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Mar: Sem 4 - Principles II > Exam 3: Immune Dysfunction > Flashcards

Exam 3: Immune Dysfunction Flashcards

1
Q

The Immune system functions to…

A

Protect the host against micro-organisms
(two types: innate and adaptive/acquired immiunity)

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2
Q

What aspect of the immune system requires no prior exposure to pathogens?

A

Innate Immunity

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3
Q

What aspect of our immune system is rapid, non-specific, and does not provide long-lasting protection?

A

Innate Immunity

has no memory, but the response is always identical

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4
Q

What are the 3 non-cellular components of innate immunity?

A
  • Epithelial and mucous membranes
  • Complement system proteins
  • Acute phase proteins

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5
Q

What are the 4 cellular components of the innate immunity system?

A
  • Neutrophils
  • Macrophages
  • Monocytes
  • NK cells (Natural Killer Cells)

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6
Q

What cell (of the innate immunity response) responds the fastest to infection?

A

Neutrophils

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7
Q

What cell (of the innate immunity response) provides a slower but more prolonged response to infection?

A

Macrophages

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8
Q

What is the Complement System?

A

Over 30 plasma and cell surface proteins that complements both innate and adaptive immunologic systems.

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9
Q

What does the Complement system do to enhance the adaptive and innate immunologic systems?

A
  • Augments phagocytes and antibodies
  • Marks pathogens for permanent destruction

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10
Q

Where are the proteins for the Complement system produced?

A

Most are produced in the Liver

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11
Q

What activates the complement system?

A

Infection of course.

C1 and C3 (Complement proteins 1 & 3).

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12
Q

What is the most numerous WBC?

A

Neutrophils

S6

Part of Innate immunity
They are Neumorous

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13
Q

What are the characteristics and actions of neutrophils?

A
  • Migrate rapidly to bacterial infections
  • Release cytokines to phagocytize
  • ½ life is 6 hours
  • Sensitive to acidic infection environments
  • Become purulent exudate

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14
Q

What type of immune cell is the largest blood cell and what is their role?

A
  • Monocytes (largest blood cell)
  • Circulates to specific tissue areas to differentiate into macrophages

not mentioned in lecture - but the chart also shows them turning into dendritic cells - and we know how tricky they like to be

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15
Q

What are the names of monocytes that have circulated to following areas:

  • Epidermis
  • Liver
  • Lungs
  • CNS
A
  • Epidermis → Langerhans
  • Liver → Kupffer
  • Lung → Alveolar cells
  • CNS → Microglia

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16
Q

What are the pertinent characteristics of monocytes/macrophages?

A
  • Mobilize just after neutrophils
  • Phagocytic destruction via NO & cytokines
  • Persist at site in chronic infections (fight infection long term)

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17
Q

So then what are all the cells a parent Granulocyte-monocyte progenitor can turn into?

A

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18
Q

What is the least common blood granulocyte? (circulating)

A

Basophils

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19
Q

What cells reside in connective tissue close to blood vessels?

A

Mast Cells

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20
Q

What are the characteristics/actions of basophils/mast cells?

A
  • Express high affinity for IgE
  • Initiate hypersensitivity reactions
  • Stimulate smooth muscle contraction i.e. bronchoconstriction

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21
Q

How do Basophils and Mast Cells initiate hypersensitivity reactions?

A
  • produce histamine
  • leukotrienes
  • Prostaglandin release
  • cytokines

His Large Prostate Crys

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22
Q

What cells play a major role in allergies, asthma, and eczema?

A

Basophils and Mast cells

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23
Q

Characteristics of Eosinophils

A
  • Heavily concentrated in GI mucosa
  • Protects against parasites
  • Degrade mast cell inflammation

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24
Q

What characteristics does Adaptive Immunity possess?

A
  • Present only in Vertebrates
  • Delayed onset of action
  • Capable of memory and specific antigen response

Vaccinations are also a form of adaptive memory

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25
Q

What type of cells do adaptive immunity cells originate from?

A

Hematopoietic stem cell on the lymphoid side (lymphoid progenitor on the chart)

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26
Q

What is the humoral component of the Adaptive Immunity system?
What does this component do?

A

B cells → produce antibodies which bind to foreign proteins of bacteria, viruses and tumors

Dr. Google says they produce IgM, IgD, IgG, IgA, and IgE antibodies, not sure if Mordacai actually said all of these - please verify

Nothing was said during lecture for this slide, I think we can delete.

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27
Q

What are the cellular components of the adaptive immunity system?

A

Helper T-cells
Cytotoxic T-cells

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28
Q

Where do T-cells originate? Where do they mature?

A

T-cells originate in the bone marrow and mature in the Thymus.

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29
Q

What are the general characteristics of T-cells?

A
  • Produce interferon and interleukin
  • Activate IgE
  • Role in chronic inflammation
  • Respond to infection

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30
Q

What is the primary example of passive immunity?

A

Maternal IgA antibodies from breast milk

Dr. M also added: IVIG intravenous immunoglobins - given to immunocompromised pts (from pooled plasma) - effective but pricy

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31
Q

How long does passive immunity last?

A

When a pt receives antibodies from someone else, the protection can last from weeks-months

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32
Q

What is the primary example of active immunity?

A

Vaccines (they trigger antibodies to be formed)

live, inactive, or recombinant

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33
Q

Describe active immunity

A
  • Pathogen deliberately administered
  • repeat exposure for a quick response to pathogens the next time

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34
Q

Is neutropenia an example of excessive or inadequate immune response?

A

Inadequate

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35
Q

Is Asthma an example of excessive or inadequate immune response?

A

Excessive

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36
Q

Are autoimmune disorders an example of excessive or inadequate immune response?

A

Trick Question!
They are a misdirection of the immune response

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37
Q

What is required for hypersensitivity development?

A

Prior sensitization (grass, latex, nuts, meds etc)

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38
Q

What is hypersensitivity?

A

Foreign antigen reaction which causes altered T-cell and antibody response

Response varies from uncomfortable rash to fatal anaphylaxis

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39
Q

What is the most common source of hypersensitivity?

A

Drugs (NMBD, ABX, PPIs, NSAIDS etc.)

Roc is #1 cause of anaphylaxis under anesthesia

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40
Q

What occurs during a Type I Allergic Response?

A
  • 1st exposure: T-Cells stimulate B cells to produce IgE immediately
  • 2ⁿᵈ exposure: Antigen releases Ca⁺⁺ → histamine, inflammatory mediators, heparin are released.

(Histamine triggers: bronchostriction, Vascular permeability, vasodilation, gastric acid)

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41
Q

What are examples of a Type I allergic response (aka immediate hypersensitivity)?

A

Anaphylaxis, Asthma, Angioedema, Conjuctivitis, Dermatitis

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42
Q

What are common drugs used to prevent the histamine effects of Type I allergic responses?

A
  • Antihistamines
  • Cromolyn Na⁺
  • Bronchodilators
  • COX Inhibitors
  • Diagnostic allergen tests
    • small doses of allergen to desensitize

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43
Q

What is another name for Type II Allergic Responses?
What mediates these types of responses?
What is the reaction severity and time?

A
  • Cytotoxic Hypersensitivity
  • Mediated by IgG, IgM, and Complement system → activate B-cells → produce antibodies.
  • Severity will vary - reaction time in minutes or hours

mediated by GMC

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44
Q

What are examples of Type II Allergic Responses?

A
  • Hemolytic Anemia
  • Myasthenia Gravis
  • Transfusion Reactions

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45
Q

What is the treatment for Type II Allergic Responses?

A
  • Anti-inflammatories
  • Immunosuppressants
  • IVIG up and coming

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46
Q

What is another name for Type III Allergic Response?

A

Immune Complex Hypersensitivity

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47
Q

What occurs with Type III Allergic Response?

A

Failure of immune system to eliminate antibody-antigen complex.

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48
Q

Where are the antibody-antigen complexes deposited in immune complex hypersensitivity?

A

Joints, kidneys, skin, eyes

causes chronic ongoing inflammation of these places

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49
Q

What antibodies mediate Type III Allergic Responses?

A

IgG and IgM

takes hours-weeks to develop

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50
Q

What are examples of Type III Allergic Responses?

A

Systemic Lupus Erythematosus and Rheumatoid arthritis

S18

51
Q

Treatment for type III allergic response?

A
  • Anti-inflammatories
  • might need immunisuppressives

S18

52
Q

What is a Type IV Allergic Response?

A

T-lymphocyte and monocyte/macrophage mediated response that does not involve antibodies.

S19

53
Q

What are examples of Type IV Allergic Responses?

A
  • Contact Dermatitis
  • Tuberculosis
  • Stevens-Johnson Syndrome

S19

54
Q

What are the most common symptoms with Type IV Allergic Responses?

A

Cutaneous symptoms

S19

55
Q

Treatment for type IV allergic reaction?

A
  • anti-inflammatories
  • immunosuppressives

S19

56
Q

Anaphylaxis

A
  • life threatening condition (oh really?)
  • about 1:5000 to 1:20,000 anesthetics
  • usually occur within 5-10 min of exposure

S21

57
Q

Symptoms of Anaphylaxis and what rhythm occurs with untreated anaphylaxis?

A
  • Systemic vasodilation
  • Hypotension
  • Extravasation of protein and fluid (bc increased vessel permeability)
  • Bronchospasm
  • PEA

S21

58
Q

What causes the loss in BP noted with anaphylaxis?

A

Vasodilation from NO release

This is from Andy - but its not anywhere on Mordacai’s slides…

59
Q

What is the pathophysiology of anaphylaxis?

A
  • Previous exposure had made IgE antibodies
  • Mast cells and basophils degranulate: release histamine, leukotrienes, prostaglandins, eosinophil/neutrophil chemotactic factor, and platelet-activating factor
  • Anaphylaxis: up to 50% of intravascular fluid extravasates

S22

lifetime prevalence 5%

60
Q

What is Biphasic anaphylaxis?

A
  • Occurs following an asymptomatic period without second exposure
  • Secondary anaphylactic episode occurring 8 - 72 hours later.

occurs is 4-5% of the pts that experience anaphylaxis

S23

61
Q

What are risk factors for a secondary anaphylactic episode?

A
  • Severe initial response
  • Initial response required multiple epi doses

S23

62
Q

What are risk factors for perioperative anaphylaxis?

A
  • Asthma (or any baseline hypersensativivity)
  • Female (not in teen years)
  • Long Anesthetic
  • Multiple past surgeries
  • Presence of other allergic conditions

FLAAM

S24

63
Q

A quick anaphylaxis diagnosis can be compromised by…

A
  • communication issues (you are trying to troubleshoot high airway pressures first etc..)
  • pt is covered by drapes

S25

64
Q

What labs can verify mast cell activation and release?

A
  • Plasma Tryptase concentration: takes 1-2 hours, and verifies mast cell activation and release
  • Plasma Histamine concentration
  • Skin testing: 6 weeks after reacion wheel and flare response

S25

65
Q

Plasma histamine concentration should be at baseline within ____ minutes of treatment.

A

60 minutes

S25

66
Q

What is the treatment for anaphylaxis?

A
  • first Call for help
  • Stop blood, drugs, colloids
  • 100% O₂
  • Epi
  • Fluids

S26

67
Q

What is the epinephrine dose for adult anaphylaxis?

A

10 mcg - 1000mcg IVP q 1-2 min

S26

68
Q

What is the epinephrine dose for child anaphylaxis?

A

1-10 mcg/kg IVP q 1-2 min

S26

69
Q

If a patient experiencing anaphylaxis is resistant to epi, what should be given?

A

Vasopressin or Methylene blue

These will inhibit NO production and thus counteract vasodilation.

S26

70
Q

What is the crystalloid dosage for anaphylaxis?

A

NS: 10 - 25 mL/kg over 20 min
repeat PRN

S26

71
Q

What is the colloid dosage for anaphylaxis?

A

10 mL/kg over 20 min
repeat PRN

S26

72
Q

Why is epinephrine the drug of choice for anaphylaxis?

A
  • ↓ degranulation of mast cells & basophils → reduced vasodilation
  • α1 = Increased blood pressure
  • β1 = positive Inotropy & chronotropy
  • β2 = Bronchodilation

S27

73
Q

What drug classes are secondary treatments for anaphylaxis?

A
  • Bronchodilators
  • Antihistamines
  • Corticosteroids

S28

74
Q

What are the antihistamines (and dosages) used as secondary treatments for anaphylaxis?

A
  • H1 → Diphenhydramine 0.5 - 1 mg/kg IV
  • H2 → Ranitidine 50 mg IV

S28

75
Q

What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?

A
  • Hydrocortisone 250 mg IV
  • Methylprednisolone 80 mg IV

S28

76
Q

What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?

A
  • Hydrocortisone 50-100 mg IV
  • Methylprednisolone 2 mg/kg IV

S28

77
Q

Type A blood will have what Antibodies, what antigens, and is compatible with what?

A

Type A blood will have
- Anti-B antibodies
- A-antigen
- compatible with A and O

S29

78
Q

Type B blood will have what Antibodies, what antigens, and is compatible with what?

A

Type B will have
- Anti-A antibody
- B antigen
- compatible with B and O

S29

79
Q

Type AB blood will have what Antibodies, what antigens, and is compatible with what?

A

Type AB will have
- no antibodies
- A and B antigens
- Universal recipient

S29

80
Q

Type O blood will have what Antibodies, what antigens, and is compatible with what?

A

Type O will have
- Anti-A and Anti-B antibodies
- No antigens
- Compatable with O (although it is the universal donor bc of lacking antigens)

S29

81
Q

Specific immune reactions: How does a transfusion reaction happen?

A
  • This is a response to surface antigen on the donor RBC
  • responds to A, B and Rh factors

S30

82
Q

Specific Immune reactions: how does transplant rejection happen?

A
  • Response to antigens on the donor organ
  • this is due to preexisting antibodies
  • can be acute or chronic

S30

83
Q

Specific immune reactions: Graves disease

A

Autoantibodies to TSH receptor
most common cause of hyperthyroidism

S30

84
Q

Specific immune responses: Multiple sclerosis

A
  • immune mediated inflammation
  • destroys myelin and underlying nerve fibers

S31

85
Q

Specific immune responses: Rheumatoid arthritis

A
  • abnormal production of proinflammatory factors
  • infection is thought to play a role

S31

86
Q

Specific immune reactions: SLE

A
  • Autoimmune and inflammatory
  • Antibodies against: RBCs, WBCs, nucleic acids, platelets, coagulation proteins
  • affects multiple organ systems

S31

87
Q

What is/are the cause(s) of hereditary angioedema?

A

C1 Esterase inhibitor deficiency/dysfunction (decreased C1) → leads to excessive bradykinin.

S33

88
Q

What factors can cause C1 esterase problems?

A
  • Menses
  • Trauma
  • Infection
  • Stress
  • Oral contraceptives

MOIST

S33

Could you of chosen another word? Perhaps Omits

89
Q

What typically limits the production of excessive bradykinin?

A

C1

C1 limits kallikrein and Factor XIIa.

S33

90
Q

What occurs anatomically with excessive bradykinin?

A
  • Laryngeal swelling
  • Vasodilation

S33

91
Q

What dose of antihistamine should be used for hereditary angioedema?

A

Trick question. Hereditary Angioedema = excessive bradykinin and is unaffected by antihistamines.

S33

92
Q

What body parts are typically effected by hereditary angioedema?

A

Legs, hands, face, upper resp tract

S33

93
Q

What is the typical cause of acquired angioedema?

A
  • ACE Inhibitors

S34

94
Q

What symptoms are conspicuously absent with acquired angioedema?

A

No Urticaria or Pruritus

S34

95
Q

What is responsible for the breakdown of bradykinin?

A

ACE

Thus ACE inhibitors = ↑ bradykinin = angioedema.

S34

96
Q

What are the treatments for Angioedema?

A
  • Airway maintenance (usually fiberoptic intubation or tracheostomy)
  • FFP (reestablish volume)
  • C1 Inhibitor concentrate
  • Epinephrine
  • Antihistamines
  • Glucocorticoids? (not first line but give later)

GA- FACE

S35

97
Q

How does the HIV infect the host?

A
  • The virus (HIV) thru reverse transcription makes a double helix DNA with all viral genetic material
  • Can change amino acid sequence; new version of the amino acids not recognized

S36

98
Q

What cells are destroyed by the HIV virus?

A

Monocytes/Macrophages and T-cells

S36

99
Q

How long does seroconversion take after inoculation with the HIV virus?

A

2-3 weeks

host experiences flu-like symptoms during the seroconversion

S37

100
Q

What are the initial signs and symptoms of HIV conversion to AIDS?

A

Weight loss and failure to thrive

S38

101
Q

How is HIV/AIDS diagnosed?

A
  • ELISA: 4-8 weeks after infection
  • Viral Load
  • CD4/Helper T lymphocytes < 200k
  • HAART agent sensitivity

S38

102
Q

Big ass list of comorbidities associated with aids, but in general….

A

In general, if our pt is immunocompromised, they are more susceptable to more diseases (duh)

S39

103
Q

Anesthesia assessment for immunocompromised: cardiac function

A
  • Abnormal EKG
  • LV dilation
  • Pulmonary hypertension
  • MI
  • Pericardial effusions (25%)

S40

104
Q

Anesthesia assessment for immunocompromised: Neuro function

A
  • Dementia
  • Increased ICP
  • Autonomic nervous dysfunction
  • Peripheral neuropathy (35%)

S40

105
Q

Anesthesia assessment: pulm

A
  • Respiratory failure
  • Pneumothorax
  • COPD

S41

106
Q

Anesthesia assessment: Endocrine/hematologic

A
  • Adrenal insufficiency
  • Glucose intolerance
  • Anemia
  • Bone marrow suppression
  • Thrombocytopenia

S41

107
Q

Anesthesia assessment: Renal

A
  • ATN
  • ESRD

S41

108
Q

Inhibition of the liver’s ____ has huge implications for anesthetic delivery in HIV/AIDS patients.

A

CYP 450’s

Affects: Hormone synthesis
Cholesterol synthesis
Vit D metabolism
Drug metabolism (prolonged)
Bilirubin metabolism (hyperbilirubinemia)

Drugs will also take much longer to clear

S42

109
Q

What s/s characterize scleroderma? (AKA: systemic sclerosis)

A
  • Inflammation
  • Vascular Sclerosis
  • Fibrosis of skin/viscera

IVF

S44

110
Q

At what age does scleroderma typically occur?
What gender is typically affected? Cure?

A
  • 20-40
  • Females
  • No cure

S44

111
Q

Where are the mobility issues and pain of scleroderma?

A
  • decreasing mobility of fingers
  • facial pain d/t vascular sclerosis affecting the facial nerve
  • Reynaud’s is common

S45

112
Q

What GI symptoms of scleroderma are particularly pertinent to anesthesia?

A
  • GI Tract Hypomotility
  • ↓ LES tone (increased risk of aspiration)

S45

113
Q

What cardiac issues is associated with scleroderma?

A
  • dysthythmias and conduction abnormalities

S45

114
Q

____ fibrosis and ____ artery stenosis are prominent considerations for anesthesia in scleroderma patients.

A

Pulmonary fibrosis and renal artery stenosis

S45

115
Q

What are the overall anesthesia implications of scleroderma?

A
  • Could have multiple organs dysfunctional
  • Arterial catheter issues i.e. may have trouble placing an Aline
  • Contracted intravascular volume
  • Aspiration risk
  • Limited neck mobility
  • ↓ pulmonary compliance

S47

116
Q

What do inhalation agents do the immune system?

A
  • Suppress NK cells
  • Induce apoptosis of T-cells
  • Impair phagocytes

Unclear effects on tumor cells - sevo stimulates renal cell carcinoma, but inhibts small cell carcinoma.

we are the knights who say “NII”

S48

117
Q

This benzodiazepine, ____, decreases the migration of neutrophils.

A

Midazolam

S48

118
Q

This induction agent, ____, will depress natural killer cell activity.

A

Ketamine

S48

K for Killer

119
Q

This induction agent, ____, decreases cytokines but promotes NK cells.

A

Propofol

S48

120
Q

What drug class will suppress NK cells?

A

Opioids

Particularly morphine and fentanyl.

S48

121
Q

What cell type plays the greatest role in chronic inflammation?

A

T-Cells

Andy

122
Q

What cell type activates IgE and produces interleukins and interferons?

A

T-Cells

Andy

123
Q

What drug class will inhibit prostaglandin synthesis?

A

NSAIDS

S48

Mar: Sem 4 - Principles II (27 decks)

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