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Pathology > Pathology 2 > Flashcards

Pathology 2 Flashcards

1
Q

What are the forms of repair?

A

Regeneration and scarring

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2
Q

What’s regeneration?

A

Repair with the growth of fully functional tissue to replace injured or dead tissue

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3
Q

What is required for total pure regeneration?

A

An intact connective tissue scaffold or only superficial injury (so it’s rare)

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4
Q

What’s a superficial injury?

A

Only affects epidermal or epithelial layer

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5
Q

Scarring replaces injured/dead tissue with ______.

A

Fibrous tissue lacking the specialized function of the tissue it replaces

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6
Q

What’s the most common scenario of wound repair?

A

A regeneration/scarring combo

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7
Q

Removal of one kidney causes _______. Is this regeneration?

A

Hyperplasia and hypertrophy of the remaining kidney, which doubles in size. Nope, not regeneration.

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8
Q

Removal of one lobe of the liver causes ______. Is this regeneration?

A

Hyperplasia and hypertrophy of the remaining lobe, which generate the same volume of fully functional liver tissue as pre-removal. Yep, regeneration.

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9
Q

What’s an ulcer?

A

A local defect in the surface of an organ or tissue produced by shedding of inflamed necrotic tissue

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10
Q

What’s an erosion?

A

Superficial sloughing of mucosa (or epidermis)

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11
Q

T or F: Ulcers are too deep to heal by regeneration.

A

T

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12
Q

What’s an adhesion?

A

An abnormal connection between any two things in the body

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13
Q

Early on, adhesions are composed primarily of _____. What is this called?

A

Fibrin, fibrinous

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14
Q

Later on, adhesions are referred to as _____.

A

Fibrous

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15
Q

What’s a fistula?

A

An abnormal opening between two places in the body

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16
Q

T or F: Fibrous adhesions are an inevitable side-effect of surgery.

A

T

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17
Q

What’s a common complication of fibrous adhesions?

A

Intestinal obstruction

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18
Q

_________ cells have self-renewal capacity.

A

Stem

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19
Q

Stem cells undergo ____ replication.

A

Asymmetric: in every division, one daughter cell retains self-renewing capacity and the other enters a differentiation pathway to a mature cell.

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20
Q

What are pluripotent stem cells?

A

They can give rise to any tissue

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21
Q

T or F: Adult stem cells can give rise to any tissue.

A

F: Limited number of tissues

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22
Q

What is the replicative capacity of labile cells?

A

They continuously lose cells and replace them by proliferation of mature cells and stem cells

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23
Q

What are examples of labile tissues?

A 
Skin and linings of the mouth
GI tract
Bladder
Vagina
Cervix
Uterus
Fallopian tubes
Exocrine gland ducts
Bone marrow
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24
Q

What is the replicative capacity of stable cells?

A

They’re composed of cells capable of proliferation, but they’re not normally called on to proliferate

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25
Q

What are examples of stable tissues?

A 
Liver
Kidney
Pancreas
Smooth muscle tissues
Blood vessel linings
Fibroblasts
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26
Q

What is the replicative capacity of permanent cells?

A

They don’t proliferate except under extraordinary circumstances

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27
Q

What are examples of permanent tissues?

A

Parenchymal cells of the brain and heart (neurons and cardiac myocytes)

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28
Q

Which tissues are particularly vulnerable to radiation injury?

A

Continuously proliferating labile tissues

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29
Q

Erythema

A

Redness

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30
Q

Pruritis

A

Itching

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31
Q

Desquamation

A

Sloughing

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32
Q

Side effects of radiation

A
  • Skin: erythema, pruritis, desquamation, loss of hair
  • Chest/Abdomen: vomiting, nausea, diarrhea
  • Bone marrow: Leukopenia
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33
Q

The process of healing is orchestrated by _____.

A

Growth factors

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34
Q

What does EGF stimulate?

A

Fibroblast migration and proliferation

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35
Q

What does FGF stimulate?

A

Fibroblast migration and proliferation
Monocyte chemotaxis
Angiogenesis

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36
Q

What does PDGF stimulate?

A

Fibroblast migration and proliferation
Monocyte chemotaxis
(more prevalent early in the process)

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37
Q

What does TGF-beta stimulate?

A

Fibroblast migration and proliferation
Monocyte chemotaxis
Collagen synthesis

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38
Q

T or F: TGF-beta is more prevalent early in the repair process.

A

F: more prevalent later in the process

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39
Q

What growth factors mediate monocyte chemotaxis?

A

PDGF, FGF, TGF-beta

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40
Q

What growth factors mediate fibroblast migration and proliferation?

A

PDGF, EGF, FGF, TGF-beta

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41
Q

What growth factors mediate angiogenesis?

A

FGF and VEGF

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42
Q

What growth factors mediate collagen synthesis?

A

PDGF and TGF-beta

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43
Q

What comprises the extracellular matrix?

A

Basement membrane and interstitium

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44
Q

Where is the basement membrane of the ECM?

A

Right underneath the epithelium and around blood vessels

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45
Q

What’s the interstitium of the ECM?

A

Supporting tissue between epithelium and vessels and between cells in connective tissue

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46
Q

What does the interstitium of the ECM contain?

A

Fibrillar collagen, fibrillin, elastin, hyaluronic acid, and proteoglycans

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47
Q

Which types of collagen are fibrillar?

A

I, II, III, and V

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48
Q

Review time! What’s the general structure of collagen?

A

3 polypeptide chains braided into a ropelike triple helix

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49
Q

What strengthens fibrillar collagen?

A

Lateral cross links

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50
Q

What are characteristics of the classical form of Ehlers-Danlos syndrome?

A
  • A disease that causes defective type V collagen, leading to hypermobile joints and hyperextensible skin
  • Autosomal dominant
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51
Q

What are characteristics of the vascular type of Ehlers-Danlos syndrome?

A
  • It causes defective type III collagen, which is prevalent in blood vessels and bowel wall
  • Autosomal dominant
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52
Q

What are characteristics of the kyphoscoliotic type of Ehlers-Danlos syndrome?

A
  • It’s due to deficiency of lysyl hydroxyls enzyme, which impairs the cross linking of type I and III collagen
  • Results in crooked spines
  • Autosomal recessive
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53
Q

Fibrillin is secreted by ______ and is a major component of _____.

A

Fibroblasts, microfibrils

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54
Q

Microfibrils serve as scaffolding for the deposition of ________, an integral component of elastin.

A

Tropoelastin

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55
Q

What are the characteristics of Marfan syndrome? :(

A
  • Caused by defects in the fibrillin gene
  • Long body, long limbs, fingers, and toes
  • Aorta prone to rupture
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56
Q

Loss of microfibrils leads to _____.

A

Excessive TGF-Beta

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57
Q

What is being evaluated as treatment for Marfans?

A

ARBs (angiotensin receptor blockers) that inhibit the activity of TGF-Beta, which is in excess in Marfan syndrome

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58
Q

What enzymes catalyze the formation of the covalent bonds cross-linking fibrillar collagen? What cofactor is needed?

A

Prolyl hydroxylase and lysyl hydroxylase; Vitamin C

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59
Q

What happens in vitamin C deficiency?

A

It weakens blood vessels, resulting in bleeding and poor wound healing

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60
Q

What pattern of inheritance do genetic defects in structural proteins tend to have?

A

Autosomal dominant

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61
Q

What pattern of inheritance do genetic defects in enzymes tend to have?

A

Autosomal recessive

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62
Q

What’s granulation tissue?

A

Healing tissue with residual chronic inflammatory cells, cellular debris, fibroblasts, neovascularization, and new collagen

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63
Q

What does granulation tissue look like?

A

Red or pink, soft, and granular

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64
Q

What are the number 1 and 2 features that are most characteristic of granulation tissue?

A
  1. Angiogenesis

2. Proliferating activated fibroblasts

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65
Q

What makes granulation tissue soft?

A

The new blood vessels of early granulation are leaky and the fluid that leaks out of them makes granulation tissue soft

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66
Q

What makes granulation tissue hard?

A

Replacement of granulation tissue by scar

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67
Q

What is organization?

A

The process replacing injured, necrotic, and inflamed tissue by healing and scar tissue

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68
Q

Who’s the key player in the process of organization?

A

Fibroblast

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69
Q

What’s the order of cell appearance in skin wound inflammation and healing?

A
  1. Neutrophils
  2. Macrophages
  3. Fibroblasts
  4. Lymphocytes
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70
Q

What’s the order of cell appearance in MI inflammation and healing?

A
  1. Neutrophils
  2. Lymphocytes
  3. Macrophages
  4. Fibroblasts
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71
Q

What do macrophages do in skin wounds?

A

Come early, peak fast, and leave fast

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72
Q

What do macrophages do in MI?

A

Come late, peak slowly, and persist for weeks

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73
Q

What’s angiogenesis?

A

The formation of new blood vessels in healing tissue, tumors, and atherosclerosis

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74
Q

What mediates angiogenesis?

A

VEGF (which also increases vascular permeability, endothelial migration, and proliferation)

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75
Q

How does angiogenesis work in skin wounds?

A

Starts early, peaks soon, and dissipates fast

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76
Q

How does angiogenesis work in MI?

A

Begins simultaneously with fibroblast infiltration on day 4, and persists for weeks

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77
Q

What are the phases of skin wound healing?

A

Inflammation
Proliferation
Maturation

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78
Q

When does healing by first intention occur?

A

When wounds are clean, uninfected, and have their edges approximated by sutures

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79
Q

When does healing by second intention occur?

A

In larger wounds with commonly irregular edges

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80
Q

In healing by first intention, on what day do all the playas come in?

A

1: Neutrophils
2: Epithelial cells
3: Macrophages
4: Fibroblasts
5: Granulation, angiogenesis
7-14: Collagen

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81
Q

What happens in healing by second intention?

A
  • A larger blood clot fills the space of the wound
  • More intense inflammation and more granulation tissue
  • Wound contraction by myofibroblasts
  • Scar formation
  • Tissue remodeling
  • Thinning of epidermal layer
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82
Q

The third phase of healing is a matter of ______.

A

Tissue remodeling, which alters the cellular content and extracellular matrix

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83
Q

What is the “high point” of healing?

A

The proliferative phase (middle phase)

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84
Q

What are the most characteristic features of the proliferative phase?

A
  1. Angiogenesis

2. Fibroblast proliferation

85
Q

What is the most important growth factor driving angiogenesis?

A

VEGF

86
Q

What do VEGF growth factors do?

A

Stimulate migration and proliferation of endothelial cells at the site of injured blood vessels, which sprout new blood vessels

87
Q

When is neovascularization harmful?

A

In some retinal diseases such as wet diabetic retinopathy, macular degeneration, and retinopathy of prematurity

88
Q

How do you treat retinal diseases where neovascularization is harmful?

A

By injecting antibody to VEGF into the eye

89
Q

What is the most important growth factor driving fibroblast migration, proliferation, and collagen synthesis?

A

TGF-beta

90
Q

Remodeling of ECM requires ________.

A

Breaking down collagen and other matrix components

91
Q

What enzymes assist in the break down of collagen and other ECM components? (5)

A 
Matrix metalloproteinases (MMP-1, 2, etc)
Cathepsin G
Plasmin
Neutrophil elastase
Serine proteinases
92
Q

Matrix metalloproteinases depend on ____ for their action.

A

zinc

93
Q

How are MMPs controlled?

A

By TIMPS (tissue inhibitors of metalloproteinases) and by tight control of their synthesis and secretion

94
Q

How does location of a wound affect its healing?

A

Relative blood supply determines how well a wound heals

95
Q

What can impair wound healing?(11)

A
  1. Infection
  2. Age
  3. Diabetes
  4. Anemia
  5. Corticosteroids
  6. Mechanical stress
  7. Poor perfusion
  8. Foreign material
  9. Obesity
  10. Chemo/radiation
  11. Fibroblast aberrancy
96
Q

What is the most important cause of impaired wound healing?

A

Infection

97
Q

How can corticosteroids delay wound healing?

A

By inhibiting protein and collagen synthesis

98
Q

How can diabetes mellitus impair wound healing?

A

Primarily because of microangiopathy (small blood vessel disease) associated with it, but it also pours excess sugar into the wound (nutrients for infecting organisms)

99
Q

How can anemia delay wound healing?

A

It decreases oxygen delivered to the site of repair

100
Q

Why was grandma right about not picking your scabs?

A

It can disrupt the underlying partial epidermal layer and granulation tissue, setting back the healing process

101
Q

What’s dehiscence?

A

Rupture of a surgical wound or anastomosis

102
Q

What’s a hernia?

A

Protrusion of a body part somewhere it doesn’t belong

103
Q

Keloid

A

Hypertrophic scar

104
Q

Contracture

A

Abnormal excess wound contraction resulting in deformity and impaired movement

105
Q

Where is contracture most common and what disease is associated with it?

A

Palms (Dupuytren’s contracture)
Soles (Lederhosen disease)
Penis (Peyronie disease)

106
Q

What’s fibrosis?

A

Excessive interstitial collagen deposition usually due to chronic inflammation, recurring injury, persistent toxin, radiation, or autoimmune attack

107
Q

What causes the WORST fibrosis? And why?

A

Autoimmune diseases because the inciting agent is continually present and can’t be limited or eliminated

108
Q

What’s scleroderma?

A

It shows how bad fibrosis can be! Progressive fibrosis of the fingers until they’re fixed into a claw hand, sometimes with gangrene of the fingertips. The face undergoes fibrosis until its frozen into an “iron mask”. It kills peristalsis to move food into the stomach. It also leads to renal failure. Basically your life is the worst.

109
Q

Who made the link of disease to malfunction at the cellular level?

A

Virchow

110
Q

What are common causes of cell injury? (7)

A
  1. Oxygen deprivation
  2. Physical agents/trauma
  3. Chemical agents and drugs
  4. Infectious agents
  5. Immunologic reactions
  6. Genetic derangements
  7. Nutritional imbalances
111
Q

T or F: All cells have potential for exhibiting both reversible and irreversible cell injury.

A

T

112
Q

If an injurious stimulus is such that a cell can recover, you’ll see ______.

A

Reduction in biochemical and physiological function

113
Q

T or F: You’ll see gross pathologic changes due to cell injury first.

A

Nope, you’ll see those last

114
Q

Atrophy

A

Decrease in the size and function of a cell or organ

115
Q

Common causes of atrophy (6)

A
  1. Disuse
  2. Loss of innervation
  3. Diminished blood supply
  4. Inadequate nutrition
  5. Loss of endocrine stimulation
  6. Aging
116
Q

What are gyri vs. sulci?

A

Gyri: brain substance
Sulci: spaces between the substance of the brain

117
Q

If you have brain atrophy, what happens to the sulci?

A

They get bigger

118
Q

Hypertrophy

A

Increase in size of a cell caused by an augmented functional demand or specific hormonal stimulation

119
Q

Growth in the size of uterine muscle fibers during pregnancy is an example of _______.

A

Physiologic hypertrophy

120
Q

Increased thickness of the left ventricular wall of the heart in systemic hypertension is an example of ______.

A

Pathologic hypertrophy

121
Q

Hyperplasia

A

Increase in the number of cells in an organ or tissue

122
Q

Increased number of lactational units in the breast during pregnancy is an example of ______.

A

Physiologic hyperplasia

123
Q

What’s an example of pathologic hyperplasia?

A

Benign prostatic hyperplasia

124
Q

Malignancy of epithelial tissue is known as ______.

A

Carcinoma

125
Q

Polyploidy

A

The state of a cell nucleus containing three or more haploid chromosomal sets

126
Q

T or F: Polyploidy may occur naturally or as cellular adaptation.

A

T

127
Q

T or F: Polyploidy is an indicator of unrestricted cell growth.

A

It’s an indicator but it doesn’t always indicate unrestricted cell growth

128
Q

Metaplasia

A

Conversion of one differentiated cell type to another differentiated cell type

129
Q

T or F: Metaplasia is irreversible.

A

F

130
Q

What are the types of metaplasia?

A

Epithelial metaplasia and mesenchymal metaplasia

131
Q

Epithelial metaplasia commonly occurs as a precursor to ______.

A

Dysplasia/neoplasia

132
Q

T or F: Mesenchymal metaplasia is commonly preneoplastic.

A

F: rarely if ever

133
Q

What effects can smoking have on respiratory epithelium?

A

Can change pseudoolumnar ciliated epithelium to squamous epithelium

134
Q

What effects can HPV have on cervical epithelium?

A

Can change columnar to squamous

135
Q

Dysplasia

A

Alteration of size, shape, and organization of the cellular components of a tissue

136
Q

What are the characteristics of dysplasia?

A
  • abnormal size and shape of cells
  • enlargement, irregularity, and hyperchromasia of the nuclei
  • disorderly arrangement of cells within the epithelium
  • generally a preneoplastic condition
137
Q

T or F: Dysplasia is almost always preneoplastic.

A

T

138
Q

Which pigments are brown?

A
  • Iron compounds
  • Lipofuschin
  • Melanin
139
Q

What entities are responsible physiologically for iron stores?

A

Ferritin and hemosiderin

140
Q

What is the principal storage form of iron?

A

Ferritin

141
Q

What does hemosiderin consist of?

A

Intracellular granules in iron-storing cells

142
Q

What is hemochromatosis?

A

A hereditary disorder in which too much iron is absorbed or retained

143
Q

What is hemosiderosis?

A

Iron overload due to systemic or local causes

144
Q

Hemosiderin is visible by _____.

A

Routine microscopy

145
Q

Hemochromatosis is an (exogenous/endogenous) disease of iron storage, and hemosiderosis is (exogenous/endogenous).

A

Hemochromatosis: endogenous
Hemosiderosis: exogenous

146
Q

What stain can be applied to brown iron pigment to make it blue?

A

Prussian blue stain

147
Q

What’s lipofuschin?

A
  • “Wear and tear pigment”
  • A brown pigment of aging
  • A polymer of oxidized lipids which are present in long-lived cells
148
Q

What’s melanin?

A
  • Brown pigment normally present in the basal layer of skin, retina, and some other ectodermal derived tissues
  • Absorbs harmful UV light
149
Q

Black pigments encountered in pathology most often include ______.

A

Carbon

150
Q

What is anthracosis?

A

Black pigment grossly and microscopically in the lungs, pulmonary lymph nodes, and in distant tissues
-Permanent but harmless as long as surrounding tissues don’t react to the carbon

151
Q

What happens when silica is inhaled at the same time as carbon?

A

Bad things happen

152
Q

What benefit does proper calcification provide?

A

Maintains our skeletal framework

153
Q

What is dystrophic calcification?

A
  • Generally localized process, related to some tissue injury

- Plasma calcium levels are normal

154
Q

What is metastatic calcification?

A
  • Generalized process, may be calcification of many tissues
  • Calcium levels may be elevated
  • May be disarrangement of the balance between calcium and phosphate
155
Q

Which is more common: dystrophic or metastatic calcification?

A

Dystrophic

156
Q

Calcium salts using _________ and _______ stain are purple.

A

Hematoxylin and eosin

157
Q

When does dystrophic calcification have a positive clinical use?

A

In mammograms

158
Q

Why might water and electrolytes leak into cells?

A

Due to vacuole formation or to hydropic swelling

159
Q

T or F: Hydropic swelling is an early indicator of cell damage.

A

T

160
Q

Which lipids may accumulate in cells under abnormal conditions?

A

Triglycerides and cholesterol

161
Q

What is xanthelasma?

A

Soft, yellow, orange-like plaques on the eyelids or on the medial canthus; they represent abnormal lipid deposition

162
Q

How are triglycerides seen grossly?

A

As yellow, greasy deposits in diseased organs whose cells are engorged with triglyceride droplets and vacuoles (Steatosis)

163
Q

Where is steatosis most common?

A

Liver (most common!), but also in heart, skeletal muscle, and kidney cortex

164
Q

What is kwashiorkor?

A
  • A disease related to a low protein/high carb diet

- Results from the lack of protein synthesis and retention of lipid components

165
Q

Abnormal deposition of cholesterol can lead to _______.

A

Can lead to severe disease or may only be a histologic curiosity

166
Q

________ may increase intracellularly in conditions such as diabetes or hypoxia.

A

Glycogen

167
Q

Where might you see a Laffora body?

A

In some severe CNS diseases

168
Q

Where might you see corpora amylaceae?

A

Typically extracellular; may be seen in the meninges, ventricles, and in the ependyma
-generally of no significance

169
Q

What is Mallory’s alcoholic hyalin?

A

Condensed cytoskeletal protein seen in the cytoplasm of patients who have been exposed to alcohol in extreme amounts over long periods of time

170
Q

Homeothermic

A

Capable of maintaining body temperature within very narrow limits

171
Q

What temperature reflects the temperature of the core of the body most accurately?

A

The esophagus at the cardia

172
Q

Normal body temperature can vary due to ___________.

A

Exogenous or endogenous factors

173
Q

What are examples of exogenous factors that can change the normal core temperature?

A 
Climatological environment
Peripheral insulation
Diet
Physical activity
Drugs
174
Q

What are examples of endogenous factors that can change the normal core temperature?

A 
Rhythms (i.e. circadian rhythm)
Gender
Age and body size
Subcutaneous insulation
Water content
Physiological state
175
Q

Most energy is lost as ____.

A

Heat

176
Q

Total energy expenditure =

A

Internal heat produced + external work performed + energy stored

177
Q

Radiation

A

Heat transmitted via electromagnetic waves

178
Q

Conduction

A

Heat transfer within a solid or between two or more solids in close contact

179
Q

Convection

A

Heat transfer in a fluid or between a fluid and a solid

180
Q

Evaporation

A

Heat transfer by means of a change in state, from a liquid to a gas.

181
Q

What factor affects evaporation?

A

Humidity – dry air increases evaporation, humid air decreases evaporation

182
Q

What is the zone of thermal neutrality?

A

The range of ambient temperature in which the body maintains its heat balance without increasing heat production or loss above their minimum level

183
Q

T or F: Higher the ratio SA/V, higher the heat loss.

A

T duhh

184
Q

What serves as the primary overall integrator of reflexes and the brain’s inner thermostat?

A

Hypothalamus

185
Q

Where are warm fibers located?

A

In Ruffini’s corpsucles

186
Q

Where are cold fibers located?

A

In the end-bulb of Krause

187
Q

What effect does epinephrine have on metabolic activity?

A

It increases metabolic activity

188
Q

(Vasodilation/Vasoconstriction) leads to reduced heat loss.

A

Vasoconstriction

189
Q

Neonatal ______ may occur if brown fat is lacking.

A

Hypothermia

190
Q

How does thyroid hormone affect metabolic rate and heat production?

A

TH acts on the sodium/potassium pump and increases O2 consumption. This increases metabolic rate and heat production.

191
Q

(Hot/Cold) temperatures activate thyroid hormone.

A

Cold

192
Q

What is the relationship between hyperthyroidism and temperature control?

A

Metabolic rate is increased so heat production increases

193
Q

What is the relationship between hypothyroidism and temperature control?

A

Metabolic rate decreases and there is decreased heat production (extreme sensitivity to cold)

194
Q

What must happen for thyroid hormones to be maximally active?

A

The sympathetic nervous system must be simultaneously activated by cold temperatures

195
Q

Sweating is accomplished through _______.

A

Specialized eccrine sweat glands found in the dermis and epidermis

196
Q

Where don’t we have eccrine sweat glands?

A

Margins of the limbs, sex organs, and ear drums

197
Q

Sweat glands consist of __________.

A

A deep coiled portion and a duct that opens on the skin

198
Q

The duct of the sweat gland aids in ________.

A

Resorption of electrolytes (mainly Na and Cl) in the sweat so that the fluid discharged onto the skin has a reduced electrolyte concentration

199
Q

Why do we shiver?

A

It results from somatic activation of skeletal muscles which asynchronously contract.

200
Q

How can you suppress shivering?

A

It’s normally involuntary, but it can be suppressed by higher cortical input (a learned process)

201
Q

What are differences in body temperature in men and women?

A
  1. Core body temperature cools more slowly in women
  2. Women can’t create as much metabolic heat through exercise or shivering
  3. The rate of cooling of the extremities is faster among women
202
Q

What does the body do during heat exhaustion?

A
  • Vasodilation

- Excess sweating –> decreases ECF volume –> decreased blood volume –> decreased arterial pressure –> fainting

203
Q

What does the body do in heat stroke?

A

The body temperature increases to a point of tissue damage

204
Q

What is malignant hyperthermia?

A

A usually hereditary condition where there is a massive increase in metabolic rate

205
Q

What are the differences between fever and hyperthermia?

A
  1. Fever is regulated, hyperthermia is an impairment
  2. Fever is independent of ambient temperature, and hyperthermia is dependent on ambient temperature
  3. Fever has increased thermopreferendum, and hyperthermia has decreased thermopreferendum
206
Q

What are some microbial stimuli that can induce fever?

A

Viruses, bacteria, mycobacteria, and fungi

207
Q

What are some non-microbial pathogenic stimuli that can induce fever?

A

Antigens, inflammatory agents, plant lectins, or host-derived stimuli

208
Q

What are the benefits of fever?

A
  • enhanced neutrophil migration and T-cell proliferation
  • enhanced phagocytosis
  • increased IFN production/activity
  • increased radical production
  • reduced growth rate and viability of iron-dependent microorganisms
  • increased survival rate
209
Q

What are some hazardous effects of high or prolonged fever?

A
  • dehydration
  • delirium
  • cardiopulmonary strain
  • negative nutrient balance
  • teratological consequences

Pathology (4 decks)

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