Path Flashcards

1
Q

Cirrhosis

A
  1. Whole liver involved
  2. Fibrosis
  3. Nodules of regenerating hepatocytes
  4. Distortion of liver vascular architecture: intra- and extrahepatic (e.g. gastroesophageal) shunting
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2
Q

Intrahepatic shunting

A

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

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2
Q

Intrahepatic shunting

A

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

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3
Q

Extrahepatic shunting

A

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.

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4
Q

CIRRHOSIS CLASSIFICATION

A

(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

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5
Q

Cirrhosis - complications

A
  1. Portal hypertension
  2. Hepatic encephalopathy
  3. Liver cell cancer
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6
Q

CIRRHOSIS MAY BE REVERSIBLE

A

If aetiology is AGGRESSIVELY treated

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7
Q

Acute Hepatitis

A
  • <6 months
  • causes
    1. Viruses (A,E mostly )
    2. Drugs
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8
Q

Acute Hepatitis

A

Spotty necrosis

Any cause

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9
Q

Chronic Hepatitis

A

> 6 months

  1. Viral (B, C, D)
  2. Drugs
  3. Auto-immune

Severity of inflammation = grade

Severity of fibrosis = stage

Stage is more important than the grade

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10
Q

Alcoholic Liver Disease

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
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11
Q

Fatty Liver (Alcohol)

A
  • Fatty change (large droplet)
  • can be caused by lots of things
  • REVERSIBLE
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12
Q

Alcoholic Hepatitis

A
  • NON-reversible

FEATURES:

  1. Ballooning (+/- Mallory Denk Bodies)
  2. Fat
  3. Pericellular fibrosis
  4. Mainly seen in Zone 3
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12
Q

Alcoholic Hepatitis

A
  • NON-reversible

FEATURES:

  1. Ballooning (+/- Mallory Denk Bodies)
  2. Fat
  3. Pericellular fibrosis
  4. Mainly seen in Zone 3
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13
Q

Viral Hepatitis

A

Mostly seen in ZONE 1

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14
Q

Non-alcoholic fatty liver disease (NAFLD) including Non-alcoholic steatohepatitis (NASH)

A
  • 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
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15
Q

Primary Biliary Cholangitis

A
  • 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
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16
Q

Primary Sclerosing cholangitis

A
  • M>F
  • Periductal bile duct fibrosis leading to loss
  • UC risk factor
  • Increased risk or cholangiocarcinoma
  • Bile duct imaging (ERCP) diagnostic
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17
Q

Haemochromatosis

A
  • Genetically determined increased absoprtion of iron
  • Gene on chromosome 6 (hFe) mutation
  • Parenchymal damage to organs secondary to iron deposition
  • pearls stain
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18
Q

Haemosiderosis

A
  • accumulation of iron in macrophages
  • blood transfusion
  • DOES NOT DAMAGE LIVER
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19
Q

Wilson’s Disease

A

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
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20
Q

Autoimmune Hepatitis

A

F>M
Active chronic hepatitis with plasma cells
Anti-smooth muscle actin antibodies in the serum
Respond to steroids

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21
Q

Alpha-One Antitrypsin deficiency

A
  • failure to secrete alpha-one antotrypsin
  • Giant cell hepatits with mutiple nuclei
  • hepatitis and cirrhosis
  • also affects lung - emphysema
22
Q

Drug related liver injury - Paracetamol

A
  • Zone 3 damage
23
Hepatic Granulomas
Specific Causes: PBC, Drugs General causes: TB, Sarcoid
24
Granuloma
Organised collection of activated macrophages
25
Liver tumour (benign)
1. Liver cell adenoma 2. Bile duct adenoma 3. Haemangioma
26
Liver tumours: Malignant
1. Secondary tumours 2. Primary tumours SECONDARY ARE MUCH MUCH MUCH MORE COMMON
27
Liver tumours Malignant (Primary)
1. hepatocellular carcinoma 2. hepatoblastoma (primitive cells) 3. Cholangiocarcinoma 4. Haemangiocarcinoma
28
Liver cell cancer
- usually associated with cirrhosis especially in the WEST
29
Cholagiocaarcinoma
Associated with PSC, Worm infection, cirrhosis Can arise in intra and extrahepatic bile duct (including gallbladder)
30
Anion gap caclulation
Anion Gap = Sodium - (Chloride + Bicarbonate)
31
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.
32
Osmolality eqution
2NA+2K+Urea+Glucose
33
Incompatible blood transfusions signs
Haemolysis ->>>>> leading to haematuria
34
Breathlessness CAUSES
GIVING TOO MUCH BLOOD in someone with poor heart
35
Commonest electrolyte abnormality in hospital
Hyponatraemia
36
What causes hyponatraemia?
Increased extracellular water
37
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
38
ADH
- Acts on V2 receptors (collecting duct) - Insertion of aquaporin-2 V1 receptors - vascular smooth muscle - vasoconstriction (higher concentration) - Alternative name "vsasopressin"
39
What are the two main stimuli for ADH secretion?
1. Increased Serum Osomolality - e.g. you don't drink all day - mediated by hypothalamic osmoreceptors - also feel thirsty 2. Reduced blood pressure/volume - mediated by baroreceptors in carotids, atria, and aorta
40
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
41
What is the main effect of increased ADH secretion on serum sodium?
HYPONATRAEMIA
42
HYPONATRAEMIA
!!!WATER PROBLEM!!! | EXCESS WATER
43
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)
44
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)
45
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
46
Hyponatraemia - what should be checked immediately?
Urine sodium
47
Clinical signs of hypervolaemia
- Raised JVP - Bibasal crackles (on chest examination) - pulmonary oedema - Peripheral oedema
48
Hyponatraemia clinical assessment
1, Hypovolaemia 2. Euvolaemia 3. Hypervolaemia
49
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
50
Hyponatraemia -> Hypervolaemic patient causes
Cardiac failure Cirrhosis Nephrotic syndrome Low urine sodium
51
Hyponatraemia -> Euvolaemic patient causes
Hypothyroidism Adrenal insufficiency SIADH HIGH urine sodium
52
Hyopnatraemia, every cause is
EXCESS ADH
53
LOW urine sodium in hypervolaemia
Cardiac failure - secondary hyperaldosteronism - aldosterone leads to sodium reabsorption in the kindeys