WGU D116 OA review
Study online at https://quizlet.com/_h1856v
1. doxazosin Cardura, Cardura XL
alpha blocker
potent and selective post-junctional alpha-1-adrenergic blocker.
This action blocks alpha 1 receptors in vascular smooth muscle & blad-
der/prostate.
causes vasodilation of arterioles and veins and relaxation of smooth muscle in the
bladder neck/prostate (to improve urinary flow in BPH) results in a decrease in
systemic blood pressure.
For: HTN, enlarged prostate in BPH by relaxing blood vessels.
-start at 1mg daily for HTN
-for BPH, 1 mg at bedtime and maintenance 4-8mg once daily
BLACK BOX: first-dose phenomenon. significant orthostatic hypotension or syn-
cope - esp after 1st dose or dose increases.
& risk of intraoperative floppy iris syndrome (IFIS) during cataract surgery.
decreases standing and supine blood pressure so monitor BP & HR.
dont give if pt has allergy to:
quinolones, alfuzosin, prozosin, tamulosin, or terazosin.
dont take if pregnant/breastfeeding, stomach/intestine problems.
dont take with sildenafil, tadalafil, or vardenafil.
dont give to pts with heart failure or elderly. dizziness, lightheadedness/fainting
may occur. dont give with hepatic impairment (extensively metabolized by liver)
drug interactions with other antihypertensives or PDE5 inhibitors (sildenafil) or
CYP3A4 inhibitors (ketoconazole, ritonavir) bc it will increase levels of doxazosin.
usual dose is 2mg-16 mg taken once a day or slow release 4-8mg once a day.
clinical pearls: not first line for HTN but can be useful if pt has HTN & BPH.
good option for older men who need help with BP and urinary flow.
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
pt should be educated to rise slowly from sitting/lying. remind pt about eye
surgery risk! must inform opthalmologist if they've ever taken this med.
avoid alcohol & hot showers. dont stop abruptly. report s/s of low BP, fainting.
DOXAZOSIN: DILATES VESSELS & DECONGESTS THE PROSTATE
2. synaptic gap synaptic cleft:
-presynpatic neuron: sends signal
-postsynaptic neuron: receives the signal
messages are passed along the nervous system.
process:
1) action potential: reaches presynaptic terminal
2) calcium influx: triggers vessicles to release NP into synaptic gap.
3) NT binds to receptors on postsynaptic neuron.
--signal is either excitatory (triggers action potential) or inhibitory (dampens
activity).
5) NT are cleared via:
~reuptake: into presynaptic cell
~enzymatic degradation (MAO, COMT)
~diffusion away
3. lithium Mood stabilizer for bipolar (type 1) effective for acute mainia, maintenance, and
reducing suicide risk. treats resistant depression, cluter headaches.
modulates serotonin, dopamine, norepi, intracellular messengers (IP3) & has
neuroprotective and neuroplastic effects.
typical dose: 600-1200 mg/day
therapeutic range:
acute mania: 0.8-1.2
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
maintenance: 0.6-1.0
toxicity: >1.5!!n/v/d, tremor, confusion.. hold dose & hydrate!
lifethreatening is >2.0! ataxia, slurred speech, worsening confusion.. er referral &
fluids
severe >2.5: seizures, coma, death, medical emergency!! ICU/dialysis
monitoring:
-Lithium: check 5-7 days after dose change or initation then q3-6 months.. trough
levels checked 12 hours after last dose!
-TSH: get baseline then check q6-12 months. lithium can cause hypothyroidism.
-renal function (BUN, CR, GFR): get baseline then q6-12 months. risk of nephro-
genic diabetes insipidus.
-Electrolytes (Na, Ca): baseline and periodically. lithium competes with sodium.
-EKG: get one on older adults or with cardiac history. can cause t-wave flattening
or arrhythmias.
s/e: common: GI upset, nausea, tremor, polyuria/polydipsia, weight gain, acne,
mild cognitive dulling
serious adverse: hypothyroidism, nephrotoxicity, tremor (coarse), arrhythmias,
tetatogenicity -- esp. ebstein's anomaly!
4. Acetylcholine ! ACh: Excitatory. in CNS and peripheral nervous system.
broken down by acetylcholinesterase in synaptic cleft.
In PNS:
-somatic system: stimulates skeletal muscle in neuromuscual junction
-autonomic nervous system:
~parasympathetic (rest & digest): ACh is released by pre & post gang neurons.
~sympathetic: pregang neurons use ACh; post gang use norepi (except for sweat
glands -- use ACh)
In CNS:
for learning, memory, arousal, attention.
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
major role in alzheimer's disease (decreased ACh). muscle activation.
Low ACh:
-AD - memory loss, treated with cholinesterase inhibitors (donepezil, rivastig-
mine).
-Myasthenias Gravis: autoimmune destruction of ACh at NM junction
Meds:
Anticholinergics: decrease ACh effects (atropine, scopalamine, ipratropium)
Used in COPD, brady, motion sickness. s/e: dry mouth, blurred vision, urinary
retention, constipation, confusion esp. elderly.
Cholinesterase Inhibitors: increase ACh (donepezil, neostigmine)
Used for AD, MG, reversing neuromuscular blockers
5. glucocorticoids Class: corticosteroids
and interactions Natural form: secreted as cortisol by the adren cortex
Synthetic form: prednisone, hydrocortisone, dexamethasone, methylpred-
nisolone, and others
Effects: anti-inflammatory, immunosuppresive, and metabolic effects
Bind to glucocorticoid receptor inside cytoplasm of target cells. once bound, they
alter gene expression leading to:
1) increased production of anti-inflammatory proteins
2) dereased production of pro-inflammatory cytokines
also effect glucose metabolism, protein synthesis, and fat distribution.
for:
-autoimmune disorders: RA, lupus, multiple sclerosis
-inflammatory conditions: asthma, COPD, IBD/crohns/UC
-adrenal insufficiency: addisons disease to replace cortisol
Study online at https://quizlet.com/_h1856v
1. doxazosin Cardura, Cardura XL
alpha blocker
potent and selective post-junctional alpha-1-adrenergic blocker.
This action blocks alpha 1 receptors in vascular smooth muscle & blad-
der/prostate.
causes vasodilation of arterioles and veins and relaxation of smooth muscle in the
bladder neck/prostate (to improve urinary flow in BPH) results in a decrease in
systemic blood pressure.
For: HTN, enlarged prostate in BPH by relaxing blood vessels.
-start at 1mg daily for HTN
-for BPH, 1 mg at bedtime and maintenance 4-8mg once daily
BLACK BOX: first-dose phenomenon. significant orthostatic hypotension or syn-
cope - esp after 1st dose or dose increases.
& risk of intraoperative floppy iris syndrome (IFIS) during cataract surgery.
decreases standing and supine blood pressure so monitor BP & HR.
dont give if pt has allergy to:
quinolones, alfuzosin, prozosin, tamulosin, or terazosin.
dont take if pregnant/breastfeeding, stomach/intestine problems.
dont take with sildenafil, tadalafil, or vardenafil.
dont give to pts with heart failure or elderly. dizziness, lightheadedness/fainting
may occur. dont give with hepatic impairment (extensively metabolized by liver)
drug interactions with other antihypertensives or PDE5 inhibitors (sildenafil) or
CYP3A4 inhibitors (ketoconazole, ritonavir) bc it will increase levels of doxazosin.
usual dose is 2mg-16 mg taken once a day or slow release 4-8mg once a day.
clinical pearls: not first line for HTN but can be useful if pt has HTN & BPH.
good option for older men who need help with BP and urinary flow.
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
pt should be educated to rise slowly from sitting/lying. remind pt about eye
surgery risk! must inform opthalmologist if they've ever taken this med.
avoid alcohol & hot showers. dont stop abruptly. report s/s of low BP, fainting.
DOXAZOSIN: DILATES VESSELS & DECONGESTS THE PROSTATE
2. synaptic gap synaptic cleft:
-presynpatic neuron: sends signal
-postsynaptic neuron: receives the signal
messages are passed along the nervous system.
process:
1) action potential: reaches presynaptic terminal
2) calcium influx: triggers vessicles to release NP into synaptic gap.
3) NT binds to receptors on postsynaptic neuron.
--signal is either excitatory (triggers action potential) or inhibitory (dampens
activity).
5) NT are cleared via:
~reuptake: into presynaptic cell
~enzymatic degradation (MAO, COMT)
~diffusion away
3. lithium Mood stabilizer for bipolar (type 1) effective for acute mainia, maintenance, and
reducing suicide risk. treats resistant depression, cluter headaches.
modulates serotonin, dopamine, norepi, intracellular messengers (IP3) & has
neuroprotective and neuroplastic effects.
typical dose: 600-1200 mg/day
therapeutic range:
acute mania: 0.8-1.2
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
maintenance: 0.6-1.0
toxicity: >1.5!!n/v/d, tremor, confusion.. hold dose & hydrate!
lifethreatening is >2.0! ataxia, slurred speech, worsening confusion.. er referral &
fluids
severe >2.5: seizures, coma, death, medical emergency!! ICU/dialysis
monitoring:
-Lithium: check 5-7 days after dose change or initation then q3-6 months.. trough
levels checked 12 hours after last dose!
-TSH: get baseline then check q6-12 months. lithium can cause hypothyroidism.
-renal function (BUN, CR, GFR): get baseline then q6-12 months. risk of nephro-
genic diabetes insipidus.
-Electrolytes (Na, Ca): baseline and periodically. lithium competes with sodium.
-EKG: get one on older adults or with cardiac history. can cause t-wave flattening
or arrhythmias.
s/e: common: GI upset, nausea, tremor, polyuria/polydipsia, weight gain, acne,
mild cognitive dulling
serious adverse: hypothyroidism, nephrotoxicity, tremor (coarse), arrhythmias,
tetatogenicity -- esp. ebstein's anomaly!
4. Acetylcholine ! ACh: Excitatory. in CNS and peripheral nervous system.
broken down by acetylcholinesterase in synaptic cleft.
In PNS:
-somatic system: stimulates skeletal muscle in neuromuscual junction
-autonomic nervous system:
~parasympathetic (rest & digest): ACh is released by pre & post gang neurons.
~sympathetic: pregang neurons use ACh; post gang use norepi (except for sweat
glands -- use ACh)
In CNS:
for learning, memory, arousal, attention.
, WGU D116 OA review
Study online at https://quizlet.com/_h1856v
major role in alzheimer's disease (decreased ACh). muscle activation.
Low ACh:
-AD - memory loss, treated with cholinesterase inhibitors (donepezil, rivastig-
mine).
-Myasthenias Gravis: autoimmune destruction of ACh at NM junction
Meds:
Anticholinergics: decrease ACh effects (atropine, scopalamine, ipratropium)
Used in COPD, brady, motion sickness. s/e: dry mouth, blurred vision, urinary
retention, constipation, confusion esp. elderly.
Cholinesterase Inhibitors: increase ACh (donepezil, neostigmine)
Used for AD, MG, reversing neuromuscular blockers
5. glucocorticoids Class: corticosteroids
and interactions Natural form: secreted as cortisol by the adren cortex
Synthetic form: prednisone, hydrocortisone, dexamethasone, methylpred-
nisolone, and others
Effects: anti-inflammatory, immunosuppresive, and metabolic effects
Bind to glucocorticoid receptor inside cytoplasm of target cells. once bound, they
alter gene expression leading to:
1) increased production of anti-inflammatory proteins
2) dereased production of pro-inflammatory cytokines
also effect glucose metabolism, protein synthesis, and fat distribution.
for:
-autoimmune disorders: RA, lupus, multiple sclerosis
-inflammatory conditions: asthma, COPD, IBD/crohns/UC
-adrenal insufficiency: addisons disease to replace cortisol
