1. Abnormal Cellular Accumulations Flashcards

1
Q

Where do abnormal cellular accumulations come from?

A

If a cell can’t metabolise something, it will remain within the cell. Products can derive from:

  • cell’s own metabolism
  • extracellular space (e.g. Spilled blood)
  • outer environment (e.g. Dust)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 main groups of intracellular accumulations?

A
  1. Water and electrolytes
  2. Lipids (triglycerides and cholesterol)
  3. Carbohydrates
  4. Proteins
  5. Pigments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hydropic swelling and why does it occur?

A
  • Accumulation of fluid in cells.
  • Occurs when energy supplies are cut off (eg hypoxia) - Na+ and water influx.
  • Indicates severe cellular distress.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is hydropic swelling a particular problem, and why?

A

Brain (cerebral oedema) as swelling presses it against skull and compromises blood supply.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is steatosis, where and why does this occur?

A
  • Accumulation of triglycerides (lipids).
  • Often seen in liver (major organ of fat metabolism).
  • Causes:
    1. Alcohol (reversible in ~10 days)
    2. Diabetes mellitus
    3. Obesity
    4. Toxins (e.g. Carbon tetrachloride)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why would cholesterol accumulate in cells and where does it often accumulate?

A
  • Cannot be broken down and is insoluble - can only be eliminated through the liver (so accumulated if liver is compromised). Excess stored in cellular vesicles.
  • Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques = foam cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are xanthomas?

A

Hereditary hyperlipidaemias - accumulation of cholesterol in macrophages of skin and tendons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are Mallory’s hyaline and when do these occur?

A
  • Damaged keratin filaments.

- Alcoholic liver disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is alpha1-antitrypsin deficiency?

A
  • Liver produces incorrectly folded alpha1-antitrypsin protein.
  • Cannot be packaged by ER - accumulates and is not secreted. Causes liver fibrosis and cirrhosis.
  • Systemic deficiency: proteases in lung act unchecked resulting in emphysema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give an example of the accumulation of exogenous pigments in cells. What are the consequences?

A
  • Air pollutants (carbon/coal dust/soot) inhaled and phagocytosed by alveolar macrophages.
  • Causes anthracosis and blackened peribronchial lymph nodes.
  • Usually harmless unless in large amounts - fibrosis and emphysema (coal worker’s pneumoconiosis)
  • Tattooing: pigments phagocytosed by macrophages in dermis and remain there. Some pigments will reach draining lymph nodes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do bruises form after trauma?

A

Leakage of blood causes local excess of iron - accumulation of haemosiderin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is haemosiderin?

A

Iron storage molecule derived from haemoglobin (yellow/brown).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is haemosiderosis? When does this occur?

A

Deposition of haemosiderin in many organs due to systemic iron overload.

Seen in haemolytic anaemias, blood transfusions and hereditary haemochromatosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hereditary haemochromatosis?

A
  • Genetically inherited disorder resulting in increased intestinal absorption of dietary iron.
  • Iron is deposited in skin, liver, pancreas heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas (can cause pancreatic insufficiency).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the symptoms of hereditary haemochromatosis?

A

Liver damage, heart dysfunction and multiple endocrine failures (esp of pancreas).
‘Bronze diabetes’ as causes tanning and pancreatic destruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for hereditary haemochromatosis?

A

Repeated bleeding

17
Q

What causes jaundice? What is this product?

A
  • Accumulation of bilirubin.

- Breakdown product of heme (stacks of broken porphyrin rings). Formed in all cells of body (cytochromes contain heme).

18
Q

How is bilirubin normally eliminated?

A

Transported from tissues to liver by albumin, and excreted in bile.

19
Q

Why does jaundice occur?

A

If bile flow is obstructed or overwhelmed, blood levels of bilirubin rise (accumulate in tissues extracellularly or in macrophages) and cause jaundice.

20
Q

What are the 4 mechanisms of intracellular accumulation?

A
  1. Abnormal metabolism (e.g. Fatty liver)
  2. Alterations in protein folding and transport (e.g. Alpha1-antitrypsin)
  3. Deficiency of critical enzymes (e.g. Lysosomal storage disease)
  4. Inability to degrade phagocytosed particles
21
Q

What is tissue calcification and what are the 2 types?

A
  • Abnormal deposition of calcium salts within tissues.
    1. Dystrophic = localised. More common, occurs in dying tissue, atherosclerotic plaques, aging or damaged heart valves, tuberculous lymph nodes, some malignancies.
    2. Metastatic = generalised.
22
Q

Why does dystrophic calcification occur?

A

Local change/disturbance favours nucleation of hydroxyapatite crystals (e.g. Cavities in TB lungs). Does not involve abnormality in calcium metabolism.

23
Q

Why does metastatic calcification occur?

A

Due to hypercalcaemia secondary to disturbances in calcium metabolism - hydroxyapatite crystals are deposited in normal tissues throughout the body (usually asymptomatic but can be lethal).

24
Q

What causes hypercalcaemia?

A
  1. Increased secretion of parathyroid hormone (PTH) resulting in bone resorption:
    - primary - due to parathyroid hyperplasia or tumour
    - secondary - due to renal failure and phosphate retention
    - ectopic - secretion of PTH-related protein by malignant tumours (eg. Lung carcinoma)
  2. Destruction of bone tissue:
    - primary tumours of bone marrow (e.g. Leukaemia, multiple myeloma)
    - diffuse skeletal metastases
    - Paget’s disease of bone - accelerated bone turnover
    - immobilisation