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Year 1 MCD > Cell Pathology > Flashcards

Cell Pathology Flashcards

1
Q

Define atrophy

A

A shrinkage in the SIZE of the cell, or organ by loss of cell substance

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2
Q

Define hypertrophy

A

An increase in the SIZE of the cell, or organ. This can be physiological or pathological.

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3
Q

Define hyperplasia

A

An increase in the number of cells

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4
Q

Define metaplasia

A

A reversible change where one adult cell type is replaced by another

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5
Q

Define dysplasia

A

This can refer to an abnormal organisation of cells in tissue, or a pre-cancerous stage.

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6
Q

What are the hallmarks of a reversible injury as seen under a light microscope?

A

Fatty change

Cellular swelling

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7
Q

Define necrosis:

A

Confluent cell death associated with inflammation.

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8
Q

What are the four types of necrosis:

A
  • Coagulative necrosis (cells die but still recognisable as cells as they maintain cellular architecture)
  • Liquefactive necrosis (cells die and become liquid)
  • Caseous necrosis (look cheesy; become granules and unrecognisable as cells)
  • Fat necrosis (enzymes become free causing Ca2+ to be released and fat to be deposited)
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9
Q

What is an ulcer?

A

An ulcer is a local defect, or excavation of the surface produced by the sloughing of necrotic inflammatory tissue.

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10
Q

What is apoptosis?

A

Apoptosis is programmed cell death that is not associated with inflammation.

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11
Q

Under whose authority does the coroner operate?

A

The Crown

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12
Q

Does the coroner’s autopsy need consent?

A

No

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13
Q

When does the doctor need to report a death to the coroner?

A

When the cause death is unnatural, or unknown. Or shortly after police custody.

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14
Q

What are hospital autopsies used for?

A
  • Audit
  • See if new treatments work
  • Teaching
  • Research
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15
Q

What are death certificates useful for?

A

Epidemiology

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16
Q

What is a bruise?

A

A bruise or contusion is a blunt trauma injury where blood has leaked from damaged small arteries, venues and veins.

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17
Q

What is an abrasion?

A

A blunt trauma injury which is a graze or scratch.

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18
Q

What is a laceration?

A

A split to the skin caused by a blunt force which overstretches the skin.

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19
Q

What is the difference between a cut and a stab?

A

They are both sharp trauma injuries. A cut is where the length is longer than the depth. A stab is where the depth is greater than the width.

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20
Q

What is acute inflammation?

A

A transient early response to injury caused by the release of chemical mediators

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21
Q

What is chronic inflammation?

A

Inflammation of prolonged duration, usually caused by persistence of injury causing agent

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22
Q

What are the components of an inflammatory reaction?

A
  • Cells (neutrophils, macrophages, lymphocytes, esosinophils, mast cells)
  • ECM (collagen, proteoglycans, fibroblasts)
  • Soluble Factors (antibodies, complement, cytokines, coagulation system)
  • Vessels
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23
Q

What are the cardinal signs of inflammation?

A
  • Calor
  • Rubor
  • Dolor
  • Tumor
  • Loss of function
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24
Q

How can mast cells cause acute inflammation?

A

Mast cell plasma membrane IgE interaction with antigen leads to degranulation of histamine. This causes vasodilation and increased vascular permeability,

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25
Q

What medications reduce inflammation?

A

Antihistamines reduce histamine levels
Aspirin reduce prostaglandin levels
Special antibodies can target IL-1 and TNF

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26
Q

What is the difference between exudate and transudate?

A

Transudate is produced when hydrostatic pressure is greater than colloid osmotic pressure. Exudate is produced by leaky vessels.

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27
Q

How is acute inflammation valuable?

A

Exudate dilutes pathogen and allows soluble mediators to spread.

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28
Q

How is acute inflammation eventually stopped?

A
  • Mediators and neutrophils have a short half-life
  • Macrophages release anti-inflammatory products
  • Stimulus is removed
  • Mast cells and lymphocytes release anti-inflammatory products
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29
Q

Give examples for causes of chronic inflammation

A
  • Persistant infection
  • Prolonged exposure to toxic agent
  • Autoimmunity
  • Foreign body
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30
Q

What cells have more of a role in chronic inflammation?

A

Macrophages, lymphocytes and plasma cells

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31
Q

What role does a macrophage play in inflammation?

A

Classically activated macrophages cause pathogenic inflammation, and have microbicidal actions.
Alternatively activated macrophages have anti-inflammatory effects and have a role in wound repair as well as fibrosis.

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32
Q

What is a granuloma?

A

A cluster of macrophages surrounded by T cells.

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33
Q

What can cause a granuloma?

A

Infection
Foreign material
Reaction to tumours
Immune diseae

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34
Q

What are the local and systemic sequelae inflammation?

A 
Locally:
- excessive tissue damage
- secondary effects on nearby tissue
Systemic:
- evolve into systemic inflammatory reaction causing multi-organ failure.
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35
Q

Compare resolution and repair

A

Resolution is where tissue architecture returns to normal. Only occurs if cells are able to regenerate and little structural damage was done.

Repair is where normal tissue is replaced with fibrous scar tissue. The scar undergoes remodelling which is the reorientation of collagen fibres for maximal tensile strength.

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36
Q

What are the factors that hinder repair?

A 
General:
- poor nutrition
- vitamin deficiency
- supressed inflammation by steroid
Local:
- poor blood supply 
- persistent foreign body
- movement across a fracture site
37
Q

What are the possible complications with tissue repair?

A
  • Keloid formation (excessive collagen deposition)
  • Contractures (fibrous scar tissue across a joint can cause poor motility)
  • Impaired organ function e.g fibrous scar in myocardium
38
Q

What is a neoplasm?

A

A new growth of abnormal tissue which is virtually autonomous and exceeds that of normal tissue.

39
Q

What are the differences between a benign and malignant tumour?

A 
Benign: 
- well differentiated
- usually slow growing
- rarely invading
- seldom metastasise 
Malignant:
- Lack of differentiation
- Rapid turnover
- Infiltrative margins 
- Metastasise
40
Q

Give examples of cancer epidemiology patterns

A
  • Stomach cancer is x7 higher in Japan vs USA
  • Melanoma rates are much higher in New Zealand and Australia
  • Higher rates of oesophageal cancer in china and Iran
41
Q

Give examples of cancer epidemiology patterns

A
  • Stomach cancer is x7 higher in Japan vs USA
  • Melanoma rates are much higher in New Zealand and Australia
  • Higher rates of oesophageal cancer in china and Iran
42
Q

Give examples of carcinogens

A
  • Chemicals
  • Radiation
  • Hormones
  • Viruses
  • Bacteria/fungi/parasites
43
Q

What are the major classes of chemical carcinogens?

A
  • Hydrocarbons
  • Amines
  • Nitrosamines
  • Azo dyes
  • Alkylating agents
44
Q

Give examples of carcinogenic viruses

A

Esptein-Barr, HPV, Hepatitis B and C

45
Q

How can viruses cause cancer?

A

Oncogenic viral DNA can be incorporated into host cell DNA, or oncogenic RNA genomes and transcribes.

46
Q

What is metabolic cancer cachexia?

A

Increased metabolic rate due to cancer leads to weight loss, fatigue and weakness.

47
Q

What is paraneoplastic syndrome?

A

Humoral factors excreted by tumour cells or by an immune response against the tumour can induce endocrinopathies, hypercalcaemia and neuropathies.

48
Q

What are the laboratory cancer diagnostic methods?

A

Histology, Tumour typing, histochemistry, PCR, FISH, DNA microarrays and tumour markers.

49
Q

What are the different stages of cancer

A

Stage I: cancer is localised
Stage II/III: cancer is locally advanced
Stage IV: cancer has metastasised

50
Q

What cancer screening and vaccination options are available in the UK?

A

Screening against cervical, breast and colorectal cancer

Vaccination against HPV and Hep B

51
Q

What is oedema?

A

Abnormal increase in interstitial fluid

52
Q

What are the possible causes of oedema?

A
  • Increased capillary hydrostatic pressure
  • Decreased capillary oncotic pressure
  • Inflammation
  • Lymphatic obstruction
53
Q

What are the likely causes of pulmonary oedema?

A

Raised hydrostatic pressure in capillary bed. Commonly caused by left ventricular failure causing increased pressure in atrium and back pressure into capillaries.

54
Q

Give an example of a non-cardiogenic pulmonary oedema

A

Acute respiratory distress syndrome.

55
Q

What are the clinical features of acute pulmonary oedema?

A

Main symptoms are breathlessness (dyspnoea) usually worse when lying flat (orthopnoea). Acute pulmonary oedema is a medical emergency due to reduced oxygen stats.

56
Q

What is a likely complication of pulmonary oedema?

A

Fluid buildup in alveolar spaced predisposing to bacterial infection in the lung (pneumonia)

57
Q

What are the different types of cerebral oedema (by type)?

A
  • Vasogenic (breakdown of blood-brain barrier)
  • Cytotoxic (derangement of Na/K pumps)
  • Osmotic (reduction in plasma osmolarity)
  • Interstitial (breakdown of CSF-brain barrier)
58
Q

What are the clinical features of cerebral oedema?

A

Cerebral oedema leads to increased inter cranial pressure, increasing risk to brain herniation. Strategies to reduce pressure include raising head and inducing dehydration.

59
Q

What is generalised oedema?

A

Widespread accumulation of fluid in subcutaneous tissues and serous cavities.

60
Q

What are the common causes of generalised oedema?

A

Left ventricular failure, nephrotic syndrome and hepatic failure. Also low renal blood flow > increased absorption of sodium and water from kidneys

61
Q

Define thrombosis

A

Thrombosis is an abnormal blood clot formation

62
Q

What are the factors which lead to thrombosis?

A

Virchow’s Triad:

  • Stasis (loss of laminar flow leads to platelets exposed to endothelium)
  • Vessel Wall Injury (exposes ECM or endothelium lose protective function)
  • Hyper-coagulability (primary is a genetic predisposition, and secondary is acquired, such as obesity)
63
Q

What is the most likely cause of a cardiac thrombosis?

A

Left atrial thrombosis is usually related to atrial fibrillation (stasis). Left ventricular thrombosis is related to prior MI.

64
Q

What is the most important complication of cardiac thrombosis?

A

Systemic embolisation

65
Q

What are the risk factors for venous thrombosis?

A

Age, malignancy, obesity, immobility.

66
Q

What is the most important complication of venous thrombosis?

A

Pulmonary embolism

67
Q

What four things can result after the formation of a thrombus?

A
  • Propagation (becomes bigger)
  • Embolisation (becomes larger and dislodges, traveling through the circulation)
  • Dissolution (destroyed by fibrinolytics)
  • Organisation and Recanalisation (inflammatory response allowing blood vessel remodelling)
68
Q

What is an embolus?

A

A detached intravascular solid, liquid or gas mass carried by the blood to a distant site from its point of origin.

69
Q

What are the most common types of emboli?

A

Fragments of dislodged thrombus (thromboemboli)

70
Q

Where do venous thomboemboli mostly originate from, and what is their most significant consequence?

A

Venous thromboemboli mostly originate from deep leg veins. The most significant consequence is a pulmonary embolism.

71
Q

What are the symptoms of a pulmonary embolism?

A

An emboli lodging in a major pulmonary vessel can cause instantaneous death.
Emboli in medium arteries can cause breathlessness
Emboli in smaller arteries can cause dizziness and chest pain.

72
Q

Where do most arterial thomboemboli originate from, and what is their most significant consequence?

A

Mostly originate from the left side of the heart, and are likely to cause stroke.

73
Q

What is haemorrhage?

A

Extravasation of blood due to vessel rupture. If enclosed within tissue, it is a haematoma.

74
Q

What are the consequences of haemorrhage?

A

Rupture of major vessel can leads to hypovolaemia, shock and subsequently death.
Rupture of a small vessel can still be fatal if it occurs in a vital site
Formation of a haematoma within the cranial cavity can be fatal by causing a rise in intercranial pressure
Chronic low grade haemorrhage can present with iron deficiency caused anaemia.

75
Q

What is shock?

A

This is where tissue perfusion is insufficient to meet metabolic demands.

76
Q

What are the most vulnerable organs to shock?

A

Brain, lungs, heart, kidneys and bowels

77
Q

What are the different types of shock?

A
  • Hypovolemic
  • Cardiogenic (impaired cardiac function)
  • Septic (vasodilation due to inflammatory response)
  • Anaphylactic (IgE mediated hypersensitivity)
  • Neurogenic (injury to sympathetic pathways
78
Q

What are the different types of shock?

A
  • Hypovolemic
  • Cardiogenic (impaired cardiac function)
  • Septic (vasodilation due to inflammatory response)
  • Anaphylactic (IgE mediated hypersensitivity)
  • Neurogenic (injury to sympathetic pathways)
79
Q

What is an infarction?

A

Infarction is tissue necrosis due to ischaemia

80
Q

What is responsible for most infarcts?

A

An obstruction of an artery. Some may be due to venous obstruction.

81
Q

What are the factors influencing the development of an infarction?

A
  • Nature of blood supply (if there are other viable blood supplies)
  • Rate of development of occlusion (collateral blood vessels can form if occlusion is lengthy)
  • Vulnerability to hypoxia (e.g neurons vs fibroblasts)
  • Oxygen content of the blood
82
Q

What are the two types of myocardial infarction?

A
  • Transmural is when the infarction extends the entire thickness of the yay.
  • Subendocardial involves a small area
83
Q

What is atherosclerosis?

A

Complex chronic disease where focal intimal accumulation of lipids and fibrous tissue is associated with smooth muscle proliferation.

84
Q

What are the risk factors for atherosclerosis?

A

Smoking, diabetes, hypertension, hyperlipidemia

85
Q

What is the inciting events leading to atherosclerosis?

A

Endothelial damage, leading to macrophage infiltration and release of cytokines.
Circulating LDLs are trapped in lesion and oxidised. Oxidised LDLs are pro-inflammatory and drives progression of the atherosclerotic plaque.
Smooth muscle cells migrate into the lesion and deposit a collagen-rich matrix that forms a protective fibrous cap.

86
Q

What are the two types of atherosclerotic plaque?

A

Stable plaque

  • less inflammation
  • well developed thick fibrous caps
  • slowly growing
  • less likely to rupture

Unstable plaque

  • more inflammation
  • lipid rich necrotic core
  • thin fibrous cap
  • more likely to rupture
87
Q

What are the two types of atherosclerotic plaque?

A

Stable plaque

  • less inflammation
  • well developed thick fibrous caps
  • slowly growing
  • less likely to rupture

Unstable plaque

  • more inflammation
  • lipid rich necrotic core
  • thin fibrous cap
  • more likely to rupture
88
Q

What are the important disease caused by a stable atherosclerotic plaque?

A

Angina, chronic lower limb ischaemia

89
Q

What are the important disease caused by an unstable atherosclerotic plaque?

A

Unstable angina, MI, stroke, acute lower limb ischaemia

Year 1 MCD (8 decks)

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