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