Exam 2

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104 Terms

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Haptens

smallest substance in the body

attach to a molecule to create something that appears antigenic

why someone has a PCN or peanut butter allergy

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Ig E mediated

anaphylaxis and allergies

type of hypersensitivity rxn

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Cytotoxic

blood transfusions

type of hypersensitivity rxn

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Delayed

latex allergy (that comes 6-48 hours later)

type of hypersensitivity rxn

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Anaphylaxis

  1. remove trigger

  2. maintain airway

  3. Oxygen

  4. IV access and circulatory volume

  5. epinephrine

  6. albuterol, corticosteroid, diphenhydramine

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Avoid allergen

primary tx for hypersen rxn

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apheresis

blood components are separated and causative agent is removed to end the flare up

autoimmunity tx

watch for hypotension and citrate toxicity

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LAIV, MMR, VAR, ZUL

vaccines not for pregnancy and immunocompromised pts

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acute infection

develop HIV-specific Ig

1-3 weeks post-exposure, lasts 1-2 weeks

general cold symp, photopia, meningitis, mono

CD4 temporarily drops then returns to normal

viral load skyrockets

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Latent phase

1 month to 8 years

viral load: 200-500

CD4 > 500

intense disease proliferation

Asymptomatic disease: fatigue, HA, low grade fever, night sweats, lymphadenopathy

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Symptomatic Phase

year 8-10

CD4: 200-500

worsened symptoms, increased infection, candidiasis, Kaposi sarcoma, oral hairy leukoplakia

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AIDS

year 10+

CD4 < 200 and opportunistic infection

P. jiroveci pneumonia, cryptococcal meningitis, cancers

wasting syndrome and dementia

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Orasure

rapid HIV testing using the gum line

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Oraquick

rapid HIV screening using blood

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4th Gen testing

used to Dx HIV for sure

tests for Ig and virus and can say for sure

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800-1200

normal CD4

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NRTIs

LATE

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NNRTIs

efavirenz

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Protease Inhibitors

ritonavir, darunavir, atazanavir

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Truvada and Descovy

given to those at risk of contracting HIV

prevent integration of viral DNA

“PreP”

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PEP

taken after possible exposure to HIV; within 72 hours

for 28 days

combo of 3 ARTs

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Widow maker

aka left coronary artery

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left anterior descending

vessel supplying the LV

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circumflex artery

supplies atria

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4-8 L

normal CO

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Preload

volume

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Afterload

resistance of vessels

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Contractility

squeeze

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MAP

Sys + 2Dia / 3

MAP > 60-65 to perfuse vital organs (we want >70)

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Pulse pressure

Sys - Dia

normal is 40-60 mmHg

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Narrowed PP

hypovolemia and bleeding

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WidenedPP

neurological emergency (if new onset), isolated sys HTN, increased ICP

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EKG

used to look at the heart’s electrical activity

at rest, stress, or continuous

dx STEMI or ischemia based ST segment

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ST elevation

indicates STEMI

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ST depression

indicates ischemia

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Xray

used to see the size of the heart

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echocardiogram

used to identify EF (Normal is 55-65%)

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CRP

normal < 1 mg/L

general inflammatory marker released during an MI

can be used to indicate need for more testing/ predictor

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CK-MB

only in cardiac muscle and nerve tissue

rises within 4-6 hours of MI

>4-6% is indicative of MI

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Troponin

GOLD STANDARD for MI

highly specific to cardiac muscle

>0.04 is indicative of MI

rises within 4-6 hrs, peaks at 10-24, normal in 4 days

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Total cholesterol

<200 mg/dL is goal

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LDL

<130 is goal, ideally <100

bad fat that sticks

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HDL

>40 men, >50 women

good, hard fat that cleans up vessels

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statins

best at lowering LDLs

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Niacin

best at lowering triglycerides

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Tricor and Lopid

fibric acid derivatives, lower LDL, resist lipoprotein production

increase the effects of warfarin (bleeding risk)

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<3.5

total Chol : HDL ratio

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<2.5

LDL:HDL ratio

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right sided PCI

through a vein

look at right sided, pulmonary

think COPD to look at oxygenation

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Left sided PCI

through an artery to LV

coronary angiography, chamber pressures, O2 content

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CAD early stage

silent, undetected endothelial damage

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CAD fatty streaks

increased fat in vessel (LDL)

considered reversible if you elevate HDLs

increase in SA as pt ages

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CAD Raised fibrous plaques

appear in coronary arteries by age 30

multi-factoral

develop after an injury

lipids are calcified causing stenosis

stable angina begins

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CAD complicated lesions

hemorrhages occur in vessels as wall stretches

layers of lipids, calcifications, thrombus, stiff necrotic tissue (stenosis is worsened)

start to see unstable angina and myocardial events

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lipitor

inhibit chol. synthesis

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Zetia

inhibit chol absorption in the intestines

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Bile acid sequestrants

bind with bile acids to form insoluble complexes and remove LDL

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STEMI

complete obstruction of coronary blood flow

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NSTEMI

incomplete obstruction—> some blood still gets through

prolonged ischemia of cardiac muscle

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angina

pain caused by cardiac tissue switching to anaerobic metabolism

lactic acid production irritates cardiac nerve fibers

reffered pain along upper thoracic posterior nerve roots

occurs when arteries are blocked >75%

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20 minutes

ischemia is reversible for this length of time

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10 sec

time for cardiac tissue to become hypoxic after occlusion

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atherosclerosis

most common cause of angina

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stable angina

chest pain that resolves with rest, decreased O2 demand, nitrates

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perfusion

determined by pedal pulses, LOC, urinary output, edema, color, VS, MAP

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microvascular angina

pain is d/t occlusion of a small distal branch

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unstable angina

pain that develops with less activity and requires more nitro to relieve

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subendocardium

first tissue to become infarcted

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4-6 hours

time for entire thickness to become necrotic

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proteolytic enzymes

released by neutrophils and macrophages post-MI

remove necrotic tissue by 4 days

lay down collagen matrix

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10-14 days post-MI

time in which there is a greatest risk for second MI

myocardium is weak as the scar tissue is vulnerable to stress

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pericarditis

inflammation of pericardial sac

pain on inspiration

friction rub

leads to cardiac tamponade as fluid builds up c

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cardiac tamponade

too many inflammatory mediators causes vasoconstriction and leaky capillaries→ excessive fluid build up that compresses the heart

pain on inspiration

muffled, distant heart sounds

do a centesis to pull off fluid

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S3

ventricular gallop

“kentucky”

fluid overload and cardiac tamponade

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S4

atrial gallop

TENN-essee

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balloon angioplasty

inflate a balloon to compress plaques and restore perfusion

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stent

straw that sits in vessel and holds it open

pt will receive antiplatelet tx after

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tPA

IV clot busting therapy

only given for STEMI (within 30 min ideally)

risk of bleeding

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CABG

construction of new conduits for blood transport between aorta and other major coronary arteries

allows for blood to flow past a blockage

sternotomy and CPB machine

graft of saphenous vein

reverse vessel so valves are open

anastamosed proximally to aorta and distally to the blocked artery

tx with ASA and statins to prevent chol build-up

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5-10 years

life expectancy of CABG vein

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Internal mammary artery

left attached to L subclavian artery and attached distal to blockage

patency is 85-95% at 10 years

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repeat CABG

use gastroepipolic/ epigastric artery

laparotomy and sternotomy

increased wound complications (2 instead of 1)

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MID CABG

minimally invasive direct

uses thorotomy to mobilize IMA using BB

shorter recovery

decreased visualization with obesity

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Off pump CABG

surgeon works on a beating heart

doesn’t use CPB

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CPBM

catheters are placed in the vena cava/RA and aorta

allows work on a still heart

pumps and oxygenates blood

used alongside hypothermia to greatly decrease O2 demand—risk of brain damage if pt is rewarmed too fast

the longer the machine time, the greater the chance of complications

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anasarca

severe generalized edema seen with RHF

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pulmonary edema

acute and life-threatening complication of HF

alveoli fill with fluid, increasing pulmonary pressures

pt becomes agitated, pale, cyanotic, dyspneic

wheezes, coughing, crackles, frothy pink sputum

feel like they’re drowning

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pleural effusion

fluid in the pleural space

requires a thoracentesis to pull off fluid and allow for lung expansion

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30 mL/hr

necessary urinary output for renal function

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digoxin

positive inotrope (increased contractility)

negative chromotrope (decreased HR)

narrow TI (1-2)

toxicity may be caused by hypokalemia (anorexia, n/v, arrythmia)

hold if HR <60

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Stage 1 HTN

130-139/80-90

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Stage II HTN

>140 / >90

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Essential HTN

90-95% of HTN

caused by SNS, DM, weight, overproduction of Na-retaining hormones and vasoconstrictors, increased sodium intake, excessive alcohol, stress

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secondary HTN

5-10% of HTN

treat the underlying cause

stenosis, endocrine disorders, cocaine, NSAIDS, OC

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infective endocarditis

infection of endocardial valve surface

turbulence within heart allows infection

treat and proph with ABX

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mitral stenosis

obstruction of flow from LA

caused by rheumatic fever

loud S1, palpitations, diastolic murmur

narrowed valve

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mitral regurgitation

backflow of blood from LV to LA

may be asymptomatic for years

can be d/t valve prolapse

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aortic stenosis

narrowed aorta d/t age, CAD, calcification, rheumatic fever

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aortic regurgitation

backflow in relation to aortic semilunar valve

d/t leaf abnormality or endocarditis

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prosthetic valves

mechanical requires anticoagulants for life

biological are made from human, pig, or cow (less durable)