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Principles > Immune Dysfunction > Flashcards

Immune Dysfunction Flashcards

1
Q

Types of immunity (2)

A

Innate immunity
adaptive (acquired) immunity

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2
Q

What is the function of the immune system?

A

Functions to protect the host against micro-organisms

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3
Q

Innate immunity characteristics (4)

A

Rapid, non-specific

Recognizes common pathogens

Requires no prior exposure

No long-lasting immunity; Has no memory but response always identical

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4
Q

What makes up innate immunity (non-cellular) (4)

A

Is made up from Non-cellular elements
Epithelial and
mucous membranes
Complement
Acute phase proteins

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5
Q

What makes up innate immunity (cellular) (4)

A

Cellular elements;
-Neutrophils; Fastest response; respond first
-Macrophages; Slower but sustained response
-Monocytes
-NK (natural killer) cells

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6
Q

Characteristics of Complement

A

Complements the role of other immune cells; Both innate and adaptive

Augments phagocytes and antibodies

Marks/tags pathogens for permanent destruction

Over 30 plasma and cell surface proteins that are involved in the complement system

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7
Q

Where are complement elements produced?

A

Most elements produced in liver
Consider liver failure/ ESLD = less good protective/ complement system

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8
Q

How are the complement cells/elements activated

A

C1 or alternately C3

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9
Q

Most numerous of WBC’s

A

neurtrophils

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10
Q

Neutrophils migrate ____ in ____ infections and release _______ that then ______ after that they become ______

A

Migrate rapidly in bacterial infections that Release cytokines->phagocytize

After they phagocytize/ release cytokines they Become purulent exudate

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11
Q

Neutrophils 1/2 life

A

6hrs

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12
Q

What are neutrophils sensitive to?

A

Sensitive to acid environments of infection

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13
Q

largest blood cells

A

Monocytes

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14
Q

Monocytes circulate to _____ then turn into ______

A

Circulate to tissue specific areas then turn into macrophages when in the specific areas

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15
Q

Macrophages on the epidermis turn to

A

Langerhans

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16
Q

Macrophages on the liver turn into

A

Kupffer cells

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17
Q

Macrophages to the lung become

A

Alveolar cells

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18
Q

Macrophages to the CNS become

A

Microglia

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19
Q

Monocytes characteristics (4)

A

-Mobilize just after neutrophils
-Phagocytic destruction
-Produce NO (VD) and cytokines
-Persist at sites of chronic infection (keep working for longer)

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20
Q

Least common blood granulocytes

A

Basophils

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21
Q

Where to mast cells reside?

A

Reside in connective tissue close to blood vessels

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22
Q

Basophils and mast cells characteristics (4)

A

Express high affinity receptors for IgE

Initiators of hypersensitivity

Stimulate smooth muscle contraction

Play major role in allergies, asthma, eczema

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23
Q

Basophils and mast cells release…..(4)

A

Histamine, leukotrienes, cytokines, prostaglandins

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24
Q

What cells are Heavily concentrated in GI mucosa

A

eosinophils

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25
Q

Characteristics of eosinophils (2)

A

Protect against parasites
Degrade mast cell inflammation

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26
Q

Adaptive immunity Characteristics (4)

A

-Present only in vertebrates

-Delayed onset of activation

-Capable of memory and specific antigen response

-Derived from hematopoietic stem cells (lymphoid precursor)

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27
Q

Adaptive immunity humoral component

A

B cells

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28
Q

B cells produce______ that bind to ___,____,____

A

Produce antibodies (IGE, IGA, IGM) that bind to foreign proteins of bacteria, viruses, and tumors

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29
Q

Adaptive immunity Cellular component

A

T cells

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30
Q

Types of T cells

A

helper and cytotoxic

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31
Q

T cells originate in the ____ and mature in the _____

A

Originate in bone marrow

Mature in thymus (thymectomy = increase risk of infection)

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32
Q

What to T cells characteristics (4)

A

Produce interferon, interleukin

Role in chronic inflammation

Respond to infection

Activate IgE

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33
Q

Active immunity

A

Pathogen deliberately administered then you expect antibodies to be created

Repeat exposure if see virus/bacteria again -> quicker response

Lasts for months to years

Vaccines
Live, inactivated, recombinant

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34
Q

Passive immunity

A

Receive antibodies from another individual (not making them)

Protection lasts few weeks to months

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35
Q

Maternal IgA antibodies via breast milk is what type of immunity

A

passive

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36
Q

Neutropenia is what type of immune response

A

Inadequate immune response

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37
Q

Asthma or eczema is what type of immune response

A

Excessive (or exaggerated)

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38
Q

Autoimmune disorders is what kind of immune response

A

Misdirection

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39
Q

what is hypersensitivity

A

Reaction to a foreign antigen

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40
Q

What does hypersensitivity cause

A

Causes altered T-cell and antibody response (IGE = long memory/response)

Response varies from uncomfortable to fatal

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41
Q

What does hypersensitivity require

A

Requires prior sensitization;
Grass, latex, gluten, nuts, medications

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42
Q

Most common hypersensitivity

A

Most common: drugs
NSAIDS, antibiotics, PPI’s, NMBD

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43
Q

Type I allergic response

A

immediate hypersensitivity

T cells stimulate B cells
IgE antibodies already produced (the memory exists)

On second exposure
Antigen releases calcium
Release of histamine, heparin, inflammatory mediators

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44
Q

Histamine triggers causes….

A

bronchoconstriction, vascular permeability, vasodilation, gastric acid

45
Q

anaphylaxis, asthma, angioedema, conjuctivitis, dermatitis are examples of…….

A

Type I allergic response/immedate hypersensitivity

46
Q

Treatment of Type I responses

A

Prevent histamine effects:

Antihistamines

Cromolyn sodium (helps with bronchconstriction)

Bronchodilators

COX pathway inhibitors

Diagnostic tests (dx what they are allergic to)

Small doses of allergen to desensitize

47
Q

Type II allergic response

A

cytotoxic hypersensitivity

IgG, IgM, and complement mediated
Activattion of B cells to produce antibodies

48
Q

Reaction time for type 2 allergic response/ cytotoxic hypersensitivity

A

minutes - hrs

49
Q

hemolytic anemia, myasthenia gravis, transfusion reactions are examples of _____

A

Type II allergic response

50
Q

Treatment for cytotoxic hypersensitivity

A

Anti-inflammatories
Immunosuppressives

51
Q

Type III allergic response

A

immune complex hypersensitivity

Failure of the immune system to eliminate antibody-antigen complex -> keep depositing the antigens/ antibodies and elements and are deposited in the
Joints, kidneys, skin, eyes

Also mediated by IgG and IgM

52
Q

Type III allergic response response time

A

Take hours-weeks to develop

53
Q

systemic lupus erythematosus (SLE), rheumatoid arthritis are examples of what type of response???

A

Type III allergic response

54
Q

Treatment for Type III allergic response

A

Anti-inflammatories
Maybe immunosuppressives

55
Q

Type IV allergic response

A

T lymphocyte, monocyte/macrophage mediated and Does not involve antibodies

56
Q

contact dermatitis, tuberculosis, Stevens-Johnson syndrome are what type of reaction

A

Type IV allergic response

57
Q

Cutaneous symptoms are most common in what reaction?

A

Type IV allergic response

58
Q

Treatment for Type IV allergic response

A

Anti-inflammatories
immuosuppressives

59
Q

Anaphylaxis prevalence

A

1 in 5000 to 1 in 20,000 anesthetics

60
Q

Symptoms of anaphylaxis (5)

A

Systemic vasodilation
Hypotension
Extravasation of protein and fluid
Bronchospasm
Untreated…PEA

61
Q

Anaphylaxis reaction time

A

Usually occurs within 5-10 minutes of exposure

62
Q

Anaphylaxis pathophysiology

A

Previous exposure creates IgE antibodies from -> Subsequent exposure to antigen->Antigen-antibody reaction->Mast cells and basophils degranulate->Release histamine, leukotrienes, prostaglandins, eosinophil/neutrophil chemotactic factor, platelet-activating factor->Symptoms of anaphylaxis->Up to 50% of intravascular fluid extravasates -> Lifetime prevalence 5%

63
Q

“Biphasic” anaphylaxis occurs in____

A

Occurs in 4-5% of patients

64
Q

“Biphasic” anaphylaxis

A

Secondary anaphylactic episode that Occurs following an asymptomatic period without second exposure

65
Q

“Biphasic” anaphylaxis time to response

A

Occurs 8-72 hours later

66
Q

Risk factors for “Biphasic” anaphylaxis (2)

A

Severe initial response

Initial response required multi doses of epi

67
Q

Risk factors for perioperative anaphylaxis (5)

A

Asthma
Longer duration of anesthesia
Females (not in teen yrs)
Multiple past surgeries
Presence of other allergic conditions

68
Q

Diagnosis of anaphylaxis can be compromised because of …..(2)

A

Communication issues
Covered by surgical drapes

69
Q

What kind of test can verify mast cell activation and release

A

Plasma tryptase concentration
1-2 hrs

70
Q

To see Baseline within 60 minutes of treatment you should run what kind of test to diagnose anaphylaxis

A

Plasma histamine concentration

71
Q

Skin testing time and response

A

6 weeks after reaction
Wheal and flare response

72
Q

Primary treatment for anaphylaxis

A

Stop administration of drugs, blood, colloids

100% oxygen

Epinephrine

fluid therapy

73
Q

Epinephrine dose for anaphylaxis adults and children

A

10mcg-1mg IVP; repeat q 1-2 minutes (adults)

1-10mcg/kg IVP; repeat q 1-2 minutes (child)

74
Q

In resistant to epi anaphylaxis use…..

A

Resistant to epi use; vasopressin, methylene blue and they
Inhibits NO production

75
Q

Fluid therapy for anaphylaxis

A

Crystalloid: NS 10-25 ml/kg over 20 minutes; repeat prn

Colloid: 10ml/kg over 20 minutes; repeat prn

76
Q

How does Epinephrine work against anaphylaxis

A

Decreases degranulation of mast cells and basophils ↓ effect of degranulation (vasodilation)

Alpha1: supports BP
Beta 1: inotropic and chronotropic effects
Beta 2: bronchodilation

77
Q

Secondary treatment for anaphylaxis (4)

A

Bronchodilators
Antihistamines
Corticosteroids
Observe for relapse
allergy

78
Q

Antihistamine meds/ dose for anaphylaxis

A

H1: diphenhydramine 0.5-1mg/kg IV
H2: ranitidine 50mg IV

79
Q

Corticosteroids meds/ dose for anaphylaxis children and adults

A

Hydrocortisone 250 mg IV or methylprednisolone 80 mg IV (adults)

Hydrocortisone 50-100 mg IV or methylprednisolone 2 mg/kg IV (child)

80
Q

Transfusion reactions characteristics

A

Response to surface antigen on donor RBC
A, B, AB and O and Rh antigens

81
Q

Transplant rejection

A

Response to antigens on donor organ
Due to preexisting antibodies
Acute or chronic

82
Q

Graves disease

A

Most common cause of hyperthyroidism

Caused by autoantibodies to the TSH receptor

83
Q

Multiple sclerosis

A

Immune mediated inflammation

Destroys myelin and underlying nerve fibers

84
Q

Rheumatoid arthritis

A

Abnormal production of pro inflammatory factors that are deposited on the skin and joints and eyes
Infection thought to play a role

85
Q

SLE

A

Autoimmune, inflammatory
Antibodies against RBC, lymphocytes nucleic acids, platelets, coagulation proteins
Affects multiple organ systems

86
Q

Angioedema is what type of reaction

A

Type 1 hypersensitivity response

87
Q

What causes Hereditary angioedema

A

C1 esterase inhibitor deficiency/dysfunction. Causes of the deficiency/ dysfunction caused by

menses
trauma
infection
stress
oral-contraceptives

and excessive production of bradykinin

88
Q

What does excessive production of bradykinin cause

A

Usually limited by C1 inhibiting kallikrein and factor XIIa
Laryngeal swelling, potent vasodilator
Not responsive to antihistamines

89
Q

What is the relationship between ACE and bradykinin

A

ACE causes the breakdown of bradykinin….ACE inhibitors block that breakdown.

ACE inhibitors
Responsible for degradation of bradykinin
Affects vascular permeability; stimulates substance P
Vasodilation and fluid extravasation

90
Q

Acquired angioedema presents with…….

A

Lip, tongue, face swelling
Urticaria and itching are absent!

91
Q

treatment of angioedema (6)

A

Airway maintenance
(tracheal intubation
Tracheostomy)

FFP

C1 inhibitor concentrate

Epinephrine

Antihistamines
glucocorticoids

92
Q

One of the most common forms of acquired immune deficiency

A

HIV/AIds

93
Q

What does HIV/AIDS

A

The virus (HIV) thru reverse transcription makes a double helix DNA with all viral genetic material
Can change amino acid sequence; new version not recognized
Destroys monocytes, macrophages, Tcells

AIDS is final stage of infection caused by HIV

94
Q

Seroconversion with HIV/Aids happens in what time frame?

A

2-3 weeks after inoculation

95
Q

Symptoms of HIV/AIds

A

Flu like;
Fever
Fatigue
Night sweats
Pharyngitis
Myalgias
Arthralgias

96
Q

How is HIV converted to aids

A

Higher basal levels of virus…..more rapid conversion to AIDS

97
Q

Initial symptoms of HIV conversion to aids….

A

Weight loss
Failure to thrive

98
Q

Diagnosis of AIDs (4)

A

-ELISA: 4-8 weeks after infection
-Viral load
-CD4/helper T lymphocytes <200,000
-HAART agent sensitivity

99
Q

What skin concerns do we have with HIV/Aids pts

A

Fat pad redistribution

make sure they are padded

100
Q

HIV/AIDs pts metabolism consideration

A

Inhibition of cytochrome P-450 (prolonged effect)
Hormone synthesis
Cholesterol synthesis
Vit D metabolism
Drug metabolism
Bilirubin metabolism

101
Q

Scleroderma other name and is characterized by …..

A

“systemic sclerosis”

Inflammation
Vascular sclerosis
Fibrosis of skin and viscera

102
Q

Scleroderma Risk factors

A

Onset 20-40, mostly women, no cure

103
Q

S/s of scleroderma

A

Localized, limited, diffuse

Decreasing mobility of fingers
Facial pain
Raynaud’s

*Hypo-motility of GI tract
*LES tone decreased

Cardiac dysrhythmias/conduction abnormalities
*Pulmonary fibrosis
*Renal artery stenosis

104
Q

Preoperative labs for Scleroderma pts (4)

A

ECG

BUN/Creatinine

CBC/Platelets

CXR/PFT’s

105
Q

Anesthesia implications of scleroderma

A

Organ system dysfunction

Arterial catheter concerns
Continue preop calcium channel blockers

Contracted intravascular volume

Aspiration risk (RSI)

Limited neck mobility/Pulmonary compliance

106
Q

Inhalation agents effect on the immune system

A

Suppress NK cells, induce apoptosis of Tcells

Impair phagocytes

Unclear impact on tumor cells
(Sevo stimulates renal cell (bad); inhibits non-small cell (good))

107
Q

Induction meds on the immune system

A

Midazolam decreases migration of neutrophils

Ketamine depresses NK cell activity

Propofol decreases cytokines, PROMOTES NK cells

108
Q

Opioids effect on the immune system

A

Suppress NK cells (especially morphine and fentanyl)

109
Q

NSAIDs affect on the Immune system

A

Beneficial; inhibit prostaglandin synthesis

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