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Clinical Pathology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is hemostasis?

A

the ability of the body system to maintain the integrity of the blood and blood vessels

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2
Q

What are the four main steps to achieve hemostasis?

A

primary, secondary, fibrinolysis, and restoration of vessel patency

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3
Q

What is primary hemostasis?

A

transient vasoconstriction with formation of platelet plug

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4
Q

What is secondary hemostasis?

A

coagulation to form mesh of fibrin

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5
Q

What is fibrinolysis?

A

removal of platelet/fibrin plug (thrombus retractin)

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6
Q

What is restoration of vessel patency?

A

tissue repair at damaged site

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7
Q

What players are involved in primary hemostasis?

A

release of endothelians by injured endothelial cells causes local vasoconstriction

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8
Q

What players are involved in secondary hemostasis?

A

series of enzymatic reactions involving clotting factors which leads to the formation of fibrin mesh which stabilizes the platelet plug

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9
Q

Where are most coagulation factors produced?

A

the liver

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10
Q

Where is factor III produced?

A

endothelial cells

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11
Q

Where are von Willebrand factors produced?

A

within endothelial cells (blood vessels / bone marrow

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12
Q

Which factors require vitamin k for activation?

A

II, VII, IX, X

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13
Q

Which of the vitamin k factors has the shortest half-life?

A

factor VII - 5 hours

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14
Q

Which factors are involved in the intrinsic pathway?

A

factors XII, XI, IX, VII

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15
Q

Which factors are involved in the extrinsic pathway?

A

factors III and VII

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16
Q

Which factors are involved in the common pathways?

A

factors X, II, I, XII

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17
Q

Define thrombocytopenia.

A

decrease in platelet count

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18
Q

Define thrombocytosis.

A

dysfunctional platelets

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19
Q

Define thrombocytopathia?

A

low blood platelet count

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20
Q

What are the 3 general ways to have thrombocytopenia?

A

decrease in production
increase in consumption
sequestration
(don’t make it, spend it, or something takes it)

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21
Q

What are 2 main causes for thrombocytosis?

A

reactionary
primary

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22
Q

What does the reactionary cause for thrombocytosis?

A

chronic inflammation
iron deficiency
bushings

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23
Q

What does the primary cause for thrombocytosis?

A

megakaryocytic leukemia

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24
Q

What does MPV stand for?

A

mean platelet volume

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25
Q

Why might a dog with a decrease in PLT count but increase in MPV not have an issue with primary hemostasis?

A

the larger platelets due to the increase in MPV could compensate for the decrease in platelet count, ensuring that primary hemostasis is not significantly impacted

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26
Q

What is the BMBT?

A

buccal mucosal bleed time

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27
Q

What does BMBT test for?

A

it tests platelet vessel interaction through primary hemostasis

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28
Q

Why is cuticle bleed time not a great test to assess platelet function?

A

it does not differentiate primary vs secondary hemostasis defect

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29
Q

Which tests can be used to assess for issues with intrinsic pathways?

A

activated clotting time (ACT)
partial thromboplastin time (PTT/aPTT)

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30
Q

Which tests can be used to assess for issues with extrinsic pathways?

A

prothrombin time (PT)

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31
Q

Which tests can be used to assess for issues with common pathways?

A

activated clotting time (ACT)
partial thromboplastin time (PTT/aPTT)
prothrombin time (PT)

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32
Q

What are congenital coagulation disorders?

A

von Willebran disease, glanzmann’s thrombasthenia, inherited platelet delta storage pool disease, hereditary coagulation factor disorders

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33
Q

What are acquired coagulation disorders?

A

immune-mediated thrombocytopenia (ITP), disseminated intravascular coagulation, liver failure, vitamin k deficiency

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34
Q

Which congenital disorders discussed in class deal with issues with primary hemostasis?

A

von Willebrand disease

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35
Q

Which congenital disorders discussed in class deal with issues with secondary hemostasis?

A

hematoma or cavity bleeds

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36
Q

What is the Type 1 von Willebrand disease?

A

low levels of circulating vWF with normal structure, autosomal dominant with incomplete penetrance

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37
Q

What is the Type 2 von Willebrand disease?

A

low levels of circulating vWF with abnormal structure, dominant inheritance

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38
Q

What is the Type 3 von Willebrand disease?

A

near absence of vWF, autosomal recessive

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39
Q

Which vWF types produce the most clinical signs?

A

type 2 & 3 result in most severe bleeding

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40
Q

Which is the deficit in Glansmann’s Thrombasthenia?

A

platelet fibrinogen receptor GPIIb / GPIIIa

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41
Q

What is the result of GPIIb / GPIIIa?

A

results in platelet aggregation defect (platelets unable to be stabilized / cross-linked by fibrinogen) and severe bleeding
ex. otterhounds and great pyrenees

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42
Q

What is the deficit in inherited platelet storage pool disease?

A

deficiency of ADP granules within platelets

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43
Q

What is the result of the platelet storage pool disease?

A

causes moderate to severe bleeding tendency
ex. American cocker spaniel

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44
Q

Which coagulation factor is deficient in hemophilia A?

A

factor VIII

45
Q

Which coagulation factor is deficient in hemophilia B?

A

factor IX

46
Q

Which coagulation test(s) would you expect to be prolonged in an animal with hemophilia A?

A

ACT (activated clotting time)
PTT (partical thromboplastin time)

47
Q

Which coagulation test(s) would you expect to be prolonged in an animal with hemophilia B?

A

ACT (activated clotting time)
PTT (partical thromboplastin time)

48
Q

Which gender is most likely to be clinical for either of the hemophilias and why?

A

males because it is a recessive gene and males only have one copy of the X chromosome

49
Q

What are examples of acquired coagulopathies?

A

immune-mediated platelet destruction, DIC (disseminated intravascular coagulation), liver failure, vitamin k deficiency (warfarin intoxications)

50
Q

How does DIC result in bleeding disorders?

A

systemic hemorrhages / microvascualr thrombosis
leads to consumption of platelets and coagulation factors

51
Q

How does liver failure result in bleeding disorders?

A

a failing liver cannot make enough clotting factors, which help blood to clot

52
Q

Why is PT the first test to be prolonged with anticoagulant rodenticide toxicity?

A

PT is the first to be prolonged due to VII having the shortest half-life

53
Q

What are the 2 branches of the immune system?

A

acquired and innate

54
Q

What are examples of physical barriers within the innate immune system?

A

skin
physical and biochemical components (nasopharynx, gut, lungs, GI tract)
bacteria that compete with the invading pathogens

55
Q

What are examples of chemical barriers within the innate immune system?

A

inflammatory response
chemical released from infected site allow neutrophils to pass into tissue to phagocytize bacteria and kill pathogens

56
Q

Is the inflammatory response part of the innate or adaptive immune response?

A

innate immune response

57
Q

What are the 5 cardinal signs of inflammation?

A

heat
redness
swelling
pain
loss of function

58
Q

What does the cardinal sign “heat” due to?

A

vasodilation

59
Q

What does the cardinal sign “redness” due to?

A

vasodilation

60
Q

What does the cardinal sign “swelling” due to?

A

increased vascular permeability

61
Q

What does the cardinal sign “pain” due to?

A

physical and chemical stimulation of nociceptors

62
Q

What does the cardinal sign “loss of function” due to?

A

secondary to pain, disruption of tissue structures

63
Q

What are some key cells of the innate immune system?

A

natural killer cells
interferons
complement system/cascade

64
Q

What do natural killer cells do in the innate immune system?

A

subset of lymphocytes in blood and lymph organs, recognize and destroy host cells infected with microbes or viruses, activate phagocytes by releasing interferon-Y

65
Q

What do interferons do in the innate immune system?

A

cytokines that elicit cellular reactions, prevent replication

66
Q

What does the compliment system do in the innate immune system?

A

helps the body fight infection and heal from injury

67
Q

What is the end result of complement activation?

A

the end result is stimulation of phagocytes to clear foreign and damaged material, inflammation to attract additional phagocytes, and activation of the cell, killing the MAC

68
Q

What is formed from the complement activation?

A

C3 converts
leads to the production of principle effector molecules

69
Q

What is the purpose of complement activation?

A

to clean up damaged cells
help your body heal after an injury or infection

70
Q

What are the 2 branches of the adaptive immune system?

A

cell-mediated (T-cells)
humoral (B-cells)

71
Q

Which main branch of the immune system is capable of a specific/targets response?

A

adaptive immune system

72
Q

What are the 5 types of immunoglobulins?

A

IgM
IgG
IgE
IgA
IgD

73
Q

Which type of immunoglobulin is formed first?

A

IgM

74
Q

Which type of immunoglobulin is most abundant in circulation?

A

IgG

75
Q

What are the main functions of antibodies?

A

neutralization reaction
coating activity
opsonization reactions
complement activation of antibodies
precipitation reactions

76
Q

Which type of lymphocyte is involved with the cell-mediated branch of the adaptive immune response?

A

T-cells

77
Q

Which type of lymphocyte is involved with the humoral branch of the adaptive immune response?

A

B-cells

78
Q

What are 2 methods of passive immunity?

A

maternal antibodies in colostrum
receive preformed antibodies by injection

79
Q

What are 2 methods of achieving active immunity?

A

animals become resistant by either having the disease and developing antibodies or by immunization
elicits an antibody response by injecting microorganism into an animal

80
Q

Is vaccination a form of active or passive immunity?

A

active immunity

81
Q

Can immune responses cause pathology?

A

yes

82
Q

Which hypersensitivity reaction is mediated by immunoglobulins?

A

type I, II, III

83
Q

Which immunoglobulin is used in type I hypersensitivity?

A

IgE

84
Q

Which immunoglobulin is used in type II hypersensitivity?

A

IgG and IgM

85
Q

Which immunoglobulin is used in type III hypersensitivity?

A

IgG > IgM

86
Q

Which immunoglobulin is used in type IV hypersensitivity?

A

t-cells

87
Q

Which hypersensitivity reaction is involved in seasonal allergies, anaphylaxis?

A

type I hypersensitivity

88
Q

Which hypersensitivity is involved with direct cytotoxicity?

A

type II hypersensitivity

89
Q

Which hypersensitivity reaction results in cellular and tissue damage due to association with antigen/antibody complexes?

A

type III hypersensitivity

90
Q

Which hypersensitivity reaction is associated with contact dermatitis or granuloma formation?

A

type IV hypersensitivity

91
Q

What is type I hypersensitivity’s sensitization phase?

A

initial exposure to antigen and binding by B lymphocytes
activation of TH2 cell and IgE class switching in B lymphocytes
productions of IgE by B lymphocytes which will bind them to mast cells

92
Q

What is type II hypersensitivity’s sensitization phase?

A

occurs as a results of the development of antibodies directed against antigens on the surface of a cell or in a tissue resulting in the destruction of that cell or tissue

92
Q

What is type III hypersensitivity’s sensitization phase?

A

occurs when the host develops an antibody response to an antigen so that the ratio of antigen to antibody is appropriate for the formation of small soluble circulating complexes that are not able to be cleared by the MMS

93
Q

What is type IV hypersensitivity’s sensitization phase?

A

occurs with the initial exposure to the antigen and results in the development of antigen specific memory T lymphocytes (TH1)

94
Q

Which hypersensitivity reaction responds to soluble antigen?

A

type III hypersensitivity

95
Q

Which hypersensitivity reaction responds to bond antigens?

A

type II hypersensitivity

96
Q

Type I hypersensitivity overview.

A

IgE is bound to mast cells. When an allergen binds to these antibodies, cross-linking of IgE induces degranulation

97
Q

Type I hypersensitivity causes?

A

causes localized and systemic anaphylaxis, seasonal allergies including hay fever, food allergies such as those to shellfish and peanuts, hives, and eczema

98
Q

Type II hypersensitivity overview.

A

cells are destroyed by bound antibody, either by activation of complement or by a cytotoxic T cell

99
Q

Type II hypersensitivity causes?

A

red blood cells destroyed by complement and antibody during a transfusion of mismatched blood type or during erythroblastosis fettles

100
Q

Type III hypersensitivity overview.

A

antigen/antibody complexes are deposited in tissues casing activation of complement, which attracts neutrophils to the site

101
Q

Type III hypersensitivity causes?

A

most common forms of immune complex disease are seen in systemic lupus erythematosus, blue eye, glomerulonephritis

102
Q

Type IV hypersensitivity overview.

A

TH1 cells secrete cytokines, which activate macrophages and cytotoxic T-cells and can cause macrophage accumulation at the site

103
Q

Type IV hypersensitivity causes?

A

most common forms are contact dermatitis, tuberculin reaction, autoimmune diseases such as diabetes mellitus type I, multiple sclerosis, and rheumatoid arthritis

104
Q

Examples of type I hypersensitivity?

A

hay fever
asthma
eczema
hives
food allergies
anaphylaxis

105
Q

Examples of type II hypersensitivity?

A

hemolytic anemias
cytopenias
auto immune diseases
drug toxicities

106
Q

Examples of type III hypersensitivity?

A

serum sickness
systemic lupus erythematosus
vasculitis
rheumatoid arthritis
post-streptococcal glomerulonephritis

107
Q

Examples of type IV hypersensitivity?

A

contact dermatitis
poison ivy
tuberculin skin test
johnes disease

Clinical Pathology (2 decks)

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