Session 1- Cell injury Flashcards

1
Q

What’s the difference between hypoxia and ischaemia?

A

Hypoxia: Not enough oxygen is reached a tissue
Ischaemia: Decrease in blood supply to the tissue

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2
Q

What are the four causes of Hypoxia

A

HHypoxaemic Hypoxia: Arterial content of O2 is low
Anaemic hypoxia: Decreased ability for haemoglobin to carry O2
Ischaemic Hypoxia: Reduced O2 supply due to interruption in blood supply
Histiocytic Hypoxia: Inability to utilise the O2 in tissue due to some disabled oxidative phosphorylation enzyme

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3
Q

How does our own immune system damage our own body cells?

A
Autoimmune response (Fails to distinguish self form non self)
Hypersensitivity (Host tissue damaged due to an overvigorous immune system
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4
Q

What are the three processes of cell death with regards to what happens to the nucleus?

A

Pykosis: The irreversible clumping of nuclear chromatin
Karyorrhesis: Nucleus breaks into fragments
Karyolysis: Nucleus dissolves in the cytoplasm and so cannot be seen

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5
Q

What reversible damage and then irreversible damage can you see under a electron microscope when a cell dies?

A
Reversible:
Blebs form
ER swells
Chromatin clumps
Mitochondria swell
Intramembranous particles aggregate on the surface of the cell

Irreversible: Lysosomes rupture
Nucleus–>Pykosism, Karyolysis or Karyorrhexis
Defects in the cell membrane appear

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6
Q

What test is used to determine the time of death?

A

Dye exclusion test

Dye enters the dead cells where the cell membrane has been ruptured. Doesn’t enter the alive ones

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7
Q

Whats the difference between oncosis and necrosis?

A

Oncosis: Cell death with swelling
Necrosis: The morphological change s that occur after a cell has been dead for some time

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8
Q

What are the two types of necrosis?

A

Coagulative- Where Denaturation of proteins dominate over the release of proteases. Ghost outline of the cells

Liquefactive: Enzyme activity greater than protein denaturation
Enzymes digest cells leaving liquefaction of tissue

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9
Q

What type of necrosis is commonly found in TB

A

Caseous necrosis

Containss structureless debris

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10
Q

What is gangrene?

A

Necrosis visible to the naked eye

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11
Q

What are the three types of gangrene

A

Dry Gangrene= Where necrosis is exposed to air
Wet gangrene= Gangrene modified by infection
Gas gangrene= Where the infection is caused by an anaerobic bacteria that produces gas

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12
Q

What is white and red infarcts?

A
White: Occurs in solid organs. 
Coagulative necrosis
Due to occlusion of an end artery (So no blood supply reaching the area of infarct, so white)
Red Infarct: Occurs in loose tissue
Number of anastomoses
Blood leaks out of blood vessels
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13
Q

What can happen if you return blood to an area of necrotic tissue

A

It can result in inflammation that can cause increased tissue injury, and oxidative damge

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14
Q

What can increasing potassium levels cause?

A

The heart to stop

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15
Q

What enzyme is the main indicator of a myocardial infarction?

A

Troponin

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16
Q

What does the presence of myoglobin in the blood indicate? What can this cause

A

Muscle tissue injury
BTW the increase of myoglobin is called Rhabdomyolysis
Can cause renal failure

17
Q

Give the process of the intrinsic pathway of apoptosis

A

P53 triggered (Eg by irreparable damage to DNA)
Mitochondrial membrane becomes leaky
Releases cytochrome C
Activates caspases
These cleave DNA and protein in the cytoskeleton

18
Q

Name 7 key differences between apoptosis and necrosis (Pattern, cell size, nucleus, plasma membrane, cellular contents, adjacent inflammation?, Buds or blebs)

A

Pattern: N: Continuous groups of cells
A: Single cells
Cell size: N:Enlarged
A:Shrink
Nucleus: N: Pyknosis, Karyorrhexis or Karyolysis
A: Karyorrhexis is seen
Plasma membrane: N: Disrupted, early lysis
A: Remains intact
Cellular contents: N:Enzymatic digestion, leak out of the cell
A: Remain intact, released into apoptotic bodies
Adjacent inflammation: N: Frequent
A: No
Budding or Blebbing: N: Blebbing
A: Budding

19
Q

Name 5 things that can accumulate in cells

A
Lipids- Steatosis
Iron- Haemochromatosis
Pigments
Proteins
Bilirubin- Jaundice
20
Q

What are the four mechanisms that result in intracellular accumulations?

A

Abnormal metabolism
Alterations in protein folding/transport
Deficiency of critical enzymes
Inability to degrade phagocytosed particles

21
Q

What is dystrophic calcification? What causes it?

A

Localised calcification

A local change that favours the nucleation of hydroxyapatite

22
Q

What causes metastatic calcification?

A

Hypercalcaemia either caused by:
Increased secretion of the parathyroid hormone–>Bone resorption
Destruction of bone tissue