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N935 Advanced Pathophysiology > Hyper- and Hypo- Immune Disorders > Flashcards

Hyper- and Hypo- Immune Disorders Flashcards

1
Q

What are the two branches of the immune system?

A
  1. Innate

2. Adaptive

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2
Q

What is the innate immune system?

A

non-specific response that targets many common pathogens;

NOT PATHOGEN SPECIFIC, limited diversity

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3
Q

Does the innate immune system need prior exposure?

A

NO

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4
Q

How does one develop an innate immune system?

A

passed on from previous generation;

does NOT need previous exposure to pathogen

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5
Q

What compromises the innate immune system?

A
  • epithelial & mucous membranes
  • complement factors
  • neutrophils
  • macrophages
  • monocytes
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6
Q

What is the adaptive immune system?

A

system that must be developed individually; develops memory & is specific towards antigens
delayed response

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7
Q

Which is faster, the innate or adaptive immunity?

A

innate,

adaptive is delayed

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8
Q

What types of cells are involved in adaptive immunity?

A

lymphocytes;

B lymphocytes
T lymphocytes

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9
Q

What are the principle cells of the innate immune system?

A

myeloid cells

→ macrophages, neutrophils, dendritic cells

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10
Q

What is the innate immune system mediated by?

A

cells and plasma proteins that are ALWAYS present

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11
Q

Is the adaptive immune system weak or powerful?

A

powerful; usually “silent” until pathogen is found

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12
Q

What creates the receptors of the adaptive immune system?

A

rearrangements of antigen-receptor genes that occur during the maturation of the lymphocytes

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13
Q

What are the principle cells of the adaptive immune system?

KNOW!!

A

B lymphocytes

T lymphocytes

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14
Q

The adaptive immune system is mediated by what TWO mechanisms?

A
  1. Humoral Immunity
    → mediated by antibodies produced by B cells
  2. Cell-Mediated
    → T cells activated by protein antigens from antigen presenting cells (APCs)
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15
Q

What type of cell mediates humoral immunity?

of the adaptive immune system

A

B cells.

antibodies

   1. NEUTRALIZE MICROBES
   2. opsonize microbes for phagocytosis
   3. activate the complement system
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16
Q

What type of cell mediates, cell-mediated adaptive immunity?

A

T cells. [2 types]

→ activated by protein antigens from antigen presenting cells (APCs)

require repeat antigen stimulation

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17
Q

What are the 2 types of T cells?

A

CD4+ helper T cells [secrete cytokines to activate macrophages; helps B cells make antibodies; stimulates inflammation]

CD8+ helper T cells [kill infected & transformed cells]

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18
Q

The three dysfunctions of the innate immune system are:

A
  1. inadequate response
  2. excessive response
  3. misdirected response
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19
Q

What are 4 types of an inadequate innate immune system response?

A
  1. neutropenia
  2. abnormal phagocytosis
  3. deficient in the complement system
  4. hyposplenism
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20
Q

What are 3 types of excessive innate immune response?

A
  1. neutrophilia
  2. monocytosis
  3. asthma

*over-reaction

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21
Q

What is one example of a misdirected innate immune response?

A

angioedema

*body responds, but edema is sent to the wrong place

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22
Q

What are 6 dysfunctions of the adaptive immune system?

A
  1. defects in antibody production
  2. defects in T lymphocytes
  3. combined immune system defects (SCIDs)
  4. allergic reactions
  5. anaphylaxis
  6. autoimmune disorders
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23
Q

” -penia”

A

lack of, poverty, deficiency

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24
Q

” -philia”

A

affinity, attraction, fondness

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25
Q

allergy

A

reactions against normally harmless environmental antigens

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26
Q

hypersensitivity

A

excessive immunologic reactions to microbes or environmental agents dominated by inflammation

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27
Q

atopy

A

propensity or genetic tendency to develop allergic reactions

[ie. lots of food and/or environmental allergies]

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28
Q

Antibody (Ab) is also known as…

A

an immunoglobulin (Ig)

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29
Q

What is an antibody?

A

large, Y-shaped, protein USED by the immune system TO IDENTIFY and NEUTRALIZE FOREIGN OBJECTS such as pathogenic bacteria and viruses

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30
Q

Where do T cells come from?

A

Thymus

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31
Q

Where do B cells come from?

A

Immature cells are released from the bone marrow; mature in the circulation

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32
Q

How are neutrophils formed?

A

by stems cells in the bone marrow

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33
Q

What % of WBCs are neutrophils?

A

40-70%

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34
Q

What are neutrophils?

A

phagocytes that are found in the blood stream;

FIRST RESPONDERS TO INFLAMMATION
[especially bacterial]

*predominant cells in pus

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35
Q

What is neutropenia?

A

neutrophil count <1500/mm3

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36
Q

What are 5 types of neutropenia?

A
  1. neonatal sepsis
  2. Kostmann syndrome (autosomal recessive)
  3. acquired defects (chemo, antivirals)
  4. autoimmune (Lupus, RA)
  5. Infection [rate of production is inadequate for consumption]
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37
Q

What are the treatments for neutropenia?

A
  1. stop causative agent
  2. granulocyte stimulating factor (filgrastim)
  3. bone marrow transplant
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38
Q

What does the spleen do?

A

primary creator of RBCs in fetal life (up to 5 months old)

  1. removes old RBCs
  2. blood reservoir (250mL)
  3. recycles iron
  4. metabolizes hemoglobin
  5. stores 1/4 circulating lymphocytes
  6. stores & clears platelets
  7. synthesizes antibodies in the white pulp
  8. removes antibody-coated bacteria
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39
Q

How is hemoglobin broken down?

A

globin is degraded into amino acids

heme is metabolized into bilirubin [which is removed by the liver]

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40
Q

How do the spleen & liver “work together”?

A

the spleen “eats” bacteria, blood flow goes to the liver where toxins are removed & “cleansed” from the blood

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41
Q

What is the size of the spleen?

A

healthy adult:
2.8in x 5.5in

between 1oz-8oz

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42
Q

Asplenia

A

absence of normal spleen function;

type of immuno-dysfunction

** sepsis risk is increased 350-fold d/t inability to clear bacteria from the blood [S.pneumoniae, E.coli, H.flu, malaria]

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43
Q

Hyposplenism

A

reduced spleen function

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44
Q

How can sickle cell affect the spleen?

A

sickle cell can cause auto-infarction, resulting in vaso-occlusive disease

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45
Q

What is leukocytosis?

A

WBC count is above normal range;

normal reaction as an inflammatory response but can be from

 - tumors
 - leukemias
 - stress
 - pregnancy
 - convulsions 
 - medications [corticosteroids, lithium, beta agonists]
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46
Q

What are the 5 types of leukocytosis?

A
  1. neutrophilia
  2. eosinophilia
  3. basophilia
  4. monocytosis
  5. lymphocytosis
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47
Q

What is eosinophilic esophagitis?

A

chronic immune system disease in which a type of WBC (eosinophil) builds up in the lining of the esophagus

→ reaction to foods, allergens or acid reflux
- inflame or injure esophageal tissue; can lead to difficulty swallowing or food to get stuck

*food aversion or non-specific s/s

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48
Q

Neutrophilia

A

> 7000/mm3

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49
Q

4 causes of neutrophilia

A
  1. pancreatitis
  2. pyelonephritis
  3. peritonitis
  4. pneumonia
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50
Q

Leukostasis; count & blood

A

> 100,000/mm3;

thick blood flow and WBC clumping, can lead to TIAs & strokes

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51
Q

Myeloproliferative disorder or hematologic malignancy

A

> 50,000/mm3

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52
Q

What is asthma?

A

exaggerated bronchoconstrictor response to stimuli

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53
Q

Cause of extrinsic asthma:

A

IgE production, allergens

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54
Q

Cause of intrinsic asthma:

A

triggers are unrelated to the immune system:

  • ETT placement
  • cold
  • exercise
  • stress
  • inhaled irritants
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55
Q

When does extrinsic asthma typically develop?

A

childhood or early adulthood

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56
Q

When does intrinsic asthma typically develop?

A

later in adulthood

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57
Q

Having a personal and/or family history of asthma is most related to which kind of asthma?

A

extrinsic asthma

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58
Q

What type of asthma is considered a hypersensitivity reaction to an allergen?

A

extrinsic

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59
Q

Increased IgE levels are most often found in what kind of asthma?

A

extrinsic

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60
Q

Does intrinsic asthma include recognizable allergens? elevated IgE levels?

A

no recognizable allergens;

normal IgE levels

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61
Q

When do s/s of intrinsic asthma appear?

A

after respiratory infection, emotional reactions, exercise, handling chemicals, taking aspirin, etc.

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62
Q

What is the hallmark sign of misdirected innate immunity?

A

angioedema

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63
Q

What are the two types of misdirected innate immunity?

A
  1. hereditary

2. acquired

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64
Q

What two types of edema form in misdirected innate immunity?

A

SQ and submucosal

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65
Q

What structures are involved in misdirected innate immunity angioedema?

A

face, extremities, GI tract

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66
Q

What is the most important thing to remember about acquired misdirected innate immunity?

A

it will NOT respond to epinephrine

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67
Q

Deficiency in ___ is the most common form of hereditary angioedema.

A

C1 esterase inhibitor

[autosomal dominant deficiency/dysfunction]

C1INH deficiency is Type 1.
C1INH dysfunction is Type 2.

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68
Q

How does a lack of C1 esterase inhibitor lead to edema?

A

absence of C1 esterase inhibitor leads to the RELEASE of VASOACTIVE MEDIATORS that increase vascular PERMEABILITY…… producing edema via bradykinin

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69
Q

How long will edema d/t C1 esterase deficiency last?

A

24-72 hours

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70
Q

How do ACEi cause bradykinin induced angioedema?

A

ACEi block bradykinin catabolism leading to elevated levels of bradykinin.

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71
Q

How does a person develop acquired bradykinin mediated angioedema?

A

Patients with lymphoproliferative disorders can develop antibodies to the C1 inhibitor… giving rise to a syndrome that closely resembles hereditary angioedema.

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72
Q

Angioedema can be caused via two different physiological mechanisms, these two pathways are…

A
  1. release of mast cell mediators

2. bradykinin release (no allergy symptoms)

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73
Q

Angioedema caused by the release of mast cell mediators is associated with what other s/s?

A

urticaria, bronchospasm, flushing, hypotension

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74
Q

What is the treatment of mast cell mediated angioedema?

A

drugs usually used to treat allergy & anaphylaxis.

  • epinephrine
  • antihistamines
  • glucocorticoids
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75
Q

What is the treatment of bradykinin mediated angioedema?

A

C1 inhibitor concentrate (is the preferred treatment).

  • kallikrein inhibitor
  • bradykinin receptor antagonist

FFP can be administered if the above are unavailable [it contains the deficient enzyme]

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76
Q

What is the treatment of ACEi mediated angioedema?

A

STOP offending drug & administer supportive care.

→ glucocorticoids have been noted to INCREASE the expression of ACE = accelerate bradykinin METABOLISM
[opposite of the ACEi]

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77
Q

What do kallikrein inhibitors do?

A

block the conversion of kininogen to bradykinin

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78
Q

What medication blocks the conversion of kininogen to bradykinin?

A

plasma kallikrein inhibitor

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79
Q

How does FFP treat bradykinin induced angioedema?

A

provides the deficient enzyme

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80
Q

What two medications are NOT effective in acute episodes of bradykinin-mediated angioedema?

A

catecholamines & antihistamines

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81
Q

When are catecholamines & antihistamines NOT effective?

A

in bradykinin mediated angioedema

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82
Q

What are the two types of immunodeficiency disorders?

aka. inadequate adaptive immunity

A
  1. Primary (congenital)

2. Secondary

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83
Q

What causes primary (congenital) immunodeficiencies?

A

gene mutations that are usually inherited

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84
Q

Gene mutation that causes a defect in T lymphocytes is known as ____ syndrome.

A

DiGeorge syndrome

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85
Q

What are secondary immunodeficiencies encountered in high income countries?

A
  • chemotherapy

- radiation

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86
Q

What are secondary immunodeficiencies encountered in low-income countries?

A
  • malnutrition

- acquired immunodeficiency syndrome (AIDS)

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87
Q

Gene mutations that cause dysfunction in T- B- or NK- cell functions, cause ____ syndromes.

A

severe combined immunodeficiency syndromes

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88
Q

What is the treatment of severe combined immunodeficiency syndromes?
(SCID)

A

bone marrow or stem cell transplant

gene therapy

enzyme replacement

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89
Q

What organ causes the immune deficiency in DiGeorge Syndrome?

How does this affect severity?

A

Thymus hypoplasia

→ degree of immunocompromise correlates with the amount of thymus tissue present

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90
Q

What organs can be affected in DiGeorge Syndrome?

A

thymus, thyroid, parathyroid
(hypoplasia)

Can also have cardiac defects & facial dysmorphisms

  • truncus arteriosus
  • TOF
  • cleft palate
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91
Q

What gene deletion causes DiGeorge Syndrome?

A

22q11.2

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92
Q

What cell level is abnormal in DiGeorge Syndrome?

A

T cells are decreased;

B cells are normal

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93
Q

Complete absence of the thymus results in what sundrome?

A

severe combined immunodeficiency syndrome (SCID)

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94
Q

Severe combined immunodeficiency syndromes (SCID) affect what cells?

A

T cells
B cells
NK cells

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95
Q

SCID is linked to what chromosome?

A

X-linked.
boys are affected
girls are carriers

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96
Q

What is the abnormality in the most common form of severe combined immunodeficiency syndrome?

A

mutation in the gene that codes for interleukin receptors

lack of interleukin receptors → lack of interleukin signaling → lack of T, B, NK cell differentiation/maturation

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97
Q

What are four categories of excessive adaptive immunity?

A
  • anaphylaxis
  • bronchial asthma
  • allergic rhinitis, sinusitis
  • food allergies
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98
Q

What are the clinical & pathological manifestations of anaphylaxis?

[may be caused by drugs, bee sting, food]

A
  • vascular dilation = fall in blood pressure (shock)

- airway obstruction d/t laryngeal edema

99
Q

What are the clinical & pathological manifestations of bronchial asthma?

A

airway obstruction d/t smooth muscle hyperactivity

inflammation & tissue injury caused by late-phase reaction

100
Q

What are the clinical & pathological manifestations of allergic rhinitis, sinusitis?

A

increased mucous secretion

inflammation of upper airways & sinuses

101
Q

What are the clinical & pathological manifestations of food allergies?

A

increased peristalsis d/t contraction of intestinal muscles = vomiting & diarrhea

102
Q

What are hypersensitivity disorders?

A

persistent, misdirected, or inadequately regulated immune reactions against a variety of antigens

“overreaction of the immune system”

103
Q

What does it mean when an individual is “sensitized”?

A

they have been exposed to and react against an antigen

104
Q

What are 3 categories of hypersensitivity disorders?

A
  1. reactions against self-antigens
  2. reactions against environmental antigens
  3. excessive reactions against microbes
105
Q

What occurs to cause autoimmunity?

A

an individual’s self-tolerance breaks down

[normally an individual is tolerant to their own antigens]

106
Q

What is an environmental allergy?

A

abnormal reaction against common and normally harmless environmental substance antigens

107
Q

What happens in a hypersensitivity disorder involving excessive reactions against microbes?

A

the microbe is unusually persistent. the immune response itself becomes the cause of tissue injury

  • example: tuberculosis
108
Q

How many major types of hypersensitivity reactions are there?

109
Q

What is Type 1 hypersensitivity reaction?

A

“allergy”
immediate, IgE mediated, mast cells

→ caused by IgE antibodies that recognize environmental antigens & sensitize mast cells leading to the release of mediators

ie. anaphylaxis

110
Q

What is Type 2 hypersensitivity reaction?

A

antibody mediated
IgG / IgM

ie. myasthenia gravis, Graves disease

111
Q

What is Type 3 hypersensitivity reaction?

A

immune complex mediated

ie. SLE (Lupus), glomerulonephritis

112
Q

What is Type 4 hypersensitivity reaction?

A

T-lymphocyte mediated
(CD4+ / CD8+ T cells)

ie. rheumatoid arthritis, multiple sclerosis, contact dermatitis, T1DM

113
Q

What is most important about the course of Type 1 hypersensitivity reactions?

A

early (w/n minutes) vascular & smooth muscle response
followed by
slow (hours) late-phase inflammatory response

→ do not let a patient go home right away

114
Q

What are localized hypersensitivity clinical features?

A

skin

GI tract

115
Q

What are systemic hypersensitivity clinical features?

A

itching, urticaria, skin erythema
profound resp difficulty/bronchoconstriction, mucous production, laryngeal edema
vomiting, abdominal cramps, diarrhea
systemic vasodilation

116
Q

What are clinical s/s a CRNA might see if a patient has an anaphylactic reaction?

A

unexplained…

↑ airway pressure, wheezing, increased & shark-fin ETCO2, ↓ BP, flushing, rash, ↑ mucous production, ↑ HR

117
Q

Anaphylaxis is ___ mediated.

A

Immune mediated - IgE (60%)

118
Q

What are life-threatening s/s of anaphylaxis?

A

CV collapse (tachycardia, hypovolemia)

Interstitial edema, urticaria

bronchospasm, laryngeal edema

119
Q

After production of antigen-specific IgE antibodies, what causes anaphylaxis?

A

subsequent exposure to antigen results in marked mast cell and basophil degranulation

120
Q

What is the difference between “anaphylactoid” reaction vs anaphylaxis?

A

“anaphylactoid” is NOT immune mediated, does NOT involve IgE

→ less common
→ not as profound
→ direct release of histamine from mast cells or basophils… no IgE involvement

121
Q

___ is a vasoactive amine.

122
Q

Where is histamine stored?

A

mast cells

123
Q

When is histamine released?

A

upon mast cell degranulation

124
Q

What does histamine cause?

A

rapid vasodilation, increased vascular permeability, smooth muscle contraction

125
Q

____ and ____ are lipid mediators of the immune system.

A

Prostaglandins & leukotrienes

126
Q

What is the most abundant immune mediator generated by the cyclooxygenase pathway in mast cells?

A

Prostaglandin D2 (PGD2)

127
Q

What mediator causes intense bronchospasm?

A

prostaglandin D2

128
Q

What are the most potent vasoactive & spasmogenic mediators?

A

the leukotrienes

129
Q

What mediators recruit, activate leukocytes & amplify the response?

A

cytokines;

→ tumor necrosis factor & chemokines

130
Q

What are 4 major risk factors to anaphylaxis during anesthesia?

A
  1. asthma
  2. atopy
  3. multiple past exposures to latex
  4. hereditary conditions (angioedema)
131
Q

What lab can be drawn to confirm anaphylactic reaction?

A

plasma tryptase concentration

132
Q

What is tryptase?

A

stored in mast cells & released during immune-mediated reactions

→ indicator of mast cell activation

133
Q

When do plasma histamine levels return to baseline after an allergic reaction?

A

30-60 minutes

134
Q

Why isn’t histamine level used to confirm anaphylactic reaction?

A

non-specific. histamine can be released from many causes

135
Q

What is the management of perioperative anaphylaxis?

A
  1. remove agent if possible
  2. reverse hypotension & hypoxemia
  3. replace intravascular fluid
  4. inhibit further degranulation by stabilizing the membrane of mast cells [steroids / benadryl
  5. inhibit release of vasoactive mediators
  6. treat inflammation
  7. relieve bronchospasm
136
Q

What medications are given during management of perioperative anaphylaxis?

A
  • oxygen
  • epinephrine
  • fluid bolus
  • phenylephrine
  • hydrocortisone
  • diphenhydramine
  • ranitidine (zantac)
  • B2 agonist
137
Q

Dose of oxygen to administer during anaphylaxis

A

ventilate with 100%

138
Q

Dose of epinephrine to administer during anaphylaxis?

A

1-10mcg/kg IV bolus for ↓BP/bronchospasm
Q1-2min
may start infusion @ 0.05-1mcg/kg/min

139
Q

Dose of fluid bolus to administer during anaphylaxis?

A

20mL/kg balanced salt solution; repeat as necessary

140
Q

Dose of phenylephrine to administer during anaphylaxis?

A

0.1mcg/kg/min IV

titrate to effect if inadequate response to epinephrine

141
Q

Dose of hydrocortisone to administer during anaphylaxis?

A

2-3mg/kg IV

Adults: 250mg IV
Child: 50-100mg IV

142
Q

Dose of diphenhydramine to administer during anaphylaxis?

A

1-2mg/kg IV

143
Q

Dose of ranitidine to administer during anaphylaxis?

A

1.5mg/kg IV

** don’t forget H2 blocker to protect GI system from histamine!!!!

144
Q

Why administer antihistamines during anaphylaxis?

A

to protect from H1/H2 receptors

→ helps decrease pruritus & bronchospasm

145
Q

What medication is a histamine 1 antagonist?

A

diphenhydramine; competes with histamine for membrane receptor sites

146
Q

What medication is a histamine 2 antagonist?

A

ranitidine

147
Q

How does epinephrine work?

A

increases intracellular cAMP → restores/stabilizes membrane permeability → decreases the release of vasoactive mediators

148
Q

What 3 medications can be given if the patient is unresponsive to epinephrine?

A
  1. vasopressin
  2. glucagon
  3. norepinephrine
149
Q

How do corticosteroids benefit during anaphylaxis?

A

may enhance B-agonist effects of other drugs or inhibition of the release of arachidonic acid responsible for production of leukotrienes and prostaglandins

→ no known effect on degranulation of mast cells or antigen-antibody interactions

** takes several hours for effect

150
Q

Intolerance of a medication:

A

inability to tolerate the adverse effects of a medication

ie. muscle pains & statins

151
Q

Idiosyncratic reaction to medication:

A

drug reactions not related to the known pharmacological properties of the drug

ie. antiepileptic drugs & dyskinesias

152
Q

Toxic reaction to medication:

A

dose dependent, having too much drug in a person’s system at one time

153
Q

Most drug reactions manifest within how many minutes?

154
Q

Reaction to ____ is typically delayed >30 minutes

155
Q

What are 5 common drugs associated with perioperative anaphylaxis?

A
  1. muscle relaxants
  2. antibiotics
  3. latex
  4. chlorhexidine
  5. dyes
156
Q

What are the 2 muscle relaxants most commonly associated with reactions?

A
  • rocuronium

- succinylcholine

157
Q

Cross sensitivity occurs between benzylisoquinoliniums & ____.

(atracurium, Cisatracurium, mivacurium)

A

aminosteroids
over the counter cosmetics (contain ammonium ions & people can produce IgE antibodies to quarternary & tertiary ammonium ions)

morphine & neostigmine (contain ammonium ions)

158
Q

Histamine from atracurium administration is immune mediated or nonimmune mediated?

A

nonimmune mediated

159
Q

Antibiotic most commonly associated with reactions?

A

penicillin

IgE antibodies can wane over time… rxn as child may disappear as an adult

160
Q

What are the two allergenic components found in penicillin?

A

beta-lactam ring (also found in cephalosporins, carbapenems, monobactams)

R-group side chain (also found in cephalosporins)

161
Q

Cross sensitivity rate between penicillin & cephalosporins:

162
Q

What antibiotic is the second most common for reactions?

A

sulfonamide;

can cause STEVENS-JOHNSON syndrome

163
Q

What is stevens-johnson syndrome?

A

severe cutaneous hypersensitivity reaction; macules spread & coalesce leading to epidermal blistering, necrosis, sloughing

164
Q

What drugs can cause stevens-johnson syndrome?

A

sulfonamides, antiseizure drugs, antibiotics

165
Q

What is the pathology of vancomycin reactions?

A

direct histamine release r/t rate of infusion.

NOT IgE mediated (has been report, but RARE)

166
Q

What makes latex an allergen?

A

several Hevea proteins cause an IgE mediated response

Latex is produced from the rubber tree Hevea brasiliensis

167
Q

What distinguishes a latex- induced reaction from other drug reactions?

A

delayed onset, typically longer than 30 minutes.

d/t absorption across skin/mucous membranes

168
Q

What 4 patient characteristics increase the risk of having/developing a latex allergy?

A
  1. spina bifida
  2. multiple previous surgeries
  3. Hx fruit allergy
  4. healthcare workers
169
Q

What food allergies are associated with a latex allergy?

A

avocado
kiwi
banana

170
Q

What piece of equipment/container must be considered when a patient has a latex allergy?

A

stopper of a drug vial

171
Q

What are the three ingredients in propofol that may trigger an allergic reaction?

A
  1. lecithin - egg
  2. sulfite (preservative)
  3. soybean oil - soy

peanut allergy?

172
Q

Is a reaction to the sulfite or 2-isopropyl-group in propofol immune mediated or nonimmune mediated?

A

thought to be immune (IgE) mediated

173
Q

Patients with ___, ___, or ___ should not receive ASA or NSAIDs.

A

asthma, hyperplastic sinusitis, nasal polyps

174
Q

If ASA/NSAIDs is given to a patient with asthma, hyperplastic sinusitis, or nasal polyps, what three s/s can occur?
and why?

A
  1. rhinorrhea
  2. bronchospasm
  3. angioedema
NOT IgE mediated
inhibiting COX1 (medication blocks the production of cyclooxygenase but pushes arachidonic acid to be formed into leukotrienes instead) =↑ synthesis of leukotrienes = basophil & mast cell degranulation
175
Q

What type of contrast agents have higher rates of reactions?

A

ionic, high-osmolar agents

→ the higher the iodine, the greater the risk of a reaction

176
Q

Nonimmune mediated reactions to contrast can be pre-medicated with what three medications?

A
  1. hydrocortisone 1-2mg/kg IV
  2. diphenhydramine 50mg IV
  3. ranitidine 50mg IV
177
Q

Nonimmediate reactions to contrast are mediated by what cells?

178
Q

What type of local anesthetics are more likely to produce allergic reactions?

A

ester-type LA

179
Q

What medications produce possible but rare allergic reactions?

A 
midazolam
ketamine
etomidate
opioids
heparin
insulin
180
Q

What 3 medications cause direct histamine release?

A

morphine
codeine
meperidine

181
Q

What reaction is caused by Halothane?

A

halothane hepatitis

d/t halide metabolites

182
Q

What is found in cosmetics that might produce prior sensitization particular medications?

A

Dye

CRNAs will give …

  • methylene blue
  • indocyanine green (ICG)
183
Q

Allergy to CHG may be ___ and under or over reported?

A

delayed;

under-reported

184
Q

Synthetic volume expanders can cause what type of reactions?

A

both immune and nonimmune mediated

185
Q

What are 4 synthetic volume expanders that can cause allergic reactions?

A
  1. dextrans
  2. gelatins
  3. albumin
  4. starch
186
Q

Anaphylaxis to blood products occurs how often?

A

1: 20,000 - 50,000 transfusions

187
Q

Type II hypersensitivity reactions occur when:

A

IgG and IgM antibodies inappropriate mark self-components as foreign; targeting them for phagocytosis or complement-mediated destruction

→ may have genetic predisposition

188
Q

What are four autoimmune disorders?

A

Systemic Lupus erythematosus (SLE)
Scleroderma
Rheumatoid arthritis
Autoimmune hepatitis

189
Q

What are three anesthetic considerations of autoimmune disorders?

A
  1. specific vulnerable organs
  2. consequences of therapy/treatment
  3. acceleration of other/related disease processes
190
Q

“marked” or “flagged” elements are destroyed by what?

A

spleen

→ this is why a splenectomy can be helpful in antibody-mediated diseases marked by low blood counts

191
Q

Antibodies that are deposited in extracellular tissues can recruit and activate:

A

neutrophils & macrophages
= acute inflammation

→ antibodies can also activate or inhibit receptors on cell surfaces

192
Q

What is the target antigen in autoimmune hemolytic anemia?

A

red cell membrane proteins

193
Q

What is the target antigen in myasthenia gravis?

A

acetylcholine receptor

194
Q

What is the target antigen in Graves disease (hyperthyroidism)?

A

TSH receptor

195
Q

What is the target receptor in pernicious anemia?

A

intrinsic factor of gastric parietal cells

196
Q

What is the mechanism of autoimmune hemolytic anemia?

A

opsonization and phagocytosis of red blood cells

197
Q

What is the mechanism of myasthenia gravis?

A

antibody inhibits acetylcholine binding, down-modulates receptors

198
Q

What is the mechanism of Graves disease (hyperthyroidism)?

A

antibody-mediated stimulation of TSH receptors

199
Q

What is the mechanism of pernicious anemia?

A

neutralization of intrinsic factor, decreased absorption of vitamin B12

200
Q

What are the clinicopathologic manifestations of autoimmune hemolytic anemia?

A

hemolysis, anemia

201
Q

What are the clinicopathologic manifestations of myasthenia gravis?

A

muscle weakness, paralysis

202
Q

What are the clinicopathologic manifestations of Graves disease (hyperthyroidism)?

A

hyperthyroidism

203
Q

What are the clinicopathologic manifestations of pernicious anemia?

A

abnormal erythropoiesis, anemia

204
Q

What is the pathology of Type III hypersensitivity? (immune complex-mediated)

A

complexes formed in the circulation deposit in blood vessels & induce inflammation.

Manifest in acute vasculitis → can lead to fibrinoid necrosis of vessel wall & neutrophilic infiltration

205
Q

What are three common locations of acute inflammation / sites of antigen-antibody complex deposition in type III hypersensitivity?

A
  1. kidneys (glomerulonephritis)
  2. synovium of joints (arthritis)
  3. blood vessels in any tissue (vasculitis)
206
Q

What is the prototypic human immune complex disease?

A

systemic lupus erythematosus (SLE)

207
Q

Type IV hypersensitivity reaction is ___ mediated.

208
Q

What are the 2 types of t cell reactions that cause tissue injury and disease?

A
  1. cytokine-mediated inflammation (aka: delayed type hypersensitivity); cytokines produced by CD4+ t cells
  2. cytotoxicity, mediated by CD8+ t cells
209
Q

What are the typical manifestations of type IV hypersensitivity reaction?

[typical manifestations of this = chronic inflammation]

A
  • rheumatoid arthritis (synovial inflammation and destruction of articular cartilage)
  • multiple sclerosis (demyelination of CNS)
  • T1DM (antigens of pancreatic islet beta cells)
  • Inflammatory bowel disease
  • psoriasis (cutaneous plaques)
210
Q

What are the 2 categories of autoimmune disorders?

A
  1. organ-specific

2. systemic

211
Q

Systemic autoimmune disease involves what two particles?

and targets what 2 types of tissue?

A
  1. immune complexes
  2. autoantibodies

target: connective tissues & blood vessels of involved organs

212
Q

What are the 5 systemic autoimmune diseases?

A
  1. SLE
  2. RA
  3. scleroderma/systemic sclerosis
  4. Sjogren syndrome
  5. Inflammatory myopathies
213
Q

Organ-specific autoimmune diseases are divided into what 3 categories?

A
  1. Diseases mediated by antibodies
  2. Diseases mediated by T cells
  3. Diseases postulated to be autoimmune
214
Q

What are 6 autoimmune diseases mediated by antibodies?

A
  1. autoimmune hemolytic anemia
  2. autoimmune thrombocytopenia
  3. autoimmune atrophic gastritis of pernicious anemia
  4. myasthenia gravis
  5. graves disease
  6. goodpasture syndrome
215
Q

What are 2 autoimmune diseases mediated by T cells?

A
  1. T1DM

2. multiple sclerosis

216
Q

What are 3 diseases postulated to be autoimmune?

A
  1. inflammatory bowel disease (Crohn dz, ulcerative colitis)
  2. primary biliary cholangitis
  3. autoimmune (chronic active) hepatitis
217
Q

What is the pathology of SLE?

A

antibody & antigen complexes are deposited in kidneys and other organs;

antibodies coat blood cells leading to phagocytosis (Type II hypersensitivity)

218
Q

What is the etiology hypothesis of SLE?

A

exposure to insult → apoptosis → improper clearance of fragments → failure of B and T cell tolerance activates lymphocytes specific for self antigens

*can affect any organ

219
Q

Findings of SLE? (8)

A

Blood vessels: diffuse necrotizing vasculitis
Kidney: proliferative glomerulonephritis, nephritis
Skin: butterfly/macular rasha long nose/cheeks
CV: pericardial effusions, pericarditis, valvular endocarditis, CHF, HTN
Serosal cavities: effusions & fibrosis, avascular necrosis
CNS: depression, anxiety, psychosis, seizures, stroke
Blood: thrombocytopenia, anemia, anti-phospholipid syndrome (hypercoagulability)
Airway: cricoarytenoid arthritis, RLN palsy

ask the patient!

220
Q

What are 3 other types of lupus?

A
  1. Drug-induced Lupus Erythematosus
  2. Cutaneous Lupus Erythematosus
  3. Neonatal Lupus
221
Q

What are 3 drugs that can trigger drug-induced lupus erythematosus?

A
  1. hydralazine
  2. procainamide
  3. isoniazid
  • s/s will disappear 6 months after drug is stopped
222
Q

How does cutaneous lupus erythematosus present? What makes it worse?

A
  • rashes & discoid lesions on face, arms, neck, shoulders, trunk

→ pigment change and hair loss

affected by sunlight & fluorescent

223
Q

What causes neonatal lupus?

A

fetus in the womb of a mother who has lupus; exposure to mom’s antibodies

224
Q

How does neonatal lupus present?

A

infant born with skin rash, liver problems, low blood counts
→ may present with congenital heart block (HR 60s-70s) = will need a pacemaker placed!!

  • disappear after some months
225
Q

Drug categories for the treatment of lupus:

A
  • tylenol
  • NSAIDs
  • immunosupressants
  • corticosteroid: prednisone (Cushing syndrome)
  • antimalarial: hydroxychloroquine, chloroquine
  • anticoagulants: aspirin, heparin, warfarin
  • monoclonal antibodies: Belimumab
  • repository corticotropin injections: Acthar
226
Q

What immunosuppressants are used in the treatment of lupus?

A

cyclophosphamide
methotrexate
azathioprine
mycophenolate mofetil

227
Q

Anesthesia implications of lupus:

A

PRE-OP TESTING/EVALUATION

  • PFTs
  • ECHO
  • EKG
  • renal function
  • labs

What drugs is the patient taking?

  • corticosteroids
  • immunosuppressants
  • anticoagulants

AIRWAY INVOLVEMENT

228
Q

What type of airway involvement can lupus have?

A

CRICOARYTENOID ARTHRITIS = hoarseness

laryngeal function (pre- & post-op)

?smaller tube needed
?airway may be “stiff”
?airway may be red/irritated

229
Q

What is scleroderma?

A

“Hard Skin”
injury to vascular endothelium results in leakage of proteins into interstitial space

inflammation → fibrosis of skin, small blood vessels, and viscera

**COLLAGEN production is not slowed down and gets deposited throughout the body

230
Q

Etiology of scleroderma:

A

Unknown:

collagen vascular disease & autoimmune characteristics

onset is 20-40 years old; women; accelerated in pregnancy

231
Q

What is CREST syndrome?

know

A

presents in scleroderma:

Calcinoses: Ca deposits
Raynaud’s phenomenon: [evaluate ulnar perfusion before radial a-line placement!]
Esophageal hypomotility
Sclerodactyly: thickened, tight skin [affects mouth opening]
Telangiectasia: dilated capillaries

232
Q

Skin & musculoskeletal manifestations of scleroderma:

A

thick skin, diffuse edema (can involve airway), contractures, skeletal muscle myopathy, arthritis & limited joint mobility, avascular necrosis

233
Q

Nervous system manifestations of scleroderma:

A

PNS & CNS neuropathies d/t nerve compression by thickened connective tissue

trigeminal neuralgia (pain to forehead, mid, & lower face)
dry eyes
234
Q

Cardiovascular manifestations of scleroderma: (7)

A
  • sclerosis of coronary arteries & conduction system
  • cardiac tissue replaced with fibrous tissue
  • systemic & pulm HTN
  • pericarditis
  • pericardial effusion
  • intermittent peripheral vasospasm
  • RAYNAUD’S PHENOMENON
235
Q

Respiratory manifestations of scleroderma:

A
  • diffuse interstitial pulmonary fibrosis (up to 80% of patients)
  • arterial hypoxemia secondary to decreased diffusion capacity
  • decreased pulmonary compliance
236
Q

Renal manifestations of scleroderma:

A
  • renal artery stenosis d/t arteriolar intimal proliferation → decreased renal blood flow → HTN
237
Q

GI manifestations of scleroderma:

A
  • dry oral mucosa
  • progressive fibrosis of GI tract
  • dysphagia
  • hypomotility
  • ↓ lower esophageal sphincter tone
  • malabsorption; vitamin K deficiency (GI tract cannot absorb nutrients)
238
Q

Anesthetic implications of scleroderma: (9)

A
  • difficult intubation d/t limited mouth opening
  • difficult IV access d/t dermal thickening
  • pulmonary HTN
  • ↓ pulm compliance & ↓ O2 diffusion
  • systemic HTN
  • aspiration risk d/t hypotonia of LES
  • SENSITVE TO RESPIRATORY DEPRESSANTS
  • protect eyes from corneal abrasion
  • renal dysfunction with altered drug elimination

*regional anesthesia may be challenging d/t contractures and ↓ joint mobility

239
Q

Sjogren Syndrome

A

chronic inflammation & destruction of lacrimal & salivary glands
→ dense infiltrates of CD4+ t cells

  • dry eyes & mouth; may also involve other exocrine glands lining the respiratory & GI tracts, vagina
240
Q

Clinical features of Sjogren syndrome:

A
  • dryness of the eyes
  • risk for corneal abrasions
  • dry mouth (xerostomia0
  • nasal dryness causing risk of bleeding/perforation with instrumentation

**patient’s need eye drops every couple of hours

241
Q

Rheumatoid Arthritis:

A

chronic, systemic inflammatory autoimmune disease; exaggerated immune response [interleukins, B cells, cytokines, collagenase, leukocyte infiltration]

particularly affects joints; genetic & environmental risk factors
Raynaud phenomenon common
→ inflammation, swelling, destruction of cartilage

242
Q

Anesthetic implications of rheumatoid arthritis:

A

atlantoaxial INSTABILITY
SUBLUXATION of the joint.

→ can impair blood flow through vertebral arteries

243
Q

Pathophysiology of RA:

A

inflammatory cytokines convert the synovium into a thick ABNORMAL LAYER OF GRANULATION TISSUE “pannus”

 →→ Macrophages stimulate the release of platelet-rich growth factor and other enzymes that result in proliferation of cartilage fibrosis & joint destruction

N935 Advanced Pathophysiology (9 decks)

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