Gastro Flashcards
hepatic causes of jaundice (high indirect bilirubin)
Gilbert’s (decr UDPG activity)
Crigler Najjar (no UDPG)
Hepatitis
Newborn jaundice (not enough UDPG or lignin to deal with incr haem catabolism from conversion of HbF to HbA)
hepatic causes of jaundice (high direct bilirubin)
Hepatitis Drugs that impair excretion Rubin Johnson syndrome (no cMOAT for excretion) Tumours Cirrhosis
Post-Hepatic causes of jaundice
Due to high conjugated bilirubin:
Gallstones
Biliary strictures/obstruction
Cholangitis
Pancreatic or biliary tree cancer
All lead to cholestasis
What happens to bilirubin when it is unconjugated in the blood and liver?
Blood - bound to albumin
Liver - bound to ligandin
What sort of bilirubin is toxic and what does it cause in the brain?
Indirect is insoluble so cannot be excreted and builds up
Kernicterus due to brain toxicity
Which enzyme conjugates bilirubin and what happens if it is not present or has decr activity?
UDPG
Decr activity: Gilbert’s
Not present: Crippler Najjar
what happens to bilirubin in the gut?
Converted to urobilinogen via gut bacteria
then 90% is converted to stercobilin and excreted in faeces
10% absorbed into portal circulation and goes back to liver. 9% of this is recycled back to gut and 1% goes to kidneys and is excreted in urine
What colour is the pee and poo with:
obstructive jaundice?
pre-hepatic jaundice?
Obstructive: Dark wee, pale poo
Pre-hepatic: dark wee and poo (overwhelm liver conjugating enzymes)
What is a potential consequence of pre-hepatic jaundice?
Excess haem from haemolysis results in excess synthesis of bile salts which can result in precipitation of GALLSTONES
-> cholestasis -> obstructive jaundice
4 categories of mechanisms of diarrhoea
Osmotic
(excess unabsorbed substrates in gut lumen retain fluids)
Secretory
(stimulation of excretory mechanisms from enterocytes)
Inflammatory
(altered membrane permeability leads to exudation of protein, blood, mucus)
Altered intestinal motility
(slow or fast)
Common underlying cause of osmotic diarrhoea
FODMAPS (IBS)
Common underlying causes of secretory diarrhoea
Bacterial toxins
- ETEC
- Cholera
Laxative abuse
Hyperthyroidism
Common underlying causes of inflammatory diarrhoea
IBD
Invasive bacteria
- Shigella
- Salmonella
- Clostridium difficile
- Campylobacter
Entamoeba histolytica
CMV colitis
Common underlying causes of altered motility diarrhoea
SLOW: Anatomical defects causing intestinal stasis -strictures -blind loops (diverticulitis) -surgery
FAST:
- IBS
- Thyrotoxicosis
- Diabetic neuropathy
Appearance of poo with - inflammatory - secretory - osmotic Diarrhoea
Inflamm - blood and mucus, small volume
Secretory: watery, >1Lvol
Osmotic: fatty,
Acute abdomen - which causes need laparotomy and which don’t
Need laparotomy:
- Generalised peritonitis (perf ulcer, diverticulum, appendix, bowel, gallbladder)
- Ruptured organ (liver, spleen, AAA, ectopic pregnancy)
Doesn’t need:
- local peritonitis (cholecystitis, diverticulitis, salpingitis)
- suspected abscess
- localised ileus
- colicky pain (patient restless)
Maybe:
-SBO
Management of Acute abdomen
Treat shock w 2 large bore cannulas w crystalloid (Hartmann's) fluids ECG Vitals Group and hold Blood cultures Antibiotics (cef and met) Analgesia (IV morphine PRN) IV fluids Plain AXR and erect CXR Nil by mouth Antiemetics
Management of abdominal trauma (blunt)
§ ABCs, fluid resus and stabilisation
§ Surgery ?
□ Hollow organ injuries -> laparotomy
□ Solid organ injuries -> laparotomy if hemodynamically unstable or high transfusion requirements
Management of abdo trauma (penetrating)
§ ABCs § Fluid resuscitation and stabilization § Gunshot wounds require laparotomy § Laparotomy if penetrating trauma and □ Shock □ Peritonitis □ Evisceration □ Free air in abdomen □ Blood in NG tube, catheter or on DRE
§ Local wound exploration in some instances
Treatment for peritonitis
IV rehydration and electrolyte balance correction
IV antibiotics (cephalosporin, tazosin or carbepenem)
Laparotomy - exploratory peritoneal lavage and correction of anatomical defects
Treatment of ascites
1st line
○ Salt restriction (>2g daily)
○ Diuretics: spironolactone, frusemide
○ Weight loss
If refractory (treatment with diuretics is inadequate)
○ Therapeutic/palliative ascitic taps
○ IV albumin
? Liver transplantComplications of ascites and the treatment
Spontaneous bacteiral peritonitis if they develop fever, chills, abdo pain, hypotension, ARF etc
Treatment: IV antibiotics (cephalosporin) and IV albumin
Investigations for a suspected hernia
Ultrasound +/- CT
List different types of hernias
Inguinal hernias (direct vs indirect)
Femoral hernia
Umbilical
Paraumbilical (below or above umbilicus)
Epigastric (through lines alba above umbilicus)
Incisional hernia
Obturator hernia
- What does reducible mean?
2. What does irreducible mean?
hernia
- contents can be pushed back into their rightful position
- hernia cannot be pushed back into their right place = stuck = incarcerated.
May or may not be strangulated
What does incarcerated mean? (hernia)
Herniated tissue is trapped in a hernial sack and cannot be pushed back into position (=irreducible)
Doesn’t imply anything about blood supply.
obstructed vs strangulated in conte
Obstructed - bowel caught in hernia obstructing the passage of bowel contents through
Strangulated - Blood supply is compromised and bowel becomes ischaemic
3 questions to ask about a lump found on examination
- Can you get above it? (no-> hernia)
- Yes -> Is it separate to the testes? (No-> testicular tumour)
- Does it transilluminate? (Yes -> fluid as in cyst or hydrocoel; no-> solid)
Direct vs indirect hernia
Direct: directly through defect in abdominal wall. older patients.
- Medial to inferior epigastric artery)
Indirect: through deep inguinal ring into inguinal canal. Associated w congenital defect in males (patent processes vaginalis). younger patients.
- Lateral to inferior epigastric artery)
What is the site that direct hernias usually occur in called and why are the anatomical landmarks?
Hasselbach’s triangle
- lateral edge of rectus sheath
- inferior epigastric vessel
- inguinal ligament
Where do femoral hernias occur?
Femoral canal: medial to femoral vein, below inguinal ligament
Which type of hernia is more common in women and what is a common complication?
Femoral hernia . More likely to be irreducible and to strangulate.
Complications of hernias
Incarceration
Strangulation
Richter’s hernia
Obstruction
Richter’s hernia - what is it? how might a patient present?
Once side of small bowel wall becomes incarcerated in a hernia which may strangulate that section of bowel wall. presents w sepsis and tachycardia + lump
When might you perform surgery for a hernia?
Emergency if hernia is strangulated.
Elective if:
- obstruction (change in bowels)
- Pain
- Nuisance, aesthetic
Contents of the spermatic cord
Vas deferens testicular artery & vein genital branch of genitofemoral nerve lymphatics cremaster muscle \+/- hernial sac
What is the management of hernia?
Do nothing if small and asymptomatic.
Surgery to prevent strangulation or evisceration, for pain or aesthetic. Laparoscopic or open mesh repair.
What genetic alleles is coeliac associated wiht?
HLA-DQ2 and HLADQ8 are found in close to 100% patients but also in 20% of the general population
What sort of hypersensitivity is coeliac disease?
Type 4 hypersensitivity against gliadin, found in gluten
Histopathology of coeliac disease: 3 features
- Villous atrophy and crypt hyperplasia
- Increased #s plasma cells and lymphocytes in LP
- Increased IELs (CD4 T cells)
What part of bowel does coeliac mainly affect? What affect does this have on absorption?
Duodenum and jejunum
Affects absorption of Vitamin B, C and folate (proximal), mostly
Protein, fat and fat soluble vitamins (A, E, D, K) distally. absorbed so only affected in severe disease.
What sort of anaemia is associated w Coeliac disease?
Iron deficiency (microcytic)
or pernicious anaemia (B12, macrocytic)
Symptoms of coeliac disease
D • Diarrhoea, steatorrhea
• Weight loss, fatigue
• Bloating, gas
• Anaemia - iron deficiency »_space; B12, folate deficiency
• Symptoms of vitamin, mineral deficiency (apthous ulcers, angular stomatitis)
• Osteoporosis in older people
• Failure to thrive in infants
• Symptoms improve with gluten free diet and relapse when gluten reintroduced
Diagnosis of coeliac
Small bowel biopsy before starting GF diet
Bloods: FBE, Iron studies, UEC, B12, folate
Serology (anti gliadin and anti tTG antibodies + IgA)
HLA-DQ typing
What does coeliac put you at risk for?
Other autoimmune conditionts (autoimmune thyroiditis, T1D)
Cancers - EATL small bowel lymphoma, adenocarcinoma of small bowel and oesophageal carcinoma
What are the main symptoms for Crohn’s vs UC
Crohns: abdominal cramps, diarrhoea, weight loss (malnutrition), fever
UC: rectal bleeding, urgency, tenesmus, abdominal cramps
Physical distribution of Crohns vs UC
Crohn’s
- anywhere from mouth to anus
- Skip lesions
- Commonly terminal ileum
UC
- rectum -> colon (not proximal to ileocaecal jan)
- continuous
- always starts in rectum
Potential complications of UC vs Crohns
Crohns:
- Strictures
- Fissures -> risk of perforation
- Abscess
- Fistulae
- Perianal disease
US
- toxic megacolon -> risk of perforation
- incr risk colon cancer
Extra colonic manifestations of Crohn’s vs UC
Crohns
- perianal fistulae and skin tags
- renal stones
- cholelithiasis
- oral ulcers
Both
- rashes, erythema nodosum
- arthritis, analysing spondylitis
- uveitis, episcleritis
- PSC
- fatty liver
Cobblestoning and mucosal islands are a feature of what IBD condition?
Crohn’s
Effect of surgery in crohn’s vs UC
Crohn’s - recurrence is common
UC - surgery can cure.
Treatment of IBD
Crohns: stop smoking + only fluids during exacerbation
- Steroids (C-oral pred; UC-IV methylpred)
- 5ASA therapy +/- antibiotics
- Immunosuppressants (azathioprine, methotrexate, infliximab)
- Surgery for:
- Crohn’s: presence of complications
- UC: failed medical therapy, toxic megacolon, bleeding, pre-cancerous change
Investigating IBD
Bloods (FBE, CRP, UEC, LFT, blood cultures)
Stool MCS (shigella, campylobacter, e coli, C. diff, salmonella -> all inflamm pattern diarrhoea)
Abdo x-ray Erect CXR (perf?)
Colonoscopy and biopsy
management of IBS
Low FODMAPS diet
Incr fibre intake
Antismasmotic (hyoscine) before meals
Reassurance, relaxation or stress reduction therapy
Red flags that rule out IBS as a DDX
Weight loss Fever Nocturnal defecation anaemia blood or pus in stool abnormal gross finding on endoscopy
What is the criteria for IBS?
Abdo pain relieved w defecation
Abdo pain assoc w change in fréquency OR consistency of stool
+/- bloating, passing mucus, straining, urgency, incr or decr stool frequency
Managing an acute abdomen
- ABCDE
- Airway, breathing, circulation
- Disability: BSL, GCS
- E: expose patient (Evidence for trauma/aneurysm/GI bleed?) - insert 2 large bore (18 or 16gu) cannulas
- Bloods: blood cultures, group and hold, FBE, UEC, LFT, CRP, ABG, Trop, beta HCG
- ECG
- Check obs: pulse, BP, JVP, saO2
- ECG if > 50
- Ceftriaxone and metronidazole
- IV morphine PRN, metaclopramide
- IV fluids: hartmann’s
- FAST scan +/- Portable plain erect CXR and AXR
- Call surgical reg
- Prep for theatre
Preparation for theatre
- Nil by mouth
- DVT prophylaxis: LMWH, 3. TEDs
- Catheterise (IDC)
- NGT (decompression and prevents aspiration)
- PPIs
+/- analgesia, antiemetic, anxiolytic
Management of abdominal trauma
- ABCDE primary surgery (+/- O2 or intubation)
- secondary surgery + NGT, IDC
- Bloods (incl group and hold), urinalysis
- FAST scan (free fluid), Abdominopelvic X-ray (bone breaks, pneumoperitoneal, air fluid levels, hernias) , CT (not if haemodynamically unstable)
- Fluid resuscitation (2 large bore cannulas w hartmann’s )
- Surgery - laparotomy
Management of appendicitis
IV fluids + electrolyte correctance
Prompt appendectomy
Metronidazole +ceftriaxone pre-op
Complications of appendicitis
Perforation
Abscess
Examination tests for appendicitis
Tenderness at McBurney’s point (1/3 from ASIS to umbilicus)
Rovsing’s sign: when LIF is pressed, pain felt more strongly in RIF than left
Psoas sign = retrocaecal appendix (pain on flexion of hip against resistance OR passive hyperextension of hip)
Obturator sign =pelvic appendix (flexion then external or internal rotation about R hip causes pain)
Where does diverticular disease usually affect? where is the pain generally felt?
Sigmoid colon
LLQ
Management of diverticular disease
Diverticulosis: high fibre diet, avoid seeds and nuts.
Diverticulitis (acute episode):
- Conservative: NPO, IV fluids and IV cef and met
- surgical treatment is Hartmann procedure if refractory to medical MX, or complications present.
What is hartmann’s procedure
Surgical resection of sigmoid and rectum w closure of rectal stump and formation of end colostomy.
Colostomy can be later reversed and the 2 ends of bowel sewed together.
What side of body are ileostomies vs colostomies?
Colostomies: LIF
Ileostomies: RIF
Complications of diverticulitis
Recurrence Abscess Fistulae Perforation Bleeding Obstruction
Investigations for suspected diverticulitis
FBC
CT
Erect AXR (pneumoperitoneum)
Colonoscopy or flexible sigmoidoscopy
Investigating suspected ectopic pregnancy + mX
beta HCG
Transvaginal US
Laparoscopic surgery (or methotrexate if beta HCG low and ectopic is small)
Courvoisier’s law
in a patient w painless jaundice and a palpable RUQ mass, the cause is unlikely to be gallstones -> more likely to be obstructing pancreatic or biliary neoplasm
Charcot’s triangle - what is it for and what is that?
for ascending cholangitis (infection of CBD caused by bacteria)
- fever
- jaundice
- RUQ pain
Reynold’s pentad
for ascending cholangitis
- fever
- jaundice
- RUQ pain
- Mental state changes
- Hypotension
Does bleeding happen more commonly in diverticulitis or diverticulosis?
Diverticulosis
Bleeding v rare with diverticulitis.
Key features of bowel obstruction
- Vomiting, nausea, LOA
- Constipation (distal obstruction - no faeces or flatus passed; prox obstruction - some faeces or flatus may be passed)
- Distension
+/- Colicky pain (from peristalsis)
Causes of Small bowel obstruction
Functional (ileus)
Mechanical obstruction
- Adhesions
- Bulge (Hernias)
- Cancer (adenocarcinoma)
Rare causes
- foreign body
- intusseption (prox segment of bowel collapses into distal bowel lumen, commonly ileum through ileo-caecal valve)
- CD (IBD) stricture
- Gallstone ileus (stone lodges in ileocaecal valve - v rare!!)
Causes of large bowel obstruction
Functional (ileus)
Mechanical obstruction
- Cancer
- Diverticulitis
- Volvulus
Rarer causes
- Adhesions
- Constipation
- Volvulus (sigmoid or caecal)
How to distinguish between small and large bowel on AXR?
Small bowel - plicae circulares (valvulae conniventes), more centrally located. no larger than 3cm
Large bowel - No larger than 6cm. Has haustra which don’t completely cross lumen.
What sorts of SBO do you manage conservatively vs perform emergency surgery?
Conservative:
- Partial SBO
- Ileus
- Adhesions
- Crohn’s stricture
Emergency surgery
- LBO
- Strangulation
- Complete or recurrent SBO
What are potential complications of bowel obstruction
Strangulation -> ischaemic bowel
Perforation -> peritonism, fever, incr WCC
What is achalasia? what appearance do you get on barium swallow?
Oesophageal motility disorder characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.
Barium swallow -> dilated oesophagus tapering to beak-like narrowing
Investigations for motility disturbance w dysphagia?
Upper GI endoscopy - rule out malignancy
Barium swallow (older patients, rule out pharyngeal pouch)
Esophgeal manometer (assesses competence of oesophageal sphincters and oesophageal motility)
+/- CT if significant weight loss to rule out malignant infiltration
Treatment achalasia
Pneumatic dilatation - first line, + PPI
OR: Botulinum toxin (Decr tone of LES transiently)
Gastritis - common causes of acute flares
Alcohol
ASpirin/NSAIDs
Stress
H. Pylori
Diagnosis of H pylori
Urea breath test
Serology and stool Ag test
Biopsy -> histology, rapid urease test
Treatment of H pylori
Triple therapy for 7-14 days
- PPI
- Amoxicillin
- Clarithromycin
Potential complications of H pylori gastritis
peptic ulcer - 15% gastric malignancy (carcinoma and MALT lymphoma) - 0.5%
Predisposing factors for colon cancer
Neoplastic polyps FAP or HNPCC genes IBD Smoking and alcohol HX cancer
most common form of colon cancer.
adenocarcinoma
What is the sreening program for bowel cancer?
people 60-75 years old are screened using Faecal occult blood home testing kits. NOT diagnostic -> need colonscopy if postive
What common cause of iron deficiency anaemia in people over 50
Colon cancer until proven otherwise.
Where does colon cancer go to commonly ?
liver, lung, bone
What is the name of the staging criteria for bowel cancer? What are the stages?
Duke’s
○ A: Limited to muscularis mucosae
○ B: extension through muscularis mucosae
○ C: involvement of regional lymph nodes
○ D: Distant metastases
When would you use radiotherapy and chemotherapy with bowel cancer?
Radiotherapy
- palliative mostly
- post-op for tumours with high chance of recurrence
Chemo
- dukes B and C
- palliation
RIsk factors for acute pancreatitis
Alcohol Middle aged women; young-middle aged men Gallstones Hyperlipidaemia Causative meds ERCP HIV/AIDS SLE
Causes of acute pancreatitis
"I GET SMASHED" Idiopathic Gallstones Ethanol Trauma Scorpion/spider bite Malignancy/mumps (and other infections) Autoimmune Steroids Hyperlidaemia/hypercalcaemia/hyperparathyroidism ERCP Drugs
Causes of chronic pancreatitis
ALCOHOL IS #1!!!
Then CF, protein malnutrition, genetics etc rarer causes
3 clinical features of chronic pancreatitis
Severe upper abdo pain radiating to back
Steatorrhea
Diabetes
Complications of pancreatitis
○ Pseudocyst complications • Persistence of pseudocyst • Haemorrhage • Infection • Rupture ○ CBD obstruction ○ Duodenal obstruction
MX of chronic pancreatitis
Alcohol abstinence!!!
Analgesia
+/- pancreatic enzyme replacement
Surgery
MX of acute pancreatitis
IV fluids Nutritional support (enteral feeds of TPN) \+/-: Analgesia Antiemetics O2 NG tube Ca, Mg replacements Antibiotics if infected Insulin Benzo and vitamin, mineral replacement if alch-induced
Surgery if gall-stone induced
- cholecystectomy
- ERCP w sphincterotomy
In what cases would you genetic test for hereditary polyposis in colon cancer?
DNA test if FHX of FAP of HNPCC or cancer DX before age 50
What are the 2 main hereditary forms of colon polyps?
FAP - onset at puberty, surgery by 17-20
HNPCC - onset from 20
Treatment for FAP and HNPCC
Surgery: Total colectomy with ileorectal anastomosis
With yearly endoscopy surveillance
FAP: also chemotherapy
Which form of hereditary polyposos is associated w 100s of 1000s of polyps by age 20?
FAP
What are SX of volvulus due to?
Obstruction
Bowel ischeamia
What is cirrhosis?
Describe.
Is it reversible?
Anatomical term. describes conversion of liver into state of abnormal ANATOMY, occurring with chronic renal disease (ESLD).
Description: Nodules of regenerating hepatocytes surrounded by bands of fibrous scar tissue.
Irreversible.
Causes of cirrhosis. The big 3
THE BIG 3:
- Alcohol
- HBV
- HCV
Causes of cirrhosis. The autoimmune 3
AUTOIMMUNE 3
- Autoimmune hepatitis
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
Causes of cirrhosis. The metabolic 3
METABOLIC 3
- Haemochromatosis (too much Fe)
- Wilson’s disease (too much Cu)
- Alpha-1 antitrypsin deficiency
Causes of cirrhosis. The other 3
OTHER 3:
- Nash
- Budd Chiari
- Chornic biliary obstruction (tumour, CF)
4 stages of progression of chronic liver injury to cirrhosis
○ Stage 1: enlarged portal tracts w no septa
○ Stage 2: septa extending towards central vein but not much linking between portal tracts
○ Stage 3: portal-to-portal bridging
○ Stage 4:Cirrhosis (network of nodules separated by fibrous scar tissue)
Pathophys of cirrhosis.
Chronic liver injury -> inflammation, necrosis, fibrosis
What is the coagulopathy in CLD due to?
How would you measure this - what blood test?
Lack of coagulation factors (factor VIII) due to impoaired synthetic function of liver
Low platelet count due to splenomegaly from portal HTN
-INR
What are the signs you get in the decompensation phase with CLD?
Encephalopathy -> drowsiness, metabolic flap
Jaundice
Ascitites + peripheral oedema
Leukonychia
Bruising/coagulopathy
Variceal bleeding
When ALT and AST are elevated more so over ALP and GGT, which pattern suggests acute hepatitis vs cirrhosis?
AST > ALT -> cirrhosis
ALT > AST -> acute liver disease
What scoring system is used for prognosis in CLD?
Child-Pugh score
□ Based on ascites, encephalopathy, bilirubin, albumin, prothrombin time (INR)
What is the MELD score used for?
What does it predict and what is it based on?
Used to stratify patients w CLD on transplant list.
Predict 3 month survival.
Based on creatinine (hepatorenal syndrome), INR (coagulopathy) and total bilirubin (ductal obstruction w cirrhosis).
What are the most common causes of death in cirrhosis?
Renal failure (hepatorenal syndrome)
Sepsis
GI bleed (Varicies)
Hepatocellular carcinoma
What is the diagnosis of pancreatitis based on?
2/3 things to diagnose pancreatitis - clinical decision.
- Lipase > 2x upper limit of normal
- Characteristic pain
- CT w characteristic changes (inflammation around pancreatitis)
Classic triad of features of ruptured AAA
- Pain
- Hypotension
- Pulsative abdo mass
What is hepatorenal syndrome?
Renal failure due to CLD and portal HTN.
Bc there is more blood in the portal system, less blood to kidneys -> apparent drop in renal perfusion -> chronic renal arteriolar vasoconstriction -> ischaemia and infarction of kidney
What are complications of cirrhosis?
Hepatorenal syndrome
HCC
Sodium and water retention
Osteoporosis
Hepatic hydrothorax (ascites leaks into pleural space, causing SOB on exertion)
Metabolic failure
Spontaneous bacterial peritonitis from ascites
Investigations for CLD
- Abdominal ultrasound of liver
- Bloods: FBE, UEC, LFT, INR, Albumin, serology for Hep B and C, Fe studies, Caeruloplasmin etc
- Liver biopsy
- Fibroscan
When do you refer for liver transplant
Anyone with decompensated CLD (ascites, variceal bleeding, encephalopathy, coagulopathy, hepatorenal syndrome, HCC)
When not to refer for liver tarnsplant?
Too early
Substantial co-morbid illness
Psychosocial rasons
HCC not meeting criteria for transplant
Treatment for HBV
Oral nucleos(t)ide analogues PEGlyated IFN
Treatment for HCV
Peg IFN + ribaviron +/- new agents
Do transplants work with Hep C?
No reinfection occurs 100% of the time
Why might you have a low pH in liver failure?
impaired hepatic metabolism results in lactic acidosis
Causes of acute liver failure
Paracetamol overdose - toxic dose is 10g
Ischaemic hepatitis (caused by decr blood flow due to shock, acute severe heart failure)
Acute viral hepatitis
- Hep A, D, E , EBV
Treatment of paracetamol overdose
N acetyl cysteine (NAC) for paracetamol poisoning, within 8 hours of ingestion of paracetamol
+Coagulation factors
May need liver transplant
What conditions is paracetamol overdose associated with?
Why?
Alcoholism and starvation
- Both reduce glutathione levels which mops up excess of the toxic paracetamol metabolite NAPQI
What is budd Chiari syndrome?
Autoimmune liver condition
-Obstruction in the post-hepatic venous sinusoids (draining system of liver), resulting in back pressure and damage to liver cells
What is the definition of fulminant hepatic fialure/acute liver failure?
- Rapid deterioration of liver function in previously normal liver
- Jaundice to encephalopathy within <8weeks
- INR >1.5
Pathology of fulminant hepatic failure
Fulminant hepatocellular necrosis: Widespread hepatocellular necrosis beginning in thecentrizonal distribution(zone 3, around central vein) and progressing towardsportal tracts (relative preservation of portal tracts)
Investigations for ALF (FHF)
Paracetamol levels and toxicology screen
Hep A, B, C serology; EBV PCR
Liver ultrasound
Features of ALD on histology
○ Hepatocyte necrosis with surrounding zone III inflammation
○ Mallory denk bodies
○ Chicken wire fibrosis
Inherited liver diseases
- Wilson’s disease - excess Cu (keiser fleicher rings)
- Haemochromatosis -excess Iron storage (brone/grey skin)
- Alpha 1 antitrypsin deficiency
Investigations and basic treatment of Wilson’s disease
Ix: serum ceruloplasmin, Urinary copper, incr Cu on liver biopsy, genetic analysis
Mx: chelation therapy
HAemochromatosis
- diagnosis and basic MX
FBE: transferrin saturation and ferritin elevated
Gene analysis
MX: lifelong phlebotomy if primary, or chelation therapy if secondary cause.
Clinical features of acute viral hepatitis
Most subclinical.
Flu-like syndrome (nausea, vomiting, anorexia, headaches, fatigue, myalgia, fever, arthralgia)
Some progress to icteric phase - lasts days-weeks
- pale stool, dark urine, jaundice
- hepatomegaly, RUQ pain
- splenomegaly, cervical lymphadenopathy
Treatment for ascending cholangitis
Drainage via ERCP ideally
Antibiotics: tazocin or ceftriazone and metronidazole or carbapenem
How might you get a liver abscess?
Direct spread from:
- biliary tract infection
Portal spread from GI infx
Systemic infx (endocarditis)
What is sclerosing cholangitis?
list 3 causes
Inflammation of biliary tree leads to scarring and lumen obliteration
1. Primary: assoc w IBD (UC) Secondary: 2. chronic choledocholilithiasis 3. cholangiocarcinoma 4. post-surgery/trauma/ERCP
What is primary biliary cirrhosis and what are 2 common causes
Autoimmune
chornic inflammation and fibrous obliteration of intrahepatic bile ductules
- Sjogrens
- scleroderma
treatment biliary colic vs acute cholecystitis
Bilairy colic: analgesia and rehydration with elective cholecystecomy
Acute cholecystitis:
- admit, hydrate, NPO, NG tube, analgesics
- cefazolin
- cholecystectomy early
where does most pancreatic cancer occur (what part of hte pancreas?) and how does it manifest clinically?
Head of the pancreas in 70%
- Systemic SX, obstructive jaundice, vague constant mid-epigastric pain, painless jaundice, courvoisier’s sign
+/- palpable tumour mass
what type of cancer is pancreatic cancer most of the time?
Ductal adenocarcinoma
What is a Whipple’s procedure?
Pancreaticoduodenectomy - removes - CBD -GALLbladder -Duodenum -Pancreatic head \+/- distal stomach
Clinical features of acute viral hepatitis
Mostly subclinical
Flu-like prodrome preceding jaundice by 1-2 weeks
Nausea, vomiting, anorexia, headache, fatigue, myalgia, low-grade fever
Arthralgia and urticaria (HBV)
Jaundice: Some progress to icteric phase, lasting days to weeks
Pale stool and dark urine
Hepatomegaly and RUQ pain
Splenomegaly and cervical lymphadenopathy (10-20% cases)
DDX for hepatitis
Viral (Hep A-E, EBV, CMV, YF) Alcohol Drugs Immune-mediated (autoimmune) Toxins (paracetamol)
Investigations
AST, ALT (hugely elevated)
ALP and bilirubin (minimally elevated)
Viral serology (anti - :hep, EBV, CMV, YF), IgM
Complications of Hep A
Fulminant hepatic failure and subsequent death (<5% time)
Relapse
Complications of Hep B
vs Hep C
HBV:
• Cirrhosis (8-20% of those without treatment)
• HCC
• Co or super-infection with HDV
HCV:
• 80% become chronic
• 20% of chronic cases become Cirrhosis
• HCC
• Can cause cryoglobulinemia, assoc w membranoproliferative GN, lymphoma
Blood tests for HBV what do the following mean:
HBsAg Anti-HBs HBeAg Anti-HBC IgM and IgG HBV DNA
- HBsAg is a marker of infected state!
- HBeAg is a marker of high HBV viral load!
- Anti-Hbs is a marker of resolved infection/immunity
- Anti-HBc IgM markers acute infection
- Anti-HBc IgG marks chronic or resolved infection
- HBV-DNA: viral load
Treatment for HBV
• Counselling
• Screening for HCC with ultrasound every 6 months
• Treatment goal: reduce HCV DNA to undedetectable level
• Medications: IFN, tenofovir, entacavir, adefovir
• Vaccinate against HAV
Blood and sexual precautions
Serum markers for HCV?
Treatment HCV
Serum anti-HCV and HCV-RNA (monitor response tot treatment)
- Blood precautions
- Vaccinate against HBV and HCA
- Avoid alcohol
- Direct acting anti-virals (ribavirin, sofosbuvir)
- Pegylated IGN-alpha + ribaviron
- Measure HCV-RNA @ 1 and 3 months after starting treatment
histology of chrons
Chronic inflammation and granuloma formation (epithelioid macrophages and giant cells )
