Cell Injury Flashcards

1
Q

Hypoxaemic hypoxia

A

Arterial content of oxygen is low

  • reduced inspired pO2 from atmosphere
  • reduced absorption secondary to lung disease
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2
Q

Anaemia hypoxia

A

Reduced ability of the haemoglobin to carry oxygen e.g. sickle cell anaemia

Carbon monoxide poisoning

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3
Q

Ischaemic hypoxia

A

Interruption to the blood supply

  • heart failure
  • blockage of blood supply
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4
Q

Histiocytic hypoxia

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes e.g. cyanide poisoning

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5
Q

Time taken for hypoxia in neurones

A

Few minutes

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6
Q

Time taken for hypoxia in fibroblasts

A

Few hours

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7
Q

Prolonged hypoxia

A
  • Normally the intracellular free calcium is low but the breakdown of mitochondria and endoplasmic reticulum causes calcium to increase intracellularly
  • NCX is reversed and activates enzymes such as ATPases, phospholipase, proteases and endonucleases
  • decreases ATP, phospholipids and disrupts the membrane and cytoskeleton proteins and nucleic chromatin damage which is irreversible
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8
Q

When are free radicals produced?

A
  1. During normal metabolic reactions such as oxidative phosphorylation
  2. Oxidative burst in neutrophils
  3. Radiation converts H20 into OH-
  4. Fenton reaction - contact with unbound metals within the body e.g. iron and copper
  5. Drugs and chemicals e.g paracetamol metabolism in the liver
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9
Q

Ceruloplasmin

A

Storage proteins for copper

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10
Q

How to diagnose cell death

A

Dye exclusion technique - if the dye enters the cell the cell membrane is permeable therefore the cell is dead

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11
Q

Coagulative necrosis under a microscope

A

Increased neutrophils
No nucleus in cells
Ghost outlines

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12
Q

Causes of infection other than thrombosis and embolism

A

Torsion e.g. twisted bowel on mesentery or testicular torsion

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13
Q

Where are white infarcts found

A

Solid organs such as the heart kidney and spleen

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14
Q

Where are red infarcts found

A

In the lungs and liver due to a dual blood supply

Intestines due to numerous anastomoses

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15
Q

Tumour lysis syndrome

A

Killing cancer cells releases potassium which can cause an arrhythmia

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16
Q

Three phases of apoptosis

A

Initiation
Execution
Degradation and phagocytosis

17
Q

Initiation of apoptosis

A

Activation of caspases:

  • enzymes that control and mediate apoptosis
  • causes cleavage of DNA and proteins of the cytoskeleton
18
Q

Intrinsic pathway of initiation

A
  • Initiating signal comes from within the cell

Triggered by:

  • irreparable DNA damage
  • withdrawal of growth factors or hormones
  • P53 protein is activated which results in the outer mitochondrial membrane becoming leaky
  • cytochrome C is released from the mitochondria, causing activation of caspaces
19
Q

Extrinsic pathway of initiation

A
  • Initiated by extracellular signals
  • triggered by cells in danger e.g. tumour cells or by vitally infected cells
  • TNF alpha is secreted by T killer cells and binds to cell membrane receptors (death receptor)
  • activates caspaces
20
Q

Mallory’s hyaline

A

Damage keratin filaments seen in alcoholic liver disease

21
Q

Causes of hypercalcaemia

A

Increased secretion of parathyroid hormone resulting in bone resorption:

  • primary - parathyroid hyperplasia or tumour
  • secondary - renal failure with increased retention of phosphate
  • ectopic - secretion of PTH related proteins by malignant tumours

Destruction of bone tissue

  • primary tumours of the bone marrow such as leukaemia or multiple myeloma
  • diffuse skeletal metastases
  • Paget’s disease - accelerated bone turnover - immobilisation
22
Q

In a hepatic acinar, which zone is more susceptible to ischaemic damage?

A

Zone 3 - near the terminal hepatic venue as it’s further away from the portal triad