Path Flashcards
Cirrhosis
- Whole liver involved
- Fibrosis
- Nodules of regenerating hepatocytes
- Distortion of liver vascular architecture: intra- and extrahepatic (e.g. gastroesophageal) shunting
Intrahepatic shunting
Normally blood travels from intestine - is filtered in the liver and then travels to the heart
Intrahepatic shunting
- Blood passes through the liver - It goes straight from the portal vein to the hepatic vein - bypassing hepatocytes - due to all the scarring - you get unfiltered toxic blood
Intrahepatic shunting
Normally blood travels from intestine - is filtered in the liver and then travels to the heart
Intrahepatic shunting
- Blood passes through the liver - It goes straight from the portal vein to the hepatic vein - bypassing hepatocytes - due to all the scarring - you get unfiltered toxic blood
Extrahepatic shunting
Blood cannot pass through the liver - it has to find some other way of travelling back into systemic circulation - opening up of sites of porto-systemic anastomosis - e.g. esophageal varices - can lead to bleeding.
CIRRHOSIS CLASSIFICATION
(1) According to nodular size - old school now - micro and macronodular
(2) Aetiology (more useful)
a. Fatty liver disease (alcoholic and nonalcoholic (insulin resistance) MICRO
b. Viral hepatitis (B, C, D) MACRO
Cirrhosis - complications
- Portal hypertension
- Hepatic encephalopathy
- Liver cell cancer
CIRRHOSIS MAY BE REVERSIBLE
If aetiology is AGGRESSIVELY treated
Acute Hepatitis
- <6 months
- causes
1. Viruses (A,E mostly )
2. Drugs
Acute Hepatitis
Spotty necrosis
Any cause
Chronic Hepatitis
> 6 months
- Viral (B, C, D)
- Drugs
- Auto-immune
Severity of inflammation = grade
Severity of fibrosis = stage
Stage is more important than the grade
Alcoholic Liver Disease
- Fatty liver
- Alcoholic hepatitis
- Cirrhosis
Fatty Liver (Alcohol)
- Fatty change (large droplet)
- can be caused by lots of things
- REVERSIBLE
Alcoholic Hepatitis
- NON-reversible
FEATURES:
- Ballooning (+/- Mallory Denk Bodies)
- Fat
- Pericellular fibrosis
- Mainly seen in Zone 3
Alcoholic Hepatitis
- NON-reversible
FEATURES:
- Ballooning (+/- Mallory Denk Bodies)
- Fat
- Pericellular fibrosis
- Mainly seen in Zone 3
Viral Hepatitis
Mostly seen in ZONE 1
Non-alcoholic fatty liver disease (NAFLD) including Non-alcoholic steatohepatitis (NASH)
- Histologically looks like alcoholic liver disease
- Due to insulin resistance associated with raised BMI and diabetes
- Becoming recognised as one of the commonest causes of liver disease, world-wide
Primary Biliary Cholangitis
- PBC
- F>M
- Bile duct loss associated with chronic inflammation (with granulomas)
- Diagnostic test is detection of anti-mitochondrial antibodies
- granulomatous destruction of bile duct
Primary Sclerosing cholangitis
- M>F
- Periductal bile duct fibrosis leading to loss
- UC risk factor
- Increased risk or cholangiocarcinoma
- Bile duct imaging (ERCP) diagnostic
Haemochromatosis
- Genetically determined increased absoprtion of iron
- Gene on chromosome 6 (hFe) mutation
- Parenchymal damage to organs secondary to iron deposition
- pearls stain
Haemosiderosis
- accumulation of iron in macrophages
- blood transfusion
- DOES NOT DAMAGE LIVER
Wilson’s Disease
Accumulation of copper due to failure of excretion by hepatocytes into the bile
Genes on chromosome 13
KAYSER FLEISCHER RINGS
Accumulates in liver and CNS
- recessive
Autoimmune Hepatitis
F>M
Active chronic hepatitis with plasma cells
Anti-smooth muscle actin antibodies in the serum
Respond to steroids
Alpha-One Antitrypsin deficiency
- failure to secrete alpha-one antotrypsin
- Giant cell hepatits with mutiple nuclei
- hepatitis and cirrhosis
- also affects lung - emphysema
Drug related liver injury - Paracetamol
- Zone 3 damage
Hepatic Granulomas
Specific Causes: PBC, Drugs
General causes: TB, Sarcoid
Granuloma
Organised collection of activated macrophages
Liver tumour (benign)
- Liver cell adenoma
- Bile duct adenoma
- Haemangioma
Liver tumours: Malignant
- Secondary tumours
- Primary tumours
SECONDARY ARE MUCH MUCH MUCH MORE COMMON
Liver tumours Malignant (Primary)
- hepatocellular carcinoma
- hepatoblastoma (primitive cells)
- Cholangiocarcinoma
- Haemangiocarcinoma
Liver cell cancer
- usually associated with cirrhosis especially in the WEST
Cholagiocaarcinoma
Associated with PSC, Worm infection, cirrhosis
Can arise in intra and extrahepatic bile duct (including gallbladder)
Anion gap caclulation
Anion Gap = Sodium - (Chloride + Bicarbonate)
Diabetes diagnosis
Fasting blood sugar test. A blood sample will be taken after an overnight fast. A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it’s 126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.
Osmolality eqution
2NA+2K+Urea+Glucose
Incompatible blood transfusions signs
Haemolysis -»»> leading to haematuria
Breathlessness CAUSES
GIVING TOO MUCH BLOOD in someone with poor heart
Commonest electrolyte abnormality in hospital
Hyponatraemia
What causes hyponatraemia?
Increased extracellular water
Which hormone conrtols water balnce?
ADH - antidiuretic hormone (vasopressin)
- released from posterior pituitary
- acts on distal tubules to reabsorb water through water channels (aquaporins 2)
- Increase extracellular water
ADH
- Acts on V2 receptors (collecting duct)
- Insertion of aquaporin-2
V1 receptors
- vascular smooth muscle
- vasoconstriction (higher concentration)
- Alternative name “vsasopressin”
What are the two main stimuli for ADH secretion?
- Increased Serum Osomolality
- e.g. you don’t drink all day
- mediated by hypothalamic osmoreceptors
- also feel thirsty - Reduced blood pressure/volume
- mediated by baroreceptors in carotids, atria, and aorta
Why does vomiting/diarrhoa lead to hyponatraemia?
- Drop your blood volume a little bit becuase you are loosing water -> detected by baroreceptors -> release of ADH
What is the main effect of increased ADH secretion on serum sodium?
HYPONATRAEMIA
HYPONATRAEMIA
!!!WATER PROBLEM!!!
EXCESS WATER
What is the first step in the clnical assessment of a patient with hyponatraemia?
- Clinical assessment of volume status?
Physical examination - skin turgor, blood pressure, mucous membranes, urine output, cap refill, oedema (JVP high and peripheral oedema - fluid overloaded), pulse rate
FIRST THING TO DO IS TO ASSESS WHETHER PATIENT IS
(1) Hypovolaemic (reduced tissue turgor, dry mucous membranes)
(2) Euvolaemic (difficult to establish)
(3) Hypervolaemic (peripheral oedema, raised JVP)
What are the clnical signs of hypovolaemia?
- Tachycardia
- Postural hypotension
- Dry mucous membranes
- Reduced skin turgor
- Confusion/drowsiness
- Reduced urine output
- Low urine NA+ (<20)
MOST RELIABLE INDICATOR OF Hypovolaemia
LOW URINE Sodium (<20)
Kidneys are best detectors of hypovolaemia -> If you are hypovolaemic you need to hang onto salt and water -> Hanging on to salt means you reabsorb it -> This means there will be less in urine
Hyponatraemia - what should be checked immediately?
Urine sodium
Clinical signs of hypervolaemia
- Raised JVP
- Bibasal crackles (on chest examination) - pulmonary oedema
- Peripheral oedema
Hyponatraemia clinical assessment
1, Hypovolaemia
- Euvolaemia
- Hypervolaemia
Hyponatraemia -> Hypovolaemic patient causes
Diarrhoa
Vomiting
Diuretics ( If patient is on diuretics cannot interpret urine soidum - it will be high because of diruetics)
Salt losing nephropathy
Low urine sodium
Hyponatraemia -> Hypervolaemic patient causes
Cardiac failure
Cirrhosis
Nephrotic syndrome
Low urine sodium
Hyponatraemia -> Euvolaemic patient causes
Hypothyroidism
Adrenal insufficiency
SIADH
HIGH urine sodium
Hyopnatraemia, every cause is
EXCESS ADH
LOW urine sodium in hypervolaemia
Cardiac failure - secondary hyperaldosteronism - aldosterone leads to sodium reabsorption in the kindeys
