MedSurg 301 Test # 2 Study Guide
Immunology
ANTIGENS
Antigens: surface markers
Haptens: Smallest substances a host can take in; nonproblematic until combined with other substances to
form an antigen (ie Hapten-driven drug anaphylaxis)
CELLS INVOLVED IN THE IMMUNE RESPONSE
Mononuclear Phagocytes
-Non-specific
-Engulf invaders
-Message to recruit lymphocytes
Lymphocytes: B Cells
-Immunoglobulins, aka antibodies
Lymphocytes: T cells
-T-cytotoxic cells (CD8)
-T helper cells (CD4)
Lymphocytes: Natural Killer Cells
-Non-specific, phagocytic macrophage
Dendritic Cells
-Encapsulate invaders
Cytokines
-Chemical messengers
TYPES OF IMMUNITY
Innate Immunity
-Non-specific, passed from mom-baby
-Involves inflammatory response
-Found in “natural barriers:” Skin, mucosa, macrophages, NKs
Acquired Immunity
-Active acquired immunity (ie vaccines)
oBody produces its own antibodies against a pathogen
oLong lasting (memory cells)
oSlower response
-Passive Acquired Immunity
oBody receives antibodies (via mom or administration)
oShort lived
oQuick response
TYPES OF IMMUNE RESPONSES
Humoral Immunity
-B-cells
-Bacteria fighting
-PRIMARY immune response: 4-8 days after exposure
-2ND EXPOSURE: 1-3 days; stronger and longer
FIGHTS:
-Bacteria
-Viruses (extracellularly)
-Respiratory pathogens
-GI pathogens
Cell-Mediated Immunity
-T-cells, macrophages, etc.
-Virus fighting
-Produce sensitized T-lymphocytes to kill pathogens
-Seen in transplant rejection, hypersensitivity reactions
FIGHTS
-Fungi
-Viruses (intracellularly)
-Chronic infections
-Tumor and cancer cells
-
ALTERED IMMUNE RESPONSE: OVERACTIVE
Hypersensitivity Responses: cannot practice self-limitation
Type I: IgE Mediated
- Chemical mediators released from mast cells
(Histamines, serotonin, bradykinin, kinins)
- Produces:
- increased secretions
- itching
- increased vascular permeability
- smooth muscle contraction
Seen in: ANAPHYLAXIS
S/Sx:
oHypotension
oTachycardia
oNarrowing airway, dyspnea, etc.
oUrticaria
Treatment:
- Airway
- Oxygen
- IV access
- Drugs:
Epinephrine
Albuterol (bronchodilator)
Diphenhydramine (antihistamine)
Corticosteroids (immune inhibitors)
Type II: Cytotoxic – IgG/IgM Mediated
- Targets RBC, WBC, platelets
- Seen in TRANSFUSION REJECTION
- Treated like Anaphylaxis
CHRONIC ALLERGIES
Drugs used:
-Antihistamines
-Sympathomimetic (epi, sudafed)
-Corticosteroids – an “end stage” drug
-Topical (calamine lotion)
-Mast-Cell Stabilizing Drugs (Flonase; two weeks to start working, work by coating mast cell)
LATEX ALLERGIES:
Type I:
-Occurs within minutes
Type IV
-Occurs 6-48 hours later
-Contact dermatitis
AUTOIMMUNITY
- Absence of self-recognition
- Treatment: remove triggers (Immunoglobulins) from within system
IMMUNODIFICIENCY
Primary: Caused by immune cells being poorly developed or absent
Secondary: Caused by illness or treatment
VACCINATIONS
Contraindications:
-Hx of anaphylaxis
-Immunocompromised, Pregnant (live vaccines: Varicella, Zoster, M)
-Fever
-Egg allergy (Flu, pneumonia, meningococcal)
-< 200 CD4 cells (HIV/AIDs)
HIV
CLASSIFICATION
Type I: most responsive to drugs
Type II: more resistant, found in 3rd world countries
TRANSMISSION:
- Sexual contact
- Blood contact
- Perinatal (pregnancy, birth, breastfeeding)
* 70% affected are homosexual men *
HOW IT WORKS
- Retrovirus: RNA has to change within host cell—has RNA but no DNA
1. HIV attaches to CD4 receptors (found on T-helpers, Lymphocytes, Monocytes)
2. RNA makes viral DNA via reverse transcriptase
3. New viral DNA enters cell DNA and alters genome
4. Infected cell replicates more HIV infected cells
ACUTE INFECTION
- Develop HIV antibodies
- 1-3 weeks after infection
- Lasts 1-2 weeks
- Temporary decrease in CD4, quick increased viral load
S/Sx:
- Headache
- Body ache
- Pharyngitis
- Lymphadenopathy
- Rash
- Meningitis*
- Guillan-Barre*
CHRONIC INFECTION
Asymptomatic:
-“Latent Phase”
-Lasts 2mo-8y if untreated
-Viral load: 200-500
-CD4: >500
Symptomatic:
-Early Symptomatic Phase
-From years 8-10
-Viral load: >500
-CD4: 200-500
-Symptoms/Opportunistic infections:
oPropensity to infection
oCandidiasis
oKaposi Sarcoma
oOral hairy leukoplakia (Epstein-Barr)*
AIDS:
-CD4: <200
-Opportunistic Cancers and Infections (PJP, Cryptococcal meningitis, Cytomegalovirus
retinitis)
-Wasting syndrome
-Dementia
SCREENING
OraSure
Uses gum line or saliva; screens antibodies and antigens, does not differentiate
OraQuick
Uses drop of blood
DRUG THERAPY
ARTs
NRTIs
NNRTis
Protease inhibitor
Integrase inhibitor
Fusion inhibitor
Goal:
Decrease viral load
Increase CD4
Delay symptoms and opportunistic diseases
Cardiology
CORONARY CIRCULATION
Sinuses of Valsalva: open into each coronary artery
R. Coronary Artery: supplies R. atrium and ventricle
L. Coronary Artery: branches into left main & circumflex artery, supplies L. atrium and ventricle
Ischemia: tissue hypoxia; causes angina
Myocardial Infarction: tissue death, permanent loss of blood supply
CONDUCTION SYSTEM
SA Node: pacemaker
Action Potential: Electrical impulse, travels through heart
Contraction: calcium flows into cardiac cells after depolarization
AV Node: provides break in contractions for atria to fill
Bundle of His: allows repolarization; picks up impulse and spreads over ventricles via Purkinje fibers
Repolarization: Cells returning to former state
Systole: refractory period
EKGs
P wave: atria depolarize (normal: 0.06-0.12 sec)
PR interval: time between SA node impulse and ventricle (normal 0.12-0.20 sec; indicator of AV function)
QRS interval: Depolarization of ventricles, repolarization of atria (normal 0.04-0.12 sec)
T wave: repolarization of ventricles
RHYTHMS
Normal Sinus Rhythm:
60-100 bpm
Regular rhythm
SA node pacing
Sinus Tachycardia
>100 bpm
Regular rhythm
SA node pacing
Sinus Bradycardia
<60bpm
Regular rhythm
SA node pacing
Atrial Flutter
Hot-spot in heart competing with SA node
Excessive atrial contraction
Sawtooth waves (erratic P-waves)
Regular or irregular rhythm
Atrial Fibrillation
Multiple foci competing with SA node
Atria are quivering
No discernable P-wave
Irregular rhythm
Controlled: <100 response rate
Uncontrolled: >100 response rate
Ventricular Tachycardia
Hot-spot in ventricle competing with SA node
>150bpm usually
Rapid, no discernable P wave
Bizarre QRS
Regular in rhythm
Ventricular Fibrillation
Hot-spots in atria & ventricle competing w/ SA
Ventricles quivering
No CO, BP, HR
Fast and irregular
ST-Elevation = Myocardial INFARCTION (actual tissue death)
ST-Depression = Myocardial ISCHEMIA
CARDIAC OUTPUT
CO = HR X SV; measures amount of blood pumped per min (normal: 4-8L/min)
Preload: Think “VOLUME/STRETCH”; amount of blood in ventricles at the end of diastole, before the
next squeeze; determines amount of “stretch” placed on heart
Increases with:
-Hypervolemia/fluid excess
-Valve regurgitation
-Pump failure/CHF
Decreases with:
-Hypovolemia/volume deficit/dehydration
-Bleeding
-Shock
Afterload: reflects vascular RESISTANCE
Increases with:
-Vasoconstriction
-Hypertension
Decreases with:
-Vasodilation
-Hypotension
-Shock, vasodilatory
Constriction: reflects how “in shape” cardiac MUSCLE is
Increased Contractility = Increased Stroke Volume
Increases with:
-SNS stimulation
-Positive Inotropes
-Digoxin
Decreases with:
-Age (years of muscle working)
-Heart failure
-Parasympathetic stimulation
Starling’s Law:
The more the heart is stretched, the greater the force of contraction. Increased stretch leads to
increased oxygen demand and increased cardiac muscle over time.
REGULATION
Sympathetic Beta Receptors
-Increase HR
-Increase Contractility
Parasympathetic (Vagus Nerve)
-Decreases HR
Baroreceptors
-Function
oSense pressure changes in arterial system and communicate to brainstem
-Locations:
oAortic arch
oCarotid sinus
oVena Cava
oAtria
oPulmonary arteries
BLOOD PRESSURE
Systolic: maximum pressure exerted by heart
Diastolic: minimum pressure exerted by heart
Pulse Pressure (PP):
-Measure of variance between systolic and diastolic
-Equation:
PP=systolic−diastolic
-Normal value: 40-60
-<40 = hypovolemia, bleeding
->60 = head trauma, increase ICP
Mean Arterial Pressure (MAP):
-Measure of perfusion
-Equation:
MAP=systolic+(diastolic∗2)
3
-Normal value: 70-100
-Minimum value for perfusion: >60-65
STUDIES:
Chest X-ray: structural changes, size
EKG: rest, stress test, continuous monitoring (ischemia, infarction, rhythm)
Echo: ultrasound (enlargement, regurgitation)
Nuclear Cardiology: radioactive isotope injected
Calcium Scoring CT: checking the coronary arteries
Cardiac catheterization: invasive procedure; *NPO 6-12 hr prior*
Right sided: done via VEIN, measures R chamber pressures
Left-sided: done via ARTERY, measure L chamber pressure & oxygen, risk of bleeding
CARDIAC MARKERS:
C-Reactive Protein: normal inflammatory marker, increases with MI
Normal: <1.0 mg/L
CK-MB 2 / CK-2: found in cardiac muscles and nerves; rises 4-6 hours after MI
Normal: <4%
Troponin I: GOLDEN STANDARD. Highly specific to cardiac muscle. Rises 4-6 hrs, peaks 10-24 hrs,
returns to normal in 4 days
Normal: <0.4 mg/dL
Lipids/Cholesterol
Normal total: <200 mg/dL
Normal LDL (bad): <100mg/dL; decreased by diet
Normal HDL (good): >50 mg/dL; increased by exercise
CORONARY ARTERY DISEASE: ATHEROSCLEROSIS
1. Early stage: endothelial damage, silent/undetected
2. Fatty streaks: raised fat accumulation, usually middle aged, considered reversible
3. Raised fibrous plaques: fatty streak covered with collagen; lumen narrowed; fissures develop
4. Complicated lesion: most dangerous, plaque rupture, thrombus formation, narrowing or occlusion of
vessel
Risk factors:
Age, gender, race
Family history
Diabetes
Hyperlipidemia
Drinking/Smoking
Obesity/Sedentary lifestyle
Stress
Hypertension
Meds:
Prevalite. Welchol, Colestid---------------------------
Bile Acid Sequestrant
Decreases LDL (binds w/ intestinal acids)
Interferes with digoxin, coumadin, thiazides, antibiotics
Lopid, Tricor -------------------------------
Fibric Acid Derivative
Decreases LDL synthesis/secretion
Increases HDL, triglycerides
May increase coumadin effects
Lipitor, Crestor ------------------------------
Statin
Decreases LDL, triglycerides
Increases hepatic LDL receptors, HDL (slightly)
Zetia ---------------------------------
Cholesterol Absorption Inhibitor
Decreases LDL (inhibits absorption)
Increases HDL
CORONARY ARTERY DISEASE: ANGINA
Stable (Classic):
Predictable
Stable plaque
Pain resolved within 10 min w/ nitro
Unstable (progressive):
Unpredictable
Varying strength, stability
Could become MI
Prinzmetal’s Variant (Coronary vasospasm):
Rare
Patients often have history of Reynaud’s or migraines, CAD not required
Can occur at rest or follow stress, increased physical demand, histamines
Meds + Treatment:
Beta Blockers
Calcium Channel Blockers
Stent placement
Atherectomy
THROMBINS2
T – Thienopyridines
H – Heparin/enoxaparin
R – Renin-angiotensin blocks
O – Oxygen
M – morphine
B – beta-blockers
I – intervention (aspirin)
N – Nitro
S x2- Statin, Salicylate
MYOCARDIAL INFARCTION
STEMI:
Vessel completely occluded by thrombus
NSTEMI:
Vessel partially occluded by thrombus
**Most MI’s involve L. ventricle**
Healing:
Inflammatory response within 24 hours
Enzymes remove necrosis by 4 days, leading to a thin wall.
Collateral circulation = small, new vessel formations, within 10-14 days
Considered to be healed scar tissue by 6 weeks
Reperfusion Therapy:
PCI (percutaneous coronary intervention)
- Stent, balloon ablation, etc.
Fibrinolytics (clot-busters)
- rPA/tPA (tissue plasminogen activator), used in combo with heparin
HEART FAILURE:
Compensatory mechanisms:
- SNS activation = increased O2 demands and workload
- Dilation = enlarged chambers, overstrained muscle, increased O2 demand
- RAAS = kidneys release renin > angiotensin > aldosterone > fluid retention (happens because
low cardiac output makes kidneys think there is a low circulating blood volume)
- BNP/ANP = released as diuresing hormones, don’t reach kidneys (poor circulation), leads to
increased serum levels
Complications:
- Pulmonary edema
Pink sputum, crackles
- Pleural effusion
Fluid accumulation in pleural space
- L. Ventricle thrombus (blood stagnancy)
- Hepatomegaly
Blood backed up into hepatic veins
- Renal failure
Lack of blood supply = AKI
Meds:
Diuretics
- Reduce preload
i.e. Lasix
ACE Inhibitors
- Reduce afterload
i.e. Lisinopril, enalapril, benazepril
Beta-Blockers
i.e. metoprolol, propranolol, carvedilol
Digoxin
- Increases contractility, decreases HR ( + inotrope, - chronotrope)
- narrow TPI
Morphine
HYPERTENSION
Normal: <120/<80
Elevated: 120-129/80
Stage 1: >130-139/>80-89
Stage 2: >140/>90
Meds:
1. Diuretics
2. Beta-Blockers
3. Ca+ Channel Blocker
4. ACE Inhibitors
