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Lesson 1 Flashcards

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1
Q

What are causes of cell injury?

A 
Hypoxia
Chemical agents and drugs
Infections 
Immune-mediated process
Nutritional imbalance
Genetic derangement 
Physical agents
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2
Q

What are four main types of hypoxia?

A

Hypoxaemic
Anaemic
Ischaemic
Histiocytic

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3
Q

What is hypoxaemic hypoxia?

A

Low arterial O2 content t e.g. cardiorespiratory failure or in reduced inspired O2 at high altitudes

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4
Q

What is anaemic hypoxia?

A

Decreased O2 carrying capacity in blood e.g. anaemia or CO poisoning

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5
Q

What is ischaemic hypoxia?

A

Interruption to blood supply e.g. blocked vessel or heart failure

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6
Q

What is histiocytic hypoxia?

A

unable to use O2 due to disabled oxidative phosphorylation enzymes e.g. cyanide or paracetamol poisoning

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7
Q

What are some chemical agents and/or drugs that can cause cell injury?

A

Oxygen in high/low conc.
Glucose and salt in hypertonic concentrations
Trace amounts of poisons: cyanide and arsenic
Daily exposures: air and environmental pollutants, insecticides and asbestos
Drugs: recreational (alcohol) and therapeutic drugs

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8
Q

What are some immune mediated processes that can cause cell injury?

A
  • Reaction to endogenous self antigens (autoimmune disease)

- Hypersensitivity reaction as a result of vigorous immune reaction results in host tissue damage (utricaria and hives)

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9
Q

What are some nutritional imbalances that can cause cell injury?

A 
•Dietary insufficiency
	‒Malnourished states in deprived populations
	-self imposed insufficiency (anorexia nervosa)
•Dietary excess 
	‒Obesity
	‒Diabetes 
	‒Atherosclerosis 
	‒Cancer
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10
Q

What are some physical agents that can cause cell injury?

A
  • Mechanical trauma
  • Extremes of temperature (burns and deep cold) •Sudden change in atmospheric pressure
  • Radiation
  • Electric shock
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11
Q

What are examples of free radicals (that are of biological significance)?

A

• OH• (hydroxyl ions) -the most dangerous
• O2- (superoxide anion radical)
• H2O2 (hydrogen peroxide)
• Reactive oxygen species (ROS)
• Nitric oxide (NO) made by microphages, endothelia, and
neurones

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12
Q

What is the purpose of biological free radicals (in low conc. in normal state)?

A

Required for; killing bacteria, cell signaling, attack lipids in cell membranes, damages proteins, carbohydrates and nucleic acids

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13
Q

What are some causes of free radical production?

A
  • Chemical and radiation injury
  • Ischaemia – reperfusion injury
  • Cellular ageing
  • High oxygen concentrations
  • Killing of pathogens by phagocytes (ROS)
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14
Q

What are some ultra structural changes that are responsible for morphological changes?

A
  • Cell Membranes – plasma membrane and organelle membranes
  • Nucleus - DNA
  • Proteins – structural (enzymes)
  • Mitochondria – oxidative phosphorylation
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15
Q

How is ATP produced?

A
  • produced in mitochondria via oxidative phosphorylation
  • produced by glycolysis pathway in absence of oxygen from glucose in body fluids or as a result of hydrolysis of glycogen
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16
Q

How can free radicals be produced?

A
  • Chemical and radiation injury
  • Ischaemia – reperfusion injury
  • Cellular ageing
  • High oxygen concentrations
  • Killing of pathogens by phagocytes (ROS)
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17
Q

How do heat proteins (HSP) protect against cell injury?

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A
  • heat shock response aims to ‘mend’ misfolded proteins/maintain cell viability.
  • Many HSP’s are Chaperonins – provide optimal conditions for denatured protein folding, preventing protein aggregation, label misfolded proteins for degradation.
  • e.g ubiquitin
18
Q

What are the two main processes seen in necrosis?

Study These Flashcards
A
  1. Desaturation of intracellular proteins
  2. Enzymatic digestion by lysosomes inherent to the dying cell and lysosomes of leukocytes that are part of inflammatory reaction
19
Q

What is an approximate time necrosis may be developing?

Study These Flashcards
A

4-12hr after necrosis onset

20
Q

What are types of necrosis?

Study These Flashcards
A
  1. Coagulative necrosis - protein denaturation
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fat necrosis
  5. Fibrinoid necrosis
21
Q

Provide information on coagulative necrosis?

Study These Flashcards
A
  • Most common form
  • Occurs in most organs
  • A result of protein denaturation
  • Gross: Firm, pale wedge of tissue, can be soft later on
  • Microscopy – “ Ghost cells”. Neutrophils can infiltrate but NOT a prominent feature
22
Q

Provide information on liquefaction necrosis?

Study These Flashcards
A
  • Usually seen in brain
  • Seen in infections resulting in abscess formation
  • Degradation of tissue by enzymes.
  • Necrotic material - creamy yellow because of dead leukocytes -> pus (NEUTROPHILS)
23
Q

Provide information on caseous necrosis?

Study These Flashcards
A
  • “Cheese like” gross appearance

* Amorphous debris surrounded by histiocytes -> granulomatous inflammation

24
Q

Provide information on fat necrosis?

Study These Flashcards
A
  • Destruction to adipocytes (consequence of trauma) or secondary to release of lipases from damaged pancreatic tissue.
  • Fat necrosis causes fatty acids which react with calcium -> white deposits in fatty tissue
  • Can mimic breast tumour on radiology and is biopsied to exclude cancer.
25
Provide information of fibrinoid necrosis
* Seen in immune reactions involving blood vessels. * Deposits of “immune complexes” + fibrin that has leaked out of vessels. * Bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists
26
Describe white infarct
* Solid organ- Robust stromal support limits haemorrhage into necrotic area from adjacent capillaries * Arterial insufficiency * End artery * Common site: heart, spleen , kidney
27
Describe red infarct (haemorrhaging infarct)
* Organs with dual blood supply /numerous anastamoses between capillary beds * Organs that have loose stromal support * Raised venous pressure leading to increased capillary pressure/tissue pressure -> in arterial insufficiency
28
What are three types of gangrene?
* Wet gangrene (necrosis modified by bacteria) * Dry gangrene (necrosis modified by air) * Gas gangrene (necrosis modified by gas from bacteria) Clinical term to describe Visible Necrosis
29
Describe apoptosis?
* Energy dependent programmed cell death * Characteristic non random internucleosomal cleavage of DNA * Distinct morphological features * Does not result in an inflammatory response * Apoptosis can be physiological or pathological
30
Explain physiological apoptosis
* Embryogenesis and fetal development (loss of webbing as hand develops). * Hormone dependent involution e.g. shedding of endometrium at menstruation * Cell deletion in proliferating cell populations e.g. regulation of immune system or intestinal crypts * Death of cells that have served their function (neutrophils/lymphocytes).
31
Explain pathological apoptosis
* Neoplasia * Autoimmune conditions (failure of induction of apoptosis in lymphoid cells directed against host antigens) * AIDS - HIV proteins may activate CD4 on uninfected T helper lymphocytes with apoptosis -> immunodepletion
32
What are some ways in which apoptosis can be regulated?
* Genes * Inhibitors - growth factors, extracellular cell matrix, sex steroids, some viral proteins * Inducers - growth factor withdrawal, loss of extracellular matrix attachment, glucocorticoids, viruses, free radicals, ionising radiation
33
What is the mechanism of apoptosis?
* Activation of a cascade of caspases (cysteine-dependent aspartate-directed proteases) * 2 pathways resulting in activated caspase 3 which cleave proteins -> chromatin condensation, nuclear fragmentation, blebbing * Extrinsic pathway – external “death receptors” (TNF receptors or Fas receptors) are activated by a ligand * Intrinsic pathway – withdrawal of growth factors or hormones causes molecules to be released from mitochondria (e.g. Bcl2, Bax, p53) * Apoptotic cell eventually phagocytised by macrophages/histiocytes/neighbouring cells -> no acute inflammation
34
Compare necrosis and apoptosis in relation to their pattern, cell size, nucleus and plasma membrane
``` Pattern: • N - contiguous groups of cells • A - single cells Cell size: • N - enlarged (swelling) • A - reduced (shrinkage) Nucleus: • N - pyknosis, karyorrhexis, karyolysis • A - fragmentation into nucleosome sized fragments Plasma membrane: • N - disrupted, early lysis • A - intact; altered structure (orientation of lipids) ```
35
Compare necrosis and apoptosis in relation to their cellular contents, adjacent inflammation and physiologic/pathological role
Cellular contents: • N - enzymatic digestion (may leak out of cell) • A - intact (may release into apoptotic bodies) Adjacent inflammation: • N - frequent • A - no Physiologic or pathological role: • N - invariably pathologic • A - often physiologic (eliminating unwanted cells), pathologic (some forms of cell injury - DNA damage)
36
What are molecules that are released as a result of cell injury and death?
* Potassium * Enzymes * Myoglobin
37
What can happen to the body as a result of molecules released as a result of cell injury?
* Can cause local inflammation * May have general toxic effects on body * May appear in high concentrations in blood and can aid in diagnosis
38
Explain rhabdomyolysis
This can be serious without myoglobin as a breakdown product of muscle causing damage to the kidneys/renal failure -> dialysis Typical brown urine in myoglobinuria
39
What are mechanisms of intracellular accumulations?
``` • Abnormalmetabolism • Alterationsinproteinfolding and transport • Deficiency of critical enzymes • Inability to degrade phagocytosed particles ```
40
What can intracellular accumulations be?
* Water and electrolytes • Lipids * Carbohydrates * Proteins * Pigments
41
What are the names of some disease as a result of endogenous pigments (abnormal accumulations)?
* Haemosiderin * Haemosiderosis * Hereditary haemochromatosis * Bilirubin
42
What is pathological calcification - metastatic?
* Parathyroid overactivity – tumour or hyperplasia * Vitamin D overdosage * Malignant tumours e.g. breast and lung, bone * Paget’s disease •Prolonged immobilisation

MoD (11 decks)

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