GI Flashcards
risk factors for oral malignancy
Tobacco, alcohol, HPV, cannabis
High risk sites for oral malignancy
ventral and lateral tongue
floor of mouth
signs/symptoms of oral malignancy
Erythroplakia Leukoplakia Erythroleukoplakia ulcer number feeling change in voice
GORD (reflux) and causes
Inflammation of oesophagus due to refluxed low pH gastric content and squamous epithieum
- defective sphincter mechanism +/-hiatus hernia
- Abnormal oesophageal motility
- Increased intra-abdominal pressure
Management of GORD
Lifestyle modifications Antacids - symptomatic relief H2 antagonists e.g. ranitidine PPI: Omeprazole and lansoprazole - superior surgery: nissen fundoplication
Barrett’s oesophagus
Replacement of stratified squamous epithelium by columnar epithelium in the oesophagus
typical improvement in reflux symptoms
investigations and management barrets
endoscope and biopsy (Columnar lined mucosa with intestinal metaplasia)
- Optimise PPI
- endoscopic mucosal resection
- radiofrequency ablation
Allergic oesophagitis
Personal/family history of allergy and Asthma
- Increased eosinophils
- negative ph for reflux
- endoscope - corrugated
allergic oesophagus management
steroids/ chromoglycate/ montelukast
Squamous cell carcinoma of oesophagus
Malignant Oesophageal tumours in upper 1/3rd of oesophagus
Squamous cell carcinoma of oesophagus Mx
Endoscopic Mucosal resection: Option instead of an oesophagectomy if oesophageal cancer is diagnosed very early on. It involves cutting out the tumour using a loop of wire at the end of a thin flexible tube.
radiofrequency ablation (RFA): radiowaves
Radiotherapy – quite successful – before
Surgery: If T1-T2 localised disease: radical curative transthoracic esophagectomy
Adenocarcinoma of oesophagus
lower 1/3rd oesophagus
Achalasia
Coordinated peristalsis and lower oesophageal sphincter fails to relax (degeneration of the myenteric plexus)
Achalasia management
Endoscopic balloon dilation or Hellers cardiomyopathy then PPIs
Botulinum toxin
Calcium channel blockers and nitrates to help relax the sphincter
Peptic ulceration
breach in the gastrointestinal mucosa as a result of acid and pepsin attack. edges are clear cut and punched
can be gastric or duodenal
peptic ulceration: pathology of protective layer destruction
Medications: steriods or NSAIDs Helicobacter pylori (exposes gastric mucosa to acid and ammonia to which directly damages cells)
peptic ulceration signs/symptoms
epigastric discomfort, bleeding, nausea and vomiting
Eating improves the pain of
duodenal ulcers
eating worsens pain of
gastric ulcers
rapid urease test for?
H. Pylori
eradication of H. Pylori therapy
Antacids (Gaviscon)
PPI + amoxcillin 1g bd + clarithromycin 500mg bd
PPI + metronidazole 400mg bd + clarithromycin 250mg bd
Endoscope:
DU: uncomplicated DU requires no f/u and only if ongoing symptoms
GU: f/u endoscopy at 6-8 weeks and ensure healing and no malignancy
Gastric adenocarcinoma location and pathology
In UK proximal tumours of cardia/GOJ increasing and distal and gastric body tumours decreasing
H.pylori infection chronic gastritis intestinal metaplasia/atrophy dysplasia carcinoma
gastric adenocarcinoma types
intestinal (better prognosis and diffuse (infiltrates stomach wall) e.g. signet cell cancer
virchow’s node?
gastric adenocarcinoma
gastric adenocarcinoma management
Early gastric cancer: endoscopic mucosal resection
Partial gastrectomy – advanced distal tumours
Total gastrectomy – proximal tumours
Combination chemotherapy: epirubicin, cisplatin & fluorouracil) to increase survival in advanced disease
Neo-adjuvant chemotherapy before surgery – improve survival
Surgical palliation: obstruction, pain or haemorrhage
Trastuzumab for HER-2 positive cancers
Gastric lymphoma
Derived from mucosa associated lymphoid tissue (MALT): B, T cells, Plasma cells and macrophages
associated with H. Pylori. Continuous inflammation induces an evolution into a clonal B-cell proliferation: low grade lymphoma. If unchecked evolves into a high grade B-cell lymphoma
Gastric lymphoma management
May regress with H. Pylori eradication (triple therapy)
Rituximab
Chemotherapy and radiotherapy
GIST tumour and management
soft tissue sarcoma from interstitial cells of cajal
surgery and KI (Imatibib and sunitinib)
Gastroparesis
delayed gastric emptying
Gastroparesis management
Removal of precipitating factors e.g. drugs
Liquid / sloppy diet
Eat little and often
Promotility agents
Gastric pacemaker
Acute mesenteric ischaemia
Involves the small bowel and may follow the superior mesenteric artery thrombosis, thromboembolism from heart (e.g. A.Fib) and mesenteric vein thrombosis
Pathology of acute mesenteric ischaemia
Mucosal infarct (regeneration/resolution: mucosal integrity restored)
Mural Infarct (Repair and regeneration: fibrous stricture, chronic ischaemia, ‘mesenteric angina’ and obstruction)
Transmural infarct (Gangrene: perforation, peritonitis, sepsis and death if not resected)
acute mesenteric ischaemia signs/symptoms
severe abdominal pain
constant, central and around RIF
Clinical signs are out of proportion to pain/degree of illness
acute mesenteric diagnosis
Arterial blood gases: Persistent metabolic acidosis (high lactate)
Abdominal X-ray: gasless abdomen
CT/MRI: evidence of ischaemia with CT/MRI angiography or formal arteriography if doubt remains
Laparotomy: nasty, necrotic bowel at laparotomy
acute mesenteric management
Resuscitation with fluid, antibiotics (piperacillin/tazobactam) and LMWH/heparin
Thrombolysis with angiography
Surgery: resect, renastomose and planned return if fitter
Meckel’s diverticulum
Outpouching or bulge in the lower part of the small intestine.
The bulge is congenital (present at birth) and is a result of incomplete regression of vitello-intestinal duct (leftover of the umbilical cord)
Tubular structure, 2 inches long, 2 foot above IC valve in 2% of people
Meckel’s diverticulum management
surgery
Appendicitis signs/symptoms
central abdominal pain, moves to RIF and becomes localised there
Tender in McBurneys point (1/3 distance from ASIS to umbilicus)
N&V
Rovsings sign (palpate in LIF, pain in RIF)
Rebound tenderness
WCC, pyrexia, tachycardia
appendicitis investigations
Ultrasound and CT scan
appendicitis management
analgesia, antibiotics, appendicectomy
appendix mass?
An appendix mass occurs when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa.
appendix management
supportive therapy: antibiotics
surgery when acute situation has resolved
mesenteric adenitis
inflamed abdominal lymph nodes.
presents with abdominal pain, usually in younger children. This is often associated with tonsillitis or an upper respiratory tract infection.
neoplasms of appendix
adenocarcinoma of the caecum
Lymphomas of small bowel and management
Non-Hodgkin’s lymphoma
Enteropathy associated T-cell lymphomas
Maltomas (B-cell) derived
chemotherapy, surgical resection and autologous stem cell transplant
Carcinoid tumours of small bowel
Diverse group of tumours of enterochromaffin cell (neural crest) origin capable of producing 5HT (serotonin). Commonest site is the appendix
can cause appendicitis, inteussusception, obstruction, paraneoplastic syndrome
mets to liver: carcinoid syndrome: flushing, diarrhoea and RUQ
Carcinoma of small bowel
associated with crohns and coeliac disease
adenocarcinoma: starts in cells of the bowel (epithelial cells): duodenum
risk factors for colorectal carcinoma (genetic)
familial adenomatous polyposis: a rare condition where an inherited faulty gene makes many polyps develop on the bowel lining
Lynch syndrome (Hereditary non-polyposis colorectal cancer or HNPCC): a gene fault that increases the risk of several different types of cancer at a younger age
Peutz Jeghers syndrome: an inherited condition where benign (non cancerous) polyps form in the bowel.
Crohn’s
Coeliac disease
signs/symptoms of carcinoma of small bowel
• pain or lump in your tummy (abdomen) • weight loss • feeling and being sick • diarrhoea • tiredness • dark black poo, due to bleeding in the small bowel • blockage in the bowel anaemia
management of small bowel cancer?
surgery with adjuvant chemo if not spread and fit enough
e.g. top of duodenum: pancreaticoduodenectomy
Whipples disease
GI malabsorption that affects middle age white males. Caused by Tropheryma whipplei
Whipples disease management
• IV ceftriaxone (or penicillin + streptomycin) for 2 weeks then oral co-trimoxazole for 1 year
Coeliac disease - foods
wheat, barley and rye
coeliac disease signs/symptoms
o Failure to thrive in young children
o Diarrhoea, excess flatus and discomfort
o Fatigue
o Weight loss
o Mouth ulcers
o Anaemia secondary to iron, B12 or folate deficiency
o Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
o Vitamin deficiencies
malabsorption: steatorrhea
gallstones
coeliac diagnosis
check IgA levels for IgA deficiency
anti-TTG or anti-EMA antibodies
duodenal biopsy
Types of intestinal failure
Type 1 - short term - post op, obstruction, chemo/radiotherapy
Type 2 - septic patients, abdominal fistulae, post surgery awaiting reconstruction
type 3 - chronic intestinal failure
short bowel syndrome
<200cm
Common viral gastroenteritis
rotavirus, norovirus and adenovirus
E.COLI 0157 spread
It is spread through contact with infected faeces, unwashed salads, beef (raw milk/water) but wide range
signs/symptoms of e.coli 0157
• This causes abdominal cramps, bloody diarrhoea and vomiting
what to not give in e.coli 0157
use of antibiotics increases the risk of haemolytic uraemic syndrome therefore antibiotics should be avoided if E. coli gastroenteritis is considered.
• No anti-motility drugs or NSAIDs
e.coli 0157 cause and symptoms/signs of it
HUS
abdomen pain, fever, pallor, petechiae, oliguria
e.coli 0157 diagnosis
• High white cells • Low platelets • Low HB • Red cell fragments • LDH>1.5 x normal • Stool culture • PCR enzyme immunoassay incubation 1-14
Most common cause of travellers diarrhoea
Campylobacter jejuni
- raw or improperly cooked poultry
- untreated water
- unpasteurised milk
Incubation 2-5 days
campylobacter symptoms
- Abdominal cramps/pain
- headache
- Diarrhoea often with blood
- Vomiting
- Fever
Shigella spread? Incubation?
spread by faeces contaminating drinking water, swimming pools and food.
1-2 days
shigella signs/symptoms
bloody diarrhoea, abdominal cramps, fever, tenesmus
can cause HUS
salmonella spread and incubation
raw eggs, poultry and food contaminated with infected faeces of small animals
12 hours to 3 days
salmonella signs/symptoms
- Watery diarrhoea that can be associated with mucus or blood
- Abdominal pain
- Vomiting
- Fever (12-36 hours of exposure)
- Headache
- Invasive infection: bacteraemia, sepsis, meningitis, osteomyelitis & septic arthritis
Fried rice and abdominal cramping and profuse vomiting within 5 hours of ingestion
bacillus cereus
bacillus cereus
water diarrhoea
Yersinia Enterocolitica
gram negative bacillus
raw or undercooked pork can cause infection.
spread through contamination with the urine or faeces of other mammal such as rat and rabbits.
incubation 4-7 days
YE
affects chihldren - watery/bloody diarrhoea
older children - mesenteric lymphadenitis
Unpasteurised milk products & deli counter e.g. cheese products (9-48 hours)
listeria monocytogenes
listeria - high risk groups
immunosuppression and pregnancy
listeria management
Ampicillin plus gentamicin for systemic disease
Co-trimoxazole (CNS disease)
C diff toxins and colonoscope findings
Toxin A and B
Severe = patchy pseudomembranous colitis
C diff management
Non-severe: Oral Metronidazole 400mg (10 days)
Severe: Oral/NG Vancomycin 125mg qds ± IV metronidazole (10 days)
Amoebiasis, what is it? route? complication?
- Entamoeba histolytica: a protozoa
- Faecal-oral spread, strong association with poor sanitation
- Amoebic liver abscess: Incubation period 8-20 weeks & More common in men
Amoebic management
Metronidazole/tinidazole for amoebic dysentery and invasive disease
Diloxamode furoate: luminal agent to destroy gut cysts (10 days)
Giardiasis
microscopic flagellated protozoa
Invades duodenum and proximal jejunum
These mammals may be pets, farmyard animals or humans. It releases cysts in the stools of infected mammals. These cysts then contaminate food or water and are eaten to infect a new host. This is called faecal-oral transmission.
• Incubation usually around 7 days
Giardiasis management
metronidazole or Tinidazole (7days)
Diverticula
Mucosal herniation through muscle coat (pouches in bowel wall: 0.5-1cm)
Diverticulosis
small, bulging pouches (diverticula) develop in your digestive tract without symptoms.
diverticulitis
• When one or more of these pouches become inflamed or infected,
diverticulitis investigations
barium enema, sigmoid/colonoscopy, CT scan
diverticulitis management
uncomplication: high fibre diet and weight loss
diverticulitis: admit, antibiotics, analgesia and fluid resus
complex diverticulitis: surgical resection, percutaneous drainage and hartmann’s drainage
ischaemic colitis causes
arterial: AF
venous: dvt
Collagenous colitis
thickened basement
chronic watery, non-bloody diarrhoea or loose stool, often between 3 and 20 times daily
Lymphocytic colitis
No chronic architectural changes in crypts
Intraepithelial lymphocytes are raised
No thickening of BM
microscopic colitis
both lymphocytic colitis and collagenous colitis.
Upper small bowel obstruction
acute (Hours): large volumes of gastric, pancreatic and bilary secretions
distal small bowel obstruction
colicky abdominal pain and vomiting faecal origin
ileo-caecal valve remains competent ?
caecum progressively distends with swallowed air and eventually may rupture: ‘closed loop obstruction’
ileo-caecal valve remains incompetent ?
small bowel distends, delaying the onset of symptoms.
Volvulus types
sigmoid: twists on mesentery (anti-clockwise)
caecal: counter clocker
volvulus investigations
axr and ct scan
volvulus management
endoscopic decompression
Laparotomy (Hartmann’s for sigmoid) and (right hemicolectomy for caecal)
IBS management (1st line ….
loperamide for IBS-D
Laxatives for IBS-C
Anti-spasmodic for IBS-Cramps - buscopan
Crohn’s disease
Chronic inflammatory and ulcerating condition of the GI tract with exacerbations and remissions that can affect anywhere from the mouth to the anus (segmental disease)
crohn’s diagnosis
Bloods: anaemia, B12 & ferritin, infection (WCC, CRP, ESR), TFTs, U&E and LFTs
Faecal calprotectin
Ultrasound, CT and MRI
Endoscope and biopsy
Crohn’s inducing remission
1st line: steroids
add in immunosuppressant (Azathioprine, methotrexate)
Anti-TNF therapy: infliximab and adalimumab
Crohns - maintaining remission
First line: Azathioprine or Mercaptopurine
Alternatives: Methotrexate
Anti-TNF: Infliximab or Adalimumab
Crohn’s surgery
Emergency: Failure to respond to medical therapy, small bowel obstruction, abscess, fistulae
Elective: Failure to respond to medical therapy and dysplasia of colon mucosa
Ulcerative colitis
Chronic inflammatory disorder confined to colon and rectum with unknown aetiology
Continuous and confluent extending proximally from rectum for varying lengths
UC: Truelove and Witt criteria
> 6 bloody stools/24 hour + 1 or more of
Fever (>37.8°C)
Tachycardia (>90/min)
Anaemia (Haemoglobin <10.5g/dl)
Elevated ESR (>30mm/hr) – now look at CRP and albumin (low – not responding to treatment)
UC inducing remission
IV fluids and GI rest
Mild to moderate
- aminosalicylate (5-ASAs): mesalazine (double in acute relapse)
- steroids
severe
-IV corticosteroids
2nd line: IV ciclosporin
Anti-TNF therapy
maintaining remission in UC
Aminosalicyate e.g. mesalazine
Azathioprine and meractopurine
- methotrexate (alternative)
Anti-TNF: Infliximab or Adalimunmab
surgery UC
Pan proctocolectomy
- permanent ileostomy or ileo-anal anastomosis (J pouch)
Emergency surgery UC
subtotal colectomy
Toxic megacolon
acute or acute on chronic fulminant colitis
Transverse >5.5cm and Caecum >9cm
colorectal carcinoma
adenocarcinoma: rectum and sigmoid
Genetic predisposition for colorectal carcinoma
Heriditary Non Polyposis Coli (HNPCC): <100 polyps: right sided
Familial adenomatous polyposis (FAP): > 100 polyps: throughout colon
Colorectal carcinoma investigations
Bloods: FBC (microcytic anaemia), LFT
Faecal occult blood: blood in faeces
Colonoscopy/sigmoidoscopy
CT scan and CT colonography
CT Chest for staging and MRI for rectal cancers and liver mets
Colorectal bowel screening
Scotland (50-72) and England (60-72): every 2 years: stool sample, if positive, offered colonoscopy
Causes of upper GI bleed
- Oesophageal varices
- Mallory Weiss tear
- Gastric/duodenal ulcer
- Cancers of stomach or duodenum
Rockall and Glasgow-Blatchford Score
Rockall - rebleed after endo
Glasgow: scoring system for suspected upper GI bleed (remember drop in Hb, rise in urea)
General management of haematemesis
A - ABCDE
B- Bloods (FBC, coag, U&E, LFTs, group, save and crossmatch
T - transfuse (fresh frozen plasma, platelets, prothrombin complex concentrate)
E - Endoscopy
D - Drugs
E- endoscopy
Endoscopic treatment of peptic ulcers
- Injection: adrenaline causes tamponade affect, causes vasoconstriction and tip into clot formation
- Heater probe coagulation: electric current passed through it and clot it
- Combinations: need to do duel therapy for highest rate of haemostasis e.g. adrenaline and heater probe
- Clips
- Haemospray
- Acid suppression
Endoscopic treatment of stable varices
Propranolol reduces portal hypertension by acting as a non-selective beta blocker
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation)
TIPS
Endoscopic treatment of bleeding oesophageal varices
- Terlipressin (vasopressin analogue)
- Endoscopic variceal ligation (banding)
- Sclerotherapy
- Sengstaken-Blakemore balloon
- TIPS
- Propranolol infusion
indirect inguinal hernia
frequent in males
through the deep and superficial ring
lateral to the epigastric. Above and medial to the pubic tubercle
direct inguinal hernia
weakness in the abdominal wall around Hasselbach’s triangle. protrudes directly through abdominal wall
femoral hernia
lateral and below pubic tubercle
epigastric hernia
fascia defect in the linea alba between the xiphoid process and the umbilicus
paraumbilical hernia
factors include stretching of the abdominal wall by obesity, multiple pregnancy and ascites
umbilical hernia
results from persistent elevation of intraabdominal pressure. Part of the intestine or fatty tissue bulges through the muscle near the belly button (navel, umbilicus).
Incisional hernias
Iatrogenic: bigger the incision – the bigger the risk
Commonest complication of a laparotomy (exploration of the abdomen)
Due to inadequate closure of the muscle and tissues after the incision
Spigelian hernia
hernia through the Spigelian fascia, which is the aponeurotic layer between the rectus abdominis muscle medially, and the semilunar line laterally.
Haemorrhoids
venous “vascular cushions” that have become enlarged due to increased pressure (e.g. secondary to straining in constipation)
o 1st degree: no prolapse
o 2nd degree: prolapse when straining and return on relaxing
o 3rd degree: prolapse when straining, do not return on relaxing but can be pushed back
o 4th degree: prolapsed permanently
Haemorrhoids management
anusol cream and LA Sclerosation therapy rubber band ligation Open haemorrhoidetcomy stapled haemorrhoidectomy HALO/THD procedure
Anal fissure
Tear in the anal margin due to passage of a constipated stool.
Glass passing through back passage
Anal fissure management
dietary advice and stool softeners
Pharmacological sphincterotomy: GTN - Dilate vessels helps to heal quicker
Lateral Sphincterotomy: cut the lower part of the internal sphincter muscle. This will relieve the spasm in the sphincter, allowing a better blood supply to heal the fissure.
Botox injection
Alcoholic Liver Disease Pathology
2-3 days: Fatty liver: Reversible in around 2 weeks
4-6 weeks: Hepatitis: Reversible with permanent abstinence
Mths-yrs: Fibrosis: Irreversible
Years: Cirrhosis: Irreversible
Healthy - steatosis - hepatitis
ALD Signs/symptoms
- Jaundice
- Hepatomegaly
- Spider Naevi
- Palmar Erythema
- Gynaecomastia
- Bruising – due to abnormal clotting
- Ascites
- Caput Medusae – engorged superficial epigastric veins
- Asterixis – “flapping tremor” in decompensated liver disease
ALD investigations
AUDIT questionnaire Bloods: FBC (raised MCV), LFTS (ALT/AST, GT, bilirubin), U&E (hepatorenal syndrome), clotting (PR prolonged), low albumin Ultrasound Fibroscan Endoscopy: oesophageal varices CT/MRI
ALD management
14 units, detox, B1 (THiamine), steriods (short term), complication of cirrhosis
AL withdrawal
o 6-12 hours: tremor, sweating, headache, craving and anxiety
o 12-24 hours: hallucinations
o 24-48 hours: seizures
o 24-72 hours: “delirium tremens”
Delirium tremens
Chronic alcohol user results in the GABA system becoming up-regulated and the glutamate system being down-regulated to balance the effects of alcohol.
When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity.
DT signs/symptoms
Acute confusion, severe agitation, Delusions and hallucinations, Tremor, Tachycardia
Hypertension, Hyperthermia, Ataxia (difficulties with coordinated movements) & Arrhythmias
Management of Alcohol withdrawal
Chlordiazepoxide and IV B1
Wernicke’s encephalopathy signs/symptoms
confusion
oculomotor disturbances
ataxia
Korsakoffs syndrome
memory impairment (retro and anterogreade)
NAFLD
• Non-alcoholic fatty liver disease (NAFLD) forms part of the “metabolic syndrome” group of chronic health conditions (diabetes, obesity, hyperlipidaemia) relating to processing and storing energy that increase risk of heart disease, stroke and diabetes.
signs/symptoms of liver cirrhosis
Jaundice – caused by raised bilirubin
Hepatomegaly
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic circulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
clubbing
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease
Ascites
fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and into the peritoneal cavity.
Ascites management
improve underlying liver disease, low Na diet and no NSAIDs
Prophylactic antibiotics against SBP e.g. ciprofloxacin
Spironolactone
Paracentsis or drain
TIPS or transplant in refractory
SBP organisms
E. Coli, klebsiella and staph/enterococcus
SBP diagnosis
culture and neutrophils over 250
SBP management
IV cephalosporin such as cefotaxime
• Vascular instability: Terlipressin
Hepatic encephalopathy
o The functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products.
Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.
HE management
laxatives e.g. lactulose: excretion of ammonia
antibiotics e.g. rifaximin
Hep A
RNA virus, faecal oral route
cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools
Hep B
DNA virus, direct contact with blood/bodily fluids, sex, sharing needles and vertical transmission
Hep B viral markers
Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load
Acute Hep B management
• No antivirals given
• Monitor for encephalopathy and monitor for resolution
o of Hep B or Hep C, or Hep E if immunocompromised
• Notify Public Health
• Immunisation of contacts
• Test for other infections if at risk
Chronic Hep B Mx
• OPTION 1 – more widely used
o Suppressive antiviral drug (5 licensed to date) e.g. entecavir, tenofovir
• OPTION 2 – you can identify the patients that may benefits from these
o Peginterferon alone
Hep C
RNA virus, blood and body fluids
Hep C antibody tests
- Hepatitis C antibody is the screening test. If positive test for…
- Hepatitis C RNA testing (PCR) is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype
- IgG positive (antibody), RNA negative = past infection (may still get re-infected if still injecting), will not get liver disease due to HCV unless they get re-infected
- IgG positive (antibody), RNA positive = active infection (usually chronic)
Hep C management (actual medical)
Antiviral treatment with direct acting antivirals (DAAs) is tailored to the specific viral genotype
They are typically taken for 8 to 12 weeks e.g., sofosbuvir, simeprevir, ledipasvir, voxilaprevir
Response defined by loss of HCV RNA in blood sustained to 6 months after end of therapy. Virological cure known as Sustained Virological Response or SVR
Hep D
RNA virus but requires Hep B (attaches to HBsAg)
Hep E
RNA virus, tropics, faecal oral route
Autoimmune hepatitis types
Type 1 (adults: women in late 40s or early 50s). menopause - fatigue and features of liver disease on exam
Type 2: children or teenagers or early 20s: acute hepatitis with high alt/ast and jaundice
Autoantibodies for AH
Type 1 Autoantibodies:
Anti-nuclear antibodies (ANA), Anti-smooth muscle antibodies (anti-actin) and Anti-soluble liver antigen (anti-SLA/LP)
Type 2 Autoantibodies:
Anti-liver kidney microsomes-1 (anti-LKM1), Anti-liver cytosol antigen type 1 (anti-LC1) and AMA
autoimmune hep management
prednisolone (tapered), azathioprine (immunosuppressant) and liver transplant
Primary Biliary Cirrhosis
condition where the immune system attacks the small bile ducts within the liver (unknown aetiology). INtralobular bile ducts back up, fibrosis and cirrhosis - liver failure
PBC signs/symptoms
fatigue, itching without rash (bile acids), jaundice, pale stools and dark urine, xanthelasma
PBC diagnosis
ALP raised, AMA, ANA
PBC management
Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
Colestyramine (or obeticholic acid) is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
Liver transplant
Immunosuppression (e.g. with steroids) is considered in some patients
Fat soluble vitamin deficiency may occur in PSC and PBC. Monitor levels and supplement if necessary.
Primary Sclerosing Cholangitis
large and medium sized intrahepatic or extrahepatic ducts become strictured and fibrotic
PSC diagnosis
ALP
p-ANCA, ANA, aCL
MRCP
Biopsy
PSC management
• Liver transplant
• ERCP can be used to dilate and stent any strictures (use x-rays)
• Ursodeoxycholic acid is used and may slow disease progression
• Colestyramine (bile acid sequestrate): binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
• Monitoring for complications
Fat soluble vitamin deficiency may occur in PSC and PBC
Haemochromatosis
excessive total body iron and deposition of iron in tissues (autosomal recessive gene: chromosome 6)
secondary: iron overload from diet, iron therapy and transfusions
Haemochromatosis signs/symptoms
- Type 1 Diabetes (iron affects the functioning of the pancreas)
- Liver Cirrhosis
- Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
- Cardiomyopathy (iron deposits in the heart)
- Hepatocellular Carcinoma
- Hypothyroidism (iron deposits in the thyroid)
- Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
Haemochromatosis management
venesection, monitor serum ferritin, avoid alcohol
Wilson’s disease
excessive accumulation of copper in the body and tissues. AR and chromosome 13
Wilsons disease investigations
Low serum caeruloplasmin
Liver biopsy for liver copper content
24-hour urine copper assay
Wilsons management
copper chelation using: Penicillamine and Trientene
Alpha-1-antitrypsin deficiency
autosomal recessive deficiency of a protease inhibitor called alpha 1 antitrypsin. excessive protease enzymes attacking liver and lung
Budd chiari
Thrombosis of the hepatic veins
Haemangioma
commonest, • Hypervascular tumour and usually single small well demarcated capsule. No treatment
Focal Nodular Hyperplasia (FNH)
Benign nodule formation of normal liver tissue. Congenital vascular anomaly
Hepatocellular adenoma
Benign neoplasm composed of normal hepatocytes: no portal tract, central veins or bile ducts. Maligant transformation higher in males
management of hepatocellular adenoma
stop hormones, wt loss excise for males Females: o <5cm or reducing in size - annual MRI o >5cm or increase in size - for surgical excision
Hepatocellular carcinoma signs/symptoms
Weight loss and RUQ pain (most common) and mass
• Worsening of pre-existing chronic liver disease
• Acute liver failure and ascites
• Signs of cirrhosis
• Hard enlarged RUQ mass
Hepatocellular management
Liver transplantation (Best available treatment): Removes tumour and liver o Only if single tumour less than 5cm or less than 3 tumours less than 3cm each
Resection: Feasible for small tumours with preserved liver function (no jaundice or portal HTN): <3cm
Local ablation: For non resectable and patients with advanced liver cirrhosis
Chemoembolisation: TransArterial ChemoEmbolization - TACE
Systemic therapy: sorafenib
Cholelithiasis
Gallstones form when there is an imbalance between the ratio of cholesterol to bile salts disrupting micelle formation
This can cause cholestasis: blockage to the flow of bile
Cholelithiasis risk factors
fair, fat, female and forty
Biliary colic
Stone impacts in cystic duct temporally. Intermittent right upper quadrant pain caused by gallstones irritating bile ducts (cystic duct obstruction)
Biliary colic signs/symptoms
• Gradual build-up pain in RUQ and may last between 2-6 hours
• Radiates to back / shoulder
• Associated with indigestion / nausea – after we eat
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Biliary colic investigations
ALP, ultrasound, CT scan (if USS doesn’t show ductal stones), ERCP
Biliary colic management
- Analgesia and rehydrate
- Low fat diet / lose weight if obese and observe 3-6 months
- If recurrent episodes pain / colic consider / refer for laparoscopic cholecystectomy
- Unfit – Ursodeoxycholic acid 10mg/kg/day
Acute cholecystitis
Inflammation of the wall of the gallbladder. Majority caused by gallstones (calculous cholecystitis) that impacts at the neck of the gallbladder (cystic duct)
acute cholecystitis signs/symptoms
• Murphy’s sign:
o RUQ tenderness exacerbated by deep inspiration
o Place hand in RUQ and apply pressure
o Ask patient to take deep breath in
o Gallbladder will move downwards under your hand and cause pain
• Continuous epigastric or RUQ pain (referred to right shoulder)
• Vomiting, nausea, fever and local peritonism
Acute cholecystitis Mx
- IV antibiotics and IV fluids: amoxicillin, gentamicin and metronidazole i.e. triple therapy
- Nil by mouth
- Urgent Laparoscopic cholecystectomy (Open surgery if there is GB perforation)
Cholangitis
Bile duct infection (biliary obstruction)
RUQ pain, jaundice and rigors (Charcots triad). Swinging fever
cholangitis Mx
antibiotics (triple therapy), sepsis protocol and ERCP
Gallstone ileus
Fistula between gallbladder and duodenum causing large gallstone to pass into small intestine (stone erodes through GB into duodenum and obstructs ileum)
Gallstone ileus management
urgent laparotomy and interval cholecystectomy (3 months)
Carcinoma of gallbladder
Adenocarcinoma and associated with gallstones. PSC high risk factor
Cholangiocarcinoma
Adenocarcinoma: slow growing and mostly distal extra hepatic or perihilar : bile duct cancer. UC and PSC
Cholangiocarcinoma signs/symptoms
obstructive jaundice, weight loss, malaise
cholangiocarcinoma investigations
ALP, Bilirubin, FBC
US
CT/MRI, ERCP/MRCP
Biopsy
cholangiocarcinoma management
- Surgical resection: Only chance of cure
- Bile duct and liver resection (major hepatectomy + extrahepatic bile duct excision + caudate lobe resection
- Palliation: Biliary stent – ERC/PTC insertion
Acute pancreatitis causes
• Causes (I GET SMASHED)
Iatrogenic (post ERCP), Gallstones, Ethanol, Trauma, Steroids, Mumps, autoimmune, scorpion venom, hyperlipidaemia (+ hypotension and hypercalcemia), ERCP and drugs
Main common ones: Alcohol, gallstones and post ERCP
acute pancreatitis signs/symptoms
- Sudden onset severe abdominal pain
- Cause epigastric pain radiating to the back
- Patients may be severely shocked
- Vomiting prominent
- Tachycardia, fever, jaundice, shock, ileus, rigid abdomen, tenderness
- Periumbilical bruising (Cullen’s sign) and flank bruising (grey turners sign): blood vessel autodigestion and retroperitoneal haemorrhage
acute pancreatitis Iv
Bloods: lipase, amylase and CRP AXR ABG Erect CXR CT: Complications US: Gallstones
acute pancreatitis management
- Nil by mouth (consider NJ feeding to decrease pancreatic enzyme stimulation)
- IV fluids (crystalloid) and Careful monitoring
- Escalate care according to Glasgow score
- Urinary catheter and consider CVP monitoring
- Analgesia: Pethidine or morphine (might cause sphincter of oddi to contract)
- Endoscopic drainage of large pseudocysts
- ERCP: gallstone and progressive jaundice
- Antibiotics only if evidence of infected pancreatic necrosis Surgery to remove infected pancreatic necrosis
Acute pancreatitis complications
- Pancreatitic necrosis and Pseudocysts (fluid in lesser sac): fever, a mass ± persistent increase in amylase/LFT: resolve or need drainage
- Abscess: drainage
- Bleeding: elastase eroding major vessel (splenic artery): embolization
- Thrombosis: colic branches of SMA or gastroduodenal/splenic arteries
- Fistulae
- Infection in necrotic areas
- Chronic pancreatitis
Chronic pancreatitis
• Relapsing disorder may develop insidiously or following bouts of acute pancreatitis
Progressive and irreversible damage (loss of exocrine and endocrine function)
Chronic pancreatitis Iv
- Amylase may not rise in and acute exacerbation of chronic pancreatitis because the pancreas has lost it’s ability to produce the enzyme
- Ultrasound ± CT: pancreatic calcifications
- MRCP
- AXR: Speckled calcification
- Faecal elastase
chronic pancreatitis management
analgesia
creon: enzyme replacement and fat soluble vitamins
insulin
pancreatic cancer
90% are adenocarcinomas of the head of the pancreas (ductal).
Invades duodenal wall: constrict common bile duct. direct invasion of spleen
Courvoisiers law?
Painless jaundice plus a non-tender palpable gallbladder is pancreatic cancer until proven otherwise
signs/symptoms of pancreatic cancer
- Non-specific upper abdominal/back pain
- Painless obstructive jaundice
- Unintentional weight loss
- Pale stools (due to lack of bile)
- Steatorrhoea (greasy stools due to malabsorption due to lack of bile)
- Dark urine (due to obstructive jaundice)
- Palpable mass in epigastric region
Pancreatic cancer management
whipples or total pancreatectomy
