools”
- Ix: faecal calprotectin (an inflammatory marker of GI tract = less likely to be IBS, more likely IBD)
- Mx: dietary changes, stress Mx, anti-spasmodics, probiotics, laxatives/loperamide, anti-depressants
Mesenteric ischemia:
- What is the blood supply to the GI tract?
- What area of GI tract is vulnerable to ischaemia?
- Breakdown of mesenteric ischemia? Sx? Ix? Mx?
What is the difference between Mesenteric ischemia & ischemic colitis? Sx? Ix?
Blood supply
- Coeliac axis - oesophagus, stomach, start of small intestine
- Superior mesenteric artery (SMA) - most of the small intestines up to 2/3 transverse colon
- Inferior mesenteric artery (IMA) - from 2/3 along transverse colon down to rectym
- NOTE: area 2/3 along transverse colon @splenic flexure = WATERSHED ZONE (limited supply from superior & inferior mesenteric arteries) –> vulnerable to ischaemia!!
__Mesenteric ischemia
-
Acute - occlusion of SMA by thrombus/embolus
- Sx: severe abdo pain, normal abdo exam, shock
-
Ix:
- AXR (gasless abdo)
- VBG (lactic acidosis)
-
CT abdo with contrast (if suspect mesenteric ischaemia)/CT angiogram (if LA)
- If not primary surgery –> followed by mesenteric angiography (Dx non-occlusive mesenteric ischaemia)
- Mx: resus + CCOT + NBM
- Empirical abx
- Bypass ± bowel resection
- Heparin post-op
-
Chronic - narrowing of SMA by atherosclerosis (stable angina of bowel)
- Sx: colicky post-prandial abdo pain (more work for bowel to do –> pain, just like in stable angina & exercise)
- Ix: as above
- Mx: medical optimisation + bypass (angioplasty + stent if not suitable for surgery)
Ischemic colitis
- Occlusion of inferior mesenteric artery (IMA) by thrombus/embolus
- Sx: abdo pain, PR bleeding
- Ix: sigmoidoscopy/colonoscopy
- Mx: seek GI & surgical input (can develop chr ulcerating IC)
- Mild - conservative (IV abx, fluids, bowel rest, DM control)
- Prophylactic LMWH
- Segmental resection + stoma
- Mild - conservative (IV abx, fluids, bowel rest, DM control)
Most common reason to do AXR? Most common causes of this reason by type?
AXR interpretation?
Key volvulus signs on AXR?
Reason to do AXR: worried about bowel obstruction (small/large bowel)
Small bowel obstruction on AXR:
- valvulae conniventes (from one wall to other)
- Central to image
- >3cm distension
- Causes: adhesions (surgery, sepsis), hernia, neoplasm, volvulus, IBD
Large bowel obstruction on AXR:
- Haustra (Not full width of bowel)
- Outsides of image
- >6cm distension
- Causes: neoplasm, diverticular disease, volvulus, faecal impaction
NOTE: 3/6/9 rule = upper limits of normal for bowel (small = 3cm, large = 6cm, caecum = 9cm)
Volvulus signs (twisting of loop of bowel on mesentery –> balloon animal):
- Coffee bean sign - sigmoid volvulus (large bowel just before rectum)
- Embryo sign - caecal volvulus (large bowel just after small bowel)
Acute abdo DDx lower quadrants
RLQ:
- Appendicitis
- Salpingitis (can be bilateral) - ascending inf from vagina into fallopian tubes
LLQ:
- Sigmoid volvulus
- Sigmoid diverticulitis - outpouching of mucosal tissue in sigmoid colon
Diffuse/either:
- Ectopic pregnancy
- Ovarian torsion
- Renal calculi
- Pyelonephritis (ascending lower UTI)
Acute abdo DDx upper quadrants
RUQ:
- Biliary cholic, cholecystitis, ascending cholangitis
- Perforated duodenal ulcer
- Acute hepatitis (e.g. viral)
LUQ:
- Splenic rupture
- IBS (complication - splenic flexure syndrome)
Acute abdo DDx epigastric & diffuse
Epigastric:
- Peptic ulcer disease (PUD) - worse after eating (increased HCL), nocturnal (RFs: NSAIDs, H. pylori inf)
- Pancreatitis - radiates (to back), N&V ± Cullen’s/Turner’s
- Aortic dissection - tearing, radiates (to back)
- MI - crushing, radiates (carotids & arms)
Diffuse:
- Peritonitis - distension & guarding, caused by haemorrhage/perforation
- Bowel obstruction, bowel strangulation
- Acute hepatitis
Why do patients with chronic liver disease get oedematous?
Backflow of blood into the hepatic portal vein –> increased hydrostatic pressure –> more fluid leaking out into interstitium
Less albumin produced by liver –> less oncotic pressure
Overall net fluid movement into interstitium
Decompensated chronic liver disease - what is it? what is the physical presentation?
CLD can be stable but insults such as alcohol/infection –> decompensation (liver failing to carry out normal function)
Presentation: ASCITES (+ worsening jaundice/coagulopathy/asterixis/hypoglycaemia)
At the end of abdo exam what do you offer to do?
GOR(D)
- external Genitalia
- hernial Orificies
- digital Rectal
Structures in each region of abdomen?
Exposure in abdo exam?
Ideally nipples to knees but in this case, I will do nipples to the groin due to possible patient discomfort
diarrhoea with profound hyperkalaemia + persists with fasting
what is the diagnosis?
VIPoma - neuroendocrine tumour (starts in pancreas)
IBS presentation
- Chr abdo pain + bloating + altered bowel habit but improves with defecation
- Dx of exclusion
WHat is inclusion bodies (owl eyes) associated with?
CMV colitis
IBD - UC Vs Crohn’s (epidemiology, pattern, histology)
Smoking: protects UC, worsens Crohn’s
Site: rectum (colon) in UC, terminal ileum (entire GI tract) in Crohn’s
Pattern: continuous (worse distally) in UC, skip lesions (patchy) in Crohn’s
Histology: mucosa - crypt abscesses in UC, trans-mural - non-cas granuloma in Crohn’s
Erythema nodosum is associated with which conditions?
IBD (also pyoderma gangrenosum),
Sarcoidosis
TB
Meds (OCP, sulphonamides, aspirin/NSAIDs)
What is the severity index score for acute colitis (e.g. IBD)?
Truelove & Witts’ severity index
Extra-intestinal signs of IBD
A PIE SAC
- APHTHOUS - MOUTH ULCERS (CROHNS)
- PYODERMA GANGRENOSUM
- I (EYE)- IRITIS, UVEITIS, EPISCLERITIS (CROHNS)
- ERYTHEMA NODOSUM
- SCLEROSING CHOLANGITIS (PRIAMRY- UC)
- ARTHRITIS
- CLUBBING FINGERS (CD> UC)
Peptic/duodenal ulcer - Ix? Mx? Key DDx?
Duodenal > gastric ulcers
Key Investigation:
- Stool antigen test (urea breath test not done due to COVID) to test for H. pylori
Triple therapy- 1 week
- PPI
- Clarithromycin
- Amoxicillin OR Metronidazole
DDx: Zollinger-Ellison syndrome (very rare cause): Gastrin secreting neuroendocrine tumour in pancreas - gastrinoma
- Would have FHx: MEN + multiple ulcers post-treatment
Sign most commonly suggestive of bowel obstruction
Tinkling bowel sounds
Primary Sclerosis Cholangitis (PSC) vs Primary Biliary Cholangitis (PBC)
- Associations? Ix? Tx?
-
PSC - intrahepatic & extrahepatic (horrible & progressive disease, obstructive jaundice)
- Associations: UC (10% but 80% PSC have UC), Cholangiocarcinoma
-
Ix: MRCP, pANCA
- ‘Beads on string’ on ERCP
- Tx: supportive, liver transplant
-
PBC - intrahepatic only (benign condition - middle-aged female, intractable itching)
-
Associations: AI diseases (RA, Sjogren’s, hypothyroidism)
- Sicca syndrome (70%) - dry eyes & mouth (like Sjogren’s syndrome)
- Fat malabsorption w/ steatorrhoea (incl vitamins ADEK):
- Low vit D can cause osteomalacia & proximal myopathy e.g. difficulty climbing stairs & pain in lower back
- Low vit K can cause coagulopathy
- Ix: anti-mitochondrial Ab (AMA), high cholesterol
- Tx: ursodeoxycholic acid (prognostic benefit)
-
Associations: AI diseases (RA, Sjogren’s, hypothyroidism)
Causes of hepatomegaly, splenomegaly & enlarged kidney(s)?
Hepatomegaly causes:
- Hepatitis (infective and non-infective)
- Hepatocellular carcinoma/hepatic mets
- Wilson’s disease, Haemochromatosis
- Primary biliary cirrhosis
- Leukaemia, Myeloma, haemolytic anaemia
- Glandular fever
- Tricuspid regurgitation
Splenomegaly causes:
- Portal HTN secondary to liver cirrhosis
- Splenic mets
- Haemolytic anaemia, Congestive HF, Glandular fever
Large kidney causes:
- Bilaterally enlarged: polycystic kidney disease, amyloidosis
- Unilaterally enlarged: renal tumour
What are signs of chronic stable liver disease? Some specific signs for the cause of the CLD?
Spider naevi (≥5), palmar erythema, gynecomastia, Dupuytren’s contracture (alcoholic liver disease), clubbing
NOTE - Spider naevi:
- SVC distribution (above nipples)
- Press on them and flush from inside out
Specific signs:
- Needle marks/tattoos - hep C
- Parotid swelling - alcohol-related liver disease
- Bronzed complexion/insulin injection signs - haemochromatosis
- Obesity/DM - non-alcoholic fatty liver disease
- Xanthelasma - cholestatic disorder
Different kinds of erythema?
Nodosum - pain over shins
Multiforme - target lesions (life-threatening = Steven’s Johnson Syndrome)
Ab igne - hot water bottle (chr heat exposure)
Marginatum - acute rheumatic fever
Chronicum migrans - lyme disease
Findings on abdo exam general inspection?
Abdo examination differentiating observations from inspection
- Distended abdo - CLD, hepato-splenomegaly, PCKD
- AV-fistula - renal failure on dialysis, renal transplant
- Stoma - IBD, surgical
When to admit UC case? Mx?
Severe UC (if does not meet –> managed in outpatients):
- 6+ bowel move/day
- Frank blood
- Temp ≥37.8, HR ≥90, anaemia, ESR ≥30
Hep B Serology reading?
- Active hepatitis requires HbsAg
- Anti-HBs – vaccinated or previous infection
- Anti-HBc – must have cleared infection/had in past
- Acute inf Anti-HBc IgM
- Chronic inf Anti-HBc IgG
- HBeAg +ve = high infectivity
Hep C Serology reading?
- HCV-RNA = acute
- Anti-HCV = previous infection
- Both = chronic infection
Viral hepatitis
Hep A: faecal-oral –> acute
Hep B: blood-borne –> acute/chronic –> serology
- Contains: Core Ag (cAg), E Ag (eAg), DS-DNA, surface antigens (sAg)
- eAg present if active & infective
- Infection response –> generate sAb (surface) + cAb (core)
- Vaccination gives sAg (no reproductive capacity) –> develop sAb (but not cAb)
- Serology:
- HBsAg/HBeAg - actively infecte
- IgM = acute; IgG = chronic
- eAg = highly infective
- HBsAb - protective (cleared/vaccinated)
- HBcAb - only if previously cleared
- HBsAg/HBeAg - actively infecte
- Can be assoc with Polyarteritis Nodosa (vasculitic rash) & mononeuritis multiplex
- Tx: IFN-alpha & lamivudine
Hep C: blood-borne –> chronic –> HCV RNA
- More likely to become chronic than Hep B
- Assoc w/ mixed cryoglobulinaemia (purpuric skin lesions, Raynaud’s phenomenon)
- RF +ve, low C4, normal C3
- Can have +ve anti-LKM1 ab (also in AI hep)
- Tx: PEG-IFN alpha & ribavirin
Hep D: blood-borne –> co/superinfection w/ Hep B virus
Hep E: faecal-oral –> acute, pregnancy
Dysphagia DDx? Ix?
Dysphagia - difficulty swallowing
- vs Odynophagia - painful swallowing
- vs Globus sensation - lump in throat, no pain
Oropharyngeal - difficulty initiating swallowing (± cough, choking, aspirating, regurgitation) - pressure in throat
- Oral:
- mastication (CN 5,7,11) e.g. CVA
- Low saliva e.g. Sjogren’s syndrome
- Pharyngeal:
- Neuromuscular - CVA, Myasthenia Gravis, Parkinson’s
- Upper oesophageal sphincter - decreased relaxation
Oesophageal - difficulty after swallowing - pressure in chest
- Solids & liquids - motor
- Intermittent: oesophageal dysmotility
- Progressive (solids –> both): achalasia, systemic sclerosis
- Solids only - obstructive
- Non-progressive: lower oesophageal rings/webs, oesophagitis
- Progressive: stricture, cancer
Ix:
- Barium swallow if possible proximal oesophageal lesion
- Upper endoscopy ± biopsy
- If affects solids & liquids –> manometry
