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Pathological Processes > Session 1 > Flashcards

Session 1 Flashcards

1
Q

What does the degree of cell injury depend on?

A
  • Duration of injury
  • Severity of injury
  • Type of injury
  • Type of tissue
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2
Q

What can cause cell injury?

A
  • Hypoxia
  • Toxins
  • Physical agents (eg. direct trauma, changes in temperature like burns, changes in pressure)
  • Microorganisms
  • Radiation (internal organ injury)
  • Dietary insufficiencies
  • Immune mechanisms (eg. autoimmune, allergy)
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3
Q

What is the difference between hypoxia and ischaemia?

A
  • Hypoxia: reduced oxygen supply.

- Ischaemia: loss of the blood supply into an area and therefore reduced delivery of O2 and nutrients

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4
Q

What can cause ischaemia?

A
  • Arterial occlusion

- Global hypotension (sepsis)

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5
Q

What is hypoxaemic hypoxia?

A

Low arterial content of oxygen

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6
Q

What are the causes of hypoxaemic hypoxia?

A
  • Reduced O2 partial pressures at altitude

- Reduced O2 absorption (lung disease, poor O2 exchange)

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7
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

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8
Q

What are causes of anaemic hypoxia?

A
  • Anaemia

- CO poisoning

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9
Q

What is ischaemic hypoxia?

A

Interruption to the blood supply (most important clinically!)

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10
Q

What are the causes of ischaemic hypoxia?

A
  • Blockage of a vessel

- Heart failure

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11
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes (when tissue cells are poisoned and can’t use O2)

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12
Q

What can cause histiocytic hypoxia?

A

Cyanide poisoning

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13
Q

Why can the brain not survive without oxygen for too long?

A
  • Neurones have a higher and quicker demand for O2

- Other cells (eg. fibroblasts) can survive for longer

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14
Q

How can the immune system damage cells in the body?

A
  • Hypersensitivity: overly vigorous immune reactions

- Autoimmune reactions: failure to distinguish self from non-self

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15
Q

Which cell components are most susceptible to injury?

A
  • Plasma/organelle membranes
  • Nucleus (DNA)
  • Proteins (structural, metabolic enzymes)
  • Mitochondria (oxidative phosphorylation)
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16
Q

What happens in hypoxia when the injury is reversible (short term)?*

A
  • Oxidative phosphorylation can’t function, so less ATP is produced
  • Less ATP means reduced function of sodium pump which causes an increase in Ca2+, Na+ and H2O, K+ efflux
  • Causes oncosis, blebs, ER swelling, myelin figures
  • Less ATP means increased glycolysis, causing lower pH and therefore chromatin clumping
  • Lower ATP causes less protein synthesis leading to lipid deposition
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17
Q

What happens in prolonged hypoxia?*

A 
- Increased Ca2+ inhibits: 
ATPase: reduced ATP
Phospholipase: decreased phospholipids
Protease: disruption of protein 
Endonuclease: nuclear chromatin damage
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18
Q

What are free radicals?

A

Reactive oxygen species which have a single unpaired electron in the outer orbit and therefore have an unstable configuration that can react with other molecules and produce further free radicals.

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19
Q

What are the 3 significant free radicals that can cause damage?

A
  • Hydroxyl
  • Superoxide
  • Hydrogen peroxide
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20
Q

When are free radicals produced?

A
  • Oxidative phosphorylation (can escape the electron transport chain)
  • Oxidative burst of neutrophils (inflammation)
  • Radiation causing lysis of H2O
  • Contact with unbound metals within body (Fenton reaction)
  • Drug metabolism
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21
Q

How does the body control free radicals?

A
  • Antioxidant scavengers that donate electrons to free radicals (Vit. A, C, E)
  • Metal carrier and storage proteins (transferrin, ceruloplasmin) that make metals unavailable for reactions
  • Enzymes that neutralise free radicals
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22
Q

Which enzymes neutralise free radicals?

A
  • Superoxide dismutase
  • Glutathione peroxidase
  • Catalase
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23
Q

How do free radicals injure cells?

A
  • Cause lipid peroxidation in the lipids in cell membranes

- Generates further radicals and creates a chain reaction

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24
Q

How do free radicals affect DNA?

A
  • Can oxidise proteins, carbohydrates and DNA
  • Molecules can become broken or crosslinked
  • Made mutagenic and therefore carcinogenic
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25
Q

What are heat shock proteins?*

A

A response that ‘mends’ misfolded proteins to maintain cell viability. They are unfoldases and chaperonins.

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26
Q

What is an example of a heat shock protein?

A

Ubiquitin

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27
Q

What do injured cells look like under microscope?*

A
  • Oncosis

- Paler cytoplasm

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28
Q

What do dead cells look like under the microscope?*

A
  1. PYKNOSIS - pink cytoplasm that shrinks, is darker
  2. KARYORRHEXIS - breakdown of the nucleus
  3. KARYOLYSIS - dissolved nucleus
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29
Q

What are the general features of injured and dying cells?

A
  • Cytoplasmic changes
  • Nuclear changes
  • Abnormal cellular accumulations
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30
Q

How do dead/dying cells look under the electron microscope?*

A

Look at diagram, page 20! :)

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31
Q

What can accumulate in cells?

A
  • Water and electrolytes
  • Lipids
  • Carbohydrates
  • Proteins
  • Pigments
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32
Q

Why do abnormal cellular accumulations occur?

A

When metabolic processes become deranged, especially with sublethal or chronic injury.

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33
Q

When can fluid accumulate in the cell?

A
  • During hypoxia
  • Sodium and water enter the cell
  • Big problem in the brain
  • Indicates severe cellular distress
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34
Q

How to see swelling in a brain?*

A

Less defined gyri and sulci.

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35
Q

What is steatosis?

A

Accumulation of triglycerides that is mainly seen in liver.

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36
Q

What are the causes of steatosis?

A
  • Alcohol
  • Diabetes
  • Obesity
  • Toxins
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37
Q

What does steatosis look like?

A

IRL: Liver yellow due to fat accumulation, will cause dysfunction.
Microscope: Many adipocytes present.

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38
Q

When does cholesterol accumulate in cells?

A
  • Excess that is not eliminated by conjugation with albumin and removal through liver is stored in cell in vesiclees
  • Accumulation = foam cells
  • Present in macrophages, skin and tendons of people ith hyperlipidaemias (xanthomas)
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39
Q

What does accumulation of cholesterol look like?*

A

Slide 28! :)

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40
Q

What do proteins look like when they accumulate in cells?

A
  • Eosinophilic droplets

- Aggregations in cytoplasm

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41
Q

What is Mallory’s hyaline and how does it cause protein accumulation?*

A
  • Damaged intermediate filaments within hepatocytes
  • In people with alcoholic liver disease
  • Highly eosinophilic, appear pink on H&E
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42
Q

How does alpha 1-antitrypsin deficiency cause protein accumulation?

A
  • Liver produces incorrectly folded alpha 1-antitrypsin

- Cannot be packaged or secreted so accumulates in the ER

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43
Q

How does alpha 1-antitrypsin cause systemic deficiencies?

A

Proteases in the lungs act unchecked and therefore result in emphysema as the alveoli become destroyed.

44
Q

When do pigments accumulate in cells?

A

Air pollution particles (eg. carbon/soot)
- When they are phagocytosed by macrophages

Tattooing when pigment enters skin
- Phagocytosed in dermis where it remains but also can reach the lymph nodes

45
Q

What does accumulation of pigment look like?*

A
  • Anthracosis (accumulation of carbon in lungs)

- Blackened lung, blackened peribronchial lymph nodes

46
Q

Is anthracosis harmful?

A

No, unless in large amounts, where they can cause fibrosis and emphysema

47
Q

What are endogenous pigments that can accumulate in cells?

A

Haemosiderin (an iron storage molecule), derivative of Hb (yellow/brown)

48
Q

When is haemosiderin found in cells?

A

When there is a systemic (disease) or local (bruise) overload of iron.

49
Q

What can cause accumulation of haemosiderin?

A
  • Hereditary haemochromatosis
  • Haemolytic anaemias (iron released)
  • Blood transfusion (no mechanism to remove iron)
50
Q

What is hereditary haemochromatosis and what does it look like?*

A
  • Inherited disorder
  • Increased dietary absorption of iron
  • Deposited in skin and organs (cirrhosis associated)
51
Q

What are the symptoms of hereditary haemochromatosis?

A
  • Liver damage
  • Heart dysfunction
  • Endocrine failures (pancreas)

All associated with iron overload in cells.

52
Q

What is the treatment for hereditary haemochromatosis?

A

Repeated bleeding to remove blood and therefore extra iron.

53
Q

What is jaundice and what does it look like?*

A

Jaundice is yellowing of the skin due to buildup of bilirubin, which is bright yellow

54
Q

Why can jaundice happen?

A
  • Bile flow obstructed
  • Increased bile production
    All leads to deposition extracellularly or in macrophages
55
Q

What is bilirubin?

A

Breakdown product of heme, broken porphyrin rings (released heme)

56
Q

Where is bilirubin formed and how is it removed from the body?

A
  • Formed in all cells
  • Eliminated in bile
  • Taken from tissue by albumin to liver, conjugated and then excreted in bile
57
Q

What does pleural fluid look like when jaundiced?

A

Yellow-tinged.

58
Q

What happens when molecules leak out of membranes?

A
  • Local inflammation
  • General toxic effects
  • High concentrations in blood = diagnosis?
59
Q

How do intracellular accumulations occur? List 4 ways.*

A

1) Abnormal metabolism (eg. overproduction)
2) Alterations in protein folding and transport
3) Deficiency of critical enzymes
4) Inability to degrade phagocytosed particles

60
Q

What is dystrophic calcification of tissue?

A

Abnormalities/degeneration of tissue leading to mineral calcium depositions even though levels in blood remain normal.

61
Q

What are examples of dystrophic tissue calcification?

A
  • Area of dying tissue
  • Calcification of valve leaflets
  • Atherosclerotic plaques
  • Malignancies
62
Q

What does calcification look like?*

A

See slides. :) (80/88)

63
Q

Why can dystrophic calcification occur?

A
  • Local disturbance that favours nucleation of hydroxyapatite crystals
64
Q

What can be the consequences of dystrophic calcification?

A

Organ dysfunction (atherosclerosis, heart valve calcification)

65
Q

What is metastatic calcification and why does it occur?

A
  • Deposition of calcium salts in otherwise normal tissue.
  • Caused by hypercalcaemia secondary to disturbances in calcium metabolism.
  • Hydroxyapatite crystals deposited throughout body
  • Usually asymptomatic
66
Q

Can metastatic calcification be cured?

A

Yes, if cause of hypercalcaemia is corrected.

67
Q

What causes hypercalcaemia?

A
  • Increased secretion of PTH resulting in bone resorption

- Destruction of bone tissue

68
Q

What is primary, secondary and ectopic bone resorption?

A
  • Primary: parathyroid tumour/hyperplassia
  • Secondary: renal failure and retention of phosphate
  • Ectopic: PTH related proteins secreted by malignant tumours (rectified by surgery)
69
Q

Why can bone tissue be destroyed?

A
  • Tumours of bone marrow
  • Skeletal metastases
  • Accelerated bone turnover (Paget’s disease)
70
Q

What is the definition of oncosis?

A

Cell death with swelling; changes that occur in injured cells prior to death.

71
Q

What is the definition of necrosis?

A

Morphologic changes in a living organism that occur after a cell has been dead for 12-24+ hours

72
Q

What are the 4 types of necrosis?

A
  • Coagulative
  • Liquefactive (2 main)
  • Caseous
  • Fat necrosis (2 special types)
73
Q

What is coagulative necrosis?

A
  • Necrosis caused by the ischaemia of solid organs (eg. heart, kidneys)
  • Caused by protein denaturation & hypoxia
74
Q

What is liquefactive necrosis?

A
  • Necrosis caused by ischaemia in loose tissues (eg. brain, lung)
  • Identified by presence of many neutrophils
  • Protease release
75
Q

What does coagulative necrosis look like?*

A
  • Pyknosis
  • Cell architecture preserved (Ghost outline)
  • Maintained integrity
  • Denaturation of proteins dominates over protease release
  • Pale to naked eye
  • Many neutrophils
76
Q

What does liquefactive necrosis look like?*

A
  • Cells fall apart
  • Eosinophilic pink debris left over
  • Enzymatic digestion of tissue (greater than denaturation)
  • Many neutrophils deposited
77
Q

What is caseous necrosis?

A
  • Structureless debris

- Associated with infections (eg. TB)

78
Q

What does caseous necrosis look like?*

A
  • Stains pink/purple
  • ‘Cottage cheese’ appearance before staining
  • Often has granulomatous inflammation
79
Q

What is fat necrosis?*

A
  • Adipose tissue (after injury)

- Fatty acids and calcium deposit in tissue

80
Q

When does fat necrosis occur?

A

eg. Acute pancreatitis

81
Q

What is the definition of gangrene?*

A

Necrosis visible to the naked eye

82
Q

What is the definition of infarction?

A

Necrosis caused by reduction in arterial blood flow (cause of necrosis and can cause gangrene)

83
Q

What is an infarct?

A

An area of necrotic tissue which is the result of loss of the arterial blood supply

84
Q

Why are some infarcts white and some red?

A
  • White: poor blood supply. Will occur in solid organs after occlusion of an end artery. (coagulative)
  • Red: extensive haemorrhage into dead tissue, dual blood supply, reperfusion (liquefactive)
85
Q

What is dry gangrene?*

A
  • Modified by exposure to air (coagulative necrosis)
86
Q

What is wet gangrene?

A
  • Necrosis modified by infection (liquefactive necrosis)
87
Q

What is gas gangrene?

A

Wet gangrene where the tissue became infected with anaerobic bacteria that produce palpable bubbles of gas in tissues.

88
Q

What are the most common causes of infarcts?

A
  • Emboli that break off and occlude a blood supply somewhere else.
  • Intestines twisting and occluding blood supply.
  • Testicular torsion
89
Q

What are the consequences of infarction?

A

Dependent on:

  • If there’s an alternative blood supply
  • Tissue involved
  • Blood O2 content
  • Ischaemia speed (collateral arteries develop)
90
Q

What is ischaemia-reperfusion injury?

A

Return of blood flow causing further damage

  • Increased production of radicals
  • Increased number of neutrophils = more inflammation
  • Complement pathway
91
Q

What leaks out of the cell when it is damaged?

A
  • Potassium
  • Enzymes (can indicate what organ is involved, eg. troponin)
  • Myoglobin (dead myocardium and striated muscle)
92
Q

Why is the release of myoglobin dangerous?

A
  • Can block kidney and cause renal failure

- Leads to rhabdomyolysis

93
Q

What is cell apoptosis?*

A

Programmed cell death with shrinkage, when the cell activates enzymes that degrade its own proteins and nuclear DNA. Does not elicit an inflammatory response.

94
Q

What do apoptotic cells look like under the microscope?*

A
  • Shrunken
  • Eosinophilic
  • Chromatin condensation, karyorrhexis and pyknosis seen
  • Apoptotic bodies phagocytosis so no leakage out of cell and inflammation
95
Q

What are some features of apoptosis?*

A
  • Maintained membrane integrity
  • No lysosomal enzymes
  • Quick
  • Opposite to mitosis
96
Q

When does apoptosis occur physiologically?

A
  • Embryogenesis (eg. phalanges) - Hox genes

- Maintaining a steady state

97
Q

When does apoptosis occur pathologically?*

A
  • When DNA in cell damaged

- Killing of infected cells by cytotoxic T cells

98
Q

What are the key phases of apoptosis?*

A
  • Initiation
  • Execution
  • Fragmentation
  • Phagocytosis (express proteins recognised by phagocytes)
99
Q

What is the initiation &execution phase?

A

Activation of caspases - enzymes that cause cleavage of DNA and proteins in cytoskeleton

100
Q

What is the intrinsic pathway of initiation?*

A

Signal from within cell.

  • p53 protein activated
  • mitochondrial membrane becomes leaky
  • cytochrome C release causes caspase activation
101
Q

What is the extrinsic pathway of initiation?*

A

Signal by cells that are a danger (eg. cancer)

  • TNF alpha secreted by cytotoxic T cells
  • Binds to ‘death receptor’ on cell membrane
  • Activates caspase cascade
102
Q

What is different in apoptosis compared to oncosis?*

A
  • Shrinking not swelling
  • Cell budding not blebbing
  • No inflammation
103
Q

Compare apoptosis, necrosis and oncosis.

A

Slide 71! :)

104
Q

Why do cells die?

A
  • Accumulate damage to DNA
  • Reach senescence
  • Cell can no longer divide when telomeres reach critical length
105
Q

Why can stem cells continue to replicate?

A

Contain an enzyme (telomerase) that maintains the original length of telomeres

106
Q

Why do cancer cells multiply so much?

A

They produce telomerase.

Pathological Processes (10 decks)

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