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AS - N935 Advanced Patho II > Hyper- & Hypo Immune Disorders > Flashcards

Hyper- & Hypo Immune Disorders Flashcards

1
Q

Hyper- & Hypo- Immune Disorders

A

Inadequate innate immunity
- Neutropenia, abnormal phagocytosis, complement system deficiency, hypersplenism
Excessive innate immunity
- Neutrophilia, monocytosis, asthma
Misdirected innate immunity
- Angioedema
Inadequate adaptive immunity
- T lymphocytes deficiency (DiGeorge Syndrome), SCIDs
Excessive adaptive immunity
- Allergic reactions, anaphylaxis, drug allergies
Misdirected adaptive immunity
- Hypersensitivity to self-antigens, SLE, rheumatoid arthritis, hepatitis
Anesthesia & immunocompetence
- Graft vs. host disease
- Tumor lysis syndrome

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2
Q

Innate Immunity

A

NON-SPECIFIC response that targets common pathogens
No prior exposure required to elicit response
Passed on to each generation
Epithelial & mucus membranes, complement factors, neutrophils, macrophages, & monocytes
RAPID response
Mediated via cells & plasma proteins that are always present
Principle cells = myeloid cells (macrophages, neutrophils, dendritic cells)
NOT pathogen specific

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3
Q

Adaptive Immunity

A

Developed individually
Delayed response, develops memory & specific towards antigen, B & T lymphocytes
Powerful, normally silent but active & adapt to antigens
Specialized, unique specificity
Receptors created by rearrangement antigen-receptor genes that occur during lymphocyte maturation
Principle cells = T & B lymphocytes

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4
Q

Humoral Mediated Immunity

A

Mediated by antibodies produced by B cells

Antibodies neutralize microbes, opsonize them for phagocytosis, & activate the complement system

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5
Q

Cell Mediated Immunity

A

T cells activated by protein antigens from antigen presenting cells (APCs)
Requires repeat antigen stimulation to perform their functions
CD4+ helper T cells secrete cytokines to activate macrophages, helps B cells make antibodies, & stimulate inflammation
CD8+ helper T cells kill infected & transformed cells

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6
Q

Adaptive Immune Dysfunction

A 
Defects in antibody production or T lymphocytes
Combines immune system defects (SCIDs)
Allergic reactions
Anaphylaxis
Autoimmune disorders
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7
Q

-penia

A

Lack of, poverty, deficiency

Neutropenia = lacking neutrophils

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8
Q

-philia

A

Affinity, attraction, fondness

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9
Q

Allergy

A

Reactions against normally harmless environmental signs

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10
Q

Autoimmune

A

Reactions against self-antigens

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11
Q

Hypersensitivity

A

Excessive immunologic reactions to microbes or environmental agents dominated by inflammation

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12
Q

Atopy

A

Propensity or genetic tendency to develop allergic reactions

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13
Q

Antibody (Ab)

A

Immunoglobulin (Ig) large Y-shaped protein used by the immune system to identify & neutralize foreign objects such as pathogenic bacteria & viruses

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14
Q

Neutrophils

A

Formed by stem cells in the bone marrow
Make up 40-70% all WBCs in humans
Phagocytes found in the bloodstream
FIRST RESPONDERS to inflammation - especially bacteria
Predominant cells in pus (create yellow/white-ish color)

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15
Q

Neutropenia

A

<1,500/mm^3
Types include neonatal sepsis, Kostmann syndrome, acquired defects, autoimmune, infection
Treatments include medication cessation, granulocyte colony-stimulating factor, & bone marrow transplants
ASEPSIS important

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16
Q

Spleen

A

Lymphatic system
Large lymph node - primary blood filter
Primary RBC creation site fetal up to 5mos
Function: 250mL blood reservoir, removes old RBCs, recycles iron, metabolizes hemoglobin, lymphocyte storage, clears platelets
Globin → amino acids
Heme → bilirubin (removed via liver)
Synthesizes antibodies

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17
Q

Asplenia

A

Absence normal spleen function
Type immuno-dysfunction
Increased sepsis risk 350x d/t spleen unable to clear bacteria from the blood

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18
Q

Hyposplenism

A

Reduced spleen function

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19
Q

Sickle Cell Anemia

A

Auto-infarction w/in spleen results in vaso-occlusive disease

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20
Q

Leukocytosis

A

WBC count above normal range
Normal reaction - inflammatory response
Other causes include tumor, leukemias, pregnancy, convulsions & medications

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21
Q

Left Upper Shift

A

↑ratio immature to mature neutrophils

Bone marrow trying to make more

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22
Q

Right Shift

A

↓ratio immature to mature neutrophils

Shows bone marrow suppression (radiation sickness)

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23
Q

Leukemia

A

Acute - immature WBCs present in the peripheral blood

Chronic - mature, non-functioning WBCs in peripheral blood

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24
Q

Eosinophilic Esophagitis

A

Chronic immune system disease where type WBC (eosinophil) build-up in esophagus lining
Build-up reaction to foods, allergens, or acid reflux → inflame or injure the esophageal tissue
Damaged tissue → difficulty swallowing or cause food to get stuck

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25
Q

Neutrophilia

A

Granulocytes ↑2-3x
Neutrophilia >7,000/mm^3
- Pancreatitis, pyelonephritis, peritonitis, pneumonia
Leukostasis >100,000/mm^3
- Thick blood flow & WBC clumping → TIAs & strokes
Myeloproliferative disorder or hematologic malignancy >50,000/mm^3

26
Q

Asthma

A

Exaggerated bronchoconstriction response to stimuli

27
Q

EXTRINSIC Asthma

A

IgE production

Allergens

28
Q

INTRINSIC Asthma

A

Triggers are unrelated to the immune system

Examples: ETT placement, cold, exercise, stress, inhaled irritants

29
Q

Angioedema

A

Hereditary or acquired
Subcutaneous & submucosal edema formation
Often involves face, extremities, & GI tract

30
Q

Bradykinin-Mediated Angioedema

A

Autosomal dominant deficiency/dysfunction C1 esterase inhibitor
ACEi drug-induced angioedema d/t ↑bradykinin
Acquired - lymphoproliferative disorders acquire C1 esterase inhibitor deficiency 2° antibody production
CATECHOLAMINE & ANTIHISTAMINES ARE NOT EFFECTIVE IN ACUTE EPISODES

31
Q

Acute Angioedema Treatment

A

Androgens - prophylactic therapy
Antifibrinolytic therapy inhibiting plasmin activation
C1 inhibitor concentrate
Synthetic bradykinin receptor antagonist
Recombinant plasma kallikrein inhibitor - blocks kininogen → bradykinin conversion
FFP replaces the deficient enzyme

32
Q

DiGeorge Syndrome

A

Thymic, thyroid, & parathyroid hypoplasia
Cause: 22q11.2 gene deletion
↓T cells (B cells are normal)
Cardiac malformations & facial dysmorphisms
- Truncus arteriosus & TOF
- Cleft palate
Immunocompromise degree correlates w/ amount thymus tissue present
Complete absence = severe combined immunodeficiency syndrome
Treatment: T-cell infusion or thymus transplant
Hypoparathyroidism - Ca2+ supplementation
Strict asepsis d/t infection risk

33
Q

Severe Combined Immunodeficiency

A

Genetic mutations that affect T, B, & NK cell function/maturation
X-linked form 1/58,000 births
Appear healthy at birth but highly susceptible to severe infections
All newborns screened SCIDs
Gene mutations that encode for interleukin receptors
Treatment: bone marrow or stem-cell transplant, gene therapy, or enzyme replacement

34
Q

Allergic Reactions

A

Immune-mediated
“Overreactions”
4 types:
Type I - IgE (anaphylaxis)
Type II - IgG/IgM (myasthenia gravis, Grave’s disease)
Type III - immune complex (SLE)
Type IV - T lymphocytes (rheumatoid arthritis, multiple sclerosis)

35
Q

Type I

A

IgE
Histamine release & other mediators from mast cells
Vascular dilation, edema, smooth muscle contraction, mucus production, tissue injury, inflammation
Immediate hypersensitivity
Anaphylaxis, allergies, bronchial asthma

36
Q

Type II

A

IgG/IgM production binds to antigen on target cell or tissue → phagocytosis or lysis target cell via activated complement
Leukocytes recruitment
Possibly delayed
Autoimmune hemolytic anemia

37
Q

Type III

A

Immune complex formation (antigen-antibody complexes) → complement activation
Recruit leukocytes
Inflammation, necrotizing vasculitis (fibrinoid necrosis)
Delayed
SLE, glomerulonephritis, serum sickness

38
Q

Type IV

A

Activated T lymphocytes
Release cytokines, inflammation, & macrophage activation
T cell-mediated cytotoxicity
Perivascular
Delayed
Chronic dermatitis, multiple sclerosis, type 1 diabetes, tuberculosis

39
Q

Anaphylaxis

A

Life-threatening
Cardiovascular collapse (tachycardia, hypovolemia)
Interstitial edema, urticaria (cutaneous rash)
Bronchospasm, laryngeal edema

Immune mediated IgE 60%

Non-immune mediated “anaphylactoid” IgG or IgM
Less common
Direct histamine release from mast or basophils

40
Q

Histamine

A

Vasoactive amine
Stored in mast cells
Release upon mast cell degranulation
Causes → vasodilation, ↑vascular permeability, & smooth muscle contraction

41
Q

Prostaglandins

A 
Lipid mediator
Prostaglandin D2 (PGD2) most abundant mediator generated by cyclooxygenase pathway in mast cells → intense bronchospasm
42
Q

Leukotrienes

A

Lipid mediator

Most potent vasoactive & spasmogenic agents known

43
Q

Cytokines

A

Tumor necrosis factor & chemokines

Recruit, activate, & amplify leukocytes

44
Q

Perioperative Anaphylaxis Management

A 
Remove triggering agent
Reverse/treat hypotension & hypoxemia
Replace intravascular fluid
Inhibit further degranulation 
Inhibit release vasoactive mediators
Treat inflammation
Relieve bronchospasm
45
Q

Antihistamines

A

Histamine 1 antagonist
Diphenhydramine competes w/ histamine

Histamine 2 antagonist
Ranitidine

↓pruritis & bronchospasm
Not as effective to treat anaphylaxis once vasoactive mediators have been released

46
Q

Epinephrine

A

1-10mcg/kg IV bolus
Repeat every 1-2minutes as needed
↑intracellular cAMP, restores membrane permeability, & ↓release vasoactive mediators
β agonists relax bronchial smooth muscle

UNRESPONSIVE TO EPI → VASOPRESSIN, GLUCAGON, OR NOREPINEPHRINE

47
Q

β2 Agonists

A

Albuterol delivered via MDI or nebulizer useful to treat bronchospasm

48
Q

Corticosteroids

A

Several hours to take effect
Potentially enhance β agonist effects
Inhibit arachidonic acid release (leukotriene & prostaglandin production)

49
Q

Intolerance

A

Inability to tolerate medication adverse effects

Example: muscle pain & statins

50
Q

Idiosyncratic Reactions

A

Drug reactions not r/t known pharmacological drug properties

Example: antiepileptic drugs & dyskinesias

51
Q

Toxicity

A

Dose-dependent

Too much drug present in patient system at one time

52
Q

Perioperative Anaphylaxis Causes

MUSCLE RELAXANTS

A

Rocuronium & Succinylcholine

Atracurium histamine release = non-immune mediated

53
Q

Perioperative Anaphylaxis Causes

ANTIBIOTICS

A

PCN & cross-sensitivity w/ cephalosporins (β-lactam ring)
Sulfonamide - second most common (Stevens-Johnson syndrome)
Vancomycin - non IgE mediated (direct histamine release r/t drug infusion rate)

54
Q

Perioperative Anaphylaxis Causes

LATEX

A

Delayed onset >30min after exposure

Spina bifida, multiple previous operations, fruit allergy, & healthcare workers

55
Q

Perioperative Anaphylaxis Causes

PROPOFOL

A 
Contains lecithin (derived from egg yolk) & soybean oil as emulsifying agents
Preservatives = EDTA or sodium metabisulfite/benzoate 
2-isoproyl group
56
Q

Perioperative Anaphylaxis Causes

ASA & NSAIDs

A

Rhinorrhea, bronchospasm, & angioedema
High risk patients = asthma, hyperplastic sinusitis, & nasal polyps
NON IgE mediated
Cyclooxygenase-1 inhibition promotes leukotriene synthesis → release mediators from basophils & mast cells

57
Q

Perioperative Anaphylaxis Causes

RADIOCONTRAST MEDIA

A

0.1-3%
More common w/ ionic, high-osmolar contrast agents
↑iodine ↑risk adverse reaction
Non-immune mediated pretreat w/ corticosteroid & histamine antagonists

58
Q

Perioperative Anaphylaxis Causes

OTHER

A

Midazolam, Etomidate, Ketamine, Heparin, Insulin
Opioids - Morphine, Codeine, & Meperidine directly release histamine
Local anesthetics <1%
Ester > Amide
Halothane induced hepatitis
Dyes - ICG or methylene blue
Chlorhexidine
Synthetic volume expanders - contain dextrans, gelatins, albumin, starch → both immune & non-immune reactions
Blood products

59
Q

Rejection

A

Histocompatibility determines if tissue graft will be accepted (compatible) by the receiving individual
Major histocompatibility complex (MHC) are polymorphic genes that differ among individuals
- Function to recognize T cells
Graft donor expresses MHC molecules differ from those in the recipient host
- Graft recognized as foreign by recipient T cells
- Recipient CD4+ & CD8+ T cells specific for graft antigens are activated, migrate back into transplants, & cause its rejection

60
Q

Graft Rejection Treatment

A

IMMUNOSUPPRESSION needed to prolong graft survival
- Corticosteroids, anti T-cell antibodies, T-cell function inhibition drugs
Immunosuppression → risk opportunistic fungal & viral infections
- Reactivation latex viruses (cytomegalovirus) ↑cancer risk in immunocompromised patients

61
Q

Graft vs. Host Disease

A

Syndrome commonly associated w/ bone marrow & stem cell transplants
Donor WBCs remain w/ the donated tissue (graft) recognize the recipient (host) as foreign
NOT the same as transplant rejection
Donor immune system rejects the recipient body

Treatment: T-cell suppression

  • Steroids & calcineurin inhibitors (cyclosporin & tacrolimus)
  • Suppresses pro-inflammatory cytokine synthesis
62
Q

Tumor Lysis Syndrome

A

Rare but potentially lethal
Massive lysis tumor cells results in intracellular substances release into the bloodstream
- Potassium, phosphate, uric acid
Causes: steroids & after chemoembolization or radiofrequency ablation treatments

AS - N935 Advanced Patho II (20 decks)

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