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a consistent elevation of systemic arterial blood pressure is called:
hypertension
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usually serial measurements are made before a diagnosis is made and tx is started.
tx is usually started when the...
systolic BP is:
diastolic BP is:
tx is ually stated when:
- systolic BP is: > 139
- diastolic BP is: >89
-
pts. are encouraged to adopt a healthy lifestyle change when their BPs are within which range:
- systolic: 120 -139
- diastolic: 80-89
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name the 3 factors which can influence BP:
- cardiac output
- blood volume
- peripheral resistance
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the volume of blood pumped per minute is called:
what is the equation for this term:
-
the amount of blood pumped by a ventricle in one contraction is called:
stroke volume
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CO= HR x SV is important because drugs that influence CO, SV, or HR have the potential to influnce:
blood pressure
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the inner layer of the blood vessel lining is extremely smooth, friction that reduces the velocity of blood is called:
peripheral resistance
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smooth muscles in the arteries determine how constricted the arteries are and the tone that they have, list the 2 things that can affect the amount of constriction and tone:
catecholamines and renin- angiotensin system
-
which system is are involved in regulating BP:
autonomic nervous system
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on a minute to minute basis, a cluster of neurons in the medulla oblongata that regulates BP is called:
vasomotor center
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list 2 location where receptors act as sensors to provide the vasomotor center information:
- aorta
- internal carotid artery
-
receptors that have the ability to sense pressure within the blood vessles are called:
list 2 things that can diminish the response of these receptors:
baroreceptors
diminished response: aging, or diseased states (diabetes, ect)
-
Most HTN is primary, which means not caused by a disease.
list 2 mechanisms by which BP is increased, not as a result of disease:
- long term increased catecholamines: causing increased blood vessle constriction
- volume overload: eventaully causes thickening of the arteries from smooth muscle hypertrophy, 2ndary to vessel wall edema
-
If HTN is not tx'd or the causes isnt removed, the artieral constriction becomes less easily reversed and the drugs are less likely to decrease the BP.
describe why long standing HTN is hard on the heart:
increases the afterload: the pressure the L ventricle must exceed to pump out its blood
thus
increases the work of the heart and oxygen consumption
-
list 11 things that one could recommend as a therapeutic lifestyle change to decreased BP:
- healthy diet
- DASH diet
- weight loss if needed
- exercise
- OSA tx (obstructive sleep apnea)
- decreased alcohol intake
- decreased salt intake
- decreased saturated fats
- increased fiber
- no smoking
- decreased stress
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list 6 things the drug selection is based on for the tx of HTN:
- co-morbidities
- race
- age
- willingness/likelihood of taking multiple doses/day
- degree of elevation
- response to medications
-
what type of medication is recommended as the inital drugs for mild to moderate HTN:
pts. with a more compelling condition may benifit from:
what type of medication is recommended as the inital drugs for mild to moderate HTN: diuretics
pts. with a more compelling condition may benifit from: combiniation medications
-
pts. with a more compelling condition may benifit from combination drugs.
list 3 benifits from the combination drugs:
- increase compliance
- allow decreased doses
- decreased side effects
-
anti- HTN drugs can have undesirable side effects.
explain why the pts. should be encouraged to report these:
so that dose or drug changes can be made.
rather than the pt. stopping the drug
-
describe the overall general mechanism by which diuretics decrease BP:
by increasing Na+ excretion and thus increasing uring output, producing a decreased blood volume.
-
list the 2 most commonly used diruetics:
list 1 benifit and one disadvantage of these:
thiazide and thiazide like diruetics
- benifit: inexpensive
- disadvantage: hypokalemia is common
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name the K+ sparing diruetic that acts by blocking the actions of the hormone aldosterone:
spironolactone (aldactone)
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if K+ sparing diruetics are taken with either of the following...
ACE inhibitors (or ARBs)
K+ supplements
what condition may result:
hyperkalemia
- s/sx of hyperkalemia:
- muscle weakness
- fatigue
- bradycardia
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list the adverse effects of spironolactone (aldactone) for the following..
men
women
- men:
- gynecomastia (enlarged breast tissue in males)
- testciular atrophy
- impotence
- dimished libido
- women:
- menstural irregularities
- hitsutism (excessive hairness)
- breast tenderness
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instruct the pt. who is taking K+ sparing diuretics to avoid: (3)
- foods high in K+
- do NOT use a salt subsitute (b/c many are high in K+)
- do NOT take K+ supplements
-
observe pt for sunburning if prolonged sun exposure has occured b/c:
many diuretic cause photosensitivity and an increased risk of sunburns
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monitor electrolytes, glucose, lipid profiles, liver fxn studies, creatinine, and uric acid levels of pts. on diruetics because:
most diuretics cause loss of Na+ and K+ and may increase lipid, glucose and uric acid levels
-
monitor hearing and balance for pts on diuretics b/c what condition may result:
for which drug in particular does this condition result from:
ototoxicity may occur, especially with loop diuretics (although this is reversable)
-
diuretics taken in concurrent use with digoxin increase the risk of:
- dig toxicity
- potentially fatal dysrhythmias
hypokalemia may cause dysrhythmias, pts taking digoxin must be monitored
-
when diuritics are given in concurrent use with lithium, why is there potential for toxicity:
diuretics decrease Li+ excretion, so Li+ toxicity is more likely
-
Loop diuretics are rarely used for long term tx, but are usually giving for short periods due to their ability to:
remove large amounts of excess fluid from the pt in a short amount of time
-
The most commonly used loop diuretic is:
furosemide (Lasix)
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because of loop type diuretics ability to remove large amounts of excess fluid from the pt. in a short amount of time, what other conditions other than HTN are they used to tx:
- Heart failure
- pulmonary edema
-
Because loop diuretics are so powerful and effective, there is potential for which which adverse effects: (2)
-
what is the MOA for diuretics:
decreased Na+ reabsorption by the kidney tubules with resulting increased water loss and decreased blood volume
-
serious dysrhythmias can be the result of:
potassium depletion, hyopkalemia
-
Patient care for starting a diuretic should include a check for the proper fxn of which system:
check for renal fxn
-
patient care before giving a diuretic should include checking for s/sx of dehydration because:
what 2 other situations may also increase fluid loss:
diuretics decrease blood volume
fever and exercise increase flood loss
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patient care for diurectics should including asking if the pt. is dizzy or light headed with position changes becuase:
orthostatic hypotension may occur when starting a diuretic
-
what time of the day should be avioded when giving diuretics:
avoid giving diuretics in the evening or at bedtime.
make sure pts. on these medications can get to the bathroom easily, assist prn
-
pts. on diuretics should report immediately (3):
- an increase or decrease of >2 #/24 hrs
- crackles, or a new or louder murmur
- hypokalemia while on a non K+ sparing drug
-
if a pt. is on a K+ sparing diuretic check frequently for: (3)
- hypokalemia
- hypovolemia
- hypotension
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if a pt is on IV loop diurectics, frequently check which 2 vital signs:
-
Thiazides my reduced the effectivness of due to the rx-rx interactions (3):
- anticoagulants
- sulfonylureas
- antidiabetic drugs, including insulin
-
hydrochlorothiazide (HCTZ, thiazide) increases the risk of renal toxicity from the rx-rx interactions of:
NSAIDs (steroids)
-
hydrochlorothiazide (HCTZ, thiazide) increases K+ loss when giving with which 2 rx-rx interactions:
- coricosteroids
- amphotericin B
-
contraindications for diuretics include:
- hypersensitivity to sulfonamides, thiazides, and sulfa
- chronic renal failure (execpt with loop diuretics)
-
if the pt. is on a K+ wasting diuretics (e.g. thiazides, thiazide-like, and loop diuretics) should consume foods high in K+ such as:
- strawberry
- banana
- dried fruits (prunes)
- tomatoes
- beets
- dried beans
- OJ
- grapfruit juice
- prune juice
- freash meats
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if the pt. is on a K+ sparing diurectic, they should avoid food high in K+ such as:
- salt substitutes
- gatorade
- powerade
- strawberry
- banana
- dried fruits (prunes)
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the pt. should check their BP every day before taking their diuretic, hold it, and contact their provider if the BP is:
<90/60
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teach the pt. that excessive heat conditions contribute to excessive sweating and further:
fluid and electrolyte loss
extra caution is warranted in these conditions
-
blocking Ca++ ion changles thus decreasing the Ca++ inside arterial smooth muscles (and cardiac cells if non-selective), decreasing the strength of muscle contraction is the MOA of:
calcium channel blockers (CCBs)
in arterial muscles this decreases peripheral resistance and thus lowers BP
-
K+ sparing agents diurectics (aldosterone antagonists):
sprionolactone
aldactone
-
loop diuretics:
furosemide
lasix
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CCB: selective (for arteries)
amlodipine
norvasc
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CCB: non-selective (works on arteries and the heart)
diltiazem
cardizem
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how can some CCBs worsen heart failure:
because they decrease the strength of muscle contractions of the arterioles
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CCB are the primary tx for which two groups of people:
-
what is the pregnancy category for CCBs:
pregnancy category C
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the adverse effects are generally minor and are related to vasodilation such as: (5)
- headache
- dizziness
- peripheral edeam
- flushing
- constipation
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Immediate-acting forms of CCBs can cause:
reflex tachycardia
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Do not administer immediate release formulations of CCB's if what is suspected:
if an MI is suspected or within 2 weeks following a confirmed MI
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what is the food interaction of CCB that increases the absorption of CCB's that could cause an overdose:
list (2) signs of CCB overdose:
grapefruit juice
- sigsn of OD:
- hypotension
- tachycardia
-
observe the pt. for paradoxial (absurd) increase in chest pain, heart failure, decreased level of consciousness, and dizziness before giving doses becuase:
sever hypotension may cause this and may indicate that BP has decreased too quickly or too substantially)
-
reflex tachycardia, an increased HR caused by a significant drop in the BP is more likely to occur when the CCB is administered:
IV
-
these drugs should be discontinued slowly or weaned to avoid:
rebound hypotension
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pts. on CCBs should be observed for constipation, due to decreased peristalsis.
instruct the pt. to include what into the diet to facilitate stool passage:
increase fluid and fiber intake
-
concurrent use of CCBs with a beta blocker increases the risk of:
heart failure
-
concurrent use of CCBs may increase the levels of digoxin, leading to bradycardia and digoxin toxicity which could lead to:
heart failure
-
concurrent use of CCBs with alcohol potentiates the vasodilation and could lead to:
syncope caused by a severe drop in BP (hypotension)
-
the system that helps to maintain the BP in the proper range and helps ensure adequate renal perfusion is called:
the renin-angiotensin system
-
the enzyme secreted by speicalized cells in the kidney when BP falls or there is a decrease in Na+ ions flowing thru the kidney tubules is called:
renin
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once in the blood, renin converts the inactive liver protein angiotensinogen to:
angiotensin I
-
when angiotensin I passes thru the lungs, it is converted to:
angiotensin II
one of the most important vasoconstrictors
-
the enzyme that is responsible for the final step in the renin-angiotensin system is called:
angiotensin converting enzyme (ACE)
-
angiotensin II stimulates the secretion of:
aldosterone
a hormone of the adrenal cortex
-
what is the primary action of aldosterone:
increase Na+ reabsorption in the kidney
-
list the 2 mechanisms by which angiotensin II increases blood pressure:
- direct vasoconstriction
- increased water retention via the action of alderstone
-
what is the MOA for ACE inhibitors:
what are the (2) effects of ACE inhibitors:
block the effects of angiotensin II
- effects:
- lowering peripheral resistance
- decreasing blood volume
-
what is the MOA of ARBs:
to block the action of angiotensin II after its formed
in the arteriolar smooth muscle and the adrenal gland
-
how are ACE inhibitors and ARB's the same:
- same
- they both have the same effect
- lowering peripheral resistance
- decreasing blood volume
-
how are ACE inhibitors and ARBs different:
they both have the same effects, but....accomplish such by a different mechansim
-
Because ARBs do not decrease ACE what to things are less common with ARBs than with ACEI's:
-
one of the side effects of ACEI's and ARB's is a presistant, dry cough because:
blocking ACE increases cough-producing bradykinin (a proinflammatory substance)
-
an adverse of ACEIs and ARBs that can be a major concern for pts with diabetes, renal impairment, renal artery stenosis, and pts. taking a K+ sparing diuretic is:
Hyperkalemia, increased K+
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when begining an ACEI therapy, how long would it take for angioedema to develop:
within hours or days after begining an ACEI tx
-
what are the s/sx of angioedema:
swelling around the lips, eyes, throat and other body regions
paroxysms (violent or sudden attack) of mouth or facial swelling, dry cough, stridor (high pitched musical breath sounds)
-
ACEI and ARBs may produce a first dose phenomenon, resulting in:
profound hypotension, which may result in syncope
espically if its given IV
-
neurtopenia (low count of neutrophils, WBC that help fight infections) and agranulocytosis (low level of WBC) may occur as an adverse effect of:
ACEI's
-
pt care for ACEIs and ARBs should include watching closely after the 1st few doses, as angioedema can occur and needs prompt tx.
in which group is this especially common in:
common in: african americans
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Considering ACEIs can cause neutropenia and agranulocytosis, pt. care should include:
frequent checks for s/sx of infections
-
Pt. care for pts on ACEIs and ARBs, that have renal disease, DM (diabetes Mellitus), and heart failure should be check for s/sx of:
hyperkalemia
- s/sx of hyperkalemia:
- muscle weakness
- fatigue
- bradycardia
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which class of commonly used medications can make ACEIs less effective:
NSAIDs
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what is the MOA for adrenergic antagonists:
they decrease the BP by blocking adrenergic receptors
-
because alpha 2 receptors are parasympathetic in character, alpha 2 anti hypertensives are:
agonists
-
decreasing the BP can be accomplished by any of the following mechanisms with adrenergic antagonists:
- alpha 1 or beta 1 blockade
- alpha 2 agonism
-
what is the MOA for alpha 1 blockers:
what is the overall result:
blocking alpha 1 receptors on arterial smooth muscle causes relaxation of the arteriole muscles
overall result: decreasing peripheral resistance
-
Considering alpha 1 blockers relax smooth muscle in the prostate and bladder neck enhancing urine flow, they are most often used for:
benign prostate hyperplasia
THEY ARE NOT OFTEN USED TO TX HTN!!!
-
the side effects of alpha 1 blockers can cause orthostatic hypotension and dizziness because:
alpha blockers inablility to constrict blood vessles makes the pt. less able to response do position changes
-
1st dose phenomenon can be an adverse effect of alpha 1 blockers, when the 1st dose is given or a with dose increases:
- significantly decreased BP
- dizziness
- fainting
-
what is the MOA of alpha 2 agonists:
alpha 2 receptors in the brain stem are engaged causing a decrease in NE (norepinephrine).
with this there are fewer impulses from the brain to the heart and arterioles with resulting slowing conduction and arteriole dilation
-
considering alpha 2 agonists are centrally acting, they may cause some side effects that are difficult to tolerate, list (7)
- orthostatic hypotension
- sedation
- dizziness
- impotence
- decreased libido
- edema
- dry mouth
-
what is the MOA for beta blockers:
beta 1 receptors are on the heart
such blockade decreases the C.O. and decreases the heart rate
they also decrease the impulse conduction and contracility so they are negative inotropics
-
non selective beta blockers block:
beta 2 receptors
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