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Immuno/Pathology and Physiology > Pathology Week 2 > Flashcards

Pathology Week 2 Flashcards

1
Q

What percentage water is the body? Where is the water?

A

60%. 40% of the 60% is intracellular, 15% interstitial, 5% intravascular

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2
Q

Osmolality

A

Concentration of particles in a solution

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3
Q

Osmolarity

A

Osmolality in the blood

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4
Q

Normal plasma osmolality

A

280mosm/L

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5
Q

What is driving force

A

Osmolality difference

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6
Q

What has equal osmolarity?

A

intravascular, interstitial, and intracellular spaces

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7
Q

What has equal concentration of small solutes?

A

The extracellular spaces - interstitial and intravascular

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8
Q

How are water soluble substances transported?

A

via solvent drag

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9
Q

What is oncotic pressure

A

A type of osmotic pressure created by proteins

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10
Q

What two pressures are involved in filtration (movement out of capillary)?

A

Capillary hydrostatic pressure and interstitial oncotic pressure

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11
Q

What two pressures are involved in absorption (movement in)?

A

Capillary oncotic pressure and interstitial hydrostatic pressure

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12
Q

Starling’s Equation?

A

Jv=Kf(filtration-absorption) where Jv is fluid movement, Kf is hydraulic conductance

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13
Q

Normal net fluid movement

A

Out at beginning of capillary, in at end.

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14
Q

Where does excess filtered fluid go?

A

Returned to circulation by lymphatics

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15
Q

Hypoalbuminemia

A

Oncotic pressure of capillary too low, more filtered out than reabsorbed. Comes from severe protein malnutrition and leads to Kwashiorkor

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16
Q

Congestive heart failure

A

Elevated hydrostatic pressure. Right sided failure leads to peripheral edema, left sided leads to pulmonary edema.

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17
Q

Sepsis and inflammation

A

From increased hydraulic conductance. Capillary leak syndrome in meningitis.

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18
Q

Lymphatic impairment

A

Can be surgical or mechanical, leads to lymphedema (eg post mastectomy

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19
Q

What is edema?

A

Too much interstitial fluid.

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20
Q

What is anasarca?

A

Generalized edema

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21
Q

What are effusions?

A

Excess fluid in body cavities, considered edema (eg hydrothorax/pleural effusion)

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22
Q

What is a transudate?

A

Type of edema. Accumulations of salt water with very low protein content and low specific gravity. Occurs when hydrostatic pressure pushes water and salt out of normal vessels and exceeds the ability of lymphatics to drain. Due to increased intravascular hydrostatic pressure, decreased intravascular osmotic pressure, increased sodium retention from renal dysfunction, and lymphatic obstruction. Pitting edema.

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23
Q

What is an exudate?

A

Protein rich accumulations of salt water. Occurs when vessels are permeable and leak protein. Seen with inflammation. Occurs in anaphylaxis.

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24
Q

Hemostasis

A

Arrest of hemorrhage. Blood coagulation, platelet coagulation, endothelial cell interactions

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25
Q

Thrombus

A

coagulated blood containing platelets, fibrin, and entrapped cells

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26
Q

Extrinsic clotting pathway

A

Plasma contacts Tissue Factor (imp for de novo coagulation)>Factor VII>Factor X>Prothrombin>Thrombin>Fibrinogen>Fibrin. Clotting also triggers fibrinolysis, which determines size of thrombus.

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27
Q

Intrinsic clotting pathway

A

More important in lab analysis, involves Hageman factor

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28
Q

Role of platelets in thrombosis

A

primary hemostatic plug. Von Willebrand factor binds platelets to underlying collagen. Aggregation activated by thromboxane A and ADP. Prostacyclin and nitric oxide inhibit platelet aggregation.

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29
Q

Virchow’s Triad (causes of thrombosis)

A

Endothelial injury, alteration in flow, hypercoagulable blood.

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30
Q

Examples of endothelial injury

A

Endothelial injury can come from athersclerotic plaques, inflamed cardiac valves (endocarditis), inflamed vessels (vasculitis), MI, latrogenic (caused by medical treatment - e.g. catheters), hypertension, turbulent blood flow.

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31
Q

Examples of altered blood flow

A

Atrial fibrillation (left atrium stops contracting, wiggles), aneurysms, atherosclerotic plaques, dilated cardiac ventricles, and obstruction (imp. in venous thrombi due to stasis which predisposes to thrombosis).

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32
Q

Hypercoagulable blood

A

Primary is inherited, secondary is acquired. Primary includes Factor V Leiden, prothrombin gene mutation, Protein C or S deficiency, Antrithrombin III deficiency and homocystinuria. Secondary are pregnancy and OCPS, cancer, antiphospholipids, polycythemia (too many RBCs)

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33
Q

Lines of Zahn

A

Alternating layers of fibrin/platelets and RBCs indicative of thrombus formation in flowing blood

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34
Q

Clot

A

Blood solidified outside of vascular system or postmortem. Not attached to wall or vessel. Separates into two components. No lines of Zahn.

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35
Q

Things thrombi can do

A

Propagate, lyse, organize and recanalize, become infected, embolize

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36
Q

Embolus

A

Anything other than liquid blood that can travel through and lodge somewhere.

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37
Q

Thromboemboli

A

Most common are pulmonary emboli. DVTs often source. Sudden death. Pulmonary hemorrhage.

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38
Q

Arterial emboli

A

Occlude organs. Sources are heart and atherosclerotic vessels

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39
Q

Paradoxical embolus

A

Thrombus in venous or right sided circulation that sends embolus into systemic circulation. Must shunt through heart - through atria via patent foramen oval (20-25% of people don’t have full closure). Ex: DVT of lower extremity that leads to embolic infarct of brain.

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40
Q

Atheroemboli

A

Debris from ruptured atherosclerotic plaques. Cholesterol crystals in blood vessels.

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41
Q

Air embolism

A

The bends! Can happen in delivery, chest trauma, cardiac surgery.

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42
Q

Fat embolism

A

After fractures, ortho surgery.

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43
Q

Infarction

A

Irreversible tissue necrosis due to ischemia in discrete area. Coagulative necrosis (hypereosinophilia and absence of nuclei)

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44
Q

Ischemia

A

An imbalance of oxygen supply and demand due to loss of blood flow from obstructed arterial flow or reduced venous drainage

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45
Q

White infarcts

A

Obstruction of arterial supply and single blood source and not reperfused and solid tissue.

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46
Q

Red infarcts

A

venous insufficiency or dual blood supply or reperfused and loose tissue

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47
Q

Disseminated Intravascular Coagulation (DIC)

A

Excessive secondary coagulation (from TF release of endothelial damage) from thrombi in the microvasculature - micro infarctions. Depletes clotting factors and platelets, and bleeding diathesis ensues to lack of hemostasis - shock from hemorrhage. You see schistocytes (fragmented RBCs in blood smear)

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48
Q

Shock definition and causes

A

circulatory collapse - global hypotension with hypo perfusion of tissues. 3 causes: hypovolemia (hemorrhage), cardiogenic (MI, arrhythmia), sepsis (microbial infection).

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49
Q

Shock pathophysiology

A

Lactic acidosis from anaerobic respiration. Hypotension. Tissue ischemia and necrosis. Multisystem organ failure.

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50
Q

Septic Shock

A

Secondary to infection, due to capillary leak syndrome. Vasodilation and vascular permeability. Frequently leads to DIC.

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51
Q

Stages of shock

A

Nonprogressive/compensated: blood pressure maintained, no urine output, tachycardia, peripheral vasoconstriction, recovery possible. Progressive/uncompensated: renal failure, BP down which leads to lactic acidosis. Irreversible: BP and pH down, organs die, death.

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52
Q

Pathology of shock

A

Necrosis of areas furthest from arterial supply and necrosis of vulnerable cells - neuronal cells and tubular kidney cells

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53
Q

Hypertrophy

A

Increase in size of cell due to increased # organelles. Can be caused by high blood pressure (myocardial hypertrophy), unilateral nephrectomy, pregnancy (myometrial hypertrophy).

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54
Q

Hyperplasia

A

Increase in number of cells. Can occur in nursing glandular breast tissue, chronic blood loss (erythroid hyperplasia),

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55
Q

Atrophy

A

Decrease in size and function of cell. Can also decrease number of cells. Menopause, aging, immobilization, starvation. Cells initiate autophagy for breakdown of organelles

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56
Q

Metaplasia

A

Replacement of one differentiated tissue with another differentiated tissue (reprogramming of stem cells).

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57
Q

Intracellular storage problems

A

Triglycerides in alcoholic liver, hemosiderin (breakdown product of Hgb) in hemochromatosis, sphingomyelin in Niemann Pick, precursor tyrosine metabolites in hereditary tyrosinemia, mucopolysaccharides in Hurler syndrome, partially folded precursor proteins in Alpha 1 antitrypsin deficiency (leads to liver scarring from entrapment of alpha 1 and pulmonary emphysema due to lack of alpha 1), carbon dust - pulmonary fibrosis or coal workers pneumoconiosis

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58
Q

Hydropic Changes in Cells

A

influx of sodium and water into damaged cell, reversible

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59
Q

Reversible vs. Irreversible cell injury

A

Swelling of organelles, disaggregation of ribosomes, cytoplasmic blebs all reversible, calcium deposits within mito, disrupted plasma membrane, fragmentation of organelles all irreversible

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60
Q

Dystrophic calcification

A

Occurs within injured tissues, normal serum calcium and normal calcium metabolism. Ex: heart valves, atherosclerotic blood vessels, areas of necrosis, neoplasms. Used for breast CA dx.

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61
Q

Metastatic calcification

A

Occurs within normal tissues, increased serum calcium levels, derangement of calcium metabolism (hyperparathyroidism, destruction of bone, Vit. D tox, chronic renal failure)

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62
Q

Coagulative necrosis

A

common sequela of ischemic injury. Denaturation, cells lose nuclei but retain original structure

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63
Q

Pyknosis

A

Irreversible condensation of chromatin in nucs

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64
Q

Karyorrhexis

A

Fragmentation of nucs

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65
Q

Karyolysis

A

Loss of nucs

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66
Q

Liquefactive necrosis

A

Common sequela of bacterial or fungal infection. Forms abscess (localized collection of pus), breakdown of underlying tissue

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67
Q

Caseous necrosis

A

Common sequela of tuberculosis. Can also be caused by some fungi. Looks like amorphous eosinophilic debris

68
Q

Fat necrosis

A

Usually results of released of digestive enzymes as in pancreatitis

69
Q

Fibrinoid necrosis

A

typically seen in blood vessels in response to immune-mediated or hypertensive injury

70
Q

Apoptosis

A

Look for broken nucs. Involves caspases. Membrane blebbing. No inflammation. Involves single cells, not many.

71
Q

Necroptosis

A

Does not activate caspases. Programmed signal pathway but looks like necrosis. Does result in mito injury. Can be physiologic or pathologic.

72
Q

Huchinson-Gilford Progeria and Werner Syndrome

A

Both diseases of aging - heritable. HG is due to abnl intranuclear protein lamin A, W due to abnl DNA helicase.

73
Q

Caloric restriction

A

Lowering metabolic rate decreases ROS production, inhibits insulin/IGF-1 and MTOR pathways

74
Q

Advanced glycation end products (AGEs)

A

in tasty bad foods

75
Q

Sirtuin

A

The anti-aging protein activated by resveratrol (in red wine)

76
Q

Acute inflammation

A

Neutrophils accumulate, interstitial edema. Tissue must be vascularized. 3 main components: increased blood flow (vasodilation), vascular permeability, migration of neutrophils to site (exudate). Vascular stasis and congestion can occur secondary to fluid leakage from blood vessels. IL-1 and TNF involved.

77
Q

Chronic inflammation

A

Mononuclear cells accumulate (lymphocytes, plasma cells, macrophages), mixed with granulation tissue

78
Q

Mechanisms of endothelial permeability

A

Endothelial cell contraction (histamines, leukotrienes cause, fast and short lived). Endothelial cell retractions (delayed response from cytokines IL-1 and TNF, cytoskeleton rearrangement). Direct endothelial injury (from toxins, burns, chemicals). Neutrophil/leukocyte mediated cell injury (long lived, late response).

79
Q

Extravasation

A

Delivery of neutrophils to site

80
Q

Diapedesis

A

AKA transmigration of neutrophils across endothelium

81
Q

Selectins vs. integrins vs. PECAM

A

Selectins help catch and roll (different selectins for different cells - p-selectin for platelets) most bond to sialyl Lewis X on cells on cell being caught. Integrins firmly hold, found on surface of cell being caught. PECAM is involved in migration

82
Q

Neutrophil chemotactic agents

A

leukotriene B4, IL-8.

83
Q

What do neutrophils do when they arrive at site?

A

phagocytose bad stuff, release lysosomal contents and free radicals to interstitium (degranulation)

84
Q

Opsonins important in phagocytosis

A

IgG and C3b

85
Q

Bactericidal mechanism in phagolysosome

A

Oxygen dependent: NADPase activation and conversion of hydrogen peroxide in presence of halide. There is also an oxygen independent mechanism.

86
Q

Purulent

A

Exudate with prominent neutrophils

87
Q

Suppurative

A

purulent exudate plus tissue necrosis (pus).

88
Q

Fibrinous

A

Exudate containing fibrin due to leakage of blood vessels, coagulation cascade activated

89
Q

Ulcer

A

defect of the surface of and organ or tissue due to sloughing of inflamed necrotic tissue

90
Q

Vasoactive amines example (cell derived mediators of inflammation)

A

Histamine - preformed in mast cells, basophils, platelets. One of the first mediators in inflammatory response. Functions in vasodilation and vascular permeability.

91
Q

Arachidonic acid metabolite example (cell derived mediator of inflammation )

A

eicosanoids. for short range signaling. Thromboxane A2, Leukotrienes C4, D4, and E4. Prostaglandins.

92
Q

Platelet activating factor

A

phospholipid derived mediator from mast cells and other leukocytes. For platelet aggregation, bronchoconstriction, vasodilation

93
Q

Important cytokines

A

IL2 and IL4 for lymphocyte growth and differentiation. IL10 and TGF for negative regulation of immune response. Inflammatory cytokins: TNF alpha, IL1 beta, IFN alpha and beta (type 1 interferons), IL6. IFN gamma, TNF alpha, IL5, IL10, IL12 for activation of inflammatory response. IL8 for chemotaxis. IL3, IL7, CSFs (colony stimulating factor), and stem cell factor for hematopoiesis.

94
Q

IL-1 and TNF

A

involved in hemodynamic effects of septic shock (hypotension, increased HR, decreased blood pH). Induction of adhesion molecules.

95
Q

Hageman Factor

A

Facto XII. Initiates kinin, clotting, fibrinolytic, and complement cascade

96
Q

Chronic inflammation

A

Mononuclear cells. Tissue destruction by inflammatory cells. Attempts at repair - connective tissue replacement, angiogenesis, fibrosis.

97
Q

Major basic protein

A

Found in eosinophils. Toxic to parasites and epithelial cells.

98
Q

Granulomatous inflammation

A

Activated macrophage predominates. Focal collection of macrophages/giant cells (Langhans type) surrounded by mononuclear lymphocytes. Central necrosis may be present in some granulomas (particularly in immune granulomas). Foreign body granulomas also possible.

99
Q

Regeneration vs. Healing vs. Fibrosis

A

restitution of nl structure vs. scar formation/organization of exudate vs. tissue scar (chronic inflammatory diseases)

100
Q

Extracellular matrix molecules

A

Collagens I,III, IV, GAGs, elastin, microfibrils, fibronectin, integrins

101
Q

3 Stages of healing

A

Early (thrombosis, inflammation, reepithelialization), Mid (granulation tissue at 1-3 days then wound contraction), Late (cross linking and remodeling).

102
Q

Early stage of healing

A

0-3 days. Fibrin clot, fibronectin (0-4 hours, binds to collagen, fibrin, etc), phagocytosis, chemoattraction to wound (1-4 days). Monocytes adhere to site and produce PDGF and TGFbeta. Organization (formation of new vessels, dissolution of clot, deposition of stroma).

103
Q

Mid stage of healing

A

1-10 days. Early formation of new matrix (type III collagen), dissolution of clot, phagocytosis, granulation tissue

104
Q

Granulation tissue

A

Made of macrophages, myofibroblasts, fibroblasts, capillaries (angiogenesis!). Granulation tissue is not a granuloma! Highly vascularized. Appears pale with thick-walled capillaries.

105
Q

Mitogenic cytokines

A

PDGF and FGF (most fibrogenic growth factor)

106
Q

Fibrogenic cytokines

A

TGFbeta and IL-4

107
Q

Angiogenic Cytokines

A

VEGF - vascular endothelial GF

108
Q

Epithelial proliferation cytokines

A

EGF (epidermal GF)

109
Q

Late stage of healing

A

(3-30 days) Definitive matrix of type 1 collagen, mature scar

110
Q

What is responsible for wound contraction?

A

myofibroblasts

111
Q

Reepithelialization

A

Source is hair follicle - helps close wound

112
Q

Keloid

A

thick bundles of collagen

113
Q

Wound dehiscence

A

wound breaks apart, something to do with unhydroxylated collagen

114
Q

Decubitus ulcer

A

Ischemic wound

115
Q

Role of metalloproteinases in healing

A

proteolytic enzymes requiring metal (usually zinc) that help in wound repair.

116
Q

Type I Hypersensitivity

A

Immediate (allergic). IgE mediated with deganulation of mast cells, eosinophils typical. Inflammation and edema occurs. Ex: asthma (increased production of mucous )

117
Q

Type II Hypersensitivity

A

Antibody dependent - IgG autoantibodies. Ex: Goodpasture syndrome, Graves Disease. Acute inflammation and cellular changes may be present.

118
Q

What promotes thrombus formation?

A

ADP and thromboxane A2

119
Q

What inhibits thrombus formation?

A

Antithrombin III, nitric oxide, prostacyclin

120
Q

Areas typical for red necrosis

A

testis, intestine, lung

121
Q

Areas typical for white necrosis

A

spleen

122
Q

What is aPTT?

A

Activated partial thromboplastin time. Characterizes blood coagulation.

123
Q

What are schistocytes indicative of?

A

DIC - disseminated intravascular coagulation

124
Q

What is Atrial fibrillation? What can it cause?

A

left atrium stops contracting, wiggles. Risk factor for mural thrombus formation.

125
Q

What is a typical lesion of shock?

A

coagulative necrosis

126
Q

What stains amyloid?

A

Congo red stains all amyloids reddish pink. Best when viewed under polarized light to show green-red birefringence.

127
Q

3 Subtypes of Type II Hypersensitivity

A

A: opsonization and phagocytosis, might not be immune response. B: Complement and Fc Receptor - mediated inflammation. C: Abnl physiological response esp. with receptors, no inflammation ex: Graves disease, myasthenia gravis

128
Q

Goodpasture syndrome

A

Example of Type II hypersensitivity with Subtype B Complement/Fc response. Ab directed against Type IV collagen in BM (in kidney,lung) - glomerulonephritis. RBC casts typical - take form of kidney tubules. Pulmonary hemorrhage. Look for linear immunofluorescence.

129
Q

Graves Disease

A

Example of type II hypersensitivity subtype C physiologic response. Ab stimulates TSH receptor without ligand. Hypertrophy and hyperplasia of thyroid - hyper metabolism.

130
Q

Type III hypersensitivity

A

Immune complex. IgG/C3/Antigen mediated.. Immune complexes deposit in tissues and initiate complement FcR mediated injury to tissues. Granular appearance w/ immunofluorescence. Acute inflammation is associated pathology.

131
Q

What are some Type III hypersensitivity diseases?

A

Poststrep glomerulonephritis, systemic lupus erythematous, vasculitis.

132
Q

Poststrep GN

A

Type III hypersensitivity. hypercellularity of glomerulus - intrinsic and inflammatory cells obstruct capillaries - decreased filtration leads to proteinuria, decreased albumin.

133
Q

Systemic lupus erythematous

A

Type III hypersensitivity. Butterfly shaped/malar facial rash

134
Q

ANA

A

Antinuclear antibodies. Positive means autoantibodies are present. Immune complexes deposit in skin, glomerulus, synovium, endocardium, and branch vessels – areas of mechanical trauma and high pressures.

135
Q

Vasculitis

A

Type III hypersensitivity. Neutrophils and fibrinoid necrosis present despite lack of infection or trauma.

136
Q

Type IV hypersensitivity

A

Cell-mediated (NOT ANTIBODY MEDIATED) through T cells. Granulomas and chronic inflammation are associated pathological patterns.

137
Q

Type I DM

A

Example of Type IV hypersensitivity. Target is beta islet cells.

138
Q

Sarcoidosis

A

DTH - delayed type hypersensitivity. Granulomatous with nodules in lungs (think giant cells and fibrosis)

139
Q

What is an amyloid?

A

insoluble aggregates of misfolded fibrillar proteins assuming cross-pleated beta sheet formation (tend to be hydrophobic) in extracellular space

140
Q

What are some distinguishing features of amyloid-affected organs?

A

Waxy or gritty texture, often in lymph nodes, liver, kidneys and heart. Appears glassy/hyaline and amorphous on H&E. Does NOT incite inflammatory response, should be no cells present (except trapped cells).

141
Q

What are some problems associated with amyloids?

A

Pressure atrophy and functional disruption. Deformation of organs

142
Q

What are the fibril proteins and protein precursors of the 4 most common type of amyloids? Where do the proteins come from?

A

AL (from immunoglobulin light chains from plasma cells). AA (SAA-Serum amyloid associated from liver cells). Beta amyloid (APP-amyloid precursor protein in cerebral deposits/senile cerebral). ATTR (Transthyretin TTR from mutation/genetic syndrome/senile)

143
Q

What are the two types of systemic/generalized distribution of amyloids?

A

Primary and Secondary. Primary is from plasma cell proliferation and is clinically unrecognized, ex: AL. Secondary refers to a chronic inflammatory disorder ex: AA. Systemic more common than localized (to one organ).

144
Q

What are nl cholesterol levels?

A

Total: 200mg/dL, LDL40, triglycerides <100.

145
Q

Liver enzymes to check function?

A

AST and ALT

146
Q

Ghrelin, Leptin, PYY, adiponectin

A

Ghrelin increases food intake and is secreted by stomach. PYY (from intestine) and leptin reduce food intake. Leptin also increases energy expenditure and is produced by adipocytes. Adiponectin decreases glucose production in liver, decreases fat to liver and directs fatty acids to muscle (to burn)

147
Q

PEM

A

Protein/energy malnutrition. Primary is due to unavailability of food, secondary due to coexisting disease.

148
Q

Marasmus

A

Primary PEM from global starvation. Vitamin and immune deficiencies, loss of fat and muscle, growth retardation. Wasting appearance

149
Q

Kwashiorkor

A

Primary PEM. Protein deficiency (w/ adequate caloric intake). Edema occurs from loss of oncotic pressure. Fatty liver bc you need proteins to transport fat out of liver. hair hypo pigmentation. vit/immune deficiencies. Edematous appearance.

150
Q

Cachexia

A

Extreme weight loss, fatigue, etc. esp in cancer and HIV its

151
Q

Fat Soluble Vitamins

A

A, D, E, K. Can accumulate to toxic levels.

152
Q

Water soluble vitamins

A

B, C, very rarely toxic.

153
Q

Signs of Vitamin A deficiency

A

Blindness/night blindness, immune deficiency, squamous metaplasia leading to dry eyes, pulmonary infections, kidney stones

154
Q

What is scurvy? Symptoms?

A

Vitamin C deficiency. Bleeding due to weak blood vessels, esp bleeding gums. Bone pain, poor wound healing. Healing requires collagen and vit. C is imp in collagen synthesis.

155
Q

Vitamin D deficiency

A

causes rickets (abnl endochondral bone formation), osteomalacia, hypocalcemic tetany

156
Q

Vitamin D toxicity

A

deposition of calcium in tissues, bone pain, hypercalcemia.

157
Q

Why is the mTOR pathway interesting?

A

Remember that the mTOR pathway of kinases appears to facilitate conversion to replicative senescence. All the other options protect the cell from genomic instability and/or cell arrest.

158
Q

What is the main mediator associated with Increased vascular permeability?

A

Histamine

159
Q

What is the main mediator associated with pain?

A

bradykinin

160
Q

What is the main mediator associated with fever?

A

IL-1

161
Q

What is the main mediator associated with Chemotaxis for neutrophils

A

complement fragment c5a

162
Q

What is the main mediator associated with Opsonization of bacteria for phagocytosis?

A

complement fragment c3b

163
Q

What is the main mediator associated with Neutrophilic rolling along the vascular endothelial surface?

A

selectins

164
Q

What is the main mediator associated with Neutrophilic firm adhesion to the vascular endothelial surface?

A

integrins

165
Q

What is the main mediator associated with Neutrophilic transmigration?

A

PCAM

166
Q

What is the main mediator associated with Intracytoplasmic neutrophilic killing of pathogenic organisms?

A

NADPH oxidase

167
Q

Which factor is most likely to be effective in promoting collagen formation?

A

Transforming growth factor- beta

Immuno/Pathology and Physiology (8 decks)

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