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Biology of Disease > Exam 2 > Flashcards

Exam 2 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Pinpoint hemorrhages, up to 1mm in diameter, normally on mucus membranes

A

Petechia

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1
Q

What is an extrinsic coagulation system defect (bleeding disorder)?

A

Factor VII deficiency in beagles

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1
Q

Describe fibrinous inflammation including what is in the exudate, what it looks like, where it is most visable, what causes it , and an example of it:

A

 Contents: Exudate contains abundant fibrin  Appearance: tenacious, adherent strands and sheets; can be stripped off surface.  Where found: most visible on serosal surfaces  Cause: vascular exudative process, often infectious origin Where commonly seen: walling off agent, matrix for WBC migration

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1
Q

What is a Hageman Factor?

A

Activated in first step of intrinsic coagulation cascade, activated by negatively charged surfaces Initiates generation of 4 processes: Clotting Fibrinolysis Kinin generation Complement cascade

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1
Q

What are C3b and C5b good for?

A

Opsonization

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1
Q

What does lipoxygenase produce?

A

Leukotrienes

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1
Q

What are the two types of granulomas?

A

1) Foreign body: formed in response to indigestible material, keratin, hair, plant material 2) Immune granuloma: persistent antigen with T-cell response

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1
Q

What is Von Willebrand’s factor?

A

binds subendothelial collagen, platelets bind von Willebrand’s factor via gpIb surface integrins.

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3
Q

Excess fluid in tissue interstitium

A

Edema

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3
Q

What causes DIC?

A

1) Infection-Gram negative sepsis expression of tissue factor in monos and macs, secrete IL-1, TNF, upregulate WBC binding to endothelium…etc. 2) Trauma 3) Neoplastic Disease

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4
Q

What would a tissue that is pale and anemic be caused by?

A

Arterial infarct

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5
Q

What substance is commonly found in rat poison?

A

Coumarin Poisoning which is the most common ACQUIRED bleeding disorder

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6
Q

Malignant tumor of blood

A

Hemangiosarcoma

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7
Q

Name the following examples of suppurative inflammation: 1) purulent inflammation of the subcutis 2) fluctuant pocket of pus in the subcutis 3) purulent inflammation of fascia 4) local collection of pus 5) accumulation of pus in body cavity

A

1)Cellulitis 2) Phlegmon 3) Fasciitis 4) Abscess 5) Empyema

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8
Q

Describe what suppuratitive inflammation contains, what it looks like, and what it is in response to.

A

 Contents: Dominated by neutrophils, marked vascular exudation  Appearance: tissue at site often liquified with thick creamy to yellow exudate  Cause: usually in response to infectious agent and is an immediate defensive reaction

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9
Q

Blood in urine

A

Hematuria

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10
Q

termination of blood loss from vasculature (clotting)

A

Hemostasis

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12
Q

What are the secondary effects of hemorrhage (things that the body does after hemorrhage)?

A

1) Resorption of fluid (internal hemorrhage). 2) Erythrocytes lysed and phagocytosed (getting rid of blood from where it is not supposed to be) 3) Fibrinolysis (removing fibrin from clots) 4) Potential scarring if fibrinolysis is incomplete

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14
Q

What cells are present during chronic inflammation? Chronic active? What is the hallmark of chronic inflammation?

A

Primarily mononuclear cells, macrophages CA: Includes neutrophils Neovascularization and fibrosis

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15
Q

Describe Hemophilia A and B

A

A: Sex-linked Factor VIII deficiency in cats and dogs, males bleed B: Sex-linked Factor IX deficiency in cats and dogs, males bleed

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15
Q

What is a heterophil? What fx do they lack?

A

Avian and reptile equivalent of the neutrophil (also rabbits), lack the enzymes to liquefy, hence heterophilic lesions are often caveated

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16
Q

Loss of blood from within vasculature

A

Hemorrhage

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17
Q

What digests polymerized fibrin?

A

Plasmin

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18
Q

When is Nitric Oxide up-regulated and down-regulated?

A

up: bacterial products, IL-1, TNFa, IFNg down: TGFb, IL-4, IL-10, glucocorticoids

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20
Q

Describe serous inflammation including what it looks like, where it takes place, what it does, and what causes it:

A

 Exudation of thin watery fluid is what it looks like  Body or organ surfaces is where it is mostly seen The exudate dilutes or washes away the injurious agent  Caused by envenomation, irritants, trauma, early infectious process  Fluid occupies space

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21
Q

What are the different fates of a Thrombi?

A

 Propagation: gets bigger  Fibrinolysis: gets smaller  Organization and Recanalization: The endothelial cell wall tries to grow over to try to prevent further propagation of clot  Embolism: Clot breaks off into blood (can get stuck and cause problems)

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21
Q

How can you tell a tissue has encountered an infarct?

A

Irregularly shaped, sharply demarcated (red boundary around dead tissue), peripheral zone of hyperemia, raised or depressed, anemic or hemorrhagic

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22
Q

What produces the primary hemostatic plug?

A

ADP and Thromboxane A2–promote platelet aggregation

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23
Q

What are all of the platelet aggregators (recruit platelets)?

A

ADP and Thromboxane A2, Thrombin, Collagen, Epinephrine, Immune complexes, Platelet Activating Factor

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23
Q

What are C3a and C5a?

A

Anaphylotoxins -nonvascular sm. muscle constriction -increase vasc. perm. -mast cell degranulation -activate WBC

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24
Q

Larger hemorrhages, up to a few cm, usually on mucus membrane

A

Ecchymosis

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25
Q

What acquired disease can be caused by infectious disease (Rickettsia), DIC, Neoplasia or be immune mediated?

A

Acquired Thrombocytopenia

26
Q

Mass of clotted blood outside of a vessel

A

Hematoma

27
Q

Vomiting blood

A

Hematemesis

28
Q

Blood in thorax

A

Hemothorax

30
Q

formation of a solid adherent blood clot (thrombus) within the lumen of a vessel or the heart

A

Thrombosis

30
Q

What are the chemical mediators of vascular permeability? (6)

A

Vasoactive amines Kinins Complement fragments Arachidonic Acid Mediators Cytokines Platelet Activating Factor

30
Q

What opposes the proteases involved in inflammation?

A

Alpha 2 macroglobulin inhibits all 4. Serpins inhibit serine proteases TIMPS: Tissue inhibitors of matrix metalloproteinases

31
Q

Thrombohemorrhagic disorder characterized by widespread activation of clotting mechanisms (massive release of tissue factor or thromboplastic substance) with consumption of platelets and clotting factors, activation off ibrinolysis, and widespread hemorrhage. Acquired.

A

Disseminated Intravascular Coagulation

32
Q

Benign tumor of blood (normally in spleen from rapidly dividing RBC)

A

Hemangioma

33
Q

What is granulation tissue?

A

Proliferation of fibrovascular tissue that fills tissue defect and provides framework for elaboration of fibrous tissue

34
Q

What suffix is associated with inflammation?

A

-itis

36
Q

What are the three steps of acute inflammation?

A

Hemodynamic events, changes in vascular permeability, efflux of WBC

37
Q

When and in what environment do primary granules get released?

A

late in cell activation, acidic pH

38
Q

Where do the intrinsic and extrinsic systems converge in the Coagulation system?

A

Factor X

40
Q

What is the role of eosinophils in inflammatory response?

A

Present in allergic and parasitic dz. Have granules with basic proteins which produce cytokines, chemokines, proteases, and oxidative radicals. Response to helminthic infections.

42
Q

Blood cell rupture

A

Hemolysis

43
Q

What are the granules inside platelets and what do they contain?

A

Alpha granules: contain fibrinogen, fibronectin, factors V & VIII, thrombospondin, PDGF and TGFb

45
Q

What are the different phases of wound healing?

A

1) Inflammation 2) Cell Migration 3) Matrix Deposition 4) Vascular Proliferation 5) Collagen Synthesis 6) Remodeling

46
Q

What are the two mechanisms of healing and repair?

A

1) Parenchymal regeneration 2) Replacement by fibrous tissue

48
Q

What color indicates the presence of eosinophils?

A

Green

49
Q

What is the most common inherited bleeding disorder in animals?

A

Von Willebrand’s dz, absence of Von Willebrand’s factor, can’t clot

51
Q

How is clotting controlled locally?

A

 antithrombins: prevent clot formation  Proteins C & S: prevent clot formation  Plasminogen-plasmin system: Degrades polymerized fibrin to prevent excess clotting

52
Q

What are the 4 main types of protease involved in inflammation?

A

 Serine: Elastase, Cathepsin G, Protienase 3, urinary type Plasminogen Activator  Metallo-: Involved in tissue remodeling, Zymogen forms cleaved by plasmin, Cathepsin G, bacterial proteases  Cysteine and Aspartic: Function in acid environments

53
Q

How do damaged cells recruit/bind platelets?

A

Damaged cells begin to translate proteins, P-selectin, which are incorporated into the cell’s membrane. THE RECEPTOR THAT BINDS PLATELETS IS P-SELECTIN.

54
Q

When and in what environment do secondary granules get released?

A

early in cell activation, basic pH

54
Q

What is Cox-1 v. Cox-2? What inhibits Cox?

A

1-Constitutive expression 2-expression induced in inflammation NSAIDS inhibit

55
Q

Moving material in the vasculature (not attached to the wall)

A

Embolism

56
Q

Hyperemia is an ACTIVE/PASSIVE process, primarily due to ARTERIOLAR/VENOUS dilation.

A

Active, arteriolar

57
Q

Necrosis of tissue due to absence of blood flow or low O2 in the blood

A

Infarction

58
Q

Petechiae and ecchymoses on mucus membranes

A

Purpura

60
Q

Blood in feces

A

Hematochezia

61
Q

What causes macrophage accumulation?

A

Continued recruitment (MOST IMPORTANT) -C5a, chemokines, growth factors, fibrin degradation products -local proliferation -Immobilization at site (Migration Inhibition Factor)

62
Q

What are the COX products and what do they do?

A

1)Prostacyclin (PGI2) -vasodilation, inhibits platelet aggregation 2)Thromboxane A2 -vasoconstriction, promotes platelet aggregation 3)Prostaglandins D2, E2, F2 alpha -vasodilation, promote edema

63
Q

What do C1 and C4 do?

A

Help neutralize viruses when Ab titers are low

65
Q

What form of chronic inflammation is it when “epitheliod” macrophages are predominant?

A

granulomatous inflammation

66
Q

What do platelet granules contain?

A

Histamine  Thromboxane A2  P-selectin  Growth Factors: PDGF, FGF, TGF  Enzymes

67
Q

What are the cells that can usually be found in granulation tissue?

A

1) Macrophages - remove exudate, secrete fibrogenic & angiogenic factors (growth factors) 2) Fibroblasts - lay down collagen matrix, myofibroblasts have contractile activity reducing wound volume 3) Endothelial cells - provide vascular supply (new blood vessels)

68
Q

What produces the secondary hemostatic plug?

A

Thrombin production promotes further aggregation of platelets and polymerizes fibrin

69
Q

What are some of the adverse outcomes of healing?

1) fusion of two tissues that are not normally fused
2) joint with excessive scaring that prevents the range of motion.
3) luminal structure that has scaring that reduces the lumen diameter.
4) Appendicular skeleton scarring causes limb to become permanently bent. Critical tissue replaced by fibrous tissue

A

1) Adhesion
2) Ankylosis
3) Stricture
4) Contracture

70
Q

Blood in interior chamber of eye

A

Hyphema

71
Q

What are proteins C&S dependent on and how is it activated/inactivated?

A

Vit K dependent, Activated by binding thrombomodulin/thrombin complex on endothelial cells, inhibit activated clotting factors V & VIII

72
Q

Name the leukotrienes based on fx: 1) chemotaxis, enhances adhesion, degranulation, ROS generation 2)Slow Release Substance of Anaphylaxis: vasoconstriction and bronchospasm

A

1)5-HETE & LTB4 2) Leukotrienes C4, D4, E4

73
Q

Describe catarrhal inflammation including what is in the exudate, what it looks like, what the exudate does, and what causes it:

A

 Contents: Exudate contains abundant mucus  Appearance: Shiny mucoid material coating mucosal surfaces Function of exudate: dilute, wash away agent  Cause: irritants, infectious processes

74
Q

Too much blood in a vascular bed, passive process, primarily due to venous engorgement

A

Congestion

76
Q

Blood in saliva

A

Hemoptysis

77
Q

What are the 3 phases of granulation tissue formation?

A

1) Inflammatory phase – inflammatory response initiates healing process. Cleans tissue debris. 2) Proliferative phase - rapid growth of delicate fibrovascular tissue 3) Remodeling phase - collagen fibers are replaced and reorganized, vasculature regresses.

78
Q

What are the Newly Synthesized Mediators? How are they formed? What are the two pathways?

A

-Arachidonic Acid Derivatives (autocoids) -formation stimulated by: cytokines, chemotactic peptides -formed by phospholipases acting on cell membranes -2 pathways: Cyclooxygenase and Lipoxygenase

Biology of Disease (2 decks)

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