Hyper & hypo immune disorders Flashcards
1
Q
Describe the difference between innate & adapative.
A
innate is a non-specific response that targets many common pathogens
adaptive must be developed individually
2
Q
The innate system does not need a
A
prior exposure to elicit a response
it is passed on to each generation
3
Q
The innate system is comprised of
A
epithelial & mucous membranes, complement factors, neutrophils, macrophages, & monocytes
4
Q
The adaptive response has a
A
delayed response
5
Q
The adaptive response develops
A
memory & specificity towards an antigen
6
Q
The adaptive response is composed of
A
B & T lymphocytes
7
Q
The principle cells of innate immunity include
A
myeloid cells
-macrophages, neutrophils, and dendritic cells
8
Q
The principle cells of adaptive immunity are
A
T & B lymphocytes
9
Q
The adaptive immune system is _____ as compared to the innate immune system
A
very powerful
10
Q
Describe humoral immunity.
A
component of adaptive immunity
mediated by antibodies produced by B cells
11
Q
Humoral immunity acts by
A
antibodies neutralize microbes, opsonize them for phagocytosis, and activate the complement system
12
Q
Describe cell-mediated immunity
A
T cells activated by protein antigens from antigen presenting cells (APCs)
13
Q
Cell mediated immunity requires repeat
A
antigen stimulation to perform their functions
14
Q
The innate immune dysfunction includes
A
inadequate response, excessive response, & misdirected response
15
Q
Excessive response is inclusive of
A
neutrophilia, monocytosis, asthma
16
Q
Misdirected immune response includes
A
angioedema
17
Q
Inadequate response includes
A
neutropenia, abnormal phagocytosis, deficient in the complement system, hyposplenism
18
Q
Adaptive immune dysfunction include
A
defects in antibody production, defects in T lymphocytes, combined immune system defects, allergic reactions, anaphylaxis, & autoimmune disorders
19
Q
Autoimmune means
A
reactions against self antigens
20
Q
Hypersensitivity (definition)
A
excessive immunologic reactions to microbes or environmental agents dominated by inflammation
21
Q
Atopy (definition)
A
propensity or genetic tendency to develop allergic reactions
22
Q
Antibody is a
A
large Y shaped protein used by the immune system to identify and neutralize foreign objects such as pathogenic bacteria & viruses
23
Q
Neutrophils are formed by
A
stem cells in the bone marrow
phagocytes that are found in the blood stream
24
Q
Neutrophils make up
A
40-70% of all WBCs in humans
25
First responders to inflammation (especially bacterial) are
neutrophils
26
Neutropenia is defined as
a neutrophil count <1500/mm3
27
Types of neutropenia include
neonatal sepsis, Kostmann syndrome (autosomal recessive), acquired defects (chemotherapy, antivirals), autoimmune (lupus, RA), infection- the rate of consumption exceeds production
28
Treatments for neutropenia include
the cessation of medications that cause neutropenia, granulocyte colony-stimulating factor (filgastrim), and bone marrow transplants
29
For patients with neutropenia in the periop enviroment,
respecting asepsis is particularly important
30
The spleen is part of the
lymphatic system- like a large lymph node, primary blood filter
31
The primary creator of RBCs in fetal life & up to 5 months of age
is the spleen
32
The functions of the spleen include:
removes old RBCs, a blood reservoir, recycles iron, metabolized hemoglobin, stores 1/4 of circulating lymphocytes, stores & clears platelets
synthesizes antibodies in the white pulp
removes antibody-coated bacteria
the Globin portion of hemoglobin is degraded to amino acids, and the heme portion is metabolized to bilirubin
33
Hyposplenism is the
reduced spleen function
34
Asplenia refers to
the absence of normal spleen function
causes an increase of sepsis by 350 fold
a type of immuno-dysfunction
35
Sickle cell anemia & its' relation to hyposplenism
can cause auto-infarction in the spleen resulting in vaso-occlusive disease
36
For patients with hyposplenism, they require
immunizations, travel restrictions, abx prophylaxis even with minor procedures, and alert warning bracelets
37
Leukocytosis is when the
WBC count is above normal range
a normal reaction often an inflammatory response but can also be from tumors, leukemias, stress, pregnancy, convulsions, and medications (corticosteroids, lithium, and beta agonists
38
Leukocytosis is different from
leukemia
acute leukemia- immature WBCs in the peripheral blood
chronic leukemia- mature, non-functioning WBCs in peripheral blood
39
Describe the difference between left upper shift & right shift
left upper shift- increase in the ratio of immature to mature neutrophils; bone marrow is trying to make more
right shift- decrease ratio of immature to mature neutrophils
shows bone marrow suppression (radiation sickness)
40
Eosinophilia is responsible for
allergic disorders
41
Describe eosinophilic esophagitis
chronic immune system disease in which a type of white blood cell (eosinophil) builds up in the lining of esophagus
42
The cause of eosinophilic esophagitis can be
a reaction to foods, allergens, or acid reflux, can inflame or injure the esophageal tissue
43
Damaged esophageal tissue from eosinophilic esophagitis can lead to
difficulty swallowing or cause food to get stuck when swallowing
44
Describe the difference between extrinsic and intrinsic asthma.
extrinsic- IgE production, allergens
| intrinsic- triggers are unrelated to the immune system i.e. ETT placement, cold, exercise, stress, inhaled irritants
45
Neutrophilia occurs within
hours of an infection, granulocytes increase 2-3 fold
| -mobilization of stored granulocytes and new from the bone marrow
46
Neutrophilia is defined as
neutrophils >7000/mm3
47
Neutrophilia may be a result of
pancreatitis, pyelonephritis, peritonitis & pna
48
Leukostasis is defined as & can lead to
>100,000 mm/3
| thick blood flow & WBC clumping, can lead to TIAs & strokes
49
Angioedema is can be
hereditary or acquired
results in subcutaneous & submucosal edema formation
often involves the face, extremities, & GI tract
50
Bradykinin mediated angioedema can be due to
autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
ACE-I
Acquired
51
Describe acquired bradykinin mediated angioedema.
lymphoproliferative disorders acquire C1 esterase inhibitor deficiency secondary to antibody production
52
Describe ACE-I angioedema.
drug-induced angioedema resulting from increased bradykinin availability to ACI-I mediated blockage of bradykinin catabolism
53
Describe autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
the absence of C1 esterase inhibitor leads to release of vasoactive mediators that increase vascular permeability and produce edema by bradykinin
repeated bouts of facial and/or laryngeal edema lasting 24-72 hours
54
What should not be used for bradykinin-mediated angioedema?
catecholamines and histamines are not effective
55
What is the treatment for bradykinin-mediated angioedema?
```
androgens- prophylactic therapy
antifibrinolytic therapy-inhibiting plasmin activation
C1 inhibitor concentrate
synthetic bradykinin receptor antagonist
recombinant plasma kallikrein inhibitor
FFP- replaces the deficient enzyme
```
56
Defects of T lymphocytes is known as
DiGeorge syndrome
57
Defects of combined immune system defects is known as
severe combined immunodeficiency syndromes
58
DiGeorge syndrome is a
thymic, thyroid, and parathyroid hypoplasia
| due to a gene deletion--> decreased T cells (B cells are normal)
59
S/S of DiGeorge syndrome include
cardiac malformations, facial dysmorphisms, truncus arteriosus, TOF, and cleft palate
60
With DiGeorge syndrome, the degree of immunocompromise correlates with
the amount of thymus tissue present
61
A complete absence of the thymus results in
severe combined immunodeficiency syndrome
62
Treatment of DiGeorge syndrome is
thymus transplant or infusion of T cells
63
Anesthetic considerations for DiGeorge syndrome include
SBE prophylaxis if required, calcium supplementation in hypoparathyroidism, strict asepsis due to risk for infection
64
Severe combined immunodeficiency syndromes are
genetic mutations that affect T, B, & NK cell function/maturation
lack of receptor--> lack of interleukin signaling--> lack of NK, B, & T cell differentiation/maturation
65
Babies with SCID appear
healthy at birth but are highly susceptible to severe infections
66
The only treatment for SCID is
bone marrow or stem cell transplant, gene therapy or enzyme replacement
67
Excessive adaptive immunity is inclusive of
allergic reactions, anaphylaxis, drug allergy
68
Allergic reactions are
immune-mediated
| "overreactions" of the immune system
69
The four types of allergic reactions include
Type I- IgE
type II- IgG/IgM
Type III- immune complex
Type IV- T lymphocytes
70
Type I immune mediated allergic reactions are different than other immune mediated reactions because
they are immediate
71
Anaphylaxis is a
life-threating response involving
cardiovascular collapse (tachycardia, hypovolemia)
interstitial edema, urticaria
bronchospasm, laryngeal edema
72
Anaphylaxis is caused by
immune mediated-IgE
previous exposure to antigens in drugs evokes production of antigen-specific IgE antibodies
subsequent exposure results in marked mast and basophil degranulation
73
Nonimmune mediation or anaphylactoid is
via IgG or IgM
less common
direct release of histamine from mast or basophils
74
Mediators include
vasoactive amines- histamines
lipid mediators- prostaglandins & leukotrienes
cytokines- tumor necrosis factor & chemokines
75
Describe the role of vasoactive amines.
stored in mast cells
release upon mast cell degranulation
causes rapid vasodilation, increases vascular permeability, and smooth muscle contraction
76
Describe the role of lipid mediators- prostaglandins & leukotrienes.
Prostaglandin is the most abundant mediator generated by the cyclooxygenase pathway in mast cells--> causes intense bronchospasm
the leukotrienes are the most potent vasoactive and spasmogenic agents known
77
Describe the role of cytokines.
recruit, activate leukocytes and amplify
78
Risk factors for anaphylaxis in anesthesia includes
asthma, atopy, multiple past exposure to latex, hereditary conditions (angioedema)
79
Clinical manifestations of anaphylaxis include
tachycardia, bronchospasm, laryngeal edema, & cutaneous rash
80
Plasma histamine concentrations return to
baseline 30-60 minutes after a reaction
81
Diagnosis of anaphylaxis is through
clinical manifestations, plasma tryptase concentration, plasma histamine concentrations, and skin testing
82
Describe plasma tryptase concentration.
tryptase is stored in mast cells and is released during immune-mediated reactions
indicates mast cell activation
83
Management of perioperative anaphylaxis includes
remove the agent if possible, reverse hypotension & hypoxemia, replace intravascular fluid, inhibit further degranulation, inhibit release of vasoactive mediators, treat inflammation, relieve bronchospasm
84
Describe the role of antihistamines in anaphylaxis treatment.
histamine 1 antagonist- diphenhydramine- competes with histamine for membrane receptor sites
histamine 2 antagonist- ranitidine
helps to decrease pruritus and bronchospasm
not as effective in treating anaphylaxis once vasoactive mediators have been released
85
The dose of epinephrine for anaphylaxis is
1-10 mcg/kg IV bolus, repeat every 1-2 minutes as needed
86
Epinephrine works by
increasing intracellular cAMP, restoring membrane permeability and decreasing the release of vasoactive mediators
beta agonists effect- relaxes bronchial smooth muscle
87
If a patient is unresponsive to epi-->
vasopressin, glucagon, or norepinephrine
88
The role of corticosteroids in anaphylaxis is
has no known effect on degranulation of mast cells or antigen-antibody interactions
-takes several hours for effect
may enhance the beta agonist effects of other drugs or inhibition of the release of arachidonic acid responsible for production of leukotrienes and prostaglandins
89
Beta 2 agonists can be useful
when delivered by MDI or nebulizer for treatment of bronchospasm in anaphylaxis
90
Patients with _____ are at increased risk for anaphylaxis
allergies (asthma, fruits, or medications)
91
Previous uneventful exposure does
not eliminate the possibility of anaphylaxis on second exposure
92
Anaphylaxis can occur
on first exposure due to cross-reactivity with other gents
93
Anaphylaxis is NOT
intolerance, idiosyncratic reactions, or toxicity
94
Intolerance is the
inability to tolerate the adverse effects of a medication
| -example is muscle pain & statins
95
Idiosyncratic reactions are
drug-reactions that are not related to the known pharmacological properties of a drug
-examples are antiepileptic drugs & dyskinesias
96
Toxicity is a result of
having too much drug in a person's system at one time
97
Any medication administered during anesthesia can produce
an allergic reaction
most reactions manifest within 5-10 minutes
latex is typically delayed >30 minutes because it must be absorbed through the skin
98
Common drugs associated with perioperative anaphylaxis are
muscle relaxants, antibiotics, and latex
99
The most common muscle relaxants to cause anaphylaxis are
rocuronium and succinylcholine
100
With muscle relaxants and anaphylaxis, there is
cross-sensitivity within classes
101
Some over the counter cosmetics contain ammonium ions and are capable of
sensitizing patients to developing IgE antibodies to quaternary & tertiary ammonium ions
morphine & neostigmine also contain ammonium ions
102
The histamine release from atracurium administration is
nonimmune mediated
103
The most common anaphylaxis reaction among the antibiotics is
penicillin
| - clinical illness misattributed to PCN in some cases (viral rash vs. PCN rash)
104
IgE antibodies can
wane over time- may have a reaction as a child but able to take it as an adult
105
Penicillin contains two allergenic components also present in other antibiotics:
B-lactam ring (found in cephalosporins)
| R-group side chain (found in cephalosporins)
106
The second most common antibiotic allergic reaction is
sulfonamides
| most common cause of Stevens-Johnson syndrome
107
Vancomycin may also cause
allergic reactions although most are non IgE but rather direct release related to the rate of the drug infusion
108
A feature that distinguishes latex-induced allergic reactions from other drug-induced allergic reactions is its
delayed onset, typically longer than 30 minutes after exposure
antigen from rubber gloves absorbed across mucous membranes into systemic circulation
can also be inhaled
109
At risk individuals for latex include
spina bifida, multiple previous operations, history of fruit allergy, and healthcare workers
110
Propofol was formerly advised
that it should be used in caution in patients with a history of egg, soy, or peanut allergy
it contains preservatives which are what people are typically allergic to
111
Propofol allergy is thought to be
IgE mediated with the 2-isopropyl-group or the preservative
112
The combination of these conditions preclude individuals who are taking NSAIDs to rhinorrhea, bronchospasm, and angioedema:
asthma, hyperplastic sinusitis, & nasal polyps
113
Allergies to NSAIDs are not
IgE mediated but rather due to inhibition of cyclooxygenase 1 that promotes synthesis of leukotrienes and subsequent release of mediators from basophils and mast cells
114
With NSAIDs, allergic reactions do not typically
occur with Cox-2 specific inhibitors
115
Allergic reactions to radiocontrast media are more common with
ionic, high-osmolar contrast agents
| -the higher the iodine, the greater the risk of adverse reaction
116
Allergic reactions to radiocontrast media are often
non-immune mediated & can be treated with corticosteroids and histamine antagonists
117
Allergic reactions to local anesthetics are more likely for
ester type> amide type
| most reports are the adverse events of intravascular injections or systemic absorption of additives
118
Dyes may lead to
(are found in cosmetics & soap) and may lead to prior sensitization
119
Other sources of allergic reactions include
halothane (induced hepatitis)
chlorhexidine
synthetic volume expanders
blood products
120
Autoimmune disorders include
SLE, RA, autoimmune hepatitis
121
Anesthetic considerations for misdirected adaptive immunity include
specific vulnerable organs, consequences of therapy, acceleration of other disease process (i.e. CV disease)
122
Autoimmunity is a
type of hypersensitivity to self-antigens. Antibodies inappropriately mark self-components as foreign
123
Autoimmune disease can be divided into
organ-specific or system
124
Systemic disease is
immune complexes & autoantibodies
- principally affect the connective tissues and blood vessels of involved organs
- even though the immunologic reactions are not specifically directed against constituents of connective tissue or blood vessels
125
Since the graft donor and recipient host are genetically different,
some of these differences are recognized by the immune system and are responsible for immune destruction of the graft, called rejection
126
Grafts exchanged between nonidentical individuals of the same species are called
allografts
127
Histocompatibility determines if the
tissue graft (histo=tissue) will be accepted (compatible) by the receiving individual
128
The major histocompatibility complex in humans are
polymorphic genes that differ among individuals
| -they function to recognize T cells
129
If the graft donor expresses MHC molecules that differ from those in the recipient, the graft is recognized as
foreign by the recipient's T cells leading to rejection
130
To prolong graft survival the following is needed:
immunosuppression via corticosteroids, anti-T cell antibodies, drugs that inhibit T- cell function
131
Immunosuppression carries the risk of
opportunistic fungal and viral infections
| -reactivation of latent viruses (cytomegalovirus) as well as an increased risk of cancers
132
Graft vs. host disease is a
syndrome commonly associated with bone marrow and stem cell transplants
The donor's WBCs which remain with the donated tissue (graft) recognize the recipient (host) as foreing
133
Graft vs. host disease is not
the same as a transplant rejection
| the donor's immune system reject the recipient
134
The treatment for graft vs. host disease is
to suppress T-cells via steroids & calcineurin inhibitors
| -suppress the synthesis of pro-inflammatory cytokines
135
Tumor lysis syndrome is a
rare, potentially lethal disease of massive lysis of tumor cells resulting in release of intracellular substances into the blood stream
-potassium, phosphate & uric acid
136
Causes of tumor lysis syndrome include
```
steroids
after treatments (chemoembolization, radiofrequency ablation)
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