Term
|
Definition
| an uncommon drug response resulting from a genetic predispostion |
|
|
Term
|
Definition
drug induced disease
-essentially identical to naturally occurring pathology |
|
|
Term
|
Definition
| measure the time required for ventricles to repolarize( become more -) after each contraction |
|
|
Term
|
Definition
can prolong AT interval, creating life threatening arrhythmias
-avoid in patients with bradycarida, CHF, low K, and low Mg |
|
|
Term
|
Definition
| K helps trigger depolarization of the heart. Helping it beat |
|
|
Term
|
Definition
| has the ability to block calcium from entering muscle cells, as a result, Mg can help reduce vascular resistance. |
|
|
Term
|
Definition
kindey function.
less than 2 |
|
|
Term
|
Definition
|
|
Term
|
Definition
blood supplied by hepatic artery ( oxegentated blook from aorta) and portal vein( blood with digested food from small intestine)
detoxification
protein sythesis
produces biochemicals for digestion |
|
|
Term
|
Definition
| reduction in drug responsiveness brought on by repeated dosing over a short time |
|
|
Term
|
Definition
| reduction in drug responsiveness brought on by repeated dosing over a short time |
|
|
Term
| parasympathetic nervous system uses what NT at both ganglion neurons |
|
Definition
|
|
Term
| the SNS uses what NT at Alpha and Beta receptors |
|
Definition
| NE or EPI(released from Adrenal Medulla) |
|
|
Term
| The SNS used what NT at Sweat gland with a muscarinic receptor |
|
Definition
|
|
Term
| Cholinergic receptors cause what effect |
|
Definition
| REST DIGEST. (ach is on PNS and sweat in SNS) |
|
|
Term
|
Definition
vasoconstriction in periphery
ejaculation
contraction of bladder neck and prostate
pupil dilation or mydriasis |
|
|
Term
|
Definition
periphery receptors: regulate NE release through negative feedback
CNS receptors: reduce sympathetic outflow to heart and blood vessels, relief of sever pain |
|
|
Term
|
Definition
increase HR
-force of contration
-velocity of conduction in AV node
KINDEY
- renin release causes vasoconstriction and other events associated with RAAS
HF, shock, atriovent heart block, CA |
|
|
Term
|
Definition
bronchial dilation
relaxtion of uterine muscles
vasodilation to heart
glycogenolysis
enhanced skeletal muscle contraction
dopamine dilates renal blood vessels
Asthma, delay of preterm labor, can cause hyperglycemia and tremors due to increased skeletal muscle contraction |
|
|
Term
| EPI can activate what adrenergic receptors |
|
Definition
|
|
Term
| NE can activate what adrenergic receptors |
|
Definition
| alpha 1, alpha 2, and beta 1 |
|
|
Term
| Dopamine can activate what adrenergic receptors |
|
Definition
| alpha 1, beta 1 and DOPAMINE! |
|
|
Term
|
Definition
muscarinic agonist (will cause rest and digest symptoms)
bradycardia plus all other things about resting |
|
|
Term
|
Definition
| muscarinic antagonists/ anticholinergic (will have fight or flight response bc you are doing opposite of PNS) |
|
|
Term
|
Definition
| anticholinergic (I gotta go med) |
|
|
Term
|
Definition
an adreneric agonist the has a brief DOA and is metabolized quickly by MAO and cannor cross BBB
and no PO
-NE, EPI, DOP, Isoproterenol, Dobutamine |
|
|
Term
|
Definition
adreneric agonist that is metabolized slowly by MAO can be given orally and can cause CNS effects by crossing BBB
Phenylephrine, terbutaline, ephedrine |
|
|
Term
|
Definition
all receptors
catecholamine
delays absoption of local anesthetic
control superficial bleeding
elevated blod pressure
dialation
overcome AV block
shock the heart! resore cardiac function in arrest
bronchial dilation in asthma
anaphlactic shock |
|
|
Term
|
Definition
| prevent the breakdown of EPI |
|
|
Term
|
Definition
Alpha 1 alpha 2 and beta 1
catecholamine
hypotensive states
cardiac arrests
does not promote hyperglycemia |
|
|
Term
|
Definition
beta1, beta 2
catecholamine
cardiovascular
bronchospasm |
|
|
Term
|
Definition
catecholamine
increases cardiac outpue
increases renal perusion
HF: increases myocardial contractility |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
apha 1, alpha 2, beta 2
noncatecholamine
can make meth from this |
|
|
Term
|
Definition
alpha 1 adreneric blocker
HTN and BPH |
|
|
Term
|
Definition
alpha 1 and alpha 2 blockade
treatment of pheochromacytoma
treatment of tissue necrosis followin IV |
|
|
Term
|
Definition
non selective beta blockade
HTN
Angina
Cardiac dysrythmias
MI |
|
|
Term
|
Definition
Beta 1 blockade only
HTN
angina pectoris
MI
heart failure
( can be used in DM bc of no B2) |
|
|
Term
|
Definition
activation of alpha 2 receptors located in the cardio control centers in brainstem
reduction of smpathetic outflow to blood vessels and heart
vasodialtion
decrease HR
used for
HTN
sever pain |
|
|
Term
| 3 basic functions of kidney |
|
Definition
1. cleanins ECF and maintain ECF volume and comp
2. maintenance of acid- base balance
3. excretion of metabolic wasted and foreign substances |
|
|
Term
| where does filtration occur |
|
Definition
|
|
Term
| what is the first step in urine formation |
|
Definition
| filtration at the glomerulus |
|
|
Term
| for small molecules such as elctrolytes, glucose, amino acids, drugs, and metabolic wastes, what kind of proces is filtration |
|
Definition
|
|
Term
| Large molecules are transfered where during filtration |
|
Definition
| they stay behind in the blood |
|
|
Term
| how much of water, electrolytes and nutrients undergo reabsorption |
|
Definition
|
|
Term
| what kind of transport do solutes require in order to be reabsorbed |
|
Definition
|
|
Term
| where does reasoption take place |
|
Definition
| Proximal convoluted tubule, Loop of Henle, Distal concoluted tubule (just not in collecting duct) |
|
|
Term
| where does active tubular secretion occur |
|
Definition
| proximal convoluted tubule |
|
|
Term
| what substances are actively pumped into the nephron from the plasma during active tubular secretion |
|
Definition
|
|
Term
| reabsoprtion at the proximal convoluted tubule |
|
Definition
65% of Na filtered Na+ and Cl- reabsorbed. Essentailly all HCO3- and K+ reabsorbed
water follows passively |
|
|
Term
| reabsorption in the loop of henle descending limb |
|
Definition
water drawn from loop into the interstitial space of the medulla.
freely permeable to h20 and causes urine to becom concertrated |
|
|
Term
| reabsoption in the loop of henle in the ascending limb |
|
Definition
20%of filtered Na+ and Cl- reabsorbed.
not h20 permeable. |
|
|
Term
| reabsorption at the distal convoluted tubule (early segment) |
|
Definition
| 10% of Na and C reabsorbed. water follows passively. |
|
|
Term
| late distal convoluted tubule and collecting duct |
|
Definition
Na-K exchange as influenced by aldosterone
regulation of urine concentration by ADH |
|
|
Term
|
Definition
| acts on collecting duct to increase it permeabilty to water therfore increasing reabsorption and concentration of urine |
|
|
Term
|
Definition
| lacking ADH. Water can not be reabsored in collecting duct therefore pt has large amounts of dilute urine |
|
|
Term
|
Definition
HTN
mobilize edematous fluid r/t heart failure cirhosis and kidney disease
prevent renal failure |
|
|
Term
|
Definition
| the block sodium and choride reabsorption which causes h20 to be attracted into the nephron |
|
|
Term
| adverse effects of diuretects |
|
Definition
hypovelemia
acid base imbalance
electrolyte imbalance |
|
|
Term
|
Definition
high ceiling diuretic (loop diuretic)
acts on ascending loop of henle to block reabsoption of na and cl (20%)
oral- 60 min onset, persits for 8 hours
IV- onset of 5 min. last up to 5 hours. (for ER reasons) |
|
|
Term
| Theraputic uses of Furosemide |
|
Definition
pulmonary edema with CHF
edamatous states related to hepatic renal disease
CAN PRODUCE DIURESIS EVEN WHEN GFR and RENAL BLOOF FLOW ARE LOW
HTN |
|
|
Term
| adverse effects of furosemide |
|
Definition
hyponatremia, hypochloremia and dehydration
hypotention
hypokalemia( increased secretion in distal nephron)
ototoxicity
hyperuricemia (can increase gout symptoms)
Fetal dealth |
|
|
Term
| Drug interaction of furosemide |
|
Definition
digoxin
ototoxic drugs
lithium (excretion of lithium is decreased when NA is low. can reach toxic levels)
Use cause with other HTN meds |
|
|
Term
| HCTZ (hydrocholorthiazide) |
|
Definition
thiazide
early seg distal convoluted tubule
peakes 4-6 hours
PO only
FIRST DRUG OF CHOICE IN HTN TREATMENT (cheap!!)
Edema |
|
|
Term
|
Definition
hypovelemia, hypocholeremia, dehydration
hypokelemia
no prego
hypereuricemia ( uric acid level in people pre desposed to gout)
DEPENDEDNT ON ADEQUATE KIDNEY FUNCTION |
|
|
Term
|
Definition
digoxin
use caustion with other HTN meds
lithium ( counter transport system wtih na)
no ototoxic effects |
|
|
Term
|
Definition
potassium sparing
rarely used alone from diuretic effects
ofen used to counteract potassium loss caused my thiazied or loop diuretics
blocks the effect of aldosterone on the Na/K exchange pump in the distal nephron |
|
|
Term
|
Definition
promotes Na and K homeostasis. Helps maintain intravascualr volume. promotes sodium reaboption in exchange for secreted K and H.
If blocked, K is retaiend and Na excretion is increased. (pump is reversed) ex. Spironolactone
released from adrenal cortex
regulation of blood volume and blood pressure |
|
|
Term
|
Definition
HTN
edematoes states
HF due to blockade of aldosterone receptros
primary hyperaldosteronism |
|
|
Term
| Spironolactone Side effects |
|
Definition
| hyperkalemia is most common |
|
|
Term
| spironolactone drug reactions |
|
Definition
agents that rise K levels
-salt subs
-K sups
-angiotensin converting enzyme inhibitors
angiotensin receptor blockers
direct renin inhibitors |
|
|
Term
|
Definition
huge molecule capable of large amounts of diuresis
creats osmotice force in the lumen of nephrom
undergoes minimal reabsorption
little effect of excretion of other electrolytes
MUST BE GIVEN IV |
|
|
Term
|
Definition
reduction of intracranial pressure
prevention of renal failure in sever hypotention r/t hypovolemic shock or dehydration |
|
|
Term
|
Definition
it can leak out into the interstitial space except those in brain. (EDEMA)
headache
N/V |
|
|
Term
| What should a nurse monitor while administering a diuretic |
|
Definition
hypovelmia (weight!)
Dehydration
I/O
Electrolyes, especially K |
|
|
Term
| what should the serum level of K be |
|
Definition
|
|
Term
| where is a majority of our blood at all times? |
|
Definition
|
|
Term
| when is pressure in heart the highest? |
|
Definition
| when it leaves the left ventricle |
|
|
Term
|
Definition
|
|
Term
| what 3 factors effect stroke volume |
|
Definition
1. myocardial contractility
2. cardiac afterload
3. cardiac preload |
|
|
Term
|
Definition
| arterial pressure the left ventricle must overcome to eject blood |
|
|
Term
|
Definition
| amount of tension applied to a muscle prior to contraction |
|
|
Term
| what controls stroke volume |
|
Definition
|
|
Term
| starlings law of the heart |
|
Definition
| force of contraction proportional to the muscle fiber length |
|
|
Term
| what aspect of venous return determinants can drugs directly alter |
|
Definition
| blood volume, venous tone |
|
|
Term
|
Definition
| peripheral resistance x cardiac output |
|
|
Term
| what regulates arterial pressure |
|
Definition
|
|
Term
| what does the ANS use for steady state control for arterial pressure |
|
Definition
| the ANS regulates AP by adjusting CO and peripheral resistance |
|
|
Term
| what does the ANS use for rapid control of arterial pressure |
|
Definition
|
|
Term
| How does RAAS help regulate AP |
|
Definition
angiotensin II constricts arterioles and Veins
aldosterone permits water retention in the kidneys |
|
|
Term
|
Definition
protect cardio system in event of volume overload
-atrial natriuretic peptide: produced by atrial myocytes
-B(brain)- natriuretic peptide: cardiac ventricular myocytes and some produced by brain cells
-C natriuretic peptide: produced by cells in vascular endothelium |
|
|
Term
| which natriuretic peptide promote natriuresis and therefore diuresis |
|
Definition
|
|
Term
| whic natiuretic peptides promote vasodilation |
|
Definition
|
|
Term
|
Definition
hormone released by kidney when there is a decrease in blood flow
converts angiotensinogen to angiotensin I |
|
|
Term
|
Definition
I, II, III
only type II is highly active |
|
|
Term
|
Definition
vasoconstricion
very potent: contricts everything!
acts indirectly on:
-sympathetic neurons to increase NE release
-adrenal medulla to increase to
EPI release
-CNS to increase SNS outflow
all of this mean increase HR and increase contractility
CAUSES RELEASE OF ALDOSTERONE |
|
|
Term
| Fact! HTN can cause renal damage due to angiotensin II |
|
Definition
| angiotensen II increases filtration pressure. by increasing pressure in afferent arteriole(in to nephron) *after increasing systemic arterial pressure) and by constricting the effert arteriole (out of nephron) this generates back pressure in glomerulus. initially is beneficial. Overtime is harmful |
|
|
Term
| what regulates renin release |
|
Definition
|
|
Term
| steps to form angiotensin II |
|
Definition
renin catalyzes the formation of Angiotensis I from angiotensinogen.
Angiotensin converting enzyme catlyzes I to II.
ACE is a non-specific enzyme and is known as kinase II when it acts on sunstrates or hormones known as bradykinins |
|
|
Term
|
Definition
"prils"
reduces levels of angiotensin II through inhibiton of ACE
-vasodilation
-reduce blood volume
increases levels of bradykinin through inhibition of kinase II (same as ACE)
-vasodilation
-can lead to cough and angioedema( sever swelling to the tongue, more fatal in blacks) |
|
|
Term
|
Definition
| a peptide that causes blood vessels to dilate, lowering BP, ACE inhibiors increase levels of bradykinin by inhibitation of kinase II |
|
|
Term
|
Definition
most PO only enalaprilat given IV
prolonged half lived (BID) except captopril
Prodrugs- must be converted to an active form in small intestine and liver except lisinopril
ALL are excreted by kidneys. those with renal disease require reduced doses |
|
|
Term
|
Definition
| HTN: vasodialte and reduce blood volume HF: vasodilation reduces afterload (increases CO) vasodilation reducs pulmonary congestion and edema |
|
|
Term
| Adverse effects of ACE inhibitors |
|
Definition
first dose hypotension (first dose should be small)
Cough (most common reason pts discontinue med)
-increased permeability in lung causes irritation and cough
angioedema
hyperkalemia
fetal injury |
|
|
Term
| ACE inhibitor drug interaction |
|
Definition
Diurectics- can cause first dose hypotention, stop 1 week prior to ACE inhibitor initiation and then restarted if needed
Antihypertensive agent
Drugs that raise K levels (Sporonolactone)
lithium |
|
|
Term
| ace inhibitor excreted what ion and retains what ion |
|
Definition
| exetes sodium and retains K |
|
|
Term
| which hormone can promote vascular fibrosis (which decreases arterial compliance) |
|
Definition
|
|
Term
|
Definition
selective blockade of alpha 1 adreneric receptor
HTN and BPH |
|
|
Term
|
Definition
blockade of alpha 1 and alpha 2
treatment of pheochromactyoma
treatment of tissue necrosis following IV |
|
|
Term
|
Definition
Valsartan
Losartan
blocks access of angiotensin II to systemic vessels and kidney
decreased release of aldoserone ( increase renal excretion of sodium and water and reduced excretion of potassium)
Does not inhibit kinase II so no increased levels of bradykinin. no cough! |
|
|
Term
|
Definition
HTN
heart failure
diabetic nephropaty
MI
stroke prevetion |
|
|
Term
| adverserse effects of ARBS |
|
Definition
angioedema
hyperkalemia
fetal harm |
|
|
Term
|
Definition
|
|
Term
|
Definition
DRI
inhibits renin
angioedema
cough
GI effects
hyperkalemia
fetal injury
death |
|
|
Term
|
Definition
|
|
Term
|
Definition
| greatest impackt on heart and blood vessles |
|
|
Term
| do calcium channel blockers cause vasoconstriction or vasodialation |
|
Definition
|
|
Term
| do CCB have an effect on arterials veins or both |
|
Definition
| arteriols, arteries and arterioles of the heart |
|
|
Term
| if beta 1 receptors are stimulates what happens the level of calcium |
|
Definition
|
|
Term
| when calcium channels are open does av node conduction increase or decrease |
|
Definition
|
|
Term
|
Definition
CCB
acts on vascular smooth muscle and the heart
-dialition, decrease BP, decrease HR, decrease AV, decrease FOC
has indirect reflex effects: barorecepter reflex
Net effects: only effect that appears is vasodialation , reduce BP and increase coronary perfusion |
|
|
Term
|
Definition
|
|
Term
| main adverse effect of varapamil and diltiazem |
|
Definition
constipation from decrease contraction in bowels
can also cause heart block
dizziness
facial flushing
headache
edema of ankles and feel
gingival hyperplasia |
|
|
Term
|
Definition
CCB
works on blood vessels (minimal work on heart)
CANNOT treat dysrythmias
less likely that verapmail to exacerbate pre existing cardiac disorders
because no effects on heart. the indirect effects are not oppesed and there will be an increased HR and increased contractile force. |
|
|
Term
| adverse effects of nifedipine |
|
Definition
flushing
diziness
headache
peripheral edema
gingival hyperplasia
ECZEMA
increases cardiac oxygen demand
increased angina pain (sometimes combined with beta blockers but b blockers can intensify the aderse cardiac effects of V and D (heart block) |
|
|
Term
|
Definition
vasodialator of arterioles
postural hypotenstion is minimal b/c no veins!
hypertension crisis
AE: reflex tachycardia
increase blood volume
systemic lupus erythematousus
headache, dizziness, weakness and fatigue |
|
|
Term
|
Definition
vasodilater
organic nitrate that converts into nitric oxide in the body
VIENS
cheap effective and fast acting
hypertensive emergencies |
|
|
Term
|
Definition
vasodilator
fastest acting
veins and arteries
emergencies! 230/140!!
continuous IV infusion
fast results but will stop once iv is stoped.
streat the cause not the symptoms
can cause cyanide poisoning (liver patients) |
|
|
Term
|
Definition
syntethis BNP that causes vasocntriction
suppressed the RAAS
arterioles and veins |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| what kind of stroke will be cause by hypertention |
|
Definition
|
|
Term
| what is the second most common cause of ESRD in caucastians and leading cause of EDRD in AAs |
|
Definition
| hypertensive nephrosclerosis |
|
|
Term
| in a patient with stage one or stage two hypertention what is the maintenance blood pressure goal |
|
Definition
|
|
Term
| for patients with DM or kidney disease it is important to maintain a BP below what |
|
Definition
|
|
Term
| how does microalbuminuria cause risk for hypertension |
|
Definition
| if albumin is low that is indication of renal damage which means fluid is being retained which increases BP |
|
|
Term
| what is the equation for arterial pressure |
|
Definition
| CO x peripheral resistance |
|
|
Term
| classes of antihypertensive drugs |
|
Definition
diuretics
sympatholytics(antiadrenergic drugs, beta, adrenergic blockers, direct actin vasodilators, calcium channel blockers, druges the suppress RAAS) |
|
|
Term
|
Definition
ace inhibitors (prils)
ARBS ( valsartan, losartan)
aldosterone antagonists (spironolactone)
direct renin inhibitor (aliskiren) |
|
|
Term
|
Definition
ace inhibitors (prils)
ARBS ( valsartan, losartan)
aldosterone antagonists (spironolactone)
direct renin inhibitor (aliskiren) |
|
|
Term
| sympatholytics (antiadrenric drugs) |
|
Definition
beta adrenergis blockers
alpha 1 blockers
alpha 1/ nonselective beta blockers
centrally active alha 2 agonist
direct acting vasodilators
CCB
RAAS suprresers |
|
|
Term
|
Definition
alpha and beta adrenergic blockera
should be avoided in patients wiht asthma, heart failur, AV block or bradycardia |
|
|
Term
| what anithypertensives are contradicted during pregnancy |
|
Definition
|
|
Term
| in patients with heart failure what is their prognosis dependent on |
|
Definition
| ther ejection fraction. ( should be 55-80 percent |
|
|
Term
| what happends to the heart during HF |
|
Definition
cardiac remodeling :hypertrophies, ventricles dialate
trys to reduce CO
water retention and increased blood volume |
|
|
Term
|
Definition
DIURETICS
drugs that inhibit RAAS
beta blockers
Digozin
inotropic agents
vasodilators |
|
|
Term
|
Definition
naturally occurring compund
cardiac glycoside
positive inotropic effect
not shown to prolong life
inhibits the na/k atapse which indirectly promose CA accumulation whiin the myoctyes (increase contraction)
digoxin competes with digoxin for binding to NA K so if K is low binding of digoxin increases
low TI
monitor HR frequently
antidot is digoxin immune FAB
USED ONLY FOR ATRIAL FIB |
|
|
Term
|
Definition
synthetic catecholamie
beta 1 activation adrenergic receptor
continuous IV infusion |
|
|
Term
|
Definition
phosphodieterase inhibitor
increases cAMP which increased contractility |
|
|
Term
|
Definition
vasodilator
veins!
indication patients with severs refractory HF |
|
|
Term
|
Definition
no symptoms
no structural cardiac ab
treat with cardiotoxic drug
risk factors (HTN)
REDUCE RISK!!! |
|
|
Term
|
Definition
no signs
ECG is bad
prevent symptoms
use ACE OR ARBS |
|
|
Term
|
Definition
symptoms
structural
improve quality and prolong life
dont use
-antidysrhytmic agents
-CCB
NSAIDS (can cause fluid retantion) |
|
|
Term
|
Definition
going to die
heart translplant
control fluid volume (diuretics) |
|
|
Term
| class I anridysrhythmic drugs |
|
Definition
|
|
Term
| class II antidysrhythmic drugs |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| supraventricular dysrhythmias |
|
Definition
a fib: fire randomly, stroke is big risk
atrial flutter
sustained supraventricular tachycarida (SVT): citcuit, increased HR |
|
|
Term
|
Definition
sustained ventricular tachycardia
: heart cant pump effectively, treat immediatly
v fib: impossible coordination leads to failure and death
ventricular premature beats: usually benign
Digozin induces ventricular dysrythmis
torsades de pointes" prologed QT |
|
|
Term
|
Definition
delay repolarization
quinidine |
|
|
Term
|
Definition
class IA HF agents
delay repolarization
both atrial and ventricular fib
GI upset |
|
|
Term
|
Definition
Na blockers
accelerate repolarization
Lidocaine
Ventricular fib only |
|
|
Term
|
Definition
Class IB HF agent
Accelerates repolarization
ventricular dysrhythmia |
|
|
Term
|
Definition
| used as last resort because they can make what you have worse |
|
|
Term
|
Definition
Beta blockers
propranolol
both atrial and ventricular |
|
|
Term
|
Definition
K channel blocker amiodarone
ventricular only
pulmonary toxicity is greatest concern
corneal microdeposists |
|
|
Term
|
Definition
CCB
varapamil and Diltiazem
Atrial only |
|
|
Term
|
Definition
| class III potassium channel blocker |
|
|
Term
|
Definition
inhibits cAMP induces camcum infux so no Ca for contraction.
very short half life
need to lift patients arm after giving IV |
|
|
Term
|
Definition
hmg coa reducats inhibiots
this is needed to make cholesterol
increased number of LDL receprots on heptoctys allowing more removal of LDLS from blood
AE: myopathy/ rhabdomyolosis
hepatoxicity
dosing should be once in the evening |
|
|
Term
|
Definition
reduces LDL
increases HDL more effectively than any other drug
decreased production of VLDLS |
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Term
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Definition
bile acid binding sequesterant
reduction of LDL cholesterol |
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Term
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Definition
inhibits cholesterol absorption within the the small intestine as well as colesterol secreted in the bile
reduces toal cholesterol, LDL, cholesterol and TG |
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Term
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Definition
most effective drug available for lowering TG levels
can raise HDL cholesterol
little or no effect on LDL |
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Term
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Definition
decreases plama TG content
lowers VLDL levles
Can raise HDL cholesterol
little effect on LDL
displaces warfarin from plasam albumin (check INR frequently) |
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Term
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Definition
alows cells to bing and ingest lipoproteins
activate enzymes that metabolize lipoproteins
increase the structural stability of lipoproteins |
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Term
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Definition
total: less that 200
HDL: 60 or greater
LDL: less that 100
TG: less that 150
in kids
total: 170 or less
ldl less that 110 |
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Term
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Definition
clolesterol less that 200 mg a day
sat fat to 7% of total cals
increase soluble fine to 10-25 gm/day |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
organic nitrates
beta blockers
CCB |
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Term
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Definition
| occurs in response to strain |
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Term
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Definition
coronary artery spasm
can produce pain even at rest or during sleep
CCB
orgaic nitrates |
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Term
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Definition
medical emergency
angina at rest
new onset exertional angina
intesification of existing angina
need
-anti-ischemic therapy (NTG, beta blocker, 02, morphine (reduces sympathetic response)
-antiplatelet/anticoag therapy - aspirin, clopidogrel, abciximab, eptifibatide. LMW heparin or IV heparin
-organic nitrates. tolerance can develo[p rapidly |
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Term
| what type of angina are beta blockers effective for |
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Definition
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Term
| what kind of angina are CCB used for |
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Definition
| stable and varian (vasospastic angina) not unstable! |
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Term
| revascularization therapy |
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Definition
CABG surgery
percutaneous transluminal coronary angioplasty PTCA
-used for pts with stable angina, usually involves balloon angioplasty and subsequent stent placement |
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Term
| drugs used to prevent MI infarction and death |
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Definition
antiplatelet drugs
cholesterol lowering drugs
ACE inhibitors
antianginal agents |
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Term
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Definition
stage 1- formation of platelet plug
stage 2- coag |
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Term
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Definition
| a protein the reinforces the platlet plug |
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Term
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Definition
| turned on by trauma to the vessel wall. releases tissue factor |
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Term
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Definition
| turned on when blood makes contact with exposed collagen from a damaged vessel wall |
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Term
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Definition
degrades the meshwork of the clot to remove clots
plasminogen is the precursor |
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Term
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Definition
reduce formation of fibrin (which reinforces platelet plug)
- can inhibit syntheses of clotting factors
- can inhibit activity of clotting factors |
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Term
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Definition
| enhaces antithrombin which inhibits activation of clothing factors thrombin and factor Xa |
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Term
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Definition
| development o antibodies againt heparin platelt complexes. antibodies activate platelets and damage vessel walls. = platelet aggragation. CBC monitored daily |
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Term
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Definition
not as effective as unfractionated heparin
DVT prevention, unstable angina
Sub q injection!
does not require monitoring |
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Term
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Definition
oral anticoag
blocks biosynthesis of vitamin K dependant factors
long term therapy
monitor treatment |
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Term
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Definition
(ADP receptors located on platelts) this is an ADP receptor antagonist and prevents ADP stimulated platelet aggregation
prevents blockage of coronary artery stenets |
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Term
| gycoprotein IIb/IIIA receptor antagonists |
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Definition
most effective antiplatelt drugs
super aspirins
prevents formation of fibrinogen bride |
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Term
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Definition
converts plasminogen to plasmin
thrombolytic drug
causes bleeding
ischemic stroke, PE, MI
does not cause AE or hypotension
needs to be used with in 3-4 hours for IS
and 6 hours for AMI
in order to take tPA patient can not have
-active bleeding
-hemorrhagic CVA in past 3 months
-intracranial, intraspinal or cardiac surgery in past 2 months or gen surg in past 10 days
-SBP greater that 190 or DBP greater the 115
-know intracranial neoplasms, AV malformations, aneurysms or bleeding disorders |
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