Session 1 Cell Injury Flashcards

(34 cards)

1
Q

How would villi differ in cilliac disease?

A

Short, fat and blunted.

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2
Q

What do macrophages do to dead fat cells?

A

Digest them

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3
Q

What forms in lymph cancer?

A

Glands form in lymph cancer on the outer edges. (White things)

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4
Q

How can you identify basal cell carcinomas on a histological section of skin?

A

The darker patches are where the carcinoma is.

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5
Q

What is used to fix and stain tissue?

A

Formalin used to fix
Then embedded in paraffin wax.
- remove water from tissue using alcohol and a vacuum

Stain with Haematoxycilin (stain nucleus purple) and eosin stains cytoplasm and CT pink

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6
Q

Name 3 things that can cause call injury.

A

Hypoxia
Toxins
Physical agents (trauma/extreme temperature/pressure)

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7
Q

What are the causes of hypoxia?

A

Hypoxaemic hypoxia

  • arterial content of oxygen is low
  • e.g higher altitudes and reduced absorption secondary to lung disease

Anaemic hypoxia

  • decreased ability to carry oxygen
  • anaemia or carbon monoxide poisoning

Ischaemic hypoxia

  • interruption of blood supply
  • blockage of a vessel or heart failure

Histiocytic hypoxia

  • inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes.
  • cyanide poisoning
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8
Q

How does the immune system damage Body cells?

A
  • hypersensitivity reactions = host tissue is injured secondary to an overly vigorous immune reaction
  • autoimmune reactions = immune system fails to distinguish self from non self e.g Graves’ disease of thyroid.
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9
Q

Which cell components are most susceptible to injury?

A
  • cell membranes
  • nucleus
  • proteins
  • mitochondria
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10
Q

What is happening at the molecular level in hypoxia?

A

In the case if ischaemic hypoxia

  • blockage
  • less oxidative phosphorylation in mitochondria of cell
  • less atp for protein synthesis as a result
  • increased glycolysis
  • less action of Na pump = efflux of K and cellular swelling due to influx of h2o and Na and Ca
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11
Q

What happens if hypoxia is irreversible?

A

Changes are irreversible
- mitochondria and ER release calcium into the cytosole = decrease ATP and phospholipids, disrupt cytoskeleton proteins and cause nuclear chromatin damage

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12
Q

What enzymes in the body control free radicals?

A

Superoxide dismutase
Catalase
Glutathione peroxidase

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13
Q

What is a heat shock protein? Give an example.

A

Ubiquitin

Aims to mend misfolded proteins and maintain cell viability in cell injury.

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14
Q

How does a dead cell change in appearance?

A
  • pyknosis = normal cell with dark nucleus
  • karyorrhexis = coagulation of proteins so cell looks dotty. Some proteins leak out of cell. Because of coagulation, take up stain making cytoplasm appear darker.
  • karyolysis = nucleus dissolves away = irreversible cell death.
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15
Q

How would a cell look if injury was reversible??

A
  • blebs of cytoplasm
  • clumping of nuclear chromatin
  • mitochondrial and ER swelling
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16
Q

What are the two main types of necrosis? (And name the other two)

A

Coagulative

  • ischaemia of solid organs e.g. kidney, liver, heart.
  • due to protein desaturation.

Liquefaction necrosis

  • ischaemia in loose tissues e.g brain and lungs
  • presence of many neutrophils
  • due to enzyme release

Also there’s caseous and fat necrosis.

17
Q

What does coagulative necrosis look like?

A
  • cells architecture is sort of preserved
  • darker staining
  • looks more wiggly
  • lots of dots between layers = neutrophils mopping up dead tissue
  • nuclei have undergone karyolyse
18
Q

What is the difference between oncosis and necrosis?

A
  • oncosis = the process of cell death with swelling.

- necrosis= when the cell is actually dead. What you see after it dies e.g karyolysis.

19
Q

What is caseous necrosis and what does it look like?

A
  • contains structureless debris
  • particularly associated with infections, especially tuberculosis
  • appears dense like a ball
  • in a fixed tissue appears lighter, like cheese (caseous = cheese in Latin)
20
Q

Define the terms

  • gangrene
  • infarction
  • infarct
A

Gangrene = a necrosis visible to the naked eye

Infarction = necrosis caused by reduction in arterial blood flow. Can lead to gangrene.

Infarct = an area of necrotic tissue which is a result of loss of arterial blood supply. An area of ischaemic necrosis.

21
Q

What is the difference between dry and wet gangrene?

A

Dry = necrosis modified by exposure to air (coagulative necrosis)

Wet = necrosis modified by infection (liquefactive necrosis)

22
Q

Why are some infarcts white and why are some red?

A

White

  • anaemic infarcts
  • solid organs with occlusion of end artery
  • coagulative necrosis

Red

  • haemorrhaging infarct
  • loose tissue
  • Dual blood supply
23
Q

What is ischaemia reperfusion injury?

A

if blood flow is returned to a damaged by not yet necrotic tissue, damage sustained can be worse than if blood flow hadn’t been returned.
Possible causes include:
- increased production of oxygen free radicals with reoxygenation
- increase number of neutrophils resulting in more inflammation and increased tissue injury
- delivery of complement proteins and activation of complement pathways.

24
Q

What apoptosis and When may it occur?

A

Apoptosis = cell death with shrinkage that is regulated and characteristics.
Occurs physiologically when trying to maintain a steady state and embryogenesis.
Occurs pathologically when cytotoxic T cells acting on virus infected or neoplastic cells, when cells have damaged DNA etc.

25
What are the stages of apoptosis?
1) initiation and execution - initiation signal comes from within the cell, triggered by irreparable dna damage or withdrawal of hormones/growth factors. - p53 protein activated = outer mitochondrial membrane becoming leaky - cytochrome c is released from the mitochondria and this causes activation of caspases Afterwards degradation and phagocytosis occurs.
26
How do apoptic bodies appear under a light microscope and electron microscope?
Light Cells are shrunken and appear eosinophilia Chromatin condensation ``` Electron Cytoplasmic budding (not blebbing like in oncosis) No leakage of cell contents occurs = doesnt induce inflammation. ```
27
Where can abnormal cellular accumulations be derived from and what are they most likely to be?
- the cells own metabolism - the extracellular space - the outer environment 5 main groups of intracellular accumulations: - water and electrolytes - lipids - proteins - pigments - carbohydrates
28
What is steatosis?
Accumulation of triglycerides in a cell. Organs look yellow and swelled from it. If you cut through it its like cutting through butter. Cholesterol can only be eliminated through the liver. Can appear in skin and tendons of people with hereditary hyperlipidaemia = xanthomas.
29
What is hereditary haemochromatosis?
Genetically inherited, increased intentional absorption of dietary iron It’s deposited in the skin liver pancreas and heart = associated with liver cirrhosis Treatment is repeated bleeding
30
What’s accumulating in jaundice?
Bilirubin, a breakdown product of haem. Must be eliminated in bile. Taken from tissues by albumin to liver and and excreted in bile. If bile flow is obstructed or overwhelmed, bilirubin in blood rises and jaundice results.
31
What is metastatic calcification?
- hypercalcaemia that is distributed body wide | - hydroxyapatite crystals are deposited in normal tissues
32
What causes hypercalcaemia?
1) Increased secretion of parathyroid hormone 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 tumour 2) destruction of bone tissue
33
What is dystrophic calcification?
Occurs in area of dying tissues in atherosclerotic plaques. There is no abnormality in calcium metabolism or serum calcium or potassium conc. A local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals.
34
What prevents cells dividing for forever?
Telomeres at the end of DNA chromosomes get shorter with each replication. When the telomeres reach a critical length, the cell can no longer divide.