medsurg exam 2 (HIV and immun)

immunity

organized series of actions by body to protect itself against pathological organism - resulting in destruction/neutralization of organism

fx of immune system

homeostasis, defense, surveillance

foreign substances (antigens)

bacteria, viruses, fungi, prions, parasites

haptens

smallest molecules in body; ppl have different systems

antigens

have receptor sites (what’s attached within my immune system; memory cells are built)

cells involved w immune sys

mononuclear phagocytes, lymphocytes, dendritic cells, cytokines

lymphocytes involved in immune sys

B (bursa cells), T (t cytotoxic (CD8) and t helper (CD4), and natural killer

types of immunity

innate or acquired

innate/natural immunity

exists without former antigen contact; “born w it” (human specific immunity), includes natural barriers (skin, mucus membs), involves inflamm response; NON SPECIFC

active acquired immunity

when body responds to patho org and produces antibodies against them; follows an invasion and results in sensitized antibodies; when reinvaded response is faster; can take a while to develop but lasts long time (example: vaccines)

passive acquired immunity

temporary; receives antibodies to antigen instead of making them; quick but doesn’t last long bc no memory cells; (ex: immunoglobulin from mom to fetus; injection of serum antibodies)

types of immune response

humoral and cell-mediated

humoral immunity

antigen invades causes B cells to divide and become plasma cells (differentiated B) which produce antibodies (immunoglobulin) that travel in bloodstream to communicate w other cells

humoral immunity response

primary takes 4-8 days after initial exposure; 2nd exposure takes 1-3 days (stronger, longer lasting)

cell mediated immunity

when T cells recognize antigen and start immune response; production of sensitized t-lymphocytes to kill and destroy pathologic organisms

protection from cell-mediated immunity primarily against

cancer cells, virus infected cells, fungal infections; rejection of transplanted tissue, contact hypersensitivity reactions

immuno effects on aging

decrease in fx, increase infection susceptibility, alterations in T cells, increase tumor incidence, immunity from vax may not be as strong

overacting immune response

hypersensitivity disorders; alleriges, autoimmune disorders

under responsive immune sys

severe infections, immunodeficiency diseases, malignancies

overacting classifications

Type I, II, III, IV; can’t practice self-limitation

type I classification (overact immune resp)

IgE-mediated

type II classification (overact immune resp)

cytotoxic reaction

type III classification (overact immune resp)

immune-complex reaction

type IV classification (overact immune resp)

delayed hypersens reaction

type I IGE mediated reaction

chemical mediators released from mast cells: histamine, serotonin, leukotriene, eosinophil chemotactic factor, kinins, bradykinin; symptoms: increase mucosal secretion, itching, increased vas permeability, smooth mus contraction

anaphylaxis

med emergency!, shock can occur, tx: remove trigger, maintain airway, high flow oxygen, maintain circulatory vol, IV access, epi, albuterol, corticosteroids, diphenhydramine

type II cytotoxic reaction

target cells usually red, white, and platelets; commonly involved antigens: ABO blood group, Rh factor and drugs

if pt is transfused w incompatible blood

antibodies immediately coat foreign RBCs, RBCs agglutinate, life threatening, cell lysis and possible renal failure secondary to hemoglobinuria

collab care of hypersens reactions

after allergy dx: avoid trigger/allergen, tx symptoms, desensitization through immunotherapy if necessary; document allergies, drug therapy

durg therapy for chronic allergies

antihistamines, sympathomimetic/decongestant drugs, corticosteroids, topical antipruritics, mast cell-stablizing drugs

sympathomimetic/decongestants

epinephrine (adrenalin), pseudoephedrine (sudafed)

corticosteroids

most commonly given nasally

topical antipruritic drugs

calamine lotion

mast-cell stabilizing drugs

cromolyn, nedocromil (both aval as nasal spray/inhalant neb); these don’t help immediately

latex allergies

the longer one uses, more likelihood of getting allergy; two types: IV and I; symptoms include skin rash, hives, itching, nasal/eye/sinus s/s, asthma, and shock

type I latex allergy

minutes of contact

type IV latex allergy

contact dermatitis, delayed reaction: up to 6-48 hr

autoimmunity

immune resp attacks itself bc it cannot tell self from non-self (no self-recognition); unknown cause, classified by organ and systemic diseases; tx: aphaeresis

apheresis

procedure where blood components are separated then one of those components are removed; ex: plasmapheresis - watch for hypotension and citrate toxicity

autoimmune issues

occur anywhere; known as having flare ups and remissions & our job as nurse is to try and keep pts in remission

immunodeficiency disorders

occurs when immune sys doesn’t provide adequate protection to body; one or more immune mechs impaired; primary and secondary disorders

primary immunodeficiency disorder

improperly developed/absent immune cells

secondary immunodeficiency disorder

caused by illness or tx

causes of secondary immunodeficieny

drug-induced, age, malnutrition, stress, diseases/disorders, therapies

vax

contain small amts of pathogenic organism (alt so it doesn’t cause disease) ATTENUATED VS NONATTENUATED

vax work

admin to pt, pt produces antibodies, later if pt is exposed to pathogen body can get rid of it; pt is protected from disease, hopefully, without ever having it

precautions/contrainds for adult vax

hx of anaphylactic reac, immunocomp state, pt w febrile illness, allergy to eggs

vax contraind in preg

LAIV, MMR, VAR, AND ZVL

dont give attenuated vax

to ppl who disqualify themselves (pregnant women)

type I HIV

prev in US and canada; more responsive to drugs

type II HIV

more prev in 3rd world countries; more resistant

HIV modes of transmission

sexual, blood, perinatal (during preg and birth, breastfeeding)

¼ babies of HIV+ moms

will get virus (all will have antibodies)

incidence of HIV

33 million worldwide; 1 mil in US; ~50,000 new each year; msot are men

HIV and RNA

has rna but no dna so must have host cell to duplicate; attaches to gp120 knobs to cell’s CD4 receptors

cells w CD4 receptors

T helper, lymphocytes, and monocytes

inside HIV

rna makes viral dna with reverse transcriptase; viral dna enters cells dna and alters; infected immune cell makes HIV infected cells

acute HIV infection

develop HIV specific antibodies; occurs 1-3 weeks post infec.; lasts 1-2 weeks; headaches, body aches, diarrhea, pharyngitis, etc; viral load rises quickly

chronic infection HIV

asymptomatic & symptomatic, AIDS

chronic asymptomatic inf (HIV)

also called latent phase; 1-2 months-8years; viral load bt 200-500, CD4 counts maintains above 500 cells/ul; intense disease proliferation

chronic symptomatic infection

early symptomatic phase; from year 8-year10; CD4 t-cells bt 200-500; s/s: night sweats, fever, chronic diarrhea, headaches, fatigue, thrush, kaposi sarcoma, etc

chronic infection - AIDS

year 10+; CD4 below 200; opportunistic infections - (PJP), cryptococcal meningitis, cytomegalovirus retinitis; opportunistic cancers, wasting syndrome, dementia

rapid screening for HIV

OraSure (uses gum line), OraQuick (drop of blood), both 20 min screens, positives in either require EIA confirmation

testing for HIV

based on risk factors, 4th gen testing for both antigens and antibodies; 10 day eclipse or window period; immunoassay testing

test for HIV progression

measure CD4 counts and viral loads; CD4 norm between 800-1200 (w/o disease), viral load 200-500 means early chronic phase stable; high viral 5000-10,000 progressing

drug therapy

antiretroviral agents (ARTS), drugs to tx opportunistic infections

ARTs

NRTIs (nucleoside reverse transcrip inhibs), NNRTIs (non-neucleoside …) , protease inhibitors, integrase inhibitors, fusion inhibitors

goals for drug therapy

decrease viral load; maintain or raise CD4 counts, delay dev of HIV related symptoms and opportunistic diseases

PrEP (pre-exposure prophylaxis) drugs

prescribed to ppl at risk for HIV; to prevent HIV from sexor injection drug use; work by prevent integration to CD4

PrEPs reduce

risk of getting HIV from sex by abt 99% when taken as prescribed; reduces risk of getting HIV by at least 74% (truvada (men & women) and descovy (men))

PEP (post-exposure preophylaxis)

med to prevent HIV after possible exposure; must be within 72 hrs exposure, for emergent situations (not repeated expos), combo of 3 ART meds for 28 days; CDC rec tenofovir, emtricitabine, and raltegravir or dolutegravir

valves of heart are

unidirectional

heart valves

tricuspid, pulmonic, mitral, aortic

coronary circulation

has own circ sys; blood flows during diastole, systolic = max pressure

sinuses of valsava

right above cusps of aortic valve; open into right and left cor art

right coronary artery

supplies r atrium and r ventricle (part of posterior left vent)

left coronary artery

branches into left anterior descending and left circumflex artery that supply the left atrium and left ventricle

ischemia

tissue hypoxia; inadequate blood flow to meet myocardial o2 requirements; pain that goes along w it is angina

myocardial infarction (MI)

result of permanent loss of blood supply and cellular death (tissue necrosis)

SA node

specialized nerve tissue - heart’s pacemaker; drives heart beat

action potential

electrical impulse travels through heart and leads to contraction; all cardiac muscle has this (start of heart beat)

contraction

occurs when calcium flows into cardiac cells after depolarization

depolarization

calcium coming out of cell

AV node

allows time for atria to fill by providing break in contraction

bundle of his

picks up impulse and spreads it over ventricles by way of purkinje fibers

repolarization

cells return to former state

systole

absolute refractory period during which cardiac muscle gradually recovers and is excitable again; opening of aortic valve

p wave

depolarization of atrium

PR interval

measure of time required for impulse to spread from SA node to ventricle

QRS interval

depolarization of the ventricles

t wave

repolarization of ventricles

EKG strip small box

0.04 sec

EKG large box

0.20 sec

p wave normal

0.06-0.12 sec

pr interval

0.12-0.20

QRS complex

0.04-0.12

p to p

to measure atrial rate

r to r

for ventricular rate

measure rhythm

regular, irregular, regular irregularity

rule of 10s

count each 6 sec strip for number of complexes then x10 for 60 secs