Exam 3: Immune Dysfunction Flashcards
1
Q
The Immune system functions to…
A
Protect the host against micro-organisms
(two types: innate and adaptive/acquired immiunity)
S2
2
Q
What aspect of the immune system requires no prior exposure to pathogens?
A
Innate Immunity
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3
Q
What aspect of our immune system is rapid, non-specific, and does not provide long-lasting protection?
A
Innate Immunity
has no memory, but the response is always identical
S3
4
Q
What are the 3 non-cellular components of innate immunity?
A
- Epithelial and mucous membranes
- Complement system proteins
- Acute phase proteins
S4
5
Q
What are the 4 cellular components of the innate immunity system?
A
- Neutrophils
- Macrophages
- Monocytes
- NK cells (Natural Killer Cells)
S4
6
Q
What cell (of the innate immunity response) responds the fastest to infection?
A
Neutrophils
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7
Q
What cell (of the innate immunity response) provides a slower but more prolonged response to infection?
A
Macrophages
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8
Q
What is the Complement System?
A
Over 30 plasma and cell surface proteins that complements both innate and adaptive immunologic systems.
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9
Q
What does the Complement system do to enhance the adaptive and innate immunologic systems?
A
- Augments phagocytes and antibodies
- Marks pathogens for permanent destruction
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10
Q
Where are the proteins for the Complement system produced?
A
Most are produced in the Liver
S5
11
Q
What activates the complement system?
A
Infection of course.
C1 and C3 (Complement proteins 1 & 3).
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12
Q
What is the most numerous WBC?
A
Neutrophils
S6
Part of Innate immunity
They are Neumorous
13
Q
What are the characteristics and actions of neutrophils?
A
- Migrate rapidly to bacterial infections
- Release cytokines to phagocytize
- ½ life is 6 hours
- Sensitive to acidic infection environments
- Become purulent exudate
S6
14
Q
What type of immune cell is the largest blood cell and what is their role?
A
- Monocytes (largest blood cell)
- Circulates to specific tissue areas to differentiate into macrophages
not mentioned in lecture - but the chart also shows them turning into dendritic cells - and we know how tricky they like to be
S7
15
Q
What are the names of monocytes that have circulated to following areas:
- Epidermis
- Liver
- Lungs
- CNS
A
- Epidermis → Langerhans
- Liver → Kupffer
- Lung → Alveolar cells
- CNS → Microglia
S7
16
Q
What are the pertinent characteristics of monocytes/macrophages?
A
- Mobilize just after neutrophils
- Phagocytic destruction via NO & cytokines
- Persist at site in chronic infections (fight infection long term)
S7
17
Q
So then what are all the cells a parent Granulocyte-monocyte progenitor can turn into?
A
S4
18
Q
What is the least common blood granulocyte? (circulating)
A
Basophils
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19
Q
What cells reside in connective tissue close to blood vessels?
A
Mast Cells
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20
Q
What are the characteristics/actions of basophils/mast cells?
A
- Express high affinity for IgE
- Initiate hypersensitivity reactions
- Stimulate smooth muscle contraction i.e. bronchoconstriction
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21
Q
How do Basophils and Mast Cells initiate hypersensitivity reactions?
A
- produce histamine
- leukotrienes
- Prostaglandin release
- cytokines
His Large Prostate Crys
S8
22
Q
What cells play a major role in allergies, asthma, and eczema?
A
Basophils and Mast cells
S8
23
Q
Characteristics of Eosinophils
A
- Heavily concentrated in GI mucosa
- Protects against parasites
- Degrade mast cell inflammation
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24
Q
What characteristics does Adaptive Immunity possess?
A
- Present only in Vertebrates
- Delayed onset of action
- Capable of memory and specific antigen response
Vaccinations are also a form of adaptive memory
S10
25
What type of cells do adaptive immunity cells originate from?
Hematopoietic stem cell on the lymphoid side (lymphoid progenitor on the chart)
| S10
26
What is the humoral component of the Adaptive Immunity system?
What does this component do?
B cells → produce antibodies which bind to foreign proteins of bacteria, viruses and tumors
*Dr. Google says they produce IgM, IgD, IgG, IgA, and IgE antibodies, not sure if Mordacai actually said all of these - please verify*
*Nothing was said during lecture for this slide, I think we can delete.*
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What are the cellular components of the adaptive immunity system?
Helper T-cells
Cytotoxic T-cells
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Where do T-cells originate? Where do they mature?
T-cells originate in the bone marrow and mature in the Thymus.
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What are the general characteristics of T-cells?
- Produce interferon and interleukin
- Activate IgE
- Role in chronic inflammation
- Respond to infection
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What is the primary example of passive immunity?
Maternal IgA antibodies from breast milk
*Dr. M also added: IVIG intravenous immunoglobins - given to immunocompromised pts (from pooled plasma) - effective but pricy*
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How long does passive immunity last?
When a pt receives antibodies from someone else, the protection can last from weeks-months
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What is the primary example of active immunity?
Vaccines (they trigger antibodies to be formed)
*live, inactive, or recombinant*
| S12
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Describe active immunity
- Pathogen deliberately administered
- repeat exposure for a quick response to pathogens the next time
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34
Is neutropenia an example of excessive or inadequate immune response?
Inadequate
| S13
35
Is Asthma an example of excessive or inadequate immune response?
Excessive
| S13
36
Are autoimmune disorders an example of excessive or inadequate immune response?
Trick Question!
They are a misdirection of the immune response
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37
What is required for hypersensitivity development?
Prior sensitization (grass, latex, nuts, meds etc)
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What is hypersensitivity?
Foreign antigen reaction which causes altered T-cell and antibody response
*Response varies from uncomfortable rash to fatal anaphylaxis*
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What is the most common source of hypersensitivity?
Drugs (**NMBD,** ABX, PPIs, NSAIDS etc.)
*Roc is #1 cause of anaphylaxis under anesthesia*
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What occurs during a Type I Allergic Response?
- 1st exposure: T-Cells stimulate B cells to produce IgE immediately
- 2ⁿᵈ exposure: Antigen releases Ca⁺⁺ → histamine, inflammatory mediators, heparin are released.
(Histamine triggers: bronchostriction, Vascular permeability, vasodilation, gastric acid)
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What are examples of a Type I allergic response (aka immediate hypersensitivity)?
Anaphylaxis, Asthma, Angioedema, Conjuctivitis, Dermatitis
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What are common drugs used to prevent the histamine effects of Type I allergic responses?
- Antihistamines
- Cromolyn Na⁺
- Bronchodilators
- COX Inhibitors
- Diagnostic allergen tests
- small doses of allergen to desensitize
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What is another name for Type II Allergic Responses?
What mediates these types of responses?
What is the reaction severity and time?
- Cytotoxic Hypersensitivity
- Mediated by **IgG, IgM, and Complement system** → activate B-cells → produce antibodies.
- Severity will vary - reaction time in minutes or hours
mediated by GMC
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What are examples of Type II Allergic Responses?
- Hemolytic Anemia
- Myasthenia Gravis
- Transfusion Reactions
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What is the treatment for Type II Allergic Responses?
- Anti-inflammatories
- Immunosuppressants
- IVIG up and coming
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What is another name for Type III Allergic Response?
Immune Complex Hypersensitivity
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What occurs with Type III Allergic Response?
Failure of immune system to eliminate antibody-antigen complex.
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Where are the antibody-antigen complexes deposited in immune complex hypersensitivity?
Joints, kidneys, skin, eyes
*causes chronic ongoing inflammation of these places*
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What antibodies mediate Type III Allergic Responses?
IgG and IgM
*takes hours-weeks to develop*
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What are examples of Type III Allergic Responses?
Systemic Lupus Erythematosus and Rheumatoid arthritis
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Treatment for type III allergic response?
- Anti-inflammatories
- might need immunisuppressives
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52
What is a Type IV Allergic Response?
T-lymphocyte and monocyte/macrophage mediated response that **does not involve antibodies**.
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What are examples of Type IV Allergic Responses?
- Contact Dermatitis
- Tuberculosis
- Stevens-Johnson Syndrome
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What are the most common symptoms with Type IV Allergic Responses?
Cutaneous symptoms
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Treatment for type IV allergic reaction?
- anti-inflammatories
- immunosuppressives
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Anaphylaxis
- life threatening condition (oh really?)
- about 1:5000 to 1:20,000 anesthetics
- **usually occur within 5-10 min of exposure**
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Symptoms of Anaphylaxis and what rhythm occurs with untreated anaphylaxis?
- Systemic vasodilation
- Hypotension
- Extravasation of protein and fluid (bc increased vessel permeability)
- Bronchospasm
- **PEA**
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58
What causes the loss in BP noted with anaphylaxis?
Vasodilation from NO release
| This is from Andy - but its not anywhere on Mordacai's slides...
59
What is the pathophysiology of anaphylaxis?
- Previous exposure had made IgE antibodies
- Mast cells and basophils degranulate: release histamine, leukotrienes, prostaglandins, eosinophil/neutrophil chemotactic factor, and platelet-activating factor
- Anaphylaxis: up to 50% of intravascular fluid extravasates
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## Footnote
lifetime prevalence 5%
60
What is Biphasic anaphylaxis?
- Occurs following an asymptomatic period **without second exposure**
- Secondary anaphylactic episode occurring 8 - 72 hours later.
*occurs is 4-5% of the pts that experience anaphylaxis*
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What are risk factors for a secondary anaphylactic episode?
- Severe initial response
- Initial response required multiple epi doses
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What are risk factors for perioperative anaphylaxis?
- Asthma (or any baseline hypersensativivity)
- Female (not in teen years)
- Long Anesthetic
- Multiple past surgeries
- Presence of other allergic conditions
FLAAM
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63
A quick anaphylaxis diagnosis can be compromised by...
- communication issues (you are trying to troubleshoot high airway pressures first etc..)
- pt is covered by drapes
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What labs can verify mast cell activation and release?
- Plasma Tryptase concentration: takes 1-2 hours, and verifies mast cell activation and release
- Plasma Histamine concentration
- Skin testing: 6 weeks after reacion **wheel and flare response**
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Plasma histamine concentration should be at baseline within ____ minutes of treatment.
60 minutes
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What is the treatment for anaphylaxis?
- **first** Call for help
- Stop blood, drugs, colloids
- 100% O₂
- Epi
- Fluids
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What is the epinephrine dose for adult anaphylaxis?
10 mcg - 1000mcg IVP q 1-2 min
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What is the epinephrine dose for child anaphylaxis?
1-10 mcg/kg IVP q 1-2 min
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If a patient experiencing anaphylaxis is resistant to epi, what should be given?
Vasopressin or Methylene blue
*These will inhibit NO production and thus counteract vasodilation*.
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What is the crystalloid dosage for anaphylaxis?
NS: 10 - 25 mL/kg over 20 min
repeat PRN
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What is the colloid dosage for anaphylaxis?
10 mL/kg over 20 min
repeat PRN
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72
Why is epinephrine the drug of choice for anaphylaxis?
- ↓ degranulation of mast cells & basophils → reduced vasodilation
- α1 = Increased blood pressure
- β1 = positive Inotropy & chronotropy
- β2 = Bronchodilation
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73
What drug classes are secondary treatments for anaphylaxis?
- Bronchodilators
- Antihistamines
- Corticosteroids
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What are the antihistamines (and dosages) used as secondary treatments for anaphylaxis?
- H1 → Diphenhydramine 0.5 - 1 mg/kg IV
- H2 → Ranitidine 50 mg IV
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What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?
- Hydrocortisone 250 mg IV
- Methylprednisolone 80 mg IV
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What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?
- Hydrocortisone 50-100 mg IV
- Methylprednisolone 2 mg/kg IV
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77
Type A blood will have what Antibodies, what antigens, and is compatible with what?
Type A blood will have
- Anti-B antibodies
- A-antigen
- compatible with A and O
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Type B blood will have what Antibodies, what antigens, and is compatible with what?
Type B will have
- Anti-A antibody
- B antigen
- compatible with B and O
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Type AB blood will have what Antibodies, what antigens, and is compatible with what?
Type AB will have
- no antibodies
- A and B antigens
- Universal recipient
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Type O blood will have what Antibodies, what antigens, and is compatible with what?
Type O will have
- Anti-A and Anti-B antibodies
- No antigens
- Compatable with O (although it is the universal donor bc of lacking antigens)
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Specific immune reactions: How does a transfusion reaction happen?
- This is a response to surface antigen on the donor RBC
- responds to A, B and Rh factors
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Specific Immune reactions: how does transplant rejection happen?
- Response to antigens on the donor organ
- this is due to preexisting antibodies
- can be acute or chronic
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Specific immune reactions: Graves disease
Autoantibodies to TSH receptor
most common cause of hyperthyroidism
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Specific immune responses: Multiple sclerosis
- immune mediated inflammation
- destroys myelin and underlying nerve fibers
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Specific immune responses: Rheumatoid arthritis
- abnormal production of proinflammatory factors
- infection is thought to play a role
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Specific immune reactions: SLE
- Autoimmune and inflammatory
- Antibodies against: RBCs, WBCs, nucleic acids, platelets, coagulation proteins
- affects multiple organ systems
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87
What is/are the cause(s) of hereditary angioedema?
C1 Esterase inhibitor deficiency/dysfunction (decreased C1) → leads to excessive bradykinin.
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What factors can cause C1 esterase problems?
- Menses
- Trauma
- Infection
- Stress
- Oral contraceptives
MOIST
| S33
## Footnote
Could you of chosen another word? Perhaps Omits
89
What typically limits the production of excessive bradykinin?
C1
*C1 limits kallikrein and Factor XIIa*.
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What occurs anatomically with excessive bradykinin?
- Laryngeal swelling
- Vasodilation
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91
What dose of antihistamine should be used for hereditary angioedema?
Trick question. Hereditary Angioedema = excessive bradykinin and is unaffected by antihistamines.
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What body parts are typically effected by hereditary angioedema?
Legs, hands, face, upper resp tract
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What is the typical cause of acquired angioedema?
- ACE Inhibitors
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What symptoms are conspicuously absent with acquired angioedema?
No Urticaria or Pruritus
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What is responsible for the breakdown of bradykinin?
ACE
*Thus ACE inhibitors = ↑ bradykinin = angioedema*.
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What are the treatments for Angioedema?
- Airway maintenance (usually fiberoptic intubation or tracheostomy)
- FFP (reestablish volume)
- C1 Inhibitor concentrate
- Epinephrine
- Antihistamines
- Glucocorticoids? (not first line but give later)
GA- FACE
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How does the HIV infect the host?
- The virus (HIV) thru reverse transcription makes a double helix DNA with all viral genetic material
- Can change amino acid sequence; new version of the amino acids not recognized
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What cells are destroyed by the HIV virus?
Monocytes/Macrophages and T-cells
| S36
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How long does seroconversion take after inoculation with the HIV virus?
2-3 weeks
*host experiences flu-like symptoms during the seroconversion*
| S37
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What are the initial signs and symptoms of HIV conversion to AIDS?
Weight loss and failure to thrive
| S38
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How is HIV/AIDS diagnosed?
- ELISA: 4-8 weeks after infection
- Viral Load
- CD4/Helper T lymphocytes < 200k
- HAART agent sensitivity
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Big ass list of comorbidities associated with aids, but in general....
In general, if our pt is immunocompromised, they are more susceptable to more diseases (duh)
| S39
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Anesthesia assessment for immunocompromised: cardiac function
- Abnormal EKG
- LV dilation
- Pulmonary hypertension
- MI
- Pericardial effusions (25%)
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Anesthesia assessment for immunocompromised: Neuro function
- Dementia
- Increased ICP
- Autonomic nervous dysfunction
- Peripheral neuropathy (35%)
| S40
105
Anesthesia assessment: pulm
- Respiratory failure
- Pneumothorax
- COPD
| S41
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Anesthesia assessment: Endocrine/hematologic
- Adrenal insufficiency
- Glucose intolerance
- Anemia
- Bone marrow suppression
- Thrombocytopenia
| S41
107
Anesthesia assessment: Renal
- ATN
- ESRD
| S41
108
Inhibition of the liver's ____ has huge implications for anesthetic delivery in HIV/AIDS patients.
CYP 450's
*Affects: Hormone synthesis
Cholesterol synthesis
Vit D metabolism
Drug metabolism (prolonged)
Bilirubin metabolism (hyperbilirubinemia)*
Drugs will also take much longer to clear
| S42
109
What s/s characterize scleroderma? (AKA: systemic sclerosis)
- Inflammation
- Vascular Sclerosis
- Fibrosis of skin/viscera
IVF
| S44
110
At what age does scleroderma typically occur?
What gender is typically affected? Cure?
- 20-40
- Females
- No cure
| S44
111
Where are the mobility issues and pain of scleroderma?
* decreasing mobility of fingers
* facial pain d/t vascular sclerosis affecting the facial nerve
* Reynaud's is common
| S45
112
What GI symptoms of scleroderma are particularly pertinent to anesthesia?
- GI Tract Hypomotility
- ↓ LES tone (increased risk of aspiration)
| S45
113
What cardiac issues is associated with scleroderma?
- dysthythmias and conduction abnormalities
| S45
114
____ fibrosis and ____ artery stenosis are prominent considerations for anesthesia in scleroderma patients.
Pulmonary fibrosis and renal artery stenosis
| S45
115
What are the overall anesthesia implications of scleroderma?
- Could have multiple organs dysfunctional
- Arterial catheter issues i.e. may have trouble placing an Aline
- Contracted intravascular volume
- Aspiration risk
- Limited neck mobility
- ↓ pulmonary compliance
| S47
116
What do inhalation agents do the immune system?
- Suppress NK cells
- Induce apoptosis of T-cells
- Impair phagocytes
*Unclear effects on tumor cells - sevo stimulates renal cell carcinoma, but inhibts small cell carcinoma*.
we are the knights who say "NII"
| S48
117
This benzodiazepine, ____, decreases the migration of neutrophils.
Midazolam
| S48
118
This induction agent, ____, will depress natural killer cell activity.
Ketamine
| S48
## Footnote
K for Killer
119
This induction agent, ____, decreases cytokines but promotes NK cells.
Propofol
| S48
120
What drug class will suppress NK cells?
Opioids
*Particularly morphine and fentanyl*.
| S48
121
What cell type plays the greatest role in chronic inflammation?
T-Cells
| Andy
122
What cell type activates IgE and produces interleukins and interferons?
T-Cells
| Andy
123
What drug class will inhibit prostaglandin synthesis?
NSAIDS
| S48
