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Pathology 2 Flashcards

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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
List the different types of disorders of growth
- Agenesis - Aplasia - Atresia - Hypoplasia - Dysplasia - Neoplasia
26
What is agenesis?
Complete failure of an organ to develop during embryonic growth and development due to the absence of primordial tissue
27
What is aplasia?
Lack of development of an organ where its precursor did exist at one time. Looks the same as agenesis
28
What is atresia?
Absence or closure of a normal body orifice or tubular passage such as the anus, intestine or external ear canal
29
What is hypoplasia?
Incomplete development of an organ
30
What is dysplasia?
Disordered growth, abnormal development. May be due to congenital/inherited developmental anomaly, abnormal maturation of cells within a tissue
31
What is neoplasia?
Abnormal new formation and growth of cells
32
What are the different types of intracellular accumulations?
- Lipid - Glycogen - Protein - Other
33
What are the different categories of intracellular accumulations?
- Normal cellular constituent accumulated in excess - Abnormal substance - Often pigmented
34
What are the different mechanisms of intracellular accumulation?
- Abnormal metabolism - Defect in protein folding and transport - Lack of enzyme needed for breakdown - Indigestible material
35
What is lipidosis?
Accumulation of TAGs and other metabolites (neutral fats and cholesterol) within parenchymal cells, commonly the liver
36
Why is the liver most commonly affected by lipidosis?
Is the organ most central to lipid metabolism
37
How does intracellular glycogen accumulation occur?
- 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
38
Give examples of when glycogen accumulation may occur
- Diabetes mellitus - Glycogen storage diseases - Corticosteroid therapy
39
Outline reasons for intracellular protein accumulation
- 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)
40
Give examples of other possible intracellular accumulations
- Viral inclusion bodies (intranuclear or intracytoplasmic) | - Lead inclusion bodies (intranuclear)
41
List the different types of extracellular accumulations
- Amyloid - Gout - Cholesterol
42
What is amyloid?
Chemically diverse group of extracellular proteinaceous substances that appear histologically and ultrastructurally similar
43
Describe the appearance of amyloid on HE stained tissue sections
- Hyaline - Homogenous - Eosinophilic - Glassy
44
Outline the characteristics of extracellular amyloid accumulations
- Can be primary or secondary | - Can be systemic or localised
45
Outline the key features of gout
- Deposition of sodium urate crystals or urates in tissue | - Can be articular or visceral
46
Outline key features of extracellular cholesterol accumulation
- Cholesterol crystals are by-products of haemorrhage and necrosis - usually no pathological significance, except cholosteatoma
47
What is a cholosteatoma?
A cholesterol granuloma, commonly found in teh choroid plexus of lateral ventricles of old horses/ponies
48
Describe the histological appearance of cholesterol
Clefts - cholesterol is dissolved during processing
49
What are the 2 types of pathologic calcification?
- Dystrophic | - Metastatic
50
Describe dystrophic calcification
- Occurs locally in dying/dead tissue | - very white appearance
51
Outline the causes of metastatic calcification
- 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
Give examples of exogenous pigments and give the colour and common site for accumulation
- Carbon: black, lungs - Carotenoid pigments: yellow to yellow/orange - Tetracycline: yellow/brown, teeth and bones
53
Give examples of endogenous pigments, the colour, and common site for accumulation
- Melanin: black, mainly epidermis | - Lipofuscin-ceroid: brown, aged cells
54
What leads to ceroid pigmentation?
Pathologic pigment, often in vit E deficiency
55
What do the lipofuscin and ceroid pigments consist of?
Lipid and protein | - Are same pigment but named differently depending on situation i.e. lipofuscin is non-pathologic, ceroid is pathologic
56
Give examples, colour, and common site of haematogenous pigments
- 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
What are the 3 phases of acute inflammation?
- Fluidic - Cellular - Reparative
58
What is the role of the complement cascade in inflammation?
- 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
What are the potential outcomes of acute inflammation?
- Resolution - Healing by repair - Chronic inflammation - Abscess formation
60
Describe the pathway to abscess formation following acute inflammation
- Marked neutrophilic response with tissue destruction - Abscess formed - Can then go into resolution, healing by repair or chronic inflammation pathways
61
Describe the resolution pathway following acute inflammation
- Damage neutralised - Tissue damage minimal - Inflammation resolved
62
Describe the healing by repair pathway following acute inflammation
- Damage neutralised with some tissue destruction - Organisation through phagocytosis and granulation tissue formation - Healing by repair
63
Describe the chronic inflammation pathway following acute inflammation
- Persisting damaging agent with tissue destruction - Organisation with continued inflammation - Chronic inflammation
64
Give the sequence of events of acute inflammation
- Momentary vasoconstriction - Dilation of blood vessels - Margination of leukocytes - Emigration of leukocytes - Potential induction of systemic increase in temperature
65
Describe the vasoconstriction phase of acute inflammation
- Neural reflex - Lasts only seconds - Prevents blood loss
66
Describe the dilation of blood vessels in acute inflammation
Occurs quickly, caused by the release of chemical mediators from damaged cells
67
Describe the exudation of fluid in acute inflammation
Following the slowing of blood flow and altered capillary permeability protein rich fluid exudated
68
Describe the margination of leukocytes in acute inflammation
Circulating white blood cells (especially neutrophils) begin adherence to altered endothelial surface
69
Describe the emigration of leukocytes in acute inflammation
Leukocytes, especially neutrophils, migrate via diapedesis (active process)
70
Where does the majority of leukocyte transmigration and haemorrhage occur in acute inflammation?
In the capillaries and post-capillary venules
71
Describe the pathway to the development of pyrexia
- 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
How does stimulation of the sympathetic system lead to pyrexia?
- Evokes non-shivering and shivering thermogenesis to produce body heat - Skin vasoconstriction decreases heat loss from body surface
73
Name the strongest pyrogen
LPS (endotoxin)
74
Name the endogenous pyrogens activated in the pyrexia pathway
IL-1, IL-6, TNFa
75
What is the effect of prostaglandins on pyrogen production?
Negative feedback effect on endogenous pyrogen production
76
What are acute phase proteins?
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
What is the difference between positive and negative acute phase proteins (APPs)?
- Positives: inflammatory mediators so increase | - Negatives: used up in acute inflammation so decrease
78
Give examples of positive APPs
- 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
Give examples of negative acute phase proteins (APPs)
- Albumin The following only for humans: - Transferrin, transthyretin, retinol binding protein
80
What are the key features of plasma derived chemical mediators in inflammation and give examples
- Present in plasma as precursor - Must be activated - E.g. complement proteins, kinins
81
What are the key features of cell-derived chemical mediators in inflammation?
- Sequestered in intracellular granules | - Need to be secreted or synthesised de novo
82
Give examples of cell-derived chemical inflammatory mediators, and whether they are secreted or produced de novo
- Histamine: needs to be secreted | - PG, cytokines: need to be produced de novo
83
List major cellular sources of cell-derived inflammatory mediators
- Platelets - Neutrophils - Monocytes/macrophages - Mast cells - Also some from mesenchymal cells and most epithelial cells
84
What dell-derived inflammatory mediators are produced by all leukocytes
- Prostaglandins - Leukotrienes - Platelet-activating factors - Activated oxygen species
85
What cell-derived inflammatory mediator is produced by mast cells, basophils, platelets?
Histamine
86
What cell-derived inflammatory mediators do platelets produce?
- Histamine - Serotonin - Prostaglandins
87
What cell-derived inflammatory mediator do neutrophils and macrophages produce?
Lysosomal enzymes
88
What cell-derived inflammatory mediators do macrophages produce
- Lysosomal enzymes - Nitric acid - Cytokiines
89
What cell-derived inflammatory mediators do epithelial cells produce?
- Prostaglandins - Platelet activating factors - Cytokines
90
What cell types produce cytokines?
Lymphocytes, macrophages, epithelial cells
91
What cell-derived inflammatory mediators are produced by the liver and via what system?
- Factor XII activation: kinin system (bradykinin), coagulation/fibrinolysis system - Complement activation: C3a and C5a (anaphylatoxins), C5b, C5b-9 (MAC)
92
What inflammatory mediators are principally involved in vasodilation?
- Nitric oxide - Bradykinin - Prostaglandins (PGE2)
93
What inflammatory mediators are principally involved in chemotaxis, leukocyte activation?
- Leukotrienes - C5a - Chemokines e..g IL-8, IL-5 - BActerial products e.g. LPS, teichoic acid - Defensins
94
What inflammatory mediators are principally involved in increased vascular permeability?
- Vasoactive amines like histamine - Complement factors like C5a, C3a - Leukotrienes - PGE2 - PAF< IL-1, TNF
95
What inflammatory mediators are principally involved in fever?
Cytokines e.g. IL-1, NF, IL-6
96
What inflammatory mediators are principally involved in smooth muscle contraction?
- Histamine - Serotonin - C3a - PAF
97
What inflammatory mediators are principally involved in tissue damage
- Neutrophil granule content - matrix metalloproteinases | - ROS
98
What is the role of arachidonic acid metabolites in acute inflammation?
- 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
Outline the arachidonic acid pathway production of prostaglandins
- 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
Where do NSAIDs act to reduce inflammation?
Interfere with COX enzyme to prevent production of proinflammatory PGs
101
What is the fate of arachidonic acids metabolised by 5-lipoxygenase?
Produces leukotrienes (chemokines), leading to chemotaxis, vasoconstriction, bronchospasm and increased vascular permeability
102
What happens if 5-HPETE (product of arachidonic acid 5-lipoxygenase metabolism) is metabolised by 12-lipoxygenase?
- Produces lipoxin A and B | - Inhibit neutrophil adhesion and chemotaxis
103
What is the effect of thromboxane A?
Causes vasoconstriction, promotes platelet aggregation
104
What are the different types of effusions?
Transudate and ecudate
105
What is transudation?
- Fluid leaks out of blood vessel due to increased hydrostatic pressure or decreased osmotic pressure - Only fluid leakage, no protein lost
106
What may lead to transudation?
- Increased cardiac output | - Decreased protein present in capillaries
107
What is exudation?
- Forms in inflammation due to increased vascular permeability - Increased interendothelial spaces - Proteins lost
108
What may lead to ecudation
- Inflammation
109
Give the key features of transudate
- Extravascular filtrate of plasma - Little protein present - Few or no measurable nucleated cells - Fluid appears grossly clear and watery
110
Give the key features of exudate
- Inflammatory - Extravascular fluid that is rich in protein (fibrinogen) and or cells - Grossly appears cloudy or viscous
111
What is meant by serous inflammation?
Accumulation of mucinous secretory products | - Can be catarrhal: mucosal eptihelium thickened, thick layer of clear mucus
112
What is fibrinous inflammation?
- Characterised by strands of fibrin derived from protein-rich exudate - Friable exudate,scrambled eggs appearance - Consists of fibrin plus other plasma proteins
113
What is purulent/suppurative inflammation?
- Pus | - Numerous PMNs present
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