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test 2 study guide

Study Guide for Immune, Inflammation, Infection, Adrenergics and Cholinergics

  1. Immune/Inflammation
    1. Understand passive and active immunity and which uses gamma globulins

Active- natural contact with infection

Passive- transfer for mother to child OR injectio of human GAMMA GLOBULIN

    1. Be able to differentiate your immunoglobulins (IgG, IgE, IgM, IgA….)

HUMORAL IMMUNE SYSTEM – ANTIBODIES

Type of Antibody

IgD

Present in plasma

Protects against bacterial and viral infections

IgM

Largest antibody

First made to fight a new infection

Transferred to nursing infant

IgG

Makes up 80-85% of plasma antibodies

Protects against infection

Transferred across placental barrier providing immunity to fetus Transferred to nursing infant

IgA

Found mainly in body secretions: saliva, tears, mucus, colostrum

Transferred to nursing infant

IgE

Involved in allergic reactions

Located in mucosal lining of respiratory and GI tracts

Which are passed to neonate through breastfeeding

  • A, G, E
    1. What cells are involved in immunity?

Look at MAST CELLS derived from basophils

Basophils store Histamine

    1. Understand B cells and T cells and what their roles are

B cells- produce antibodies

T cells: helper and cytoxic

Basopils: store histamine

Dendritic cell : recognize antigens as non-self

Neutrophils: are the most abundant

Memory trick: visualize antibodies as the soldiers produced by your body going to attack and neutrilaze antigens (enimes)

ACQUIRED IMMUNE SYSTEM

On test:

  • primary response: 1- 2 weeks before antibody reaches efficacy (desired therapeutic effect)
  • Secondary response: more rapid response efficacy in 1-3 days

Immune Response

Primary Cells

Functions

Protection

Humoral

(antibody-mediated)

  • B cells
    • Plasma cell
    • Memory cell
    • Creates antibodies
    • Directly disable pathogens
    • Marks pathogens for kill

Mainly bacteria

Cellular

(Cell-mediated)

  • T cells
    • Helper
    • Cytotoxic
    • Memory cell
    • Cell to cell combat
    • Direct kill of pathogens

Viruses, cancer, tumor cells & transplanted cells

Humoral Response primarily protects against bacteria and viruses

Understand autoimmunity and alloimmunity - teaching on meds for transplant

  • Autoimmune: body attacks itself
  • Alloimmunity: body rejects transplant
  • Immunosupressant - cyclosporine- helps slow downe system say you get a transplant you can this med to the body does not reject
    • CYCLOSPORINE
      • Adverse effects: kidney damage. Risk for injection
      • Do not give with grapefruit, NSAIDs, and avoid crowds
    1. What do your lymph organs do? - what is lymphadenopathy?
      1. Lymphadenopathy is the swelling of the noses secondary to autoimmune disease
    2. Hypersensitivity reaction

Hypersensitivity Reactions

Type

Antigens

Onset

Mechanism

Disorders

I

**

Pollen, foods, drugs, animal dander

Immediate

IgE binds to mast cells & basophils → releases chemical mediators

Hay Fever, asthma, food allergies, dermatitis/eczema, anaphylaxis

Type 2: blood transfusion

    1. What does histamine do? What are signs & symptoms of the presence of histamine?

, histamine & other substances are released from mast cells, basophils, and other cells in response to antigens circulating in the blood. FIght infection

  • Vasodilation
    • Flushing: face and upper body
    • If extensive can cause hypotension
  • Increased capillary permeability
    • Edema
  • Bronchoconstriction
  • CNS
  • Drowsiness, foggy-headed
  • Mucous membranes
    • Increased mucous production
    • Runny nose, teary eyes
  • Peripheral nerves
    • Itching, pain
    1. Do not memorize tasks of every chemical mediator, but know what they are

Chemical mediators: - complement, cytokines, histamine, leukotrienes, prostaglandins

    1. What does hypersensitivity look like?

Type

Antigens

Onset

Mechanism

Disorders

I

**

Pollen, foods, drugs, animal dander

Immediate

IgE binds to mast cells & basophils → releases chemical mediators

Hay Fever, asthma, food allergies, dermatitis/eczema, anaphylaxis

II

May be self or foreign

(tissue-specific)

Delayed

IgG or IgM binds to antigen on cell surface cell lysis & tissue damage

Blood transfusion (foreign), Goodpasture’s syndrome (kidney), Graves’ disease (thyroid)

III

Fungal, viral, bacterial

Immediate or delayed

IgG or IgM binds to antigen → creates immune complexes → inserts into small blood vessels, joints, & glomeruli → inflammation & tissue damage

Rheumatic fever, rheumatoid arthritis, post-strep glomerulonephritis, type I diabetes mellitus, systemic lupus erythematosus (SLE)

IV

Fungal, viral, bacterial,

foreign substances: foreign tissue, metals, rubber, plants

Delayed

Cell-mediated: sensitized T cells → attack antigen → inflammatory response

Contact dermatitis, poison ivy, transplant rejection, TB infection, PPD (TB skin test)

    1. How do you differentiate and determine anaphylaxis? - what is treatment?

Defining characteristics

-hypotension

-laryngeal edema

-bronchospasm

Severity depends on the level of response: local or systemic

Reaction is immediate & can be life-threatening

Itching, erythema, headache

Vomiting, abdominal cramps, diarrhea

Contraction of respiratory bronchioles

Laryngeal edema

Vascular collapse

**If you use an EpiPen, call 911!!!

Even if the patient seems better.

    1. In a reaction, if there is any respiratory/breathing symptom what is treatment?

EPIPEN

    1. What are side effects of antihistamine drugs?

Sedation! Especially with first gen

    1. Differentiate between 1st and 2nd generation antihistamines

ANTIHISTAMINES: FIRST GENERATION- benodryl

  • Mechanism of action
    • Compete with histamine for H1 receptors in tissues → block the actions of histamine
      • Not bullies
      • Give before (prophylactic) or early in allergic response
  • Can bind to (wet) muscarinic receptors → anticholinergic (dry) effects
    • Drying of mucous membranes , DRY mouth

ANTIHISTAMINES: 2ND GENERATION

  1. Mechanism of action
    1. Similar to1st generation
    2. do not cross/minimally cross the blood-brain barrier → much less sedation

What is angioedema?

With immunosuppression, what are our worries?

  • Getting sick

5mm TB test

Know T cells, B cells, cytokines, macrophages

Adreergic, IGG and IGM,

Drugs,: tetro-teeth

Asprin- can thin the blood you do not combine anticoag like warfarin and heparin bc too much bleedign

Celebox(NSAID) increased risk of MI and stroke

Tylenol is metabolized by LIVER and does no thave antiinflamator effects

Prednisone (glucocorticoids) is a steroid and adverse effects include hypergylcemia, PUD, and suceptibility to infection TAPER off

  1. Infections
    1. KNOW your antibiotics - their side effects specific to each, and indications or what to avoid when on them.
    2. Know how to prevent side effects for vancomycin

60-90 min slow rate

    1. Understand an infection workup and how to prioritize those tasks
    2. What do you do when you suspect an allergy to an IV drug?

STOP INFUSION CALL DR

    1. Know about interpreting TB tests
  • Tuberculin skin test (TST)
    • Positive if ≥15 mm induration in low-risk individuals
    • Immune compromised-may not respond as well to PPD
      • Reactions ≥5 mm considered positive
    1. Know about active vs latent TB
    2. Milary TB is organisms spread via bloodstream
    3. Understand HIV testing

Transmision is throught blood, semen, vaginal secretions and breast milk. It targets and kills T cells

Transmision is more likley when viral load is high

  • Viremia: large viral levels in blood for 2-3 weeks
  • Pathophysiology of GIV damage to CD4 and T cels (T helper cells_
  • When T helper cells drop to <500 NORMAL IS 800-1200

A diagnosis of AIDS cannot be made until the HIV-infected patient meets criteria established by the CDC.

AIDS is characterized by:

  • Severe immune system suppression and CD4+ T-cell counts < 200 cells/μL
  • An opportunistic infection
  • An opportunistic cancer
  • Wasting syndrome (loss of 10% or more of ideal body mass)
  • AIDS dementia complex (ADC).
    1. Understand the importance of T& CD4 cells in HIV
      1. Symptomatic infection when CD4+ T cekks trioto 200-500 normal is 800-1200
    2. Know diff b/w AIDS and HIV Cd4ct Helper T cells reduse risk of spreading and getting
    3. Understand the goal of HIV treatment with ART

Treated with antireoviral therpay for mothers to decrease viral load

Cd4+ normal range is 800-1200 cells

Nursing implications for Penicillin

  • Give IM
  • Give IV to not add or mix another drug

Cephalexan

  • give PO

Vancomyacin

  • Used fro serious infections such as C DIFF and MRSA can get Red Mans syndrome so you need to administer IV drug slowly over 60-90 min

Tetracycline: no dary products causes teeth color change

Levofloxacin - tendonitis and tendon rupture

  1. Adrenergic/Cholinergic
    1. Understand selectivity and its relationship to dosing
    2. Know your beta 1, beta 2, and alpha functions
    3. Know your muscarinic functions

Cholinergic Drugs (weT)

  1. Agents that influence the activity of cholinergic receptors
  2. The Receptors:
    1. Nicotinic N
    2. Nicotinic M
    3. Muscarinic - THIS is where our focus lies.
      1. cause contraction of ciliary eye muscles, decreased heart rate, constriction of bronchi, voiding, increased intestinal tone & motility, sweating, vasodilation

Muscarininc Agonist: Bethanechol

  • Nurisng considerations : take on empty stomach
  • Overdose: treat with atropine
  • Increases peeing
  • Rest and digest: wet response causes bradycardia

ATROPINE- drys em up so its a muscarininc antagonist

Epinephrine- activates ALL ADRENERGIC receptors

Beta 2 agonist is Albutteroll used for Asthma

Alpha 1: pupil dilation Increase BP

Alpha 2: norepinephrine release

Beta 1: increase HR

Beta 2: dilation of bronchioles

Prozasosis: 1st dose effect experience hyposttit