Exam 2

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

Ig E mediated

anaphylaxis and allergies

type of hypersensitivity rxn

Cytotoxic

blood transfusions

type of hypersensitivity rxn

Delayed

latex allergy (that comes 6-48 hours later)

type of hypersensitivity rxn

Anaphylaxis

1. remove trigger

2. maintain airway

3. Oxygen

4. IV access and circulatory volume

5. epinephrine

6. albuterol, corticosteroid, diphenhydramine

Avoid allergen

primary tx for hypersen rxn

apheresis

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

autoimmunity tx

watch for hypotension and citrate toxicity

LAIV, MMR, VAR, ZUL

vaccines not for pregnancy and immunocompromised pts

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

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

Symptomatic Phase

year 8-10

CD4: 200-500

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

AIDS

year 10+

CD4 < 200 and opportunistic infection

P. jiroveci pneumonia, cryptococcal meningitis, cancers

wasting syndrome and dementia

Orasure

rapid HIV testing using the gum line

Oraquick

rapid HIV screening using blood

4th Gen testing

used to Dx HIV for sure

tests for Ig and virus and can say for sure

800-1200

normal CD4

NRTIs

LATE

NNRTIs

efavirenz

Protease Inhibitors

ritonavir, darunavir, atazanavir

Truvada and Descovy

given to those at risk of contracting HIV

prevent integration of viral DNA

“PreP”

PEP

taken after possible exposure to HIV; within 72 hours

for 28 days

combo of 3 ARTs

Widow maker

aka left coronary artery

left anterior descending

vessel supplying the LV

circumflex artery

supplies atria

4-8 L

normal CO

Preload

volume

Afterload

resistance of vessels

Contractility

squeeze

MAP

Sys + 2Dia / 3

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

Pulse pressure

Sys - Dia

normal is 40-60 mmHg

Narrowed PP

hypovolemia and bleeding

WidenedPP

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

EKG

used to look at the heart’s electrical activity

at rest, stress, or continuous

dx STEMI or ischemia based ST segment

ST elevation

indicates STEMI

ST depression

indicates ischemia

Xray

used to see the size of the heart

echocardiogram

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

CRP

normal < 1 mg/L

general inflammatory marker released during an MI

can be used to indicate need for more testing/ predictor

CK-MB

only in cardiac muscle and nerve tissue

rises within 4-6 hours of MI

>4-6% is indicative of MI

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

Total cholesterol

<200 mg/dL is goal

LDL

<130 is goal, ideally <100

bad fat that sticks

HDL

>40 men, >50 women

good, hard fat that cleans up vessels

statins

best at lowering LDLs

Niacin

best at lowering triglycerides

Tricor and Lopid

fibric acid derivatives, lower LDL, resist lipoprotein production

increase the effects of warfarin (bleeding risk)

<3.5

total Chol : HDL ratio

<2.5

LDL:HDL ratio

right sided PCI

through a vein

look at right sided, pulmonary

think COPD to look at oxygenation

Left sided PCI

through an artery to LV

coronary angiography, chamber pressures, O2 content

CAD early stage

silent, undetected endothelial damage

CAD fatty streaks

increased fat in vessel (LDL)

considered reversible if you elevate HDLs

increase in SA as pt ages

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

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

lipitor

inhibit chol. synthesis

Zetia

inhibit chol absorption in the intestines

Bile acid sequestrants

bind with bile acids to form insoluble complexes and remove LDL

STEMI

complete obstruction of coronary blood flow

NSTEMI

incomplete obstruction—> some blood still gets through

prolonged ischemia of cardiac muscle

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%

20 minutes

ischemia is reversible for this length of time

10 sec

time for cardiac tissue to become hypoxic after occlusion

atherosclerosis

most common cause of angina

stable angina

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

perfusion

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

microvascular angina

pain is d/t occlusion of a small distal branch

unstable angina

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

subendocardium

first tissue to become infarcted

4-6 hours

time for entire thickness to become necrotic

proteolytic enzymes

released by neutrophils and macrophages post-MI

remove necrotic tissue by 4 days

lay down collagen matrix

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

pericarditis

inflammation of pericardial sac

pain on inspiration

friction rub

leads to cardiac tamponade as fluid builds up c

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

S3

ventricular gallop

“kentucky”

fluid overload and cardiac tamponade

S4

atrial gallop

TENN-essee

balloon angioplasty

inflate a balloon to compress plaques and restore perfusion

stent

straw that sits in vessel and holds it open

pt will receive antiplatelet tx after

tPA

IV clot busting therapy

only given for STEMI (within 30 min ideally)

risk of bleeding

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

5-10 years

life expectancy of CABG vein

Internal mammary artery

left attached to L subclavian artery and attached distal to blockage

patency is 85-95% at 10 years

repeat CABG

use gastroepipolic/ epigastric artery

laparotomy and sternotomy

increased wound complications (2 instead of 1)

MID CABG

minimally invasive direct

uses thorotomy to mobilize IMA using BB

shorter recovery

decreased visualization with obesity

Off pump CABG

surgeon works on a beating heart

doesn’t use CPB

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

anasarca

severe generalized edema seen with RHF

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

pleural effusion

fluid in the pleural space

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

30 mL/hr

necessary urinary output for renal function

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

Stage 1 HTN

130-139/80-90

Stage II HTN

>140 / >90

Essential HTN

90-95% of HTN

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

secondary HTN

5-10% of HTN

treat the underlying cause

stenosis, endocrine disorders, cocaine, NSAIDS, OC

infective endocarditis

infection of endocardial valve surface

turbulence within heart allows infection

treat and proph with ABX

mitral stenosis

obstruction of flow from LA

caused by rheumatic fever

loud S1, palpitations, diastolic murmur

narrowed valve

mitral regurgitation

backflow of blood from LV to LA

may be asymptomatic for years

can be d/t valve prolapse

aortic stenosis

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

aortic regurgitation

backflow in relation to aortic semilunar valve

d/t leaf abnormality or endocarditis

prosthetic valves

mechanical requires anticoagulants for life

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