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156 Cards in this Set
- Front
- Back
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right heart path
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PA
RV TRI RA S/IVC |
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left heart path
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A
LV MItral LA PV |
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common location of artherosclerosis
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Left main coronary
left or right coronary artery |
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tunica externa is
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outer
loose Connective tissue |
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Tunica media is
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middle
smooth muscle |
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Tunica intima
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inner
simple squamous epi |
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Artery vs Vein
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round flat
muscle less valves none |
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SA is located in
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R atrium near S vena cava
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AV located
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Base or R atrium
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during diastole open valves are
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Tri and mitral
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During systome open are
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aorta and PV
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liver releases
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angiotensinogen
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Renin is released from the
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kidney
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kinase II turns
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AG I to agII and
Bradykinin to inactive |
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angiotensinogen and bradykinogen are turned to what by what
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renin and kallikrenin/ ang I and bradykinin
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non-renin alternate path is/ by what
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angiotensionogen to ang II
t-p factor cathepsin P tonin |
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non- Ace alternate path is/ by what
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angI to angII
chymase cage cathepsin P |
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angII at1 causes
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negative
Vascular smooth muscle growth I CNS I CO I aldosterone from adrenal cortex I GFR/ filtration fraction I ADH and thirst and h20 in |
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angII ag2 causes
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postive changes
vasoD anti-proliferation Cell differentation Tissue repair |
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aldosterone causes
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myocardial fibrosis, arrhythmias,LVH
Na retention, MG/K+ loss hypertension, endothelial dysfunction, d NO synthesis, prothrombotic S activation, P inhibition |
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I CO causes
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b1, b2,a1, NOT a2
overstimulation= myocyte death, arrhythmias, b1 downregulation |
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I sym causes
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Na retention
BV constriction |
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=HR*SV
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cardiac output
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=CO/BSA
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CI= cardiac index
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SV/EDV*100 =
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EF= ejection fraction
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CO*SVR+CVP=
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MAP
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= 2*DIASTOLIC PRESSURE + SYSTOLIC PRESSURE/3
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MAP
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pulmonary pressure ~
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35/20
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systemic pressure =
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120/80
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ACEi _____ preload and afterload
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reduce
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preload causes
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enlarged liver
jvd edema peripheral crackles s3 heart sound dry mucous mem/ skin turgor daily weight |
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Afterload causes
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1. vascular diastolic pressure (greater afterload = greater DP)
2. pulse pressure (difference b/w systolic pressure and diastolic pressure. the smaller the difference, the greater the afterload) 3. pulses (increased SNS and RAAS stimulation --> decreased peripheral pulse strength). |
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swan ganz catheter
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measure pulmonary artery pressure in actue decompensated heart failure, after load
1. preload/end diastolic pressure 2. ejection fraction |
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arteriosclerosis is
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hardening of arteries
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arTHEROsclerosis
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formation of artheroma (fatty plaques
subset of arteriosclerosis |
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IHD
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lack of O2
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Endothelial dysfunction is/ cause
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d ability to regulate vascular tone, clotting and inflammation
cause:age, sex, smoking, family history of chd, dyslipidemia, obesity, DM, htn,↑ homocystine, |
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Fatty streak formation is mostly and how
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mostly asymptomatic/ macrophates engluf lipoproteins forming foam cells
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macrophates and foam cells release ____ and result in also what step
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Fatty streak
growth factors and cytokines that cause:cell proliferation, inflammation and matrix degradation |
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Fibrous plaque X% = symptom at exertion
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50
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Thrombus formation: causes/process
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02 mismatch
plaque leak- platelet recruited - thrombous or clot- stabilized by thrombin conversion of fibrinogen to fibrin |
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02 supply
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coronary blood flow
O2 extraction O2 availability |
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O2 demand
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Heart RAte
Contractility Wall tension |
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early mycardial remodeling is
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wall thinning and ventricular dilation
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latemycardial remodeling is
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fibrosis
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acute MI % with symptoms/ death
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1/3 no symptoms/ 50% die
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STEMI
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most common, >30min, nitro has no effect
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NSTEMI
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<30 min,
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CHD risk equivalents
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1. Symptomatic CAD /stroke/Transient Ischemic attack TIA/>50% obstruction of carotid artery\
2.Peripheral artery disease 3. Abdominal aortic aneurysm 4. Diabetes 5. 2+ major risk factors + 10yrs of hard CHD>20% |
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Major risk factors
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1.cigarette
2.hypertension ctrl still counts 3.Low HDL <40mg/dl 4.Family history of CHD 1st degree in male w/ CHD <55yo 1st degree in female w/CHD <65yo 5.Age Men >45 Women >55 |
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ApoB/ApoA-1
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bad-over good 5:1 = 3.25 increase bad things happenen
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Exercise
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.86 = good things
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BMI
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-18.5-25-30-35-40-
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bmi calc
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= kg/m2 lb/2.2=kg inch/.39=cm
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NCEP ATPIII Metabolic syndrome criteria >/=3
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Abdominal obesity >102cm/40in men >88cm/35 in women
Triglycerides > 150 HDL <40 m <50 f blood pressure <130/85 fasting glucose >100mg/dl |
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Metabolic Syndrome
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Central Obesity + Insulin Resistance
Inflammation Thrombosis Hyperglycemia Hypertension Dyslipidemia Thrombosis |
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Proinflammatory and prothrombotic mediators in metabolic syndrome
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↑IL-6 TNF-a, PAI-1
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not a disease
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insulin resistance
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PR interval
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atria through AV nodes to ventricles
digoxin, beta blockers, nono-dihydropyridine calcium blockers ↑ conduction times |
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QRS duration
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conduction time from proximal bundle of his to completion of ventricular depolarization
Na+/K+ blocking drugs |
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QT interval
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Ventricular repolarization time
Na+/K+ channel blocking drugs can prolong |
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ST segment
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elevated = acute
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QRS Voltage
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Measure of left ventricular mass (hypertrophy)
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Holter Monitor
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chronic pt
evaluate baseline heart rhythms 24-48 hours |
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Echocardiography
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ejection fraction issue
left ventricular problems 2d and 3d TEE= invasive TTE= noninvasive use with dobutamine to find left ventricular function issues |
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Stress Test who and how
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diagnosis of obstructive CAD
echo and ekg family history very high post revascularization, is pci working? rhythm disorders women 85% of HR should be reached if you cant use dobutamine inotrop or vasodialtor HR=220-Age no LV diagnosis |
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vasodilators for stress test
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dipyridamole
adenosine |
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Coronary AngioGraphy for?
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for suspected CAD
Xray and dye |
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Coronary angioplasty/PCI Percutaneous coronary intervention for? symptoms?
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STEMI and NSTEMI
only imporoves symtomes not outcome |
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only operation that improves outcome
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CABG
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nicotine in acid is
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ionized and poorly absorbed
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nicotine in base is
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unionized and absorbed
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bioavail of nicotine is
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low because of acid and 1st pass metabolism
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per cig xmg
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1 mg/cigarette
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T1/2 of nicotine
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2hr
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T1/2 of cotinine
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16 hours
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excretion of nicotine is
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through the kidneys and breast milk
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Nicotine causes vaso
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contrition
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drugs that have decreased effect due to induction of cyp1a2
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caffeine and theophylline
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drugs that have increased effect due to induction of cyp1a2
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clopidogrel
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What smokers can not take what drug why
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combined hormonal contraceptives because of stroke, MI, thromboembolism, 35yrs and older smoke at least 15c/day
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PAH is
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polycyclic aromatic hydrocarbons interact with many drugs.
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name two generic drugs and spell
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bupropion, Varenicline
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when to use drugs to quit
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at over 10c/day
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drugs should not be used to quit
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pregnant, smokeless, light under 10c/d and adolescents
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nrt can be used in 18 and under but
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requires prescription
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bupropion effects
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NE and dopa
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Varenicline moa
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partial nicotinic agonist bind a4b2, blocks and activates
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Central agents
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clonidine
methyldopa moxonidine rilmenidine |
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clonidine moa/ effect/ SE
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a2 antagonist at cns and peri
reset baroreceptors baroreceptor intact no orthostatic hypotension dry mouth, sex dysfx, rebound hypertension, |
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methyldopa
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a2 action in cns,
prodrug, good for pregnancy d Vasc Resis little effect on HR or CO SE:heptotoxicity messes up Coombs test |
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moxonidine and rilmenidine
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imidazoline I1 agonist in CNA and a2 agonist but weak
SE less dry mouth vs clonidin sedation no rebound hypertension |
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Adrenergic neuron blockings
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Reserpine
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Reserpine
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destroys vescicles
d CO d PVR Sympathetic reflexes intact d CNS Sympathetic outflow MAO unk SE diarrhea, GI cramps, I acid secretion at GI normally P>S after S>P Parkinsonian Sexual dysfunction mental depression effect last after stopage inexpesnsive |
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Adrenoceptor blocking drugs
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a block and b block
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Prazosin, Terazosin, doxazosin, trimazosin
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block vasoconstrictor effect of CCA on Arterioles and Veins
d BP t I HR t I Cardiac contractility I renin I fluid retention d S outflow MAO unk SE dizziness, HA fatigue, Peripheral edema orthostatic hypotension overtime SE d d plasma tri d total and LDL i HDL GOOD!! |
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b-adrenoceptor antagonist
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NSB props tims nads
SB meto ate bison NSBISA pendi cartel pinch SBISA ace NSBISAO lab NSBO cart SBO neb |
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nsb initial /over time
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initiall: dHR dcontractility
time: CO returns to normal and d PVR d renin secretion i plasma triglycerides d HDL cholesterol SE mental depresion, fatigue rebound tach, I BP on discontinuation use w/ care in: asthma, HF,DM, PVR (use SB) |
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NSB effects on blood lipids
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i plasma triglycerides
s total and ldl d HDL cholesterol |
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NSB effects on blood lipids
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s plasma triglycerides
s total and ldl i HDL cholesterol |
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Vasodilators types
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CCB
dhp ndhp hydralazine minoxidil NaNitroprusside |
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type of CCB
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ROC/VOC
receptor operated channels and voltage |
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4 types of VOC
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TLNP
transient, long, neural, P___ t= skeleatl and heart L, most common vasc CM cardiac SM , sk SM N= blocked by omega-conotoxin |
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ndhp (2)
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verapamil diltiazem
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NDHP moa etc
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bind strongly to inactive state
use dependent,, more active the strong the drug selective Arteriole>venous by blocking voltage operated Ca2 channels. ca influx = d intracellular Ca t decrease contractin t I vasoD Arterial d t d PVR t d BP no fluid retention SE cardiac depression constipation |
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DHP ends in the letters
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ipine
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DHP moa etc
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lack cardiac blocking activity t reflex tachacardia
no fluid retention SE reflex tach for DHP IR nifedipine causes d BP too fast |
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Hydralazine moa etc
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releases arteriolar SM via
endothelium dependent NO hyperpolarization of vascular SM dPVR d BP t Sympathetic reflex t use B blocker dBP I fluid retention t use diuretic SE LUPUS more common in men secondary tachyphlaxis,, drug stops working, need second drug low oral bio N acetylation metabolizym many phenotypes NOT for long term solo USE with B block and diuretic |
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Minoxidil moa etc
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prodrug
cell hyperpolarization via atp sensitive K+ channels relaxes arteriolar SM by hyperpolarization of vascular SM d PVR d BP I sympathetic reflex I fluid retetion SE I potent renin Na+ water retention use with care in CHF hypertrichosis Use for BALD guys |
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Vasopeptidase inhibitors
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ACEi
AngII receptor antagonists Vasopeptidase inhibitors Renin inhibitors Endothelin receptor antagonists |
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ACEi ends in
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pril
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Angiotensin II receptor antagonists- end in
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artan
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Vasopeptidase inhibitors -ends in
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atrilat
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Renin inhibitors- end in
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kiren
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ACEi SE
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SE
ACEi also degreades bradykinin increased bradykinin t I cough. cough angioedema tetragenic hypotension acture renal failure hyperkalemia |
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prr binds to
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pro-renin to make renin (localized)
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ang 1-7 activates
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Mas then diamerize turn off ATIIreceptor-1
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ARB (artan) moa/se
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inhibit angiotensin II type I receptors
SE no dry cough diarrhea, dizziness, insomnia, nasal congestion, teratogenic hyperkalemia, htn, angioedema |
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Vasopeptidase inhibitors -atrilat moa/se
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inhibit ACE and neutral endopeptidase
neutral endopeptidase inhibits: BK adrenomedullin, anp SE cough facial redness, flusing, dizziness, severe angioedema vasoD fail drug |
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Renin inhibitors -kiren moa/se
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block formation of angI and angII from angiotensinogen
renin is rate limiting step in formation SE diarrhea cough 1/3 of acei poor bioAvail 2.5% poop it out teratogenic |
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Essential hypertension is
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no identifiable cause, most common
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Secondary HTN is
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<10% of all cases,
Drug or disease releated can be reversible |
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disease that cause 2nd htn
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CKD, suhings, sleep apnea, parathyroid disease, aldosteronism
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Drugs that cause 2nd htn
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amphetamines, alkaloids, nsaids, cocaine, ephedra, nicotine , sodium ethanol and licorice.
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normal and other BP ranges
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-120-140-160-
-80-90-100- N#PH#ST1#ST2 |
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diagnose htn requires
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2 measurements at 2 visits.
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htn pts presentation
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appear healthy for the most part
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htn target organs
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brain- stroke
eyes-retinopathy heart-lvd kidney-ckd peri vascularture-peri arterial disease |
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goal for primary htn
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140/90
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special htn goal for what conditions
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ckd/dm 130/80
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stage 1 use,
stage 2 use |
monotherapy: ace/arb/Thaizide
two drug: Ace/Arb+thiazide or Ace/Arb + CCB |
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LVD use
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1.Diuretic with ACE then BB2. Aldosterone antagonist or arb
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Post-MI use
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1.BB then add ACE/ARB
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CAD use
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1.BB then add ACE/ARB
2. CCB or Diuretic |
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DM use
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1. ACE or ARB
2. Diuretic 3. CCB or BB |
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CKD use
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ACE or ARB
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Stroke prevention use
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Diuretic with ACEi
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LVD BB that can be used
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metoprolol XL 12.5-25/ 200
carvedilol 3.125 /25-50 Bisoprolol 1.25/10 double dose q 2 weeks in stable lvd |
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CCB therapy in genreal redueces
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ischemic symptoms
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Thiazide diuretic therapy only__
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lowers BP
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CKD is defined ast
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<60ml/min/1.73m2
albuminuria >300mg/day or >200 mg alb/g creat 2x measure in 3 mo |
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very old pts target for htn
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80 years old 145/90
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Saseen
4 thiazides |
Chlorthalidone
Hydrochlorothiazide INdapamide Metolazone |
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SE of thiazides
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hyopK/NA/MG, dehydration, GOUT
I glucose and cholesterol |
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S, ACEi
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SE:
cough hyperK angioedema I lithium tetragen I SCR but this is good up to 30% 1/2 starting dose for LVD/ hyperNA or vol depletion/elderly |
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S arb
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SE: HyperK, renal fail in bilateral renal artery stenosis, I lithium
teratogenic/ btw: no dry cough, I scr, 1 generic losartan |
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S CCB dhp
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SE:HA, peri edema, flushing, reflex tach, worsen, GERD
contraindicated in: LVD (except amlodi+felodipine mostly used for HTN |
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s ccb ndhp
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d HR/block/ constipation(vera)/peri edema/ worsen GERD
interaction: Vera and diltiazem p450 3a4, I cyclosproine/ I block rish with BB or digoxin |
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S bb
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BB come after thiazide in noncompelling
SE: exercise intolerance/ d HR/block/ beware at 55-60bpm/ED with ISA/ mask signs of DM/ angina w/ cocaine/ risk of HB with dhp and digoxin contradict: 2-3rd heartblock/acute LVD/asthma/isa in post MI/ |
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S aldo antagonist
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used in LVD
SE: hyperK esp w/ ckd/orthostatic hyoptension/ hyopNa/ man boobs/ I lithium |
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favor/unfavor/avoid: diuretic
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osteoporis,high K/ gout, low K
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favor/unfavor/avoid:ACEi
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low K, preDM/highK /preg bilat renal artery stenosis
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favor/unfavor/avoid:arb
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low K, preDM/ high K/ pregnancy/ bilat renal artery stenosis
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favor/unfavor/avoid: ccb dhp
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raynauds/ peri edema high hr, tach/lvd except amlo/feldipine
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favor/unfavor/avoid: ccb ndph
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raynaulds, ha, /peri edema low hr/ 2nd or 3rd lvd
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resistant treatment use:
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chlorthalidone/ Aldoanta/ consider loop/ if bb use carve or lab/
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