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Pharmacology Exam 3 Final > Immune Dysfunction > Flashcards

Immune Dysfunction 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 immunity

The 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 Immunity

Requires 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 Arthritis
Diabetes Mellitus type 1
Systemic Lupus Erythematous
Multiple sclerosis
Infectious disease
Asthma
HIV/AIDS
Hematologic 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 Erythematous
Rheumatoid Arthritis
Lymphoma
Myleproliferative disease
Severe 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 do we worry about when Neutrophils exceed 100,000/mm3?

A

An increase in the granulocyte count does not produce specifc symptoms or signs unless the count exceeds 100,000/mm3. Such marked leukocytosis can produce leukostasis (extremely elevated blast cell count and symptoms of decreased tissue perfusion), resulting in splenic infarction and reduction in the 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 Reaction: Associated with urticaria, bronchospasm, flushing and hypotension

Bradykinin Release: No Allergic Reaction Symptoms

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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 or dysfunction of the autosomal dominant esterase inhibitors, C1 Inhibitor. The absence of C1 esterase inhibitor leads to the release of vasoactive mediators that increase vascular permeability and produce edema via bradykinin.

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20
Q

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

A

Increased permeability
Edema, 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.

This drug-induced angioedema is thought to result from increased availability of bradykinin made possible by the ACE inhibitor–mediated blockade of bradykinin catabolism.

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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

Androgens: “Mainstay of prophylactic therapy.” Believed to INCREASE hepatic synthesis of C1 esterase inhibitor.

Antifibrinolytic Therapy (Aminocaproic Acids or Aprontinin): Thought to act by inhibiting plasmin (Degrades Fibrin to reduce clots) activation.

FFP (2-4 Units) replaces the deficient enzyme (C1-Inhibitor) 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

-Avoid Catecholamines, antihistamines, and antifibrinolytics during acute episodes…NOT USEFUL FOR ACUTE EPISODES OF ANGIOEDEMA

  • Tracheal intubation may be required
  • Be prepared for tracheostomy
  • Regional anesthetics well tolerated
  • Minimize suctioning
  • Have Cl inhibitor IV INFUSION ready
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27
Q

Hypersensitivity Reaction Type I induces reactions by which physiologic responses?

A

Type I allergic reactions are IgE mediated and involve mast cells and basophils. The majority of cases of anaphylaxis are IgE-mediated events.

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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.

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32
Q

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

A

IgG or IgM

Type II reactions mediate cytotoxicity via IgG, IgM, and complement. Type II reactions usually manifest as hemolytic anemia, thrombocytopenia, or neutropenia, since these are the cell types most often affected. Clinical presentation and severity vary widely, and presentation may be delayed for several days.

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33
Q

Blood Transfusion reactions are which type of hypersensitivity reaction?

A

Type II

Type II reactions usually manifest as hemolytic anemia, thrombocytopenia, or neutropenia, since these are the cell types most often affected.

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34
Q

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

A

Rh-Negative Mother to Rh-Positive Fetus

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35
Q

PCN Reaction is what type of Hypersensitivity reaction?

A

Type II

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36
Q

Readministration of PCN would result in which type of reaction?

A

Type I

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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.

Type II reactions usually manifest as hemolytic anemia, thrombocytopenia, or neutropenia, since these are the cell types most often affected.

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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. Antigen-antibody complexes attached to basement membranes then bind to complement, which stimulates the release of cytotoxins by neutrophils at the site of attachment. This results in damage to tissues.

Type III reactions produce tissue damage via immune complex formation and deposition and often lead to glomerulonephritis, urticaria, vasculitis, and arthralgias.

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39
Q

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

A

Innate Immunity

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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.

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41
Q

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

A

Adaptive Immunity

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42
Q

Adaptive immunity is non-specific (T/F)

A

False.

Adaptive immunity is specific

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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

Hereditary Angioedema resulting in facial and laryngeal edema can be 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

Type III reactions produce tissue damage via immune complex formation and deposition and can lead to glomerulonephritis in more severe forms.

Binding of antigen-antibody complexes to basement membranes of glomerulus lead to activation of complement which results in release of cytotoxins by neutrophils at the site of attachment…In this case, leading to glomerulonephritis.

60
Q

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

A

Uticaria, vasculitis and arthralgias

Type III reactions produce tisssue damage via immune complex formation and deposition and often lead to urticaria, vasculitis, and arthralgias in less intense forms.

61
Q

What is Type IV Hypersensitivity reaction?

A

Type IV reactions are marked by T lymphocyte–mediated DELAYED hypersensitivity and are typically drug reactions.

62
Q

What are 3 cutaneous examples of Type IV hypersensitivity reaction.

A

Contact dermatitis (Steven-Johns Syndrome)
Epidermal necrosis
Poison 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 mediated

Type 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

Epinephrine, by increasing intracellular concentrations of cAMP, increases intracellular Ca++ which increases constrictions and restores membrane permeability and decreases the release of vasoactive mediators. The β-agonist effects of epinephrine relax bronchial smooth muscle and reverse bronchospasm.

Stimulates Alpha-adrenoceptors to increase Peripheral Vascular Resistance and Blood Pressure and Coronary perfusion; reversing peripheral vasodilation and decreasing angioedema

Stimulates 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, decreasing the release of inflammatory mediators.

70
Q

How long does it take anaphylaxis to occur?

A

Within 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. Albuterol for Bronchospasm.

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 EMERGENT

0.3 - 0.5 mg SQ if NOT life-threatening

May repeat every 1-2 minutes until satisfactory blood pressure response achieved.

75
Q

What medications should be considered in cases where cardiovascular collapse is unresponsive to epinephrine?

A

In cases where cardiovascular collapse is unresponsive to epinephrine, alternative vasopres- sors such as vasopressin, glucagon, or norepinephrine should be considered.

76
Q

Both Diphenhydramine (Benadryl) and Corticosteroids are effective as first line treatment against Anaphylaxis. (T/F)

A

False.
Both are effective for prevention and can be used to supplement Epinephrine (First Line), but not as first line treatment for anaphylaxis.

77
Q

What is the MOA of Diphenhydramine in the treatment os Anaphylaxis?

A

Competes with histamine receptors and may displace the histamine from its receptors…Remember, it is COMPETITIVE, so it may not be successful in the presence of excessive histamine.

78
Q

Why is Diphenhydramine used as a supplemental treatment for anaphylaxis?

A

Benadryl is an H1 antagonist, and if it successful, it will decrease pruritus and bronchospasm.

Histamine is a powerful stimulant of sensory nerve endings, specifically those mediating pain and itching.
H1 receptors also mediate inflammatory and allergic reactions:
-Vascular: Vasodilation
-Smooth Muscle: Bronchoconstriction
-Neurons: Sensory Nerve Endings
-CNS: Neurotransmitters that stimulate “wakefulness and appetite suppression.”

79
Q

Diphenhydramine is only effective once vaso-mediators have been releases. (T/F)

A

False.
Diphenhydramine is NOT effective once vaso-mediators have been released. It should be given as pre-treatment in patient with known allergic reactions.

80
Q

What is the action of Corticosteroids in Anaphylaxis?

A

There is not evidence indicating corticosteroids as useful in the treatment of anaphylaxis. The action may be related to enhancement of beta agonist effects of other pharmacological treatment or inhibition of the release of arachidonic acid responsible for production of leukotrienes and prostaglandins.

Corticosteroids may, however, be uniquely helpful in patients experiencing life-threatening allergic reactions resulting from activation of the complement system.

81
Q

What should be used as treatment for bronchospasm in anaphylaxis?

A

Albuterol

82
Q

When does a true drug reaction occur and what is an exception to this?

A

True drug reactions occur within 5-10 minutes after drug administration

Exception: Latex, which is 30 minutes

83
Q

What type of Hypersensitivity Reaction is exhibited by urticaria at the injection site?

A

None, reaction around injection site is not an allergy.

84
Q

A patient with a Penicillin allergy is at greater risk for any drug allergy. (T/F)

A

True

PCN allergy increases risk to any drug by 3-4x

85
Q

What should be considered as an allergen when allergic reactions occur during the operative maintenance phase?

A

Latex
Volume Expanders: Especially Colloids
Dyes

86
Q

60% of allergic drug reactions in anesthesia are from ______.

A

Muscle Relaxants. Especially Succ’s and Roc.

87
Q

What is the allergic affect of Atricuium?

A

Atricuruium has histamine release, but it is NOT an allergic reaction

88
Q

Allergic reactions to Muscle Relaxants are mediated by _____.

A

IgE

89
Q

Why might a patient have a true allergic reaction to Muscle Relaxants on FIRST exposure?

A

Patients may develop sensitivity to quaternary and tertiary ammonium ions that are found in many OTC drugs and cosmetics. A patient may become sensitized by use of these OTC’s, then exhibit true allergic reaction on first exposure to Muscle Relaxants.

90
Q

What should be done pre-op if a patient has a history of allergic reaction to one Muscle Relaxant?

A

A skin test should be done pre-op.

However, if a patient is allergic to one MR, they are likely allergic to all, so may want to avoid MR’s or pretreat with Diphenhydramine and steroids.

91
Q

A patient may have a reaction to MR on first exposure. (T/F)

A

True.

A patient may become sensitized and may react to MR on first exposure.

92
Q

Which 2 drugs used in anesthesia could trigger an allergic reaction due to presence of ammonium ions?

A

Morphine and Neostigmine.

Pretreat with antihistamines and steroids

93
Q

Benzy Isoquinolinines cause true allergic reactions. (T/F)

A

False.
The innate property of these drugs cause direct mast cell degranulation and histamine release, but they are not IgE mediated so are not true allergic reactions.

94
Q

Which 3 Benzyl Isoquinolinines cause direct mast cell degranulation?

A

D-tubocurarine, atracurium and mivacurium

95
Q

Which drugs used for induction are noted to cause allergic reactions?

A 
Most Common: Barbituates
Very Rare:
     Midazolam
     Etomidate
     Ketamine

Propofol: Caution in patients with history of allergic reactions to egg or soy; BUT does not mean you cannot use it!

96
Q

What property of Propofol makes it a drug to use with caution in patients with egg or soy allergies?

A

Lecithins are the culperate.

97
Q

Local Anesthetics are the most common anesthetics associated with allergic reactions. (T/F)

A

False.
Allergic reaction to LA’s is RARE. Reactions to LA’s are NOT allergic, but related to direct intravascular injection or absorption of the added epinephrine.

98
Q

True allergic reactions to Local Anesthetics are exhibited by:

A

Uticaria, laryngeal edema and bronchoconstriction

99
Q

Which type of Local Anesthetic is most likely to cause an allergic reaction?

A

Ester type; due to the additive preservative methylparaben

100
Q

What is methylparaben?

A

The preservative added to ester local anesthetics which is the cause of allergic reactions

101
Q

Why is it rare to have a true allergy to opioids.

A

Because opioids are seen by the body as a naturally occurring endorphin.

102
Q

Which opioids evoke histamine release but do not cause a true allergic reaction?

A

Morphine, Codeine and meperidine.

103
Q

Which opioid does not stimulate mast cell degranulation?

A

Fentanyl

104
Q

Which Volatile Anesthetics may cause a severe allergic reaction involving the liver?

A

Halothane Hepatitis

105
Q

What is Halothane Hepatitis?

A

An allergic reaction to the volatile anesthetic Halothane. Previous exposure may illicit antibody formation due the to reaction of reactive oxidative metabolites with the hepatic microsomal proteins.

This reaction may not be seen on first administration but seen on second, so know it is a true allergic reaction.

106
Q

Which other Volatile Anesthetics may induce Hepatitis?

A

Minimal Risk: Isoflurane and Desflurane

107
Q

Which Volatile Anesthetic does NOT cause hepatitis, and why?

A

Sevoflurane does not produce the oxidative metabolites that cause the reaction in the liver.

Pharmacology Exam 3 Final (2 decks)

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