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Med Year 5 > Path > Flashcards

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
Q

Hepatic Granulomas

A

Specific Causes: PBC, Drugs

General causes: TB, Sarcoid

24
Q

Granuloma

A

Organised collection of activated macrophages

25
Q

Liver tumour (benign)

A
  1. Liver cell adenoma
  2. Bile duct adenoma
  3. Haemangioma
26
Q

Liver tumours: Malignant

A
  1. Secondary tumours
  2. Primary tumours

SECONDARY ARE MUCH MUCH MUCH MORE COMMON

27
Q

Liver tumours Malignant (Primary)

A
  1. hepatocellular carcinoma
  2. hepatoblastoma (primitive cells)
  3. Cholangiocarcinoma
  4. Haemangiocarcinoma
28
Q

Liver cell cancer

A
  • usually associated with cirrhosis especially in the WEST
29
Q

Cholagiocaarcinoma

A

Associated with PSC, Worm infection, cirrhosis

Can arise in intra and extrahepatic bile duct (including gallbladder)

30
Q

Anion gap caclulation

A

Anion Gap = Sodium - (Chloride + Bicarbonate)

31
Q

Diabetes diagnosis

A

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
Q

Osmolality eqution

A

2NA+2K+Urea+Glucose

33
Q

Incompatible blood transfusions signs

A

Haemolysis -»»> leading to haematuria

34
Q

Breathlessness CAUSES

A

GIVING TOO MUCH BLOOD in someone with poor heart

35
Q

Commonest electrolyte abnormality in hospital

A

Hyponatraemia

36
Q

What causes hyponatraemia?

A

Increased extracellular water

37
Q

Which hormone conrtols water balnce?

A

ADH - antidiuretic hormone (vasopressin)

  • released from posterior pituitary
  • acts on distal tubules to reabsorb water through water channels (aquaporins 2)
  • Increase extracellular water
38
Q

ADH

A
  • Acts on V2 receptors (collecting duct)
  • Insertion of aquaporin-2

V1 receptors

  • vascular smooth muscle
  • vasoconstriction (higher concentration)
  • Alternative name “vsasopressin”
39
Q

What are the two main stimuli for ADH secretion?

A
  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
Q

Why does vomiting/diarrhoa lead to hyponatraemia?

A
  • Drop your blood volume a little bit becuase you are loosing water -> detected by baroreceptors -> release of ADH
41
Q

What is the main effect of increased ADH secretion on serum sodium?

A

HYPONATRAEMIA

42
Q

HYPONATRAEMIA

A

!!!WATER PROBLEM!!!

EXCESS WATER

43
Q

What is the first step in the clnical assessment of a patient with hyponatraemia?

A
  • 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
Q

What are the clnical signs of hypovolaemia?

A
  • Tachycardia
  • Postural hypotension
  • Dry mucous membranes
  • Reduced skin turgor
  • Confusion/drowsiness
  • Reduced urine output
  • Low urine NA+ (<20)
45
Q

MOST RELIABLE INDICATOR OF Hypovolaemia

A

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
Q

Hyponatraemia - what should be checked immediately?

A

Urine sodium

47
Q

Clinical signs of hypervolaemia

A
  • Raised JVP
  • Bibasal crackles (on chest examination) - pulmonary oedema
  • Peripheral oedema
48
Q

Hyponatraemia clinical assessment

A

1, Hypovolaemia

  1. Euvolaemia
  2. Hypervolaemia
49
Q

Hyponatraemia -> Hypovolaemic patient causes

A

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
Q

Hyponatraemia -> Hypervolaemic patient causes

A

Cardiac failure
Cirrhosis
Nephrotic syndrome
Low urine sodium

51
Q

Hyponatraemia -> Euvolaemic patient causes

A

Hypothyroidism
Adrenal insufficiency
SIADH
HIGH urine sodium

52
Q

Hyopnatraemia, every cause is

A

EXCESS ADH

53
Q

LOW urine sodium in hypervolaemia

A

Cardiac failure - secondary hyperaldosteronism - aldosterone leads to sodium reabsorption in the kindeys

Med Year 5 (3 decks)

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