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N935 Pathophysiology > Hyper and Hypo Immune Disorders > Flashcards

Hyper and Hypo Immune Disorders Flashcards

1
Q

innate system definition

  • onset
  • principle cells
  • does it need prior exposure to elicit response?
  • how is is acquired
A

non specific response that targets many common pathogens. not pathogen specific

  • rapid onset
  • myeloid cells are principle cells
  • does need prior exposure to elicit response
  • passed on to each generation
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2
Q

what is the innate system comprised of (7)

A 
epithelial membranes
mucous membranes
complement factors
neutrophils
macrophages
monocytes
dendritic cells
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3
Q

adaptive system definition

  • onset
  • principle cells
  • how are receptors created
A

must be developed individually. active, powerful, but silent and adapts to antigens. specialized, unique specificity, cloning themselves with unique receptors/antigens

  • onset is delayed
  • principle cells are T and B lymphocytes
  • receptors are created by rearrangements of antigen receptor genes that occur during maturation of lymphocytes
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4
Q

2 types of adaptive immunity

A

humoral immunuty

cell mediated immunity

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5
Q

humoral immunity definition

A

mediated by antibodies produced by B cells.

antibodies neutralize microbes, opsonize them for phagocytosis, and activate the complement system

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6
Q

cell mediated immunity definition

2 types and what they do

A

T cells activated by protein antigens from antigen presenting cells (APC’s)
requires repeat antigen stimulation to perform their functions
1. CD4 helper T cells (secrete cytokines to activate macrophages, helps B cells make antibodies, and stimulate inflammation)
2. CD8 helper T cells (kill infected and transformed cells)

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7
Q

Innate Immune Dysfunction can be divided into 3 categories

A
  1. inadequate response
  2. excessive response
  3. misdirected response
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8
Q

inadequate response of innate immune dysfunction examples (4)

A

neutropenia
abnormal phagocytosis
deficiency in complement system
hyposplenism

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9
Q

excessive response of innate immune dysfunction examples (3)

A

neutrophilia
monocytosis
asthma

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10
Q

misdirected response of innate immune dysfunction example

A

angioedema

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11
Q

Adaptive Immune Dysfunction examples (6)

A 
defects in antibody production
defects in T lymphocytes
combined immune system defects (SCIDS)
allergic reactions
anaphylaxis
autoimmune DO's
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12
Q

-penia

A

lack of, poverty, deficiency

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13
Q

-philia

A

affinity, attraction, fondness

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14
Q

allergy

A

reactions against normally harmless environmental antigens

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15
Q

autoimmune

A

reactions against self antigens

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16
Q

hypersensitivity

A

excessive immunologic reactions to microbes or environmental agents dominated by inflammation

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17
Q

atopy

A

propensity or genetic tendency to develop allergic reactions

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18
Q

antibody (Ab)

A

also known as immunoglobin (Ig), is a large Y shaped protein used by immune system to ID and neutralize foreign objects such as pathogenic bacteria and viruses

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19
Q

what are neutrophils formed by
what % of WBC’s?
function of neutrophils

A

formed by stem cells in bone marrow
make up 40-70% of all WBC’s in humans
are phagocytes and are found in the blood stream
first responders to inflammation, especially bacterial. predominant cells in pus, creating yellowish/white color

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20
Q

neutropenia neutrophil count

A

<1500/mm^3

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21
Q

types of neutropenia (5)

A

neonatal sepsis
kotsmann syndrome (autosomal recessive)
acquired defects (chemotherapy, antivirals)
autoimmune (lupus, RA)
infection (rate of consumption exceeds production)

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22
Q

neutropenia treatments

A

cessation of medication causes, granulocyte colony stimulating factor (filgrastim), bone marrow transplants. respecting asepsis in the periop environment is important

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23
Q

what system is spleen a part of
role of spleen
where its located

A

part of lymphatic system, primary blood filter. located in left upper abdomen

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24
Q

functions of spleen

A

removed old RBC’s, blood reservoir, recycles iron, metabolizes HGB, stores 1/4 of circulating lymphocytes, stores and clears PLTs. globin portion of HGB is degraded to amino acids, and the heme portion is metabolized to bilirubin, which is removed by the liver. synthesized antibodies in the white pulp. removes antibody coated bacteria.

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25
Q

asplenia

A

absence of normal spleen function, type of immune dysfunction. increase of sepsis risk is 350 gold, due to inability to clear bacteria from the blood.

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26
Q

hyposplenism

A

reduced spleen function

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27
Q

hyposplenism and sickle cell anemia

A

can cause auto infarction of spleen resulting in vaso occlusive disease

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28
Q

prevention of infection for hyposplenism patients

A

immunizations are important. travel restrictions, antibiotic prophylaxis even with minor procedures, alert warning bracelets

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29
Q

leukocytosis definition

A

WBC count above normal range. normal reaction often in inflammatory response but can also be from tumors or leukemias, stress, pregnancy, convulsions and medications (corticosteroids, lithium, beta agonist)

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30
Q

acute leukemia presentation

A

immature WBC’s in peripheral blood

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31
Q

chronic leukemia presentation

A

mature, non functioning WBC’s in peripheral blood

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32
Q

types of granulocytes (4)

A

basophils, neutrophils, eosinophils, mast cells

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33
Q

types of lymphocytes (2)

A

T cells and B cells

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34
Q

neutrophilia (type of leukocytosis) associated with these (4) diagnoses or insults

A

bacterial infections
inflammation
MI
burns

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35
Q

eosinophilia (type of leukocytosis) associated with these 8 clinical diseases or presentations

A 
asthma
hay fever
drug allergies
allergic skin diseases
parasitic infections
malignancy
hodgkins lymphoma
some forms of lupus
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36
Q

basophilia (type of leukocytosis) associated with

A

myeloproliferative diseases (blood cancers)

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37
Q

monocytosis (type of leukocytosis) associated with these 3 chronic infections and 3 inflammatory DO’s

A

chronic infections: TB, bacterial endocarditis, malaria

inflammatory disorders: UC, SLE, RA

38
Q

lymphocytosis (type of leukocytosis) associated with these 4 chronic infections

A

chronic infections: TB, hepatitis, CMV, pertussis

39
Q

eosinophilic esophagitis definition, triggers, pathophysiology

A

chronic immune system disease in which a type of white blood cell (eosinophil) builds up in the lining of esophagus.
this buildup, which is a reaction to foods, allergens, or acid reflex, can inflame or injure the esophageal tissue
damaged esophageal tissue can lead to difficulty swallowing or cause food to get stuck when swallowing
-may need dilation

40
Q

neutrophilia

  • neutrophil count
  • onset
  • result of (4 p’s)
A

> 7000/mm^3
within hours of infection, granulocytes increase 2-3 fold. mobilization of stored granulocytes and new from bone marrow
-pancreatitis, pyelonephritis, peritonitis, pnuemonia

41
Q

leukostasis

A

> 100,000/mm^3 neutrophil/WBC count. thick blood flow and WBC clumping can lead to TIA’s and strokes. also decreases O2 diffusion via lungs

42
Q

neutrophil count associated with myeloproliferative DO or hematologic malignancy

A

> 50,000/mm^3

43
Q

asthma

A

exaggerated bronchoconstrictor response to stimuli

44
Q

extrinsic asthma

A

associated with IgE production and allergies. associated with (+) skin test.

45
Q

intrinsic asthma

A

triggers are unrelated to immune system. include ETT placement, bronchospasm, cold, exercise, stress, inhaled irritants.

46
Q

angioedema

  • two types
  • what is involved
A

histamine mediated: autoimmune. mast cell mediators released. urticaria, bronchospasm, skin flushing, HoTN seen
bradykinin mediated: C1 esterase inhibitor dysfunction. includes ACEI and acquired.
-involves face, extremities and GI tract. SQ and submucosal edema formation

47
Q

bradykinin mediated angioedema can result from 3 ways

A
  1. autosomal dominant deficiency/dysfunction of C1 esterase inhibitor.
  2. ACEI’s. blocks breakdown of bradykinin
  3. acquired. lymphoproliferative DO’s acquire C1 esterase inhibitor deficiency secondary to antibody production
48
Q

what happens in the absence of C1 esterase inhibitor

A

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

49
Q

treatment of acute angioedema (6 options)

A
  1. androgens (long term and preop, increase hepatic synthesis of C1 esterase inhibitor)
  2. antifibrinolytic therapy (inhibiting plasmin activation, TXA, aminocarpmroic acid, aprotonin)
  3. C1 inhibitor concentrate
  4. synthetic bradykinin receptor antagonist
  5. recombinant plasma kallikrein inhibitor (blocks conversion of kininogen to bradykinin)
  6. FFP (2-4U, replaces deficient enzyme)
50
Q 
C1INH Concentrate (Berinert and Cinryze)
dose
MOA
sx relief
FDA approval
notes
A 
dose 20U/kg IV
MOA: C1INH concentrate
sx relief: .5-1h
FDA approval: cinryze as prophylaxis
notes: can be given at home, do not shake vial
51
Q 
Recombinant C1INH (Ruconest)
dose
MOA
sx relief
FDA approval
notes
A 
dose 50U/kg (<84kg), 4200U(>84kg)
MOA: C1INH
sx relief: 1-1.5h
FDA approval: HAE
notes: can be given at home, take note of rabbit allergies?
52
Q 
Ecallantide (Kalbitor)
dose
MOA
sx relief
FDA approval
notes
A 
dose: 10mg SQ at 3 sites (total 30mg)
MOA: kallikrein inhibitor
sx relief: .5-4 hours
FDA approval: HAE
notes: can be given at home
53
Q 
Icatibant (Firazyr)
dose
MOA
sx relief
FDA approval
notes
A 
dose: 30mg SQ in abdomen
MOA: bradykinin B2 receptor blocker
sx relief: 2 hours
FDA approval: HAE
notes: possible affect coronary BF
54
Q 
FFP
dose
MOA
sx relief
notes
A

dose: 2U
MOA: contains C1NH and ACE
sx relief: unclear
note: no RCTs for HAE or ACEI-AAE

55
Q

DiGeorge Syndrome

A

thymic, thyroid, parathyroid hypoplasia due to a gene deletion.

  • will see decreased T cells but B cells are normal
  • may also include cardiac malformations and facial dysmorphisms, truncus arteriosus and TOF, cleft palate
  • degree of immunocompromised correlates with amount of thymus tissue present
  • complete absence=SCIDS
  • tx: thymus transplant or infusion of T cells
  • anesethetic considerations: may need SBE prophylaxis, higher dose of abx, calcium supplementation if they have hypoparathyroidism, strict asepsis due to risk for infection
56
Q

SCIDS (Severe Combined Immunodeficiency Syndromes)

A
  • genetic mutations that affect T, B, and NK cell function/maturation
  • X linked form most common
  • lack of receptor -> lack of interleukin signaling ->lack of NK/B/T cell differentiation/maturation
  • appear healthy at birth but are highly susceptible to severe infections
  • newborns in US are screened for this
  • tx: only tx is bone marrow or stem cell transplant, gene therapy or enzyme replacement
57
Q

anaphylaxis clinical and pathologic manifestations

A 
cardiovascular collapse (tachycardia, hypovolemia), interstitial edema, urticaria, bronchospasm, laryngeal edema
(immune mediated aka IgE or non immune mediated aka IgG or IgM and are "anaphylactoid", direct release of histamine from mast cells or basophils)
58
Q

bronchial asthma clinical and pathologic manifestations

A

airway obstruction caused by bronchial smooth muscle hyperactivity, inflammation, and tissue injury caused by late phase reaction

59
Q

allergic rhinitis, sinusitis (hay fever) clinical and pathologic manifestations

A

increased mucous secretion, inflammation of upper airway and sinuses

60
Q

food allergies clinical and pathologic manifestations

A

increased peristalsis due to contraction of intestinal muscles, resulting in vomiting and diarrhea

61
Q

Type 2 allergic reactions are mediated by which antibodies?
examples
timing

A

IgG/IgM, “antibody mediated, cytotoxic”
MG, graves, autoimmune hemolytic anemia
delayed

62
Q

Type 3 allergic reactions are mediated by which antibodies?

examples

A

immune complex
SLE, glomerulonephritis, vasculitis
delayed

63
Q

Type 4 allergic reactions are mediated by which antibodies?

examples

A

T lymphocytes “delayed hypersensitivity”
RA, MS, chronic transplant rejection, TB test
delayed

64
Q

Type 1 allergic reactions are mediated by which antibodies?
examples
timing

A

IgE
anaphylaxis, bronchial asthma
immediate (5-10m)

65
Q

histamine

A

vasoactive amine
stored in mast cells, released upon mast cell degranulation
causes rapid vasodilation, increases vascular permeability and smooth muscle contraction

66
Q

prostaglandins and leukotrienes

A

lipid mediators.
prostaglandin D2 is the most abundant mediator generated by the cyclooxygenase pathway in mast cells, causes intense bronchospasm.
-leukotrienes are the most potent vasoactive and spasmogenic agents known

67
Q

cytokines

A

tumor necrosis factor and chemokine recruit and activate leukocytes and amplify

68
Q

risk factors for anaphylaxis

A

asthma, atopy, multiple past exposures to latex, hereditary conditions (angioedema)

69
Q

diagnosis of anyphylaxis

A
  • clinical manifestations
  • plasma tryptase concentration (typtase is stored in mast cells and released during immune mediated reactions. indicates mast cell activation).
  • plasma histamine concentrations. return to baseline 30-60m after a reaction. nonspecific
  • skin testing
70
Q

management of perioperative anaphylaxis

A

remove agent if possible, reverse HoTN and hypoxemia, replace intravascular fluid, inhibit further degranulation, inhibit release of vasoactive mediators, treat inflammation, relieve bronchospasm

71
Q

epinephrine administration dosage for anaphylaxis

A

10-100mcgIV bolus q1-2m then IV infusion .05-1mcg/kg/min

kids: 1-10mcg/kg by IV bolus

72
Q

anaphylaxis resistant to epinephrine: consider the following drugs

A

glucagon 1-5mg IV bolus followed by 1-2.5mg/h IV infusion
NE .05-.1mcg/kg/min IV infusion
vasopressin: 2-10unit IV bolus followed by .01-.1units/min IV

73
Q

secondary treatment drugs for anaphylaxis: 3 categories and their drugs/dosages

A
  1. bronchodilator (B2 agonist, albuterol metered dose or neb)
  2. antihistamines (H1 antagonist, diphenhydramine .5-1mg/kg IV. H2 antagonist, ranitidine 50mg IV)
  3. corticosteroids (adults hydrocortisone 250mg IV or methylprednisone 80mg IV) (kids hydrocortisone 50-100mg IV or methylprednisone 2mg/kg IV). may enhance B agonist effects or inhibition of release of arachidonic acid responsible for production of leukotrienes and prostaglandins
74
Q

patients with allergies to these things are at increased risk for drug allergies to anesthesia

A

asthma, fruits including kiwi and banana, medications

75
Q

intolerance definition

A

inability to tolerate the adverse effects of a medication ex)muscle pain and statins

76
Q

idiosyncratic reactions

A

drug reactions not related to the known pharmacological properties of a drug ex) dyskinesias and anti epileptic drugs

77
Q

muscle relaxants and anesthesia drug allergies

A

rocuronium and succinylcholine
cross sensitivity among classes: benzylisoquinoliniums, amino steroids, OTC cosmetics contain ammonium ions and are capable of sensitizing patient to developing IgE antibodies to quaternary and tertiary ammonium ions.
-morphine and neostigmine also contain ammonium ions
-the histamine release from atracurium administration is non immune mediated

78
Q

antibiotics and anesthesia drug allergies

A
  • PCN most common, sulfonamides second most common and most common cause of SJS
  • IgE antibodies can wane over time, may have reaction as a child, but able to take it as an adult
  • negative predictive value of PCN skin testing is high
  • PCN contain two allergenic components also present in other abx (B lactic ring, R group side chain)
  • Vanc: more of a histamine release related to infusionlat
79
Q

B lactam ring also found in

A

cephalosporins carbapenems and monobactams

80
Q

R group side chain also found in

A

ceopalosporins

81
Q

latex allergy
what tree causes it
at risk individuals (4)

A
  • produced by rubber tree hevea brrasiliensis
  • several hevea proteins can cause IgE mediated antibody response
  • a feature that distringuishes latex induced allergic reactions from other drug induce allergic reactions is delayed onset
  • at risk individuals include spina bifida, multiple previous operations, hx fruit allergy, healthcare workers
82
Q

propofol allergy

A
  • contains lecithin and soybean oils as emulsifying agents
  • contains preservatives
  • thought to be IgE mediated predominantly
83
Q

ASA and NSAIDS allergy

A
  • rhinorrhea, bronchospasm, angioedema can occur in at risk individuals. includes those with asthma, hyper plastic sinusitis, nasal polyps
  • not IgE mediated, rather due to inhibition of cyclooxygenase 1 that promotes synthesis of leukotrienes and subsequent release of mediators from basophils or mast cells
  • does not occur with COX 2 specific inhibitors
84
Q

Radiocontrast media allergy

A

more common with ionic, high osmolar contrast agents the higher the iodine, the greater the risk of adverse reaction
-often non immune mediated, can pretreat with corticosteroids and histamine antagonists. hydrocortisone 1-2mg/kg IV, diphenhydramine 50mg IV, ranitidine 50mg IV

85
Q

organ specific autoimmune diseases mediated by antibodies (6)

A 
autoimmune hemolytic anemia
autoimmune thrombocytopenia
autoimmune atrophic gastritis of pernicious anemia
MG
graves
goodpastuer syndrome
86
Q

systemic autoimmune disease mediated by antibodies

A

SLE

87
Q

allografts

A

grafts exchanged between nonidentical individuals of the same species

88
Q

MHC (major histocompatibility complex)

A

polymorphic genes that differ among individuals and function to recognize T cells mediates this. Transplant is recognized as foreign by recipients T cells. CD4 and CD8 is activated, migrate to implant, cause rejection

89
Q

treatment of graft rejection

A

immunosuppression (corticosteroids, anti T cell antibodies, drugs that inhibits T cell function)

90
Q

graft v host disease

A

commonly associated with bone marrow and stem cell transplant. the donor WBCs recognize recipient host as foreign. not same as transplant rejection.
tx: suppress t cells, steroids and calcineurin inhibitors

91
Q

tumor lysis syndrome
3 things released into blood
2 causes

A

massive lysis of tumor cells results in release of intracellular substances into the blood stream. potassium, phosphate, uric acid are released.
-caused after treatments and on steroids.

N935 Pathophysiology (12 decks)

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