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Summary 3rd year MBChB Core Conditions
- Vak
- Instelling
Summary of all of the core conditions studied during 3rd year of medicine at the University of Leeds (85 pages)
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core conditionsabdominal
ACUTE HEPATITIS
Hepatocyte injury with cell death, inflammation and regeneration without structural change to
the liver
NOTIFY PUBLIC HEALTH
Virus Route Markers Treatment
Hep RNA FO Anti-HAV IgM Basic analgesia
A Food/water Vaccination
NOTIFIABLE DISEASE
Hep DNA IV HBsAg, HBeAg Vaccination with HBsAg – 3x of 3 doses
B Sex anti-HBcAb, anti- Antivirals to slow progression and ↓
Sharing HBsAb infectivity
needles HBV DNA Liver transplant for end-stage liver
disease
Hep RNA IV Anti-HCV Education – ↓ smoking, alcohol
C HCV RNA Direct acting antivirals (DAAs)
Liver transplant for end-stage liver
disease
Hep RNA IV Anti-HDV IgM No specific treatment
D
Hep RNA FO Anti-hepatitis E No specific treatment
E virus
Epidemiology
- Hep A is most common viral hepatitis worldwide – rare in UK, seen in people returning from
holiday or gay men
- Hep B is uncommon in UK – vaccination
- Common in MSM, sexual contact with someone with viral hepatitis, countries where hep
virueses are common
Types
- Hep A: can cause cholestasis (slowing of bile through biliary system) with dark urine and pole
stools + hepatomegaly
- Hep B: can be passed from mother to baby (vertical transmission). Most people fully recover
within 2 months, but 10% become chronic Hep B carriers - virus integrated into their DNA and
so they continue to produce viral proteins.
- Hep C: no vaccine, ¼ makes a full recovery, rest develop chronic hepatitis liver cirrhosis +
hepatocellular carcinoma
- Hep D: can only survive in patients who also have a Hep B infection
- Hep E –No vaccine - Very rare in the UK. Normally it produces only a mild illness, the virus is
cleared within a month and no treatment is required. Rarely it can progress to chronic
hepatitis and liver failure.
- Autoimmune – Rare cause of chronic hepatitis - triggered by environmental factors that
causes a T-cell mediated response against the liver cells – treat with prednisolone and
azathioprine
- Alcohol: can lead to cirrhosis and liver failure
Cause Risk factors
- Viruses (Hep A, B + E) - Most common - IVDU – Hep C
cause - Alcohol intake
- Drug induced (e.g. paracetamol - Diet – reduce fat content
overdose) - Hygiene - some viruses are FO transmission
- Autoimmune hepatitis - Travelling – get vaccine
- Alcoholic hepatitis
- Non-alcoholic fatty liver disease
Symptoms Signs
- Abdominal pain/Right upper quadrant - Hepatomegaly
pain - Pain in RUQ
- Fatigue - Jaundice
- Pruritis (itching) Similar conditions:
- Joint and muscle pain Cirrhosis, Primary biliary sclerosis,
- Fever (viral hepatitis) Haemochromatosis, Wilsons disease , Alcoholic
- Nausea and vomiting liver disease
,Investigations: AST/ALT ↑ , Bilirubin ↑ (causes jaundice), USS of abdo to asses for carcinoma
- HbsAg (Surface antigen) – Shows that there is an acute, active infection
- HBeAg (E antigen) – Marker of viral replication and implies high infectivity
- HBcAb (Core antibody) – IgM shows recent/current infection, IgG shows past infection
- HBsAb (Surface antibody) – Implies vaccination or past or current infection
- HBV DNA (Hepatitis B virus DNA) – This is a direct count of the viral load
- HCV RNA testing used to confirm diagnosis, calculate the viral load and assess for the
individual genotype
- Autoimmune: Various autoantibodies, diagnosis can be confirmed using a liver biopsy
- Alcohol: ↑ MCV, ↑ GGT, AST:ALT>2
Other
Family/pt: could become chronic or progress to cancer, pt may need to give up alcohol, may get
clotting abnormalities
Complications: Acute liver failure, chronic hepatitis, cirrhosis, portal hypertension and
hepatocellular carcinoma
HCPs: Pharmacists, Radiologists, Doctors, Infectious disease department, Nurses
ACUTE and CHRONIC PANCREATITIS
Acute – pancreas becomes inflamed, is reversible, Chronic – permanent damage over many
years, irreversible
ACUTE CHRONIC
Epidemiol M =F, avg age is 60yrs M>F 4:1, avg age is 40yrs
ogy People with excessive alcohol intake
Cause Gallstones or alcohol misuse Obstruction, alcohol and epigenetic
factors
Obstruction in sphincter of Oddi activation of pancreatic enzymes
autodigestion inflammation
Causes of acute pancreatitis that progresses to chronic – Tumours, trauma, cystic
Risk - Gallstones & Alcohol abuse - Alcohol
factors - Hypertriglyceridemia - Smoking
- Use of causative drugs - Family history
- ERCP - Coeliac disease
- Trauma - Genetic abnormalities (GGT1, CFTR,
- SLE, Sjogren’s syndrome SPINK1)
Symptom Sudden onset epigastric pain that Epigastric pain that radiates to the back
s radiates to the back, nausea, vomiting, (improves on sitting forwards),
fever, anorexia steatorrhoea
Signs Cullen’s sign – bruising of the subcutaneous fatty tissue around the umbilicus (in
severe cases)
Grey turner’s sign – bruising in flanks which is a sign of retroperitoneal
haemorrhage (in severe cases)
Chvostek’s sign – Facial muscle spasm when the facial nerve is tapped (acute)
Epigastric tenderness but soft abdomen Epigastric tenderness
Guarding and the abdomen may be rigid Signs of malabsorption
Hypovolaemia, hypotension, abdo Signs of pseudocysts (masses in the
distention epigastrium)
Differenti PUD, Perforated viscus, Oesophageal spasm, Intestinal obstruction, AAA,
als Cholangitis
Investiga Serum lipase (diagnostic if 3x upper ↑ Blood glucose
tions value of norm) CT scan, abdominal USS, abdominal x-
AST and ALT ray
FBC, CRP, haematocrit ERCP, MRCP
ABG, abdominal plain film, Faecal elastase-1, faecal fat, steatocrit
CXR, trans-abdominal ultrasound, ↑ IgG4 levels
ratio of serum lipase: amylase
Complicat Necrosis, pseudocyst, abscess, fistulae, Malabsorption, diabetes, pseudocysts,
ions vascular complication and sepsis stenosis of common bile duct,
pancreatic cancer
Treatment
Acute
,- 1st line: Initial resuscitation (IV Hartmann’s or saline) + analgesia + nutritional
support
- Consider: Supplemental O2, antiemetic, calcium replacement therapy, magnesium
replacement therapy, insulin
- Cholecystectomy or ERCP to remove gallstones
- KADE vitamins
- Necrosectomy – if necrosis
Chronic
- Acute episodic pain: 1st -line: Analgesics
- Ongoing: 1st -line: Alcohol + cigarette smoking cessation with lifestyle modifications, ↓ fat,
↑ carb
- Pancreatic enzymes + PPI
- If pseudocysts – Antioxidants, If biliary complications – Pseudocyst decompression
- Surgery – Pancreatectomy
Pathophysiology
- Acute pancreatitis –sudden inflammation and haemorrhaging of pancreas due to
destruction by autodigestion
- Chronic pancreatitis – Caused by changes to the structure of the pancreas (fibrosis,
atrophy + calcification)
- Endocrine– makes insulin and glucagon and secreted these into the bloodstream.
- Exocrine– Acinar cells secrete digestive enzymes to help digest food.
- To protect itself, the pancreas secretes inactive enzymes (pro-enzymes or zymogens) -
activated by proteases
- Digestion - zymogens released pancreatic duct small intestine where they are
activated by trypsin.
- If these enzymes become activated too early it causes acute pancreatitis.
- Any injury to the acinar cells or blocking secretion of proenzymes into the duodenum
Pancreatitis
- Alcohol ↑ zymogen formation but ↓ fluid and bicarbonate production – the pancreatic
juices become thick and viscous and can block the duct. Pancreatic juices start backing up,
↑ the pressure.
- Pancreatic inflammation blood vessel leakage (causing fluid build-up) and lipases destroy
fat – can cause the pancreatic tissue to liquefy (liquefactive haemorrhagic necrosis)
Chronic pancreatitis symptoms: I – Idiopathic
- Steatorrhoea (↓ digestive enzymes, patients are G – Gallstones
deficient in Vitamins KADE (fat soluble) greasy E – Ethanol
stools) T – Trauma
- Weight loss + malnutrition, nausea + vomiting, S – Steroids
- DM M – Mumps
- Pain is exacerbated by fatty foods A – Autoimmune
- Some individuals develop pancreatic pseudocysts S – Scorpion sting
(often the result of ductal obstruction). H–
Hypercalcaemia/hypertriglyceridemia
E – ERCP (Used to diagnose + treat)
D – Drugs
Other
Family/Pt:
Mortality rate: Ranges from 1-25% for acute pancreatitis
HCPs: Gastroenterologist, Endocrinologist, Surgeon, Pharmacist, Radiologist,
Nutritionists/dietician, OT
HERNIAS
A protrusion of part of or a whole organ through a weakening in the abdominal wall.
FEMORAL INGUINAL
Epidemio 5% of abdo hernias MOST COMMON TYPE – 75% of abdo
logy F>M, 3:1 hernia
M>F
Risk ↑ age, pregnancy, ↑ intra-abdo ↑ age, smoking, fam history, AAA,
factors pressure chronic cough
, Symptom Soft lump, which may be reducible, the lump may protrude on coughing (raised
s intraabdominal pressure) or standing (pulled out by gravity), aching or dragging
sensation
Lump in groin – infer-lateral to pubic Lump in groin- superomedially to pubic
tubercle tubercle
Signs Tightness of the femoral ring means Groin discomfort or pain with bulge,
that the hernia is unlikely to be groin mass, abdo discomfort or pain,
reducible acute abdomen (tender, distended
abdomen with absent bowel sounds
Cough impulse indicates a strangulated hernia),
nausea and vomiting, constipation
Investiga Diagnosis usually clinical but can use USS
tion
Treatme Surgery to ↓ chance of strangulation Don’t always need surgery but not
nt Reduction of hernia and surgical repairing the hernia increases the
narrowing of femoral ring chance of complications
Surgery can be below or above Open mesh repairs are preferred for
inguinal ligament those with primary inguinal hernias and
is deemed the most cost-effective
Reducible hernia: will disappear when the patient lies down or the abdomen is under less
pressure
Direct hernia: occur when a protrusion occurs directly through a weakness in the abdominal
wall
Indirect hernia: a protrusion through the deep inguinal ring.
Examination
- Identify the ASIS and the pubic tubercle. Then identify the superficial inguinal ring (superior
and medial to the pubic tubercle) and the deep inguinal ring (roughly half-way across and
superior to the inguinal ligament).
- Ask the patient to cough – if there is a cough impulse this suggests herniation
- See if the lump is tender and see if you can reduce the hernia in the inguinal region
- Ask the patient to cough again – if the hernia fails to re-appear but removing your hand
reveals the hernia again after coughing, you are demonstrating the ability to control the
hernia at the deep ring – Hernia is likely to be indirect inguinal
Similar conditions: Other hernias, Lipoma, Femoral raised lymph node, Saphena varix
Other
Family/Pt: may need time off work, can’t carry out daily activities or heavy lifting – can lead to
depression
HCPs: Doctors, Radiographers, Nurses, Anaesthetist, Surgeon
Complications:
- Incarceration –irreducible, bowel is trapped in herniated position obstruction and
strangulation
o Painful, tender and erythematous
- Obstruction –hernia causes a blockage in the passage of faeces through the bowel, present
with signs of obstruction (vomiting, absolute constipation, abdominal pain).
- Strangulation: irreducible and tender tense lump associated with signs of bowel obstruction.-
MEDICAL EMERGENCY and the bowel will die quickly if not corrected with surgery.
SMALL AND LARGE BOWEL OBSTRUCTION
SMALL LARGE
Most common in elderly, occurs in neonates 2o to meconium ileus
Epidemio
More common than large Can be congenital - Hirschsprung's
logy
disease
Cause Adhesions (more common), hernias Malignancy, diverticular disease,
volvulus
Features Central, ileum may be tubeless Peripheral, presence of haustration
Nausea, vomiting, dysphagia, colicky pain and failure to pass bowel movements
The more distal the obstruction is, the later the signs of vomiting.
Symptom The more proximal the obstruction the later the constipation will be
s
colicky pain becomes constant “red flag” that ischaemia
may be developing
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