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What is HIV?
a retrovirus that attacks WBC
What are AIDS?
HIV Stage 3
CD4+ cells are less than 200
Risk factors w/ HIV
sharing needles
unprotected sex
contact w/ blood
breast feeding or birthing
Prevention for HIV
pre-exposure prophylaxis (ARV meds)
condoms
HIV testing
What does HIV target within the body?
CD4+ receptors on T-lymphocytes, monocytes, dendritic cells, & brain microglia
Stage 0 of HIV
Period of Infection - Development of HIV-specific antibodies
may not test positive
replication occurs
contagious
Stage 1 of HIV
Acute HIV
detect HIV RNA & antibodies
nonspecific symptoms (fever, rash, fatigue)
HIV established as antibodies cannot fight off infection
dramatic drop of CD4 T cells
When is the best time to start treating HIV?
Stage 1 to preserve the immune system
What is a viral set point?
equilibrium of HIV levels & immune response (CD4 increases to stable levels)
Stage 2 of HIV
Chronic HIV
viral set point
asymptomatic
Stage 3 of HIV
AIDS
CD4 T cells < 200
immunocompromised
deadly w/ no treatment
Stage unknown HIV
no data & AIDS symptoms are not present
HIV Diagnostic Tests
antibody
antigen/antibody
nucleic acid
blood
Which HIV diagnostic test detects HIV?
antigen/antibody & nucleic acid
Adverse effects of ARV
hepatoxicity
nephrotoxicity
osteopenia
cardiovascular disease
Reasons for ARV drug resistance
reg-resistant HIV at initial infection
selective drug resistance in pts
inconsistent adherence to HIV meds
Immune reconstitution inflammatory syndrome
an inflammatory reaction from a recovery immune system to an opportunistic infection
occurs beginning of ARV therapy
high morbidity
treatment: anti-inflammatory (cortisone)
S/S of Immune reconstitution inflammatory syndrome
fever
respiratory & abdominal S/S
worsening S/S of opportunistic infection
Respiratory S/S of HIV
SOB
dyspnea
cough
chest pain
fever
Respiratory Infections from HIV
pneumonia
TB
CMV
GI S/S of HIV
loss of appetite
N/V
oral candidiasis
chronic diarrhea
GI conditions from HIV
candidiasis
HIV wasting syndrome (severe weight loss)
What is Systemic Lupus Erythematosus (SLE)?
an inflammatory, autoimmune disorder where the body is attacking the nucleus of all cells
Risk factors of SLE
female gender
smoking
alcohol
UV rays
medications
stress
S/S of SLE
fever
fatigue
weight loss
discoid rashes
joint pain & swelling
pericarditis
lupus nephritis (major cause of mortality)
Treatment of SLE
management of chronic conditions, pain management, nonspecific immunosuppression
Medications for SLE
methylprednisolone - for acute autoimmune exacerbations
acetaminophen
hydroxychloroquine - anti malaria drug for skin lesions & flare ups
topical cortisone
methotrexate - common for lupus
Diagnostic for SLE
Positive ANA
Pancytopenia (low blood cells)
What is myasthenia gravis?
autoimmune disorder affecting the neuromuscular junction
(antibodies block ACh receptor sites —> muscle weakness)
Ocular Myasthenia gravis
only eyes are affected
diplopia
ptosis (drooping eyelids)
Generalized myasthenia gravis
facial weakness (bland expressions)
dysphonia (voice impairment)
dysphagia
generalized weakness
respiratory weakness
Diagnosis of Myasthenia gravis
Tensilon Test (admin edrophonium chloride IV —> S/S resolve)
ice test (see if ptosis resolves)
positive ACR antibody
Medications for Myasthenia gravis
ACh inhibitors
immunosuppressants
IVIG (for myasthenic crisis)
Treatment for myasthenia gravis
therapeutic plasma exchange (to remove antibodies)
removing thymus
Complications of myasthenia gravis
myasthenic crisis (exacerbation of weakness)
neuromuscular respiratory failure
treatment: endotracheal intubation & mechanical ventilation
Education of myasthenia gravis
conserve energy
rest before meals
take ACh meds w/ meals to avoid aspiration
soft foods
S/S of myasthenic crisis
respiratory distress
dysphagia
dysarthria
eyelid ptosis
diplopia
muscle weakness
S/S of Cholinergic crisis
Salivation & sweating
Lacrimation
Urination
Diarrhea
GI cramps
Emesis
Medications for myasthenia gravis
methylprednisolone - for acute autoimmune exacerbation
respiratory therapy
pyridostigmine - to prevent cholinergic crisis
eye patch - for double vision
What is multiple sclerosis (MS)?
A progressive disease of the CNS that attacks the myelin sheath
Risk factors of MS
higher northern latitudes
Vit D deficiency
smoking
obesity
Epstein-Barr infection
Phenotypes of MS
relapse-remitting
secondary progressive
primary progressive
Common S/S of MS
lesions
muscle weakness
impaired gait/balance
sensory loss in face or limbs
bladder issues
Lhermitte sign (electrical shock down back/limbs)
visual disturbances
fatigue
pain
spasticity (muscle resistance to stretch)
Diagnostic of MS
CNS lesions
elevated immunoglobulins in CSF
myeline plaques in brain MRI
Medications for MS
interferon - disease modifying therapy
methylprednisolone - for autoimmune acute exacerbation
amantadine - stimulant for fatigue
eye patch - for double vision
Normal Conduction of Cardiac Cycle
SA node - initiates electrical impulse
atrial myocardium - impulse spreads & causes atrial depolarization
AV node - impulse slows
Bundle of His - impulse speeds up
L&R Bundle Branches - conduct impulses to ventricles
Purkinje fibers - distribute impulses through ventricular walls
P wave
atrial depolarization
Q wave
depolarization of interventricular septum
R wave
depolarization of ventricles
(must be present to determine regularity)
S wave
last phase of ventricular depolarization; atrial repolarization
T wave
ventricular repolarization
U wave
final ventricular repolarization
PR Interval
AV conduction
QRS complex
ventricular depolarization
ST interval
ventricles contract & pump blood; action potentials in ventricles plateau
Approx HR
Count R waves on a 6-sec strip (30 big boxes) & multiple by 10
Enhanced automaticity
cells outside SA node become hyperexcitable —> ectopic beats or tachycardia
Suppressed automaticity
SA node dysfunction can cause bradycardia or sinus arrest
Early afterdepolarizations (EAD)
occur during repolarization & can trigger torsades de pointes (tachycardia)
delayed afterdepolarizations (DAD)
occur after repolarization; can cause premature ventricular contractions
Anatomical Reentry
impulse circulates around a fixed obstacle —> atrial flutter or ventricular tachycardia
Functional Reentry
occurs without a fixed anatomical obstacle (atrial fibrillation)
Blocks
impaired impulse conduction —> heart block
Accessory pathways
bypass normal conduction routes —> pre-excitation syndromes
Fibrosis/Scarring
structural changes in the heart that can slow conduction or blockages (promote reentry)
Hypertrophy
alters cellular electrophysiology & increases arrhythmia risk
How does potassium affect the heart?
affects resting membrane potential & repolarization
How does calcium affect the heart?
influences contractility & automaticity
Sympathetic stimulation of the heart
can increase automaticity & triggered activity
Parasympathetic stimulation of the heart
can slow SA node firing & AV conduction
Ischemia & Infarctions
alter cellular electrophysiology & create slow conduction or blocks (tachy/bradyarrhythmia)
Sinus Bradycardia
<60 bpm w/ reg rhythm
Cause of Sinus Bradycardia
increased vagal tones
hypothyroidism meds
sleep
Treatment for Sinus Bradycardia
atropine (if symptomatic)
pacemaker (if persistent)
Premature Ventricular Contractions
early beat
wide QRS complex
no preceding P wave
Cause of Premature Ventricular Contractions
caffeine
alcohol
stress
electrolyte imbalance
heart disease
Treatment for Premature Ventricular Contractions
antiarrhythmic meds, avoid triggers
Atrial Fibrillation
irregular rate & rhythm
absent P waves
risk of thromboembolism d/t ineffective atrial contraction
Cause of Atrial Fibrillation
HTN
heart disease
hyperthyroidism
alcohol
Treatment for Atrial Fibrillation
rate control (B blockers, Ca channel blockers)
rhythm control (antiarrhythmics)
anticogulation
Atrial Flutter
similar to atrial fibrillation; fast but regular rhythm; sawtooth P waves
Ventricular Tachycardia
100-250 bpm; regular rhythm
wide WRS complex
non-visible P waves
potential for hemodynamic instability; can degenerate to ventricular fibrillation
Cause of Ventricular Tachycardia
coronary artery disease
cardiomyopathy
electrolyte imbalance
Treatment for Ventricular Tachycardia
antiarrhythmic meds
cardioversion
ICD (implantable cardioverter-defibrillator)
Ventricular Fibrillation
chaotic electrical activity; no discernable waves
Causes of Ventricular Fibrillation
acute myocardial infarction
electrolyte imbalance
drug toxicity
Treatment of Ventricular Fibrillation
CPR
advanced cardiac life support
Asystole
no electrical activity; flat line
Cause of Asystole
end stage of arrhythmias
severe acidosis
Treatment of Asystole
CPR
epinephrine
What is stroke volume?
the amount of blood ejected from the left ventricle
How is stroke volume determined?
preload
contractility
afterload
What is preload?
initial stretching of the heart muscle cells right before contraction
What is contractility?
strength of cardiac contraction
What is afterload?
pressure or resistance the ventricles must overcome to eject blood through the semilunar valves into the systemic circulation
What is Mean Arterial Pressure (MAP)?
indicator of cardiac output & tissue perfusion
Range is 70-100
What is heart failure?
When the heart is unable to pump enough blood to meet the body’s metabolic needs
Risk Factors of HF
male
60+
cigarettes
excess weight
poorly managed diabetes
metabolic syndrome
What is associated with left-sided HF?
pulmonary congestion
What is associated with right-sided HF?
systemic congestion