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DIT > 1F Foundations 6 - Cellular Suffering & Death > Flashcards

1F Foundations 6 - Cellular Suffering & Death Flashcards

1
Q

Physiologic situations of apoptosis?

A
  • Embryogenesis
  • Cell breakdown (during menstruation)
  • Proliferation of cell populations (to keep cell populations constant)
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2
Q

Pathologic situations of apoptosis?

A
  • DNA damage (e.g. radiation, hypoxia)
  • Misfolded proteins (e.g. gene mutations, exposure to free radicals)
  • Infections (e.g. HIV)
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3
Q

Descriptive histological characteristics of apoptosis?

A
  • Shrinkage
  • Pyknosis (condensation of nuclear chromatin –> shrinkage of the nucleus. Makes the nucleus look more basophilic (darker))
  • Membrane blebbing
  • Karyorrhexis (Nuclear fragmentation
  • Apoptotic bodies
  • No inflammation
  • Phagocytosis
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4
Q

Ultimate initiators of apoptosis?

A

Caspases

  • Exist in inactive form
  • Active when cleaved
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5
Q

What is the function of the Bcl-2 protein family?

A
  • Closely regulate the permeability of the mitochondrial membrane
  • “Anti-apoptotic”
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6
Q

What is the function of Bax?

A
  • To go into the mitochondrial membrane and create channels to allow contents of the mitochondria to flow out
  • “Pro-apoptotic”
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7
Q

What is let out of the mitochondria during the apoptotic process to start cellular breakdown?

A

Cytochrome c

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8
Q

Cytochrome c activates what to start apoptosis?

A

Cytosolic caspases

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9
Q

Receptors in the extrinsic apoptotic pathway?

A
  • Fas-R (CD95)

- TNF

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10
Q

Ligands that activate receptors in the extrinsic apoptotic pathway?

A
  • Fas - Ligand

- TNF - alpha

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11
Q

Mechanism of Killer T cell extrinsic pathway?

A

Cytotoxic (killer) T cells release Perforin (punctures wholes in the cell) and Granzyme B (enters cell and activate caspases directly)

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12
Q

Where does p53 arrest the cell in the cell cycle?

A

Between G1 and S

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13
Q

tumour suppressor protein p53 prompts what to DNA in G1?

A

Repair by enzymes or destruction if damage is irreparable

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14
Q

Where and what? Coagulative necrosis

A
  • Heart
  • Liver
  • Kidney
  • Gelatinous substance in dead tissue
  • Occurs in low oxygen environments (e.g. infarction)
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15
Q

Where and what? Liquefactive necrosis

A
  • Brain
  • Bacterial abscesses
  • Pleural effusions
  • Viscous liquid mass
  • Major inflammatory response
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16
Q

Where and what? Caseous necrosis

A
  • TB
  • Systemic fungal infections
  • Coagulative + liquefactive
  • “Clumpy cheese”
17
Q

Where and what? Fatty necrosis

A
  • Peripancreatic fat (saponification via lipase)

- Activation of lipases

18
Q

Where and what? Fibrinoid necrosis

A
  • Blood vessels

- Immune-mediated vascular damage

19
Q

Where and what? Gangrenous wet necrosis

A
  • Extremities
  • GI tract

-Bacterial infections

20
Q

Where and what? Gangrenous dry necrosis

A
  • Toes and feet

- Ischemic coagulative

21
Q

What cellular by-products can you detect in serum when following is injured? Cardiac myocytes

A
  • Myoglobin
  • CPK
  • CKMB
  • Troponin I
22
Q

What cellular by-products can you detect in serum when following is injured? Skeletal myocytes

A
  • CPK
  • Aldolase
  • Myoglobin
23
Q

What cellular by-products can you detect in serum when following is injured? Hepatocytes

A
  • AST
  • ALT
  • Alkaline phosphatase
  • GGT
24
Q

What cellular by-products can you detect in serum when following is injured? Salivary gland cells

A

-Amylase

25
Q

What cellular by-products can you detect in serum when following is injured? Pancreatic exocrine cells

A
  • Amylase

- Lipase

26
Q

What cellular by-products can you detect in serum when following is injured? RBCs

A

Heme–> Bilirubin

27
Q

Characteristics of reversible (with O2) cell injury?

A
  • Decreased ATP synthesis
  • Cellular swelling
  • Nuclear chromatin clumping
  • Decreased glycogen
  • Fatty change of the liver (or of the cell)
  • Ribosomal detachment (decreased protein synthesis)
28
Q

Characteristics of Irreversible cell injury?

A
  • Nuclear pyknosis, karyolysis, karyorrhexis
  • Ca2+ influx –> Caspase activation
  • Plasma membrane damage
  • Lysosomal rupture
  • Mitochondrial permeability
29
Q

Mechanisms of cell injury?

A
  • ATP depletion: due to decreased oxygen/nutrients and toxins (cyanide)
  • Mitochondrial damage: impairs ATP production and can induce apoptosis (Can happen by: apoptotic signal–>programmed cell death, Increase of cytosolic Ca2+, Reactive Oxygen species, Oxygen deprivation, Mutations in mitochondrial genes)
  • Influx of calcium (caused by e.g. ischemia and cytosolic toxins): increases mitochondrial permeability and can activate phospholipases, proteases, endonucleases and ATPases
  • Accumulation of oxygen-derived free radicals: cell damage through membrane lipid peroxidation, protein modification and DNA breakage
  • Multiple causes like radiation exposure, metabolism of drugs, redox reactions, nitric oxide, transition metals, leukocyte oxidative bursts, iron overdose, reperfusion injury.
30
Q

Free radical degradation pathways

A
  • Catalase
  • Superoxide dismutase
  • Glutathione peroxidase
  • Spontaneous decay
  • Antioxidants
31
Q

Definition of infarction and reason

A

Tissue death caused by a local lack of O2. Usually cause by obstruction of blood flow

32
Q

Red infarct. What and where?

A

Loose tissues with collaterals.

  • Liver
  • Lungs
  • Intestine
  • Follows reperfusion
33
Q

Pale infarct. What and where?

A

Solid tissues with single blood supply

  • Heart
  • Kidney
  • Spleen

DIT (11 decks)

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