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PVS > Pathology > Flashcards

Pathology Flashcards

1
Q

Define pathology

A

The study of structural, biochemical and functional changes in cells, tissues and organs that underlie disease

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2
Q

Define systemic pathology

A
  • Pathology of organ systems
  • The study of alterations in specialised organs and tissues that are responsible for disorders that involve these organs
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3
Q

Define anatomic pathology

A
  • Examination of tissues taken during life (biopsy) or after death (necropsy)
  • Examines nature and extent of disease process
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4
Q

Define clinical pathology

A

Examination of blood and other body fluids, as well as cells (cytology) during life

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5
Q

List the 4 aspects of disease

A
  • Aetiology
  • Pathogenesis
  • Molecular and morphologic changes
  • Clinical manifestation
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6
Q

What is meant by aetiology?

A
  • Cause of disease
  • Can be internal (e.g. aging, immunologic defects) or external (e.g. external agents or deficiencies)
  • Most commonly multifactorial
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7
Q

What is meant by pathogenesis?

A
  • Mechanism of disease development
  • Sequence of events in response of cells or tissues to aetiologic agent from initial stimulus to ultimate expression of disease
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8
Q

What is meant by molecular and morphologic changes in disease?

A
  • Biochemical (molecular) and structural (morphologic) alterations induced in cells and organs
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9
Q

Outline the clinical manifestation aspect in disease

A
  • Functional consequences of molecular and morphologic changes
  • End results of genetic, biochemical and structural changes in cells and tissues are functional abnormalities
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10
Q

What is the difference between symptoms and signs?

A
  • Symptoms: what the animal is feeling (nausea)

- Signs: what the clinician sees (vomiting)

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11
Q

List the major processes of pathology

A
  • Inflammation
  • Healing
  • Thrombosis
  • Neoplasia
  • Metabolic dysfunction
  • Necrosis
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12
Q

What are the “pillars of inflammation”

A
  • Heat
  • Redness
  • Swelling
  • Pain
  • Loss of function
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13
Q

What is the process and function of inflammation?

A
  • Vascular and interstitial tissue changes that develop in response to tissue injury
  • Designed to sequester, dilute and destroy causal agent
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14
Q

What are the processes involved in healing?

A
  • Angiogenesis
  • Fibrosis
  • Regeneration
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15
Q

What is epithelisation?

A

Regenerative process that covers defects in injured skin and other epithelial surfaces

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16
Q

What is thrombosis?

A

Interaction of blood coagulation system and platelets to form (within a vascular lumen) an aggregate of fibrin and platelets (thrombus)

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17
Q

What leads to neoplasia?

A
  • Intrinsic genetic mutations in somatic cells that underlie abnormal mechanisms for control of mitosis, differentiation and cell-to-cell interactions
  • Leads to uncontrolled mitosis and expanding mass of uncontrolled cells
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18
Q

What is the effect of neoplasia?

A

Impinges on adjacent normal tissue

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19
Q

What is the role of metabolic dysfunction in pathology?

A
  • Abnormalities/imbalances of carb, fat and protein metabolism in cell leads to accumulation of glycogen, fat or protein
  • Also complexes of abnormally folded and branched proteins, lipoproteins and amyloid
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20
Q

What is necrosis?

A

Death of cells and tissues in living animals

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21
Q

What is the definition of diagnosis?

A

Conclusion concerning the nature, cause or name of a disease

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22
Q

List the different types of diagnosis

A
  • Clinical
  • Clinical pathologic
  • Morphologic (lesion)
  • Aetiologic
  • Disease
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23
Q

Outline what is meant by a clinical diagnosis

A
  • Based on data obtained from case history, clinical signs and physical examination
  • i.e. severe acute contagious blood diarrhoea
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24
Q

Outline what is meant by clinical pathologic diagnosis

A
  • Based on changes observed in chemistry of fluids and haematology, structure and function of cells collected from living patient
  • i.e. severe leukocytosis
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25
Q

Outline what is meant by morphologic diagnosis

A
  • Based on predominant lesions in tissue

- Can be macroscopic (gross) or microscopic (histologic)

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26
Q

What is included in a morphologic diagnosis?

A
  • Severity
  • Duration
  • Distribution
  • Location (organ or tissue)
  • Nature (degenerative, inflammatory, neoplastic)
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27
Q

Outline what is meant by aetiologic diagnosis

A

Names the specific cause of the disease

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28
Q

List methods that can be used to reach a diagnosis

A
  • Morphology
  • Molecular biology
  • Microbiology
  • Immunology
  • Genetics
  • Informatics
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29
Q

What is a biopsy?

A

Removal and examination of tissue sample from a living animal body for diagnostic purposes

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30
Q

What is a necropsy?

A

Methodical examination of the dead animal

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31
Q

What is meant by a macroscopic examination?

A
  • Observation by the unaided eye

- Observe deviations in size, colour, texture, location from normal organs/tissues

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32
Q

What is meant by microscopic examination?

A
  • Light microscopy (histopathology, often stained, specialised microscopes e.g. dark field)
  • Electron microscopy: trans or scanning
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33
Q

List molecular techniques that can be used in diagnosis

A
  • PCR
  • In situ hybridisation (ISH)
  • Genomics (DNA sequencing, DNA microarrays)
  • Transcriptomics (RNA sequencing)
  • Proteomics, metabolomics, immunological approaches
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34
Q

What are molecular techniques used for in diagnosis?

A

Detection of, or detection of alterations from normal, in nucleic acids and protein

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35
Q

What is putrefaction?

A

Colour and texture changes, gas production, odours produced by post-mortem bacterial metabolism and dissolution of host tissues (decomposition)

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36
Q

What is rigor mortis?

A

Contraction of muscles after death

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37
Q

What causes rigor mortis and on what timescale does it occur?

A
  • Depletion of ATP and glycogen

- Starts 1-6 hours after death, persists for 1-2 days

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38
Q

What is algor mortis?

A

Gradual cooling of the cadaver

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39
Q

Why may gradual heating of the cadaver occur following death?

A

Bacterial processes

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40
Q

What is livor mortis?

A
  • Hypostatic congestion

- Gravitational pooling of blood on one side of the animal

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41
Q

When and where does post-mortem clotting occur?

A
  • Heart and blood vessels

- Within several hours after death

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42
Q

What is haemoglobin imbibition?

A

Red staining of tissues

43
Q

How does haemoglobin imbibition occur?

A
  • Integrity of blood vessel walls lost
  • Hb released by lysed RBCs
  • Penetrates vessel walls
44
Q

What is bile imbibition?

A

Staining of tissues a yellow/green/brown colour

45
Q

How does bile imbibition occur?

A

Bile in gall bladder penetrates wall and stains tissues

46
Q

What is psuedomelanosis?

A

Blue-green discolouration of tissue by iron sulphide (FeS)

47
Q

How does pseudomelanosis occur?

A

Formed by the reaction of hydrogen sulphide (H2S) generated by putrefactive bacteria and iron from haemoglobin released from lysed erythrocytes

48
Q

How does bloating post mortem occur?

A

Bacterial gas formation in the lumen of teh GIT

49
Q

Why does softening occur post mortem?

A

Softening of tissue results from autolysis of cells and connective tissue, often aided by putrefactive bacteria

50
Q

When might lens opacity occur post mortem?

A
  • When carcass very cold or frozen

- Reverses when warms up

51
Q

List common causes of cell injury

A
  • oxygen deprivation
  • Physical agents
  • Chemical agents and drugs
  • Infectious agents
  • Immunologic reactions
  • Genetic derangements
  • Nutritional imbalances
52
Q

What may lead to oxygen deprivation of a cell?

A
  • Reduced blood flow (ischaemia)
  • Inadequate oxygenation of blood (cardiorespiratory failure)
  • Decreased oxygen carrying capacity of blood (anaemia, CO poisoning, blood loss)
53
Q

What physical agents may cause cell injury?

A
  • Mechanical trauma
  • Extremes of temperature
  • Radiation
  • Electric shock
54
Q

What chemical agents or drugs may cause cell injury?

A
  • Hypertonic concentrations of simple chemicals (glucose, salt)
  • Poisons
  • Environmental pollutatns (insecticides, herbicides)
  • Therapeutic drugs
55
Q

What infectious agents may cause cell injury?

A
  • Viruses and prions
  • Bacteria
  • Fungi
  • Parasites
56
Q

What immunologic reactions might lead to cell injury?

A
  • Immune reactions to external agents (microbes) and environmental substances
  • Immune reactions to endogenous self-antigens (autoimmune diseases)
57
Q

What genetic deficiencies may lead to cell injury?

A
  • Deficiency of functional (e.g. enzymes) or structural proteins (errors of metabolism, accumulation of damaged DNA or misfolded proteins)
  • Influence the susceptibility of cells to injury by chemical and other environmental insults
58
Q

Give examples of reversible cell injury

A
  • Depletion of cellular energy stores
  • Cellular swelling
  • Alterations of intracellular organelles
  • Fatty change
59
Q

What leads to fatty changes in cells?

A
  • Abnormal accumulations of neutral lipids within parenchymal cells
  • Often liver
  • Excessive production/mobilisation of lipids, defective metabolism and export of lipids (due to toxins or hypoxia for example)
60
Q

What conditions may lead to excessive production or mobilisation of lipids, leading to fatty change in cells and how?

A
  • Starvation
  • Diabetes mellitus
  • Depleted carb sotres, breakdown of fat and protein = increased FFAs
61
Q

What is the difference between necrosis and apoptosis?

A
  • Necrosis is always pathologic, cell membranes damaged, often with inflammation
  • Apoptosis: may be pathologic or physiologic, cell membranes in tact, no inflammation, is programmed cell death
62
Q

Outline the process of necrosis

A
  • Swelling of endoplasmic reticulum and mitochondria
  • Denaturation of intracellular proteins and enzymatic digestion of injured cell
  • Breakdown of plasma membrane, organelles and nucleus
  • Leakage of cellular contents
63
Q

What enzymes and proteins released from necrotic cells can be detected in the blood?

A
  • Creatine kinase

- Alkalin phosphatase

64
Q

What molecular and biochemical mechanisms are involved in necrosis?

A
  • Depletion of ATP
  • Mitochondrial damage
  • Influx of calcium and loss of calcium homeostasis
  • Accumulation of oxygen-derived free radicals
  • Defects in membrane permeability
  • Damage to DNA and proteins
65
Q

How does ATP depletion in necrosis occur?

A

Reduced supply of oxygen and nutrients, mitochondrial damage or toxins

66
Q

How does ATP depletion contribute to necrosis?

A
  • ATP required for virtually all synthetic and degradative processes within the cell
  • E..g membrane transport, protein synthesis, lipogenesis
67
Q

How does mitochondrial damage in necrosis occur?

A

Hypoxia and toxins are major causes

68
Q

How does mitochondrial damage contribute to necrosis?

A
  • Leads to reduced ATP

- Release of pro-apoptotic proteins e.g. cytochrome C

69
Q

How does influx of calcium and loss of calcium homeostasis occur in necrosis?

A

Ischaemia and toxins are major causes

70
Q

How does calcium influx and loss of calcium homeostasis contribute to necrosis?

A
  • Increases mitochondrial permeability (reduced ATP, induction of apoptosis)
  • Activation of multiple cellular enzymes e.g. phospholipases, proteases, endonucleases, ATPases
71
Q

How does accumulation of oxygen-derived free radicals (ROS) occur in necrosis?

A
  • Inflammation
  • Radiation
  • Chemicals
  • Reperfusion injury
72
Q

How does the accumulation of oxygen derived free radicals contribute to necrosis?

A

Damage to lipids, proteins and DNA

73
Q

How may defects in membrane permeability occur in necrosis?

A
  • Ischaemia
  • Toxins
  • Viruses
  • Physical/chemical agents
74
Q

How do membrane defects contribute to necrosis?

A

Consequences in:

  • Mitochondrial membrane (ATP production, apoptosis)
  • Plasma membrane (loss of cellular contents and osmotic balance)
  • Lysosomal membranes (leakage of enzymes leading to enzymatic digestion of proteins, DNA/RNA, glycogen)
75
Q

What cytoplasmic morphologic alterations seen on microscopy may occur in necrosis?

A
  • Increases eosinophilia

- Cytoplasmic vacuolation

76
Q

What nuclear morphologic changes seen on microscopy may occur in necrosis?

A
  • Karyolysis (nuclear fading)
  • Pyknosis (nuclear shrinkage)
  • Karyorrhexis nuclear fragmentation)
77
Q

What are the different patterns of tissue necrosis that may be seen?

A
  • Coagulative necrosis
  • Liquefactive necrosis
  • Gangrenous necrosis
  • Caseous necrosis
  • Fat necrosis
78
Q

What is an infarct?

A

A localised area of coagulative necrosis caused by ischaemia due to vascular obstruction

79
Q

Outline the key features of coagulative necrosis

A
  • Architecture of tissue preserved
  • Firm texture
  • Dark colour
80
Q

How does coagulative necrosis occur?

A

Injury denatures structural proteins but also enzymes, blocking proteolysis of dead cells so architecture maintained

81
Q

Outline the key features of lliquefactive necrosis

A
  • Liquid viscous mass
  • Enzymatically digested dead tissue, architecture not preserved
  • Mainly in microbial infections
  • Pus or malacia
82
Q

Why might liquefactive necrosis occur in microbial infection

A

Accumulation of leukocytes liberates enzymes

83
Q

What is malacia?

A

A type of necrosis of the central nervous system (liquefactive)

84
Q

Outline the key features of gangrenous necrosis

A
  • Variant of coagulative necrosis

- Usually applies to a limb that has lost its blood supply

85
Q

What are the types of gangrenous necrosis?

A
  • Dry
  • Moist
  • Gas
86
Q

Outline the key features of caseous necrosis

A
  • Conversion of dead cells into friable mass resembling cheese
  • Typically more chronic than coagulative necrosis
  • E.g. TB, pseudotuberculosis
87
Q

Outline the key features of fat necrosis

A
  • Focal areas of fat destruction (no specific pattern of necrosis)
  • Fat appears white, firm, chalky, resembles flecks of soap
88
Q

How does fat necrosis occur?

A
  • Typically results from release of pancreatic lipases

- TAG esters metabolised by lipases to fatty acids, react with calcium leading to fat saponification

89
Q

What fragments do apoptotic cells split into?

A
  • Apoptotic bodies

- Intact plasma membrane

90
Q

How are apoptotic bodies removed?

A

Removed by phagocytes, usually macrophages

91
Q

Give examples of physiologic causes of apoptosis

A
  • Embryogenesis
  • Involution of hormone-dependent tissues
  • Cell loss in proliferating cell populations
  • Elimination of self-reactive lymphocytes
  • Leukocytes after inflammatory response
92
Q

Give examples of pathologic causes of apoptosis

A
  • DNA damage
  • Accumulation misfolded proteins
  • Certain viral infections
  • Atrophy in organs due to disuse/compression
93
Q

What molecular/biochemical mechanisms are involved in apoptosis?

A
  • Activation of caspases
  • DNA and protein breakdown
  • Membrane alterations and recognition by phagocytes
94
Q

Outline the activation of caspases in apoptosis

A
  • Enzymatic cleavage of inactive pro-enzymes to become active
  • Are apoptosis specific enzymes that lead to breakdown of cytoskeleton
95
Q

Give potential causes of DNA and protein breakdown in apoptosis

A
  • Drugs
  • Radiation
  • Oxidative stress
  • Inherited diseases
96
Q

How does DNA and protein breakdown occur in apoptosis?

A
  • DNA broken down into small pieces by endonucleases activated by caspases
  • Protein also broken down by caspases
97
Q

What is the function of membrane alterations in apoptosis?

A
  • Recognition by phagocytes

- Removal of dead cells by phagocytosis

98
Q

What microscopic morphologic changes are seen in apoptosis?

A
  • Cell shrinkage
  • Chromatin condensation
  • Cytoplasmic blebs and apoptotic bodies
  • Phagocytosis of apoptotic cells or cell bodies
99
Q

What are the 2 pathways of apoptosis?

A
  • Intrinsic (mitochondrial)

- Extrinsic (death receptor-initiated)

100
Q

Outline the intrinsic pathway of apoptosis following injury

A
  • Injury leads to DNA damage
  • enzyme p53 activated, increases permeability of mitochondrion membrane (or direct activation of executioner caspases)
  • Release of proapoptotic molecules e.g. cytochrome C
  • Initator caspases activated
  • Executioner caspases activated
  • Leads to endonuclease activation and breakdown of cytoskeleton and cytoplasmic bud forms
101
Q

Outline the mitochrondrial pathway of apoptosis following withdrawal of growth factors or hormones

A
  • Withdrawal leads to activation of proapoptotic molecules e.g. cytochrome C
  • Initiator caspases activated, activate executioner caspases
  • Endonuclease activation or breakdown of cytoskeleton
  • Cytoplasmic bud formation
102
Q

Outline the extrinsic pathway of apoptosis following receptor-ligand interactions

A
  • Binding of ligand (Fas, TNF) to receptor
  • Adapter proteins activated
  • Initiator caspases activated, executioner caspases activated
  • Endonuclease activation, breakdown of cytoskeleton
  • Cytoplasmic bud forms
103
Q

Outline the pathway of apoptosis initiated by cytotoxic T lymphocytes

A
  • Granzyme B activated
  • Activates executioner caspases directly
  • Endonuclease activation
  • Breakdown of cytoskeleton

PVS (23 decks)

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