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Pathology 2 Flashcards

1
Q

What are the possible responses of cells to reversible cellular injury?

A
  • Hypertrophy

- Hyperplasia

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2
Q

What are labile cells?

A
  • Cells that routinely proliferate

- e.g. epidermis, intestinal epithelium, bone marrow

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3
Q

What are stable cells?

A
  • Cells that have an intermediate ability to regenerate/divide
  • e.g. bone, cartilage, smooth muscle
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4
Q

What are permanent cells?

A
  • Cells that have little or no capacity to regenerate

- e.g. neurons, cardiac/skeletal muscle cells

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5
Q

What cell types are capable of hypertrophy?

A
  • Most organs and tissues

- mainly in stable or permanent cells

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6
Q

What cell types are capable of hyperplasia?

A
  • Only in organs/tissues with dividing cells

- Labile cells > stable cells > permanent cells

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7
Q

What is meant by adaptation with regards to cell injury?

A

Reversible functional and structural responses to more severe physiologic stresses and some pathologic stimuli, allowing cell to survive and continue to function
- Cell injury occurs once limits of adaptive responses are exceeded

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8
Q

What are the potential cellular adaptations following injury?

A
  • Hypertrophy
  • Hyperplasia
  • Atrophy
  • Metaplasia
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9
Q

What is hypertrophy?

A

Increase in cell size by production of more organelles, resulting in increase in size of organ

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10
Q

What stimuli may lead to hypertrophy?

A
  • Increased functional demand
  • Stimulation by hormones
  • Growth factors (and some viruses)
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11
Q

What is the function of hypertrophy following cell injury?

A

Commonly protective, limited and reversible e.g. gravid uterus vs normal uterus

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12
Q

Give an example and cause of pathologic hypertrophy

A
  • Hypertrophic cardiomyopathy

- Blood supply not increased adequately to severe increased mass of myocytes

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13
Q

What is hyperplasia?

A
  • Increased number of cells in organ or tissue
  • Results in increased mass/size of organ/tissue
  • Can be physiologic or pathologic
  • Organisation of cells maintained
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14
Q

Give examples of physiologic hyperplasia

A
  • Hormonal hyperplasia e.g udder enlargement

- Compensatory hyperplasia

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15
Q

Outline pathologic hyperplasia

A
  • Usually due to excess of hormones of growth factors
  • Certain viral infections e.g poxvirus, papilloma virus
  • Can be diffuse (whole organ) or localised (nodular)
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16
Q

What is atrophy?

A

Decreased cell size and number, results in reduced size of organ or tissue

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17
Q

What causes atrophy?

A

Decrease in nutrients/stimulation

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18
Q

What are some physiological examples of atrophy?

A
  • Embryonal/foetal development

- Uterine atrophy after parturition

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19
Q

What are some pathologic causes of atrophy?

A
  • Decreased workload (atrophy of disuse)
  • Loss of innervation (denervation atrophy)
  • Diminised blood supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure (e..g hydronephrosis)
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20
Q

What is metaplasia/dysplasia?

A
  • A potentially reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type
  • Most commonly columnar to squamous change
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21
Q

What is the difference between metaplasia and dysplasia?

A
  • Metaplasia is organised

- Dysplasia has disorderly arrangement of cells

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22
Q

What are potential causes of metaplasia/dysplasia?

A
  • Chronic irritation
  • Deficiencies e.g. vit A
  • Result of cell/tissue injury
  • OEstrogen toxicity
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23
Q

Outline how deficiency may lead to metaplasia

A

Vit A deficiency leads to squamous metaplasia of conjunctival epithelium in tortoises

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24
Q

Outline connective tissue metaplasia

A
  • Formation of cartilage, bone or adipose tissue in tissues that do not normally contain these elements
  • e.g. bone within meningeal tissue (osseous metaplasia)
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25
Q

List the different types of disorders of growth

A
  • Agenesis
  • Aplasia
  • Atresia
  • Hypoplasia
  • Dysplasia
  • Neoplasia
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26
Q

What is agenesis?

A

Complete failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue

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27
Q

What is aplasia?

A

Lack of development of an organ where its precursor did exist at one time. Looks the same as agenesis

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28
Q

What is atresia?

A

Absence or closure of a normal body orifice or tubular passage such as the anus, intestine or external ear canal

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29
Q

What is hypoplasia?

A

Incomplete development of an organ

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30
Q

What is dysplasia?

A

Disordered growth, abnormal development. May be due to congenital/inherited developmental anomaly, abnormal maturation of cells within a tissue

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31
Q

What is neoplasia?

A

Abnormal new formation and growth of cells

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32
Q

What are the different types of intracellular accumulations?

A
  • Lipid
  • Glycogen
  • Protein
  • Other
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33
Q

What are the different categories of intracellular accumulations?

A
  • Normal cellular constituent accumulated in excess
  • Abnormal substance
  • Often pigmented
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34
Q

What are the different mechanisms of intracellular accumulation?

A
  • Abnormal metabolism
  • Defect in protein folding and transport
  • Lack of enzyme needed for breakdown
  • Indigestible material
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35
Q

What is lipidosis?

A

Accumulation of TAGs and other metabolites (neutral fats and cholesterol) within parenchymal cells, commonly the liver

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36
Q

Why is the liver most commonly affected by lipidosis?

A

Is the organ most central to lipid metabolism

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37
Q

How does intracellular glycogen accumulation occur?

A
  • Variable amounts of glycogen normally stored in hepatocytes and myocytes
  • Leads to excessive amounts of glycogen present in animals with abnormal glucose or glycogen metabolism
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38
Q

Give examples of when glycogen accumulation may occur

A
  • Diabetes mellitus
  • Glycogen storage diseases
  • Corticosteroid therapy
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39
Q

Outline reasons for intracellular protein accumulation

A
  • Proteinuria: protein resorption droplets in renal proximal tubular cells
  • excessive production of normal protein (Mott cells in particular)
  • Defects in protein folding (e.g. Alzheimer’s disease in man, TSEs/prion diseases)
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40
Q

Give examples of other possible intracellular accumulations

A
  • Viral inclusion bodies (intranuclear or intracytoplasmic)

- Lead inclusion bodies (intranuclear)

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41
Q

List the different types of extracellular accumulations

A
  • Amyloid
  • Gout
  • Cholesterol
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42
Q

What is amyloid?

A

Chemically diverse group of extracellular proteinaceous substances that appear histologically and ultrastructurally similar

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43
Q

Describe the appearance of amyloid on HE stained tissue sections

A
  • Hyaline
  • Homogenous
  • Eosinophilic
  • Glassy
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44
Q

Outline the characteristics of extracellular amyloid accumulations

A
  • Can be primary or secondary

- Can be systemic or localised

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45
Q

Outline the key features of gout

A
  • Deposition of sodium urate crystals or urates in tissue

- Can be articular or visceral

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46
Q

Outline key features of extracellular cholesterol accumulation

A
  • Cholesterol crystals are by-products of haemorrhage and necrosis
  • usually no pathological significance, except cholosteatoma
47
Q

What is a cholosteatoma?

A

A cholesterol granuloma, commonly found in teh choroid plexus of lateral ventricles of old horses/ponies

48
Q

Describe the histological appearance of cholesterol

A

Clefts - cholesterol is dissolved during processing

49
Q

What are the 2 types of pathologic calcification?

A
  • Dystrophic

- Metastatic

50
Q

Describe dystrophic calcification

A
  • Occurs locally in dying/dead tissue

- very white appearance

51
Q

Outline the causes of metastatic calcification

A
  • In normal tissue can be secondary to hypercalcaemia
  • Renal failure
  • Vit D toxicosis
  • paraThormone and PTH-related protein
  • Destruction of bone from primary or metastatic neoplasms
52
Q

Give examples of exogenous pigments and give the colour and common site for accumulation

A
  • Carbon: black, lungs
  • Carotenoid pigments: yellow to yellow/orange
  • Tetracycline: yellow/brown, teeth and bones
53
Q

Give examples of endogenous pigments, the colour, and common site for accumulation

A
  • Melanin: black, mainly epidermis

- Lipofuscin-ceroid: brown, aged cells

54
Q

What leads to ceroid pigmentation?

A

Pathologic pigment, often in vit E deficiency

55
Q

What do the lipofuscin and ceroid pigments consist of?

A

Lipid and protein

- Are same pigment but named differently depending on situation i.e. lipofuscin is non-pathologic, ceroid is pathologic

56
Q

Give examples, colour, and common site of haematogenous pigments

A
  • Haemoglobin: red (oxygenated), blue (unoxygenated), normal pigment of erythrocytes
  • Haemosiderin: yellow/brown (protein-iron complex)
  • Bilirubin: yellow, breakdown of erythrocytes leading to icterus of many tissues
57
Q

What are the 3 phases of acute inflammation?

A
  • Fluidic
  • Cellular
  • Reparative
58
Q

What is the role of the complement cascade in inflammation?

A
  • Helps innate immune system clear pathogens from organism
  • Plasma complement proteins C1-C9 activated and induce inflammation and further activation of immune system
  • End result is cell-killing Membrane Attack Complex (MAC)
59
Q

What are the potential outcomes of acute inflammation?

A
  • Resolution
  • Healing by repair
  • Chronic inflammation
  • Abscess formation
60
Q

Describe the pathway to abscess formation following acute inflammation

A
  • Marked neutrophilic response with tissue destruction
  • Abscess formed
  • Can then go into resolution, healing by repair or chronic inflammation pathways
61
Q

Describe the resolution pathway following acute inflammation

A
  • Damage neutralised
  • Tissue damage minimal
  • Inflammation resolved
62
Q

Describe the healing by repair pathway following acute inflammation

A
  • Damage neutralised with some tissue destruction
  • Organisation through phagocytosis and granulation tissue formation
  • Healing by repair
63
Q

Describe the chronic inflammation pathway following acute inflammation

A
  • Persisting damaging agent with tissue destruction
  • Organisation with continued inflammation
  • Chronic inflammation
64
Q

Give the sequence of events of acute inflammation

A
  • Momentary vasoconstriction
  • Dilation of blood vessels
  • Margination of leukocytes
  • Emigration of leukocytes
  • Potential induction of systemic increase in temperature
65
Q

Describe the vasoconstriction phase of acute inflammation

A
  • Neural reflex
  • Lasts only seconds
  • Prevents blood loss
66
Q

Describe the dilation of blood vessels in acute inflammation

A

Occurs quickly, caused by the release of chemical mediators from damaged cells

67
Q

Describe the exudation of fluid in acute inflammation

A

Following the slowing of blood flow and altered capillary permeability protein rich fluid exudated

68
Q

Describe the margination of leukocytes in acute inflammation

A

Circulating white blood cells (especially neutrophils) begin adherence to altered endothelial surface

69
Q

Describe the emigration of leukocytes in acute inflammation

A

Leukocytes, especially neutrophils, migrate via diapedesis (active process)

70
Q

Where does the majority of leukocyte transmigration and haemorrhage occur in acute inflammation?

A

In the capillaries and post-capillary venules

71
Q

Describe the pathway to the development of pyrexia

A
  • Exogenous factors or endogenous stimulate neutrophils and macrophages
  • Endogenous pyrogens activated
  • Activate arachidonic acid pathway, PGE2 release
  • PGE2 acts on neurons in preoptic area via prostaglanding E receptor 3
  • Stimulation of sympathetic system
72
Q

How does stimulation of the sympathetic system lead to pyrexia?

A
  • Evokes non-shivering and shivering thermogenesis to produce body heat
  • Skin vasoconstriction decreases heat loss from body surface
73
Q

Name the strongest pyrogen

A

LPS (endotoxin)

74
Q

Name the endogenous pyrogens activated in the pyrexia pathway

A

IL-1, IL-6, TNFa

75
Q

What is the effect of prostaglandins on pyrogen production?

A

Negative feedback effect on endogenous pyrogen production

76
Q

What are acute phase proteins?

A

Plasma proteins synthesised by the liver that change serum concentration by >25% in response to systemic inflammatory cytokines. Are considered part of innate immune system

77
Q

What is the difference between positive and negative acute phase proteins (APPs)?

A
  • Positives: inflammatory mediators so increase

- Negatives: used up in acute inflammation so decrease

78
Q

Give examples of positive APPs

A
  • C-reactive proteins
  • Serum Amyloid A (SAA)
  • Ceruloplasmin

The following only for humans:

  • Haptoglobin
  • a2-macroglobulin
  • a1-Acid glycoprotein (AGP)
  • Fibrinogen
  • Complement (C3, C4)
79
Q

Give examples of negative acute phase proteins (APPs)

A
  • Albumin

The following only for humans:
- Transferrin, transthyretin, retinol binding protein

80
Q

What are the key features of plasma derived chemical mediators in inflammation and give examples

A
  • Present in plasma as precursor
  • Must be activated
  • E.g. complement proteins, kinins
81
Q

What are the key features of cell-derived chemical mediators in inflammation?

A
  • Sequestered in intracellular granules

- Need to be secreted or synthesised de novo

82
Q

Give examples of cell-derived chemical inflammatory mediators, and whether they are secreted or produced de novo

A
  • Histamine: needs to be secreted

- PG, cytokines: need to be produced de novo

83
Q

List major cellular sources of cell-derived inflammatory mediators

A
  • Platelets
  • Neutrophils
  • Monocytes/macrophages
  • Mast cells
  • Also some from mesenchymal cells and most epithelial cells
84
Q

What dell-derived inflammatory mediators are produced by all leukocytes

A
  • Prostaglandins
  • Leukotrienes
  • Platelet-activating factors
  • Activated oxygen species
85
Q

What cell-derived inflammatory mediator is produced by mast cells, basophils, platelets?

A

Histamine

86
Q

What cell-derived inflammatory mediators do platelets produce?

A
  • Histamine
  • Serotonin
  • Prostaglandins
87
Q

What cell-derived inflammatory mediator do neutrophils and macrophages produce?

A

Lysosomal enzymes

88
Q

What cell-derived inflammatory mediators do macrophages produce

A
  • Lysosomal enzymes
  • Nitric acid
  • Cytokiines
89
Q

What cell-derived inflammatory mediators do epithelial cells produce?

A
  • Prostaglandins
  • Platelet activating factors
  • Cytokines
90
Q

What cell types produce cytokines?

A

Lymphocytes, macrophages, epithelial cells

91
Q

What cell-derived inflammatory mediators are produced by the liver and via what system?

A
  • Factor XII activation: kinin system (bradykinin), coagulation/fibrinolysis system
  • Complement activation: C3a and C5a (anaphylatoxins), C5b, C5b-9 (MAC)
92
Q

What inflammatory mediators are principally involved in vasodilation?

A
  • Nitric oxide
  • Bradykinin
  • Prostaglandins (PGE2)
93
Q

What inflammatory mediators are principally involved in chemotaxis, leukocyte activation?

A
  • Leukotrienes
  • C5a
  • Chemokines e..g IL-8, IL-5
  • BActerial products e.g. LPS, teichoic acid
  • Defensins
94
Q

What inflammatory mediators are principally involved in increased vascular permeability?

A
  • Vasoactive amines like histamine
  • Complement factors like C5a, C3a
  • Leukotrienes
  • PGE2
  • PAF< IL-1, TNF
95
Q

What inflammatory mediators are principally involved in fever?

A

Cytokines e.g. IL-1, NF, IL-6

96
Q

What inflammatory mediators are principally involved in smooth muscle contraction?

A
  • Histamine
  • Serotonin
  • C3a
  • PAF
97
Q

What inflammatory mediators are principally involved in tissue damage

A
  • Neutrophil granule content - matrix metalloproteinases

- ROS

98
Q

What is the role of arachidonic acid metabolites in acute inflammation?

A
  • Inflammation leads to cell injury, cell membrane lipids rapidly rearranged to create variety of biologically active lipid mediators derived from arachidonic acid
  • Effects short-lived because these metabolites decay rapidly, or destroyed by enzymes
99
Q

Outline the arachidonic acid pathway production of prostaglandins

A
  • Tissue damage leads to acute inflammation
  • Cell membrane lipids released, metabolised by phopholipases into arachidonic acid cascade
  • Arachidonic acid metabolised by COX-1 and COX-2 to produce prostaglandins - are proinflammatory mediators
100
Q

Where do NSAIDs act to reduce inflammation?

A

Interfere with COX enzyme to prevent production of proinflammatory PGs

101
Q

What is the fate of arachidonic acids metabolised by 5-lipoxygenase?

A

Produces leukotrienes (chemokines), leading to chemotaxis, vasoconstriction, bronchospasm and increased vascular permeability

102
Q

What happens if 5-HPETE (product of arachidonic acid 5-lipoxygenase metabolism) is metabolised by 12-lipoxygenase?

A
  • Produces lipoxin A and B

- Inhibit neutrophil adhesion and chemotaxis

103
Q

What is the effect of thromboxane A?

A

Causes vasoconstriction, promotes platelet aggregation

104
Q

What are the different types of effusions?

A

Transudate and ecudate

105
Q

What is transudation?

A
  • Fluid leaks out of blood vessel due to increased hydrostatic pressure or decreased osmotic pressure
  • Only fluid leakage, no protein lost
106
Q

What may lead to transudation?

A
  • Increased cardiac output

- Decreased protein present in capillaries

107
Q

What is exudation?

A
  • Forms in inflammation due to increased vascular permeability
  • Increased interendothelial spaces
  • Proteins lost
108
Q

What may lead to ecudation

A
  • Inflammation
109
Q

Give the key features of transudate

A
  • Extravascular filtrate of plasma
  • Little protein present
  • Few or no measurable nucleated cells
  • Fluid appears grossly clear and watery
110
Q

Give the key features of exudate

A
  • Inflammatory
  • Extravascular fluid that is rich in protein (fibrinogen) and or cells
  • Grossly appears cloudy or viscous
111
Q

What is meant by serous inflammation?

A

Accumulation of mucinous secretory products

- Can be catarrhal: mucosal eptihelium thickened, thick layer of clear mucus

112
Q

What is fibrinous inflammation?

A
  • Characterised by strands of fibrin derived from protein-rich exudate
  • Friable exudate,scrambled eggs appearance
  • Consists of fibrin plus other plasma proteins
113
Q

What is purulent/suppurative inflammation?

A
  • Pus

- Numerous PMNs present

PVS (23 decks)

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