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Pharmacology Exam 3 > Immune system > Flashcards

Immune system Flashcards

1
Q

What are the 2 Types of Immunity?

A

Innate and Adaptive

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2
Q

What is Innate Immunity?

A

Our natural immunityThe first response to an insult to the immune system

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3
Q

What are the effectors of Innate Immunity?

A

Effectors: complement, granulocytes, monocytes and macrophages, natural killer cells, mast cells and basophils

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4
Q

What is Adaptive Immunity?

A

Learned ImmunityRequires identification of antigens after 2nd exposure.

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5
Q

What are the effectors of Adaptive Immunity?

A

B Lymphocytes (antibodies) and T Lymphocytes as helper, cytolytic or regulator (suppressors) cells

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6
Q

List the Immune System Disorders causing Epidemic

A

Rheumatoid ArthritisDiabetes Mellitus type 1Systemic Lupus ErythematousMultiple sclerosisInfectious diseaseAsthmaHIV/AIDSHematologic and solid tumors

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7
Q

What is neutropenia?

A

Neutrophil granulocyte count less than 1500mm

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8
Q

What is Neonatal Sepsis

A

Infants born to mothers with immune disorders

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9
Q

Which immune dysfunctions or cancers are associated with neutropenia in adults?

A

Systemic Lupus ErythematousRheumatoid ArthritisLymphomaMyleproliferative diseaseSevere liver disease

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10
Q

How does decreasing WBC result in sepsis?

A

The bone marrow can not provide new cells to replace the granulocytes being used

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11
Q

What is Neutrophilia?

A

When neutrophil count is greater than 7000/mm3

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12
Q

What results when Neutrophils exceed 100000/mm3?

A

Infarcted SpleenReduced Oxygen Diffusion in the Lungs

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13
Q

What is the next step when a patient has sustained granulocyte counts in excess of 50,000?

A

Want to rule out noninfectious malignant disease processes such as a hematologic malignancy.

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14
Q

How does prednisone effect innate immunity?

A

Patients on prednisone may have granulocyte counts as high as 15,000 to 20,000mm3. Yet they show no signs of infection because the body is unable to mount a response.

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15
Q

Is angioedema hereditary or acquired?

A

Both

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16
Q

What are the 2 types of “release” that result in angioedema?

A

Mast Cell Release: Allergic ReactionBradykinin Release: No Allergic Reaction

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17
Q

Allergic Reaction Angioedema results from _____.

A

Mast Cell Release

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18
Q

Non-Allergic Reaction Angioedema results from _____.

A

Bradykinin Release

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19
Q

Hereditary Angioedema results from ______.

A

a deficiency of esterase inhibitors resulting in a release of vasoactive mediators.

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20
Q

What physiologic effects do the release of vasoactive mediators have on angioedema?

A

Increased permeabilityEdema, facial and laryngeal edema….triggered by menses, trauma, infection, stress or estrogen containing birth control pills.

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21
Q

Which classification of drugs can trigger angioedema?

A

ACE Inhibitors: Some patients will trigger after they have been on the medications for extended periods of time.

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22
Q

Angioedema is triggered by first contact with ACE Inhibitors. (T/F)

A

False.Some patients will trigger after they have been on the medications for extended periods.

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23
Q

What are the treatments for ACE Inhibitor triggered Angioedema?

A

AndrogensAminocaproic AcidAprontininFFP (2-4 Units) replaces the deficient enzyme and is a preferred treatment for an acute episode.

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24
Q

What is the preferred treatment for an acute episode of ACE Inhibitor triggered Angioedema?

A

FFP (2-4 Units)

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25
Q

What should be avoided during acute episodes of angioedema?

A

Avoid Catecholamines, Antihistamines, and Antifibrinolytics

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26
Q

What are some Anesthesia considerations related to angioedema?

A

NAME?

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27
Q

Hypersensitivity Reaction Type I induces reactions by which physiologic responses?

A

Response from IgE, Mast Cells and Basophills

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28
Q

Which Hypersensitivity reaction results from immediate reaction to drugs, insects, food or drugs?

A

Type I response with IgE, Mast Cells and Basophils

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29
Q

Systemic Anaphylaxis is an extreme ______ reaction.

A

Type I

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30
Q

Which type of hypersensitivity reactions require immediate medical attention?

A

Type I

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31
Q

Type II Hypersensitivity Reactions result from ______.

A

formation of antigen antibody complexes.

32
Q

Type II Hypersensitivity results from the reaction between foreign antigens and which immunoglobulins?

A

IgG or IgM

33
Q

Blood Transfusion reactions are which type of hypersensitivity reaction?

A

Type II

34
Q

Describe a “mother-fetus” reaction that would result in a Type II Hypersensitivity Reaction.

A

Rh-Negative Mother to Rh-Positive Fetus

35
Q

PCN Reaction is what type of Hypersensitivity reaction?

A

Type II

36
Q

Readministration of PCN would result in which type of reaction?

A

Type I

37
Q

Describe the Type II PCN reaction.

A

PCN binds to RBC or other tissue and forms a “neoantigen” which will cause complement mediated red cell lysis.

38
Q

How do Type III Hypersensitivity Reactions arise?

A

Elevated levels of antigen-antibody complexes from the blood stream deposit on basement membranes in tissue and vessels

39
Q

What is the first response to an insult to the immune system?

A

Innate Immunity

40
Q

Innate immunity is immature at birth. (T/F)

A

True.We are born with innate immunity but it is not mature at birth. It matures over the course of our lifetime.

41
Q

Which Immune system is specific, systemic, and has a memory?

A

Adaptive Immunity

42
Q

Adaptive immunity is non-specific (T/F)

A

False. Adaptive immunity is specific

43
Q

Adaptive immunity has memory. (T/F)

A

TRUE

44
Q

What is the key difference between adaptive and innate immunity?

A

Adaptive immunity has the ability to remember specific pathogens.

45
Q

How are antibodies formed in adaptive immunity?

A

When we are exposed to a bacteria for the first time we cannot give a real immune response, but the body identifies it as an invader and develops antibodies specific to the pathogen. So, the next time we are introduced to said pathogen, our bodies respond rapidly and overwhelmingly.

46
Q

Why is there an epidemic of immune system disorders?

A

Because we are becoming resistant to antibiotics.

47
Q

How does a NORMAL immune system respond to cancers.

A

We all have cancer, but our bodies are able to regulate the overgrowth of cells. Cancer is a problem with the immune systems ability to regulate cells that are replicating “out-of-control.”

48
Q

Edema (facial and laryngeal) is triggered by what?

A

Menses, trauma, infection, stres or estrogen containing birth control pills.

49
Q

What is C1 Inhibitor

A

A plasma protein that down regulates several inflammatory cascades.

50
Q

Deficiency in quantity or quality of C1 Inhibitor results in ____.

A

episodes of edema

51
Q

What is the inflammatory pathway that results from absence of C1 Inhibitor?

A

Upregulation of pro-inflammatory mediators and overproduction of Bradykinin which are responsible for increased vascular permeability leading to ANGIOEDEMA

52
Q

What is the MOA of C1 Inhibitors?

A

Inactivates C1, thus stops production of proteolytic fragments and inflammatory inducing complexes. Also inhibits thrombin which affects the coagulation cascade.

53
Q

Where is C1 Inhibitor synthesized?

A

Mainly in the liver, but also by monocytes and other cells in response to pro-inflammatory cytokine stimulation.

54
Q

Severe systemic anaphylaxis occurs in which type of Hypersensitivity reactions?

A

Type 1

55
Q

A Type 1 reaction may be exhibited approximately 20 minutes after administration of a drug. (T/F)

A

False. True Type 1 reactions are immediate, occurring within 5min.

56
Q

All Type 1 Hypersensitivity reactions are considered anaphylactic reactions. (T/F)

A

False.Not all Type 1 reactions are anaphylaxis, but if a reaction progresses to anaphylaxis, then it is considered an extreme Type 1 reaction and IMMEDIATE intervention is required.

57
Q

What effect does Type III Hypersensitivity reactions have on the vasculature?

A

Vascular permeability is increased.

58
Q

When does expression of Type III hypersensitivity reactions occur.

A

2-3 days after exposure

59
Q

What results from a severe form of Type III hypersensitivity reaction?

A

Glomerulonephritis

60
Q

What is typically exhibited from less intense forms of Type III Hypersensitivity reactions.

A

Uticaria, vasculitis and arthralgias

61
Q

What is Type IV Hypersensitivity reaction?

A

A delayed-type of hypersensitivity

62
Q

What are 3 cutaneous examples of Type IV hypersensitivity reaction.

A

Contact dermatitis (Steven-Johns Syndrome)Epidermal necrosisPoison Ivy

63
Q

What is triggered during Type IV hypersensitivity reactions.

A

Involves activation of T cells (T lymphocytes), which release cytokines and chemokines, and macrophages.

64
Q

What is the difference between hypersensitivity reactions in terms of mediators.

A

Type I, 2, 3 are antibody mediatedType 4 is T-cell mediated.

65
Q

What is Anaphylaxis?

A

Life Threatening, Immune or Non-Immune mediated response to the re-exposure to an antigen in which antigen specific Ig-E antibodies are released.An exaggerated response from foreign substances. Must have had a previous exposure and is not related to a sudden exposure. The reaction is mediated by Ig antibodies.

66
Q

What is Anaphylactoid?

A

Non-immune anaphylaxis caused by the release of a mediator from mast cells and basophils, and is cause by a reaction to a drug rather than an immune system activation. Triggered by direct stimulation of Mast Cells causing histamine release. Does not require prior exposure or IgE. Causes breakdown of mast cell and basophil membranes resulting in histamine release.

67
Q

What is the key difference in the treatment of anaphylaxis and anaphylactoid?

A

None. The two are treated the same.

68
Q

In immune mediated anaphylaxis 60% of reactions are mediated by ______.

A

IgE anibodies

69
Q

Why is Epinephrine used to treat Anaphylaxis?

A

Stimulates Alpha-adrenoceptors to increase Peripheral Vascular Resistance and Blood Pressure and Coronary perfusion; reversing peripheral vasodilation and decreasing angioedemaStimulates Beta1 Adrenoceptors resulting in positive ionotripic and chronotripic cardiac effects.Stimulates Beta2 resulting in bronchodilation and increased intracellular cAMP production in mast cells and basophils…resulting in the release of inflammatory mediators.

70
Q

How long does it take anaphylaxis to occur?

A

Wishing 5-10 minutes

71
Q

What are risk factors for Anaphylaxis?

A

Female, Asthma and other allergic conditions, Repeated exposure to latex (other surgeries)….Multiple surgeries increases previous exposure to latex so have increased concern for that patient.

72
Q

Why is proximity to exposure and reaction time so important in anaphylaxis?

A

Because they increase the likelihood of tachycardias, bronchospasm, and laryngeal edema.

73
Q

What is the treatment for anaphylaxis?

A

Epinephrine! Supplement epinephrine with benadryl, H2 blocker, steroids and volume replacement. Reverse hypotension and hypoxemia with IVF (crystalloid or colloid) wide open and 100% O2

74
Q

What is the dosing strategy for Epi in anaphylaxis?

A

Epinephrine 10 - 100 mcg IV if EMERGENT0.3 - 0.5 mg SQ if NOT life-threatening

75
Q

What medications should be considered if Epi is ineffective?

A

Norepinephrine and vasopressin

Pharmacology Exam 3 (2 decks)

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