PHARM 1 EXAM #4 Flashcards
Differentiate between the two groups of drugs: antipsychotics and anxiolytics
Antipsychotics = shh’s the brain from being/having it out of touch with reality
Anxiolytics = lysis anxiety
Two types of FGAs: Phenothiazines + Nonphenothiazines
Subtypes of Phenothiazines
chlorpromazine (Thorazine)
Side effects: strong sedation, severe orthostatic hypotension, moderate EPS, some antiemetic effect
fluphenazine (Prolixin)
Side effects: low sedation, strong antiemetic effect, severe EPS
Thioridazine HCl (Mellaril)
Side effects: sedation, few EPS, low risk of orthostatic hypotension, no antiemetic effect
Differences between treating psychosis vs. treating depression/anxiety
— When treating psychosis we block or antagonize the action of neurotransmitters.
— When treating depression (chapter 23) or anxiety we enhance the action of neurotransmitters.
What are the MAJOR side effects when taking Phenothiazines?
— Sedation
— Orthostatic HoTN
— EPS
— Antiemetic
these drugs lower seizure threshold = bad for epileptics
Thorazine used to tx persistent hiccups
Name the 4 neurotransmitters (NTs) targeted by psychopharmacologies agents are
- GABA — inhibitory; calms; lack —> anxiety
- Serotonin — sleep/wake cycles, mood, delusions & hallucinations; lack —> depression
- Dopamine — cognition, movement, emotion; lack —> Parkinson’s
- Norepinephrine — arousal, attention, vigilance, mood affect
Contrast the action, uses, side effects, and adverse effects of traditional/typical and atypical antipsychotics
What is depression?
A mood d/o that involves: A mood disorder that involves
— Depressed mood, despair, insomnia, hypersomnia
— Loss of interest in normal activities
— Fatigue, decreased ability to think
— Suicidal thoughts
___________________
Pathophysiology
— Insufficient amount of monamine neurotransmitters (norepinephrine, serotonin, dopamine) | want to INCREASE amount of NTs
________________
Other etiology
— Genetic predisposition
— Social and environmental factors
Types of Depression
Reactive
— Usually sudden onset resulting from precipitating event (e.g., death of a loved one)
Major
— Characterized by loss of interest in work or home
— Inability to complete tasks
— Deep depression
Bipolar
— most difficult to tx
— Mood swings between manic (euphoric) and depressive (dysphoria)
Herbal Supplements for Depression
Useful for _mild _depression
St. John’s wort
— Can decrease reuptake of the neurotransmitters serotonin, norepinephrine, and dopamine
Gingko biloba
— The use of these and many herbal products should be discontinued 1 to 2 weeks before surgery.
— The patient should check with the health care provider regarding herbal treatments.
Major Depression
— May be primary or secondary to a health problem
— Difficulty sleeping or excess sleeping
— Feelings of fatigue and worthlessness
Major Antidepressant Agents
Tricyclic antidepressants (TCAs)
Selective serotonin reuptake inhibitors (SSRIs) & Serotonin norepinephrine reuptake inhibitors (SNRIs)
— If we inhibit reuptake (stopping the reabsorption process), we actually INCREASE the availability NT in that synapse
Atypical antidepressants
Monoamine oxidase inhibitors (MAOIs)
— MAO = enzyme that breaks down the NTs (includes norepinephrine); increase amount of NT available by DECREASING its breakdown
TCA’s Action + Use
Action
— Blocks uptake of neurotransmitters norepinephrine and serotonin in brain
— Blocks histamine receptors
— Elevates mood, increases interest in ADLs, decreases insomnia
Use
Major depression and agitated depression
Examples
amitriptyline (Elavil)
iImipramine (Tofranil)
trimipramine (Surmontil)
doxepin (Sinequan)
desipramine (Norpramin)
nortriptyline (Pamelor, Aventyl)
protriptyline (Vivactil)
fluphenazine (Prolixin)
Action: Blocks dopamine receptors in brain
Use: Manages symptoms of schizophrenia
Interactions
— Increase depression when taken with alcohol or other CNS depressants; kava kava may increase EPS.
Side effects:
— Sedation, dizziness, headache, seizures
— Dry mouth, nasal congestion, blurred vision,
photosensitivity, urinary retention
— GI distress, peripheral edema, tachycardia, EPS
*Dopamine involved in regulation of cognition, emotional responses, and motivation
Administration:
— given IM in a slow release formulation q2-4 wks; very thick so Z-track in deep muscle to help prevent soreness/inflammation at injection site
— Oral liquid = cause contact dermatitis, so avoid contact with skin
Interactions + Side Effects +Drug Examples for taking TCA’s
Amitriptyline (Elavil)
Interactions
— Increased CNS effects with alcohol and other CNS depressants
— Increased sedation and anticholinergic effects with phenothiazines, haloperidol
Side effects/adverse reactions
— Sedation, dizziness, blurred vision, dry mouth and eyes, urinary retention, constipation, weight gain, GI distress, sexual dysfunction, seizures
— Orthostatic hypotension, dysrhythmias, EPS, blood dyscrasias
Greatest fear is the patient can now act on and is focused enough to carry out their suicide ideations
Use + Contraindications for Phenothiazines vs. Nonphenothiazines for Antipsychotics
Phenothiazines = fluphenazine (Prolixin)
Use: manages S/Sx of schizophrenia
Side effects:
— Sedation, dizziness, headache, seizures
Dry mouth, nasal congestion, blurred vision,
photosensitivity, urinary retention
GI distress, peripheral edema, tachycardia, EPS
Nonphenothiazines = Haloperidol (Haldol)
Use:
Treats acute and chronic psychoses, dementia
Treats schizophrenia
Treats Tourette’s syndrome
Contraindications:
Narrow-angle glaucoma
Sedation
Severe liver, kidney, and cardiovascular disease
Blood dyscrasias: High dosing or long-term use of some antipsychotics can cause or worsen blood dyscrasias
Extrapyramidal Syndrome (EPS)
Antipsychotic drugs are well known for evoking EPS in patients
Pseudoparkinsonism symptoms
— Stooped posture
— Masklike features
— Rigidity
— Tremors at rest
— Shuffling gait
— Bradykinesia
— Pill-rolling motion of the hand
Adverse Effects when taking TCA’s
Seizure threshold is decreased with TCAs
Most common adverse effects: orthostatic hypotension, sedation, anticholinergic effects anticholinergic (dry mouth, blurry vision, constipation); sedation; orthostatic hypotension; EPS.
Most dangerous adverse effect: cardiac toxicity; dysrhythmias; may increase risk of suicide early in treatment
SSRI’s Action + Uses + Drug Examples
Action
— Block uptake of neurotransmitter serotonin
Uses
— Major depression
— Anxiety disorders
—Obsessive-compulsiveness
— Panic
— Phobias
— Prevention of migraine headaches
Examples
fluvoxamine (Luvox)
fluoxetine (Prozac)
sertraline (Zoloft)
paroxetine (Paxil)
citalopram (Celexa)
escitalopram (Lexapro)
Anything that changes the brain chemistry, may now have multiple uses
Foods HIGH in K+
Lima beans, strawberries, potatoes
What are the advantages of taking an SSRI compared to taking TCA’s?
— SSRIs do not cause as much sedation, HoTN, anticholinergic S/Eff, not as cardio toxic compared to TCAs
— They also aren’t as harmful regarding overdosing when dealing with a suicide ideations patient
— Most SSRIs have stimulant properties, and hence can cause insomnia and agitation
— TCAs cause sedation
SSRIs Interactions + Side Effects
Interactions
— Increased CNS effects with alcohol and other CNS depressants
Side effects/adverse reactions
— Headache, nervousness, restlessness
— Insomnia, tremors, seizures
— GI distress
— Sexual dysfunction
— Suicidal ideation
Side effects often decrease over 1 to 4 weeks, so let the patient’s know this
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs) Action + Use + Drug Examples
Norepinephrine is associated with control of arousal, attention, vigilance, mood, affect, and anxiety.
This transmitter is involved with thinking, planning, and interpreting
Action: Inhibit the reuptake of serotonin and norepinephrine, increasing these substances in nerve fibers
Use: Major depression as well as generalized anxiety disorder and social anxiety disorder
Examples
venlafaxine (Effexor)
duloxetine (Cymbalta)
desvenlafaxine (Pristiq)
SNRI Venlafaxine (Effexor): Side Effect + Adverse + Interactions
Venlafaxine (Effexor)
Side effects: drowsiness, dizziness, insomnia, headache, euphoria, amnesia, blurred vision, photosensitivity, and ejaculation dysfunction
Adverse effects: hyponatremia, bleeding, hypertension, angioedema, blood dyscrasias, suicidal ideation, and Stevens-Johnson syndrome
Interactions: concurrent interaction of venlafaxine and St. John’s wort may increase the risk of serotonin syndrome and neuroleptic malignant syndrome
Atypical Antidepressant Drug Examples
Primary use: major depression, reactive depression, and anxiety
Examples: amoxapine (Asendin), maprotiline (Ludiomil), nefazodone (Serazone), trazodone (Desyrel)
Action: affect one or two of the three neurotransmitters: serotonin, norepinephrine, and dopamine.
Interaction:
— Do not take with MAOIs and do not use within 14 days after discontinuing MAOIs
— Trazodone may have a potential drug interaction with ketoconazole, ritonavir, and indinavir that may lead to increased trazodone levels and adverse effects.
Monoamine Oxidase Inhibitors (MAOIs) Use + Action + Drug Examples
Make the NTs more available in the brain because will inhibit breakdown by inhibiting MAO
Big problem with these drug are the interactions therefore NEVER a 1st line option
Examples: tranylcypromine sulfate (Parnate), isocarboxazid (Marplan), selegiline (Emsam), phenelzine sulfate (Nardil)
Action: monamine oxidase enzyme inactivates norepinephrine, dopamine, epinephrine, and serotonin.
Use: depression not controlled by TCAs and second-generation antidepressants
The go drug IF suffering refractory depression, not being controlled with other medications
MAOIs Interactions
Drug interactions:
Vasoconstrictors and cold medications containing phenylephrine and pseudoephedrine can cause a hypertensive crisis when taken with an MAOI.
Food interactions:
Foods that contain tyramine
Some cheeses, cream, bananas, avocados, raisins, Italian green beans, liver, pickled foods, sausage, soy sauce, yeast, beer, and red wines, can cause a hypertensive crisis.
________________
Coffee (caffeine) does not contain tyramine, but intake should be limited to 2- 8 oz. beverages, because it can increase BP significantly when combined with MAO-Is.
Overripe fruits are higher in tyramine.
MAOIs Side/Adverse Effects
— Agitation, restlessness, insomnia
— Anticholinergic effects
— Orthostatic hypotension
Hypertensive crisis from fatal tyramine or drug interaction
Plan nursing interventions, including patient teaching, for the patient taking antipsychotics
and anxiolytics
Antidepressant Agents RN Interventions
— Monitor vital signs.
— Monitor mood for drug effectiveness.
— Monitor for suicidal tendencies, seizures.
— Warn that foods that contain tyramine can cause a hypertensive crisis with MAOIs.
— Encourage taking drug as prescribed.
— Encourage avoiding alcohol, CNS depressants, and cold medicines.
— Teach to take drug with food if GI distress occurs.
— Warn patient against driving or using dangerous mechanical equipment until drug effect is known.
— Warn patient against abruptly stopping drug
— Instruct patient to take drug at bedtime (may make you drowsy)
— Advise patient that a therapeutic response usually occurs in 2 to 4 weeks (but chemistry changes are effected immediately)
— Inform patient that herbs (e.g., St. John’s wort, ginseng) may interact with antidepressants.
Mood Stabilizers Drug Examples
Used to tx bipolar d/o for the switching of euphoria —> dysphoria, making it difficult to treat
Lithium (Lithibid)
Carbamazepine (Tegretol)
Divalproex (Depakote, Valproate)
Lamotrigine (Lamictal)
Olanzapine (Zyprexa)
Ziprasidone (Geodon)
Aripiprazole (Abilify)
Normally used in conjunction with an antidepressant
What is Bipolar Disorder?
Bipolar affective disorder was formerly known as manic-depressive illness.
Definition of bipolar disorder (BPD)
— Cyclic disorder
— Recurrent fluctuations in mood
— Episodes of mania and depression persist for months without treatment
In patients with bipolar depression, using an antidepressant alone may induce mania—although the risk appears lower than previously believed. Nonetheless, to minimize any risk mania, antidepressants should not be used alone; rather, they should be combined with a mood-stabilizing drug.
Mood Stabilizer: LITHIUM
LITHIUM (ESKALITH)
also known as an antimania drug, was the first drug used to manage bipolar affective disorder
Therapeutic serum range: 0.5 to 1.5 mEq/L
— Serum lithium levels greater than 1.5 to 2 mEq/L are toxic.
— Changes in fluid balance will alter these levels, making it hard to manage; Li+ follows Na+
Action
— Alteration of ion transport in muscle and nerve cells
— Increased receptor sensitivity to serotonin
Use
— Treat manic episodes in bipolar psychosis
Overhydrated = Lithium will be flushed = below therapeutic range = drug failure
Dehydrated = Lithium will be saved = will enter toxic ranges
Lithium Interactions + Side/Adverse Effects
Interactions
— Increased lithium level with thiazides, methyldopa, haloperidol, NSAIDs, antidepressants, theophylline, phenothiazines
Side effects/adverse reactions
— Headache, drowsiness, dizziness
— Hypotension, dysrhythmias
— Restlessness, slurred speech
— Dry mouth, metallic taste, GI distress
— Tremors, muscle weakness
— Edema of hands and ankles
— Increased urination, blood dyscrasias, nephrotoxicity
LITHIUM (ESKALITH) RN Interventions
— Monitor vital signs, sodium levels.
— Monitor for drug effectiveness, suicidal tendencies.
— Monitor urine output, renal function tests.
— Encourage adequate fluid intake (1 to 2 L daily)
— Take with food to decrease GI irritation
— Monitor lithium levels every 1 to 2 months (0.8 to 1.5 mEq/L); toxic range is greater than 2 mEq/L
— Toxic side effects: persistent nausea, vomiting, severe diarrhea, blurred vision, tinnitus, ataxia, increasing tremors, confusion, dysrhythmias, seizures
— Teach patient to wear medical alert identification.
— Teach patient to take drug as prescribed and keep medical appointments.
— Warn against driving motor vehicles or operating dangerous equipment until drug effect is known.
— Advise patient that drug effect may take 1 to 2 weeks.
— Encourage patient to avoid caffeine, crash diets, NSAIDs, diuretics.
— Advise patient against getting pregnant because of teratogenic effects
Serotonin Syndrome (SS) vs. Neuroleptic Malignant Syndrome
SS:
— EXCESS of neurotransmitters (NTs)
NMS: LACK of NTs…we inhibited too much..yikes
Side Effects look very similar to one another
—INCREASE (temp, BP), diaphoretic, twitchy, muscle cramps, nauseous
So how do you tell? By what they’re taking:
— Antipsychotic = NMS
— Antidepressants = SS
For both drugs, a couple doses WILL be held
Purpose in Psychosis vs Depression
In psychosis/mania, we try to inhibit neurotransmitters (NTs)
In depression, we try to ENHANCE NTs
Foods HIGH in Tyramine when taking MAOIs
Apply the nursing process to the patient taking an atypical antipsychotic, a typical antipsychotic, and an anxiolytic
Psychosis Characteristics
— Losing contact with reality
— Manifested in a variety of mental or psychiatric disorders
— Usually characterized by more than one symptom: difficulty in processing information and coming to a conclusion, delusions, hallucinations, incoherence, catatonia, and aggressive or violent behavior
Barbiturates + Benzodiazepines correlation of GABA
Barbiturates ADD to the cup (GABA)
Benzodiazepines IMPROVE your GABA; takes the “edge” off
Contrast the various categories of different antidepressants, giving an example of one drug for each category
Characteristics of Schizophrenia
—Chronic psychotic d/o; usually occurs in adolescence or early adulthood
(+) Sx’s:
—agitation
—delusion
—paranoia
—hallucinations
—incoherent speech
(-) Sx’s:
—poor self-care
—poverty of speech
—social withdrawal
Positive (+) and Negative (-) Symptoms are characterized by…
— Positive symptoms: characterized by exaggeration of normal function
— Negative symptoms: characterized by decrease or loss of function and motivation
— Negative symptoms tend to be more chronic, persistent and refractory to treatment.
— FGAs don’t treat negative symptoms effectively, only SGAs seem to help.
First-generation antipsychotics (FGAs) vs. Second-generation antipsychotics (SGAs)
FGAs
— Block receptors for dopamine in CNS (D2 receptors)
— Cause serious movement disorders (extrapyramidal symptoms [EPS])
(SGAs)
— Produce moderate blockade of dopamine receptors
Strong blockade for serotonin (5-HT2 receptors)
Fewer EPS
Antipsychotic Agents: Conventional (Typical) FIRST Generation
— haloperidol (Haldol)
— fluphenazine (Prolixin)
— thiothixene (Navane)
— pimozide (Orap)
— loxapine (Loxitane)
— chlorpromazine (Thorazine)
— thioridazine (Mellaril)
Antipsychotic Agents: Atypical SECOND Generation
— clozapine (Clozaril)
— risperidone (Risperdal)
— paliperidone (Invega)
— olanzapine (Zyprexa)
— zipradisone (Geodon)
— quetiapine (Seroquel)
— aripiprazole (Abilify)
— asenapine (Saphris)
— lurasidone (Latuda)
What are some cognitive symptoms regarding Schizophrenia?
Disorganized thinking, memory difficulty
Decreased ability to focus attention
Describe the side effects and adverse reactions of antidepressants
Plan nursing interventions, including patient teaching, for antidepressants (tricyclic antidepressants [TCAs], monoamine oxidase inhibitors [MAOIs], selective serotonin
reuptake inhibitors [SSRIs], selective norepinephrine reuptake inhibitors [SNRIs], and atypical antidepressants
Explain the uses of lithium and its serum/plasma therapeutic ranges, side effects and adverse reactions, and nursing interventions
Antidepressant Agents: RN Interventions
— Monitor vital signs + mood for drug effectiveness; suicidal tendencies, seizures.
— Warn that foods that contain tyramine can cause a hypertensive crisis with MAOIs.
— Encourage taking drug as prescribed.
— Encourage avoiding alcohol, CNS depressants, and cold medicines.
— Teach to take drug with food if GI distress occurs
— Warn patient against driving or using dangerous mechanical equipment until drug effect is known.
— Warn patient against abruptly stopping drug.
— Instruct patient to take drug at bedtime.
— Advise patient that a therapeutic response usually occurs in 2 to 4 weeks.
— Inform patient that herbs (e.g., St. John’s wort, ginseng) may interact with antidepressants.
Apply the nursing process to the patient taking lithium, carbamazepine, and valproic acid
Compare the action and uses of thiazide, loop, and potassium-sparing diuretics
Thiazide action:
Loop action:
Potassium-sparing diuretic action:
Calcium channel action:
Drugs that suppress RAAS:
— ACE-I = prevents angiotensin I from becoming angiotensin II
— ARBs (targets BVs & adrenal medulla) = angiotensin II receptors BLOCK receptors in vasculature and adrenal gland —> “-sartan”
— Aldosterone antagonist = K+ sparing diuretics; antagonists aldosterone (save Na+)
— Direct renin inhibitors = stops system at the very beginning (Renin); may not have the efficacy that other meds [above] have
Diuretic Antihypertensive Therapy Drugs
— Thiazide diuretics: HCTZ = used for BP
— High-ceiling (loop) diuretics: furosemide (Lasix) = heart failure
— Potassium-sparing: spironolactone (Aldactone) = w/ combination in effort to INCREASE urine output w/o depleting K+ further
Differentiate side effects and adverse reactions related to thiazide, loop, and potassium-sparing diuretic
Location of diuretics used
Proximal tubule —
Descending loop —
Loop of Henle (high-ceiling) — Loop diuretics, e.g. furosemide (Lasix) —> will lose MORE electrolytes
Distal (ascending) tubule — Thiazides, e.g. HCTZ
Collecting tubule — K+ sparing, e.g. triamterene
Non selective VS. selective Beta-adrenergic blockers/Sympatholytics/Sympathetic Depressants
Nonselective beta blockers
— Propranolol & Carvedilol stop all sympathetic input to the heart (d/t bleed over from heart disease)
— WATCH lungs b/c can be impacted
Selective beta blockers
— Contraindications: patients w/ DM when taking BBers b/c MASK S/Sx of HYPOglycemia
Purpose: HTN, angina and dysrhythmias + SLOW heart down (allow for vasodilation) + DECREASE HR
Explain the nursing interventions, including patient teaching, related to thiazide, loop, and potassium-sparing diuretics
K+ wasting vs. K+ sparing: what to watch out for
K+ wasting: watching for HYPOkalemia
K+ sparing: watching for HYPERkalemia
Side Effects for Beta-Adrenergic Blockers
MUST know BP + HR BEFORE ADMINISTRATION
— Marked decrease in blood pressure
— Insomnia
— Depression
— Nightmares
— Sexual dysfunction (impotence)
RN Intervention for Beta-Adrenergic Blockers
Do not abruptly stop taking beta blockers: rebound hypertension may result
— Monitor vital signs
— Blood glucose
— Renal and liver laboratory results (especially BUN, serum creatinine, AST, and LDH)
— Suggest that patient wear a MedicAlert bracelet
— Advise patients to avoid over-the-counter drugs without first checking with a health care provider.
Apply the nursing process for the patient taking thiazide, loop, and potassium-sparing diuretics
Differentiate the pharmacologic action of the various categories of antihypertensive drugs
Sympatholytics/Sympathetic Depressants
Turning ON alpha 2 receptors, stopping Sympatholytics input leading to vasodilation; WANT to agonize this one
— Methyldopa (Aldomet) = drug of choice for pregnant woman
— Clonidine (Cadapres) = affect alpha 2 agonists, leading to vasodilation; fluid retention possible, so used with diuretic to avoid this
— Guanabenz =
— Guanfacine =
Compare the side effects and adverse reactions to sympatholytics, direct-acting vasodilators, and angiotensin antagonists
Apply the nursing process including nursing interventions and patient teaching, related to antihypertensives
Describe the blood pressure guidelines for determining hypertension.
An example of secondary HTN
_ Pheochromocytoma:_ is a rare tumor of adrenal gland tissue. It results in the release of too much epinephrine and norepinephrine, hormones that control heart rate, metabolism, and blood pressure
What are the 2 types of HYPERTENSION?
Primary = essential HTN
— No identifiable cause
— Chronic, progressive disorder
— Population: older adults, African Americans, Mexican Americans, postmenopausal women
— Treated but not cured (lifelong condition)
— Referred to as “essential hypertension”
_______________
Secondary
— Identifiable primary cause
— Possible to treat the cause directly
— Some individuals can actually be cured
What is malignant hypertension?
— A very high blood pressure that comes on suddenly and quickly
—The lower (diastolic) blood pressure reading, which is normally less than 80 mmHg, is often above 130 mmHg.
How do you measure BP?
— Seat quietly for 5 minutes in chair
— Feet on floor, arm supported at heart level
— No caffeine, exercise or smoking for 30 minutes prior
— Cuff bladder encircle at least 80% arm circulation
— At least 2 measurement and average
— Inflate 20-30mmHg above pulse extinction
— Deflate at rate of 2mmHg/sec
— Cuff size: too narrow = false high BP (extra pressure to compress artery); too wide/loose =
Differentiate between SBP vs. DBP
BP is the force of the blood pushing against the side of its container, the vessel wall. The strength of the push changes with the event in t he cardiac cycle.
Systolic BP = SBP: maximum pressure felt on the artery during left ventricular contraction, or systole = onset of 1st Karotkoff sound
Diastolic = DBP: the elastic recoil, or resting, pressure that the blood exerts constantly b/w each contraction = disappearance of Karotkoff sounds
What regulates your BP?
Baroreceptors: sensitive to pressure changes in the vasculature, will stimulate vasoconstriction and tachycardia when B/P drops in effort to maintain perfusion
ADH: hormone produced in the hypothalamus stimulates the kidneys to conserve and retain water when there is a fluid volume deficit; in fluid overload ADH secretion is inhibited and the kidney then excrete more water
ANP (hormone secreted from atria in response to fluid overload/atria stretching) and BNP (hormone secreted from ventricles in response to fluid overload/ventricle stretching) both work to increase urine output and lower vascular volume.
Purpose of peptides: atrial natriuretic peptide (ANP) + brain natriuretic peptide (BNP)
— Diurese you = make you pee
— Lowers BP
BNP serum is used to quantify heart failure b/c peptides are released when the heart is stretched; the more volume of blood/stretch to ventricles, the MORE the peptides will be released
secreted by ventricles of heart; Normal = <100
RISK FACTORS FOR HTN
Physiologic:
— Excessive intake of saturated fat and simple carbohydrates
— Alcohol: increases renin secretions
Cultural responses to antihypertensive agents:
— African Americans, Asian Americans, Mexican-Americans
Hypertension in older adult
Cultural
African Americans – who are more likely to develop HTN earlier do not respond well to beta blockers, ACE inhibitors, or diuretics (as monotherapy); usually treated with alpha1 blockers and calcium channel blockers, can use diuretic in combination with these.
Asian Americans – twice as sensitive to antihypertensives, doses may need to be reduced
Older Adults – aging increases HTN risk; more at risk of side effect of orthostatic (postural) hypotension….think safety!
Guides for Determining Hypertension
Category Systolic Diastolic
NORMAL <120mmHg <80mmHg
PREHTN 120 to 139mmHg 80 to 89mmHg
STAGE 1 HTN 140 to 159mmHg 90 to 99mmHg
STAGE 2 HTN >160mmHg >100mmHg
Hypertension leads to _____ ____ _____. What are further consequences?
end organ damage.
— Can have heart failure, a stroke, kidney failure, poor circulation to limbs (amputation) if continued pressure builds up
Consequences of Hypertension
Heart disease
Myocardial infarction (MI)
Heart failure
Angina pectoris
Kidney disease-end organ damage
Stroke end organ damage
Sympatholytics (Antiadrenergic) Antihypertensive Therapy Drugs
turning OFF fight-or-flight in order to VASODILATE + DECREASE BP
________________
Beta-adrenergic blockers – end in olol
Central acting alpha2 agonists – methyldopa, clonidine
Alpha1 blockers – doxazosin (Cardura), terzosin (Hytrin)
Alpha & beta blockers – carvedilol (Coreg) and labetalol
Adrenergic neuron blockers – only 1 – reserpine
Direct-Acting vasodilators
work directly on the blood vessels to dilate them
Calcium-channel blockers
calcium are in seashells + pine trees (-ipines) are found outside
promote dilation of arteries.
Location of diuretics used
RN Intervention for
