Atorvastatin - what does it do?
- HMG Co-A reductase inhibitor
- Lowers lipid/cholesterol levels and prevents plaque formation and promotes plaque regression
Atrovastatin - how does it work?
- Blocks hepatic cholesterol synthesis and causes intracellular cholesterol levels to drop
- Hepatocyte upregulates LDL receptors that remove LDL from blood stream
Atorvastatin - uses
- Primary and secondary prevention of ASCVD (by lowering LDLs and TGs and raising HDLs)
- Beneficial to those with ASCVD because Atorvastatin promotes plaque stability, causes anti-inflammatory activity, and improves endothelial function, including dilati
Atorvastatin - side effects
- Metabolic syndrome (cluster of conditions associated with increased ASCVD; diagnosed if three or more of the following are present: HDL <40 (M) or <50 (F); high BP; waste size >35" (F) or >40" (M); TG >150; FBS >100)
- Statin associated muscle symptoms
Atorvastatin - nursing considerations
- Lifetime therapy (drug and lifestyle management)
- Monitor for muscle weakness
- Evening dosing w/o regard to meals
- Category X drug
Ezetimibe - what does it do?
- Lowers total cholesterol, LDLs, TGs, and apolipoprotein B.
- Increases HDL cholesterol
Ezetimibe - how does it work?
- Inhibits dietary cholesterol absorption and reabsorption of cholesterol from bile
Ezetimibe - nursing considerations
- Not a first line therapy
- More expensive than statins
What do BBs, ACEi/ARBs, and CCBs have in common?
Lower blood pressure and decrease myocardial oxygen demand. They are often used to manage angina and ischemia heart disease.
Nitroglycerin - what does it do?
- Preferential venous vasodilator --> decreases preload (diastolic volume/pressure) --> decreases cardiac output --> decreases BP --> decreases myocardial oxygen demand
*NOTE: nitroglycerin has little/no beneficial effect on coronary blood flow/myocardial
Nitroglycerin - how does it work?
- Nitroglycerin converts nitrate to nitric oxide in vascular smooth muscle. This causes the dephosphorylation of myosin, which results in vasodilation
Nitroglycerin - uses
- Stable angina and variant agina
- Acute coronary symptoms (morphine and nitroglycerin used to control ischemic pain)
Nitroglycerin - routes of administration
- Immediate onset (acute angina) = sublingual, aerosol, IV
- Gradual onset (chronic angina) = oral, dermal
Nitroglycerin - side/adverse effects
- Headache (especially early on, but pt. will develop tolerance)
- Orthostatic hypotension --> SNS stimulation --> reflect tachycardia --> increased oxygen demand and BB (beta blocker?)
Nitroglycerin - nursing considerations
- Important to allow nitrate free time to prevent tolerance (longer-lasting drugs should be given with 8 hour nitrate free time to allow sulfhydryl groups to replenish)
- Risk of orthostasis when taking nitroglycerin and other antihypertensives at the sam
How/where are drugs absorbed?
- Primarily via the GI tract (oral), but sometimes there are other sites of administration (eg, dermal, topical, sublingual, IV-)
What are the common sites for drug metabolism?
- Primarily the liver, but also the kidney. Less common sites for drug metabolism are their sites of action
What are the mechanisms by which drugs pass through membranes?
- Direct membrane penetrations (drugs in lipid form can pass directly through the lipid bilayer)
- T-glycoprotein transporters allow certain drugs to cross from the outside to the inside
- P-glycoprotein transporters allow certain drugs to cross from the
What are some barriers to drugs trying to cross membranes?
- Polar state (water soluble; charges in molecule are balanced but
unevenly distributed
)
- Ionization (ions are molecules with a net charge; AIB & BIA)
What are issues with blood flow that affect movement of drug through body?
- Any kind of shock state (decreased perfusion)
- Abscess (need to incise and drain first)
- Tumors (solid tumors do not have good blood flow)
When does the blood brain barrier (BBB) become active in life?
- 1 year old
What is important about drugs that bind to albumin?
- Certain drugs bind to protein (albumin). When bound to albumin, the drug is inactive (so there is less free, active drug in the system). Thus, patients with low albumin levels (eg, liver failure patients) should be given less drug because there are less
What is the importance of the cytochrome P450 system?
- This system is responsible for the metabolism/enzymatic alteration of drugs (the enzymes prepare the drug for excretion).
- When drugs are prepared for renal excretion, they are converted from lipid to polar/water soluble forms
What are factors that affect drug metabolism?
- Liver function (AST/ALT enzymes are a measure of this)
- Age (age --> liver decline)
- First pass effect (certain drugs are a high first pass effect, aka the liver metabolizes the majority of the drug before it can have an effect)
- Drug drug interactio
How/where are drugs excreted from the body?
- Drugs are primarily excreted by the kidneys, but can also be excreted through the biliary system
- Kidneys need to function well for excretion to occur effectively (look for GFR [125], BUN [7-18] and Creatinine [0.6-1.2] levels)
What is the difference between minimum effective concentration, therapeutic range, and toxic concentration?
- Minimum effective concentration is the minimum amount of drug needed in the body for it to have a therapeutic effect, therapeutic range is the concentration in which the drug is therapeutic, and toxic concentration is the point at which you have too muc
What is a drug's half-life?
- The time required for the amount of the drug in the body to decrease by 50%
When is a drug's plateau level reached?
- When the amount of drug eliminated is equal to the amount of drug administered
- Time to plateau is approximately 4 half lives (and time from plateau to elimination is also 4 half lives)
- A loading dose can be administered to speed up the time to plate
What is maximal efficacy?
- The largest effect a drug can achieve (indicated by the height of the dose response curve)
What is relative potency?
- The amount of drug needed to achieve a clinical effect, indicated by the position of the dose response curve on the X axis
What is an agonist?
- A drug that occupies receptor sites and mimic the effect of neurotransmitter
- Agonists stimulate/activate
What is an antagonist?
- A drug that blocks receptor sites and prevent the neurotransmitter from activating the receptor
- Antagonists block/inhibit
What is a negative outcome of repeatedly giving doses of agonists?
- This can cause receptor desensitization (down regulation), so higher and higher doses of the drug will be needed over time (eg, opioids and addiction)
What is a negative outcome of repeatedly giving doses of antagonists?
- This can cause receptor supersensitization (up regulation); this explains the rebound effect when drugs are discontinued (eg, beta antagonists being given for hypertension causes up regulation of beta receptors; when drug is discontinued suddenly recept
What is therapeutic index?
- The ratio of lethal dose (LD50)/effective dose (ED50)
- It has important ramifications on patient safety (a more narrow therapeutic index = more dangerous)
Explain the effects of inhibitors and inducers of CYP
- Inhibitors of CYP cause more drug to be in the system because the drug isn't able to be broken down
- Inducers of CYP cause less of a drug to be in the system because it is being metabolized more than normal
What is a key food drug interaction to be aware of?
- Grapefruit juice is one of the most common foods that effect drugs. Grapefruit juice inhibits cytochrome CYP3A4, which results in toxic levels of drugs that use the enzyme for metabolism (eg, viagra, SSRIs)
Why is it important to avoid potassium-based salt substitutes when taking drugs that block aldosterone (ARB, ACE-I)?
- Because aldosterone leads to hyperkalemia; adding high levels of potassium from your diet can lead to dangerous levels of potassium (this can stop your heart!)
If a drug should be taken on an empty stomach, at what time of day should you take it?
- In the morning, about 2 hours before breakfast
What is an idiosyncratic reaction?
- An uncommon and unpredictable reaction
What is a latrogenic reaction?
- A reaction caused by provider error
Which types of drugs are hepatotoxic?
- Drugs whose clinical action occurs in the hepatocyte ("statins")
- Acetaminophen if excessively dosed or when drinking alcohol
Which drugs lead to nephrotoxicity/renal injury?
- "Mycin" type antibiotics
What is a genetic alteration that affects metabolization of warfarin?
- CYP2C9 (people without this enzyme cannot metabolize warfarin, so they should only be given small doses)
What is a gender issue specific to digoxin?
- Digoxin increases mortality in women with heart failure
How do women metabolize alcohol differently than men?
- Women metabolize alcohol more slowly than men
Why are neonates and infants (less than one year old) more susceptible to drug toxicity than older adults?
- Faster gastric emptying time
- Muscle blood flow
- Decreased levels of albumin
- Incomplete development of BBB
- Decreased hepatic function (decreased production of hepatic enzymes for metabolism)
- Decreased renal function
What are nursing considerations for geriatric patients, in terms of pharmacokinetics and pharmacodynamics?
Pharmacokinetics
- Delayed GI motility (absorption)
- Decreased lean body mass and body water
- Malnourishment and albumin
- Declining liver function (poor metabolization of drugs)
- Excretion (declining renal function)
Pharmacodynamics
- Polypharmacy
What is the pathophysiology of heart failure?
- Dilation and hypertrophy of the heart lead to decreased CO, inadequate tissue perfusion, and volume overload.
- Cardiac related factors (HTN, MI)
- Non-cardiac factors (DM, obesity, metabolic syndrome)
What role do beta blockers ("olol" drugs) play in treating heart failure?
- Beta blockers protect the heart from excessive sympathetic activity
What role do ACE-I "pril"/ARB "sartan"/spironolactone play in treating heart failure?
- These drugs block the renin angiotensin aldosterone system (RAAS)
- Either enalapril or valsartan should be used in ALL patients with HF
What role do furosemide, hydrochlorothiazide, and spironolactone play in treating heart failure?
- These diuretics block fluid retention and increased blood volume
- Choice between furosemide and hydrochlorothiazide based on severity of fluid retention and kidney function (both drugs cause hypokalemia)
- Spironolactone can be combined with furosemide
What role do neprilysin inhibitors (sacubitril) play in treating heart failure?
- Neprilysin inhibitors activate the natriuretic system
Which drugs should be discontinued for heart failure patients?
- NSAIDS (due to sodium retention and peripheral vasoconstriction)
- CCBs
What lab test is used to diagnose heart failure?
- BNPs (should be <100)
What kind of drug is digoxin?
- Inotropic agent
Digoxin - what does it do?
- Decreases sympathetic tone (failing heart doesn't have to work so hard)
- Increased renal blood flow (decreases congestion)
- Decreases renin release (decreases angiotensin/aldosterone effects)
- Negative chronotropic (decreases HR)
- Dromotropic (decre
Digoxin - how does it work?
- Inhibition of Na-K ATPase enzyme
- blocks K from entering cardiac myocyte --> blocks Na from leaving --> Na accumulates in myocyte so much that additional Na cannot enter --> because Na cannot enter cell, Ca cannot leave --> Ca accumulates in cell
Digoxin - uses
- Treatment of symptoms of HF (fatigue and exercise intolerance) only in selected patients (d/t its positive inotropic effect)
- Treatment of atrial fibrillation (d/t it's negative chronotropic/dromotropic effects)
Digoxin - nursing considerations
- Very narrow therapeutic range (0.5-(0.8)-2.0 ng/ml)
- Toxic range = > 2ng/ml
- Must be interpreted in presence of potassium (K normal range = 3.5 - 5.0); hypokalemia sensitizes patient to digoxin toxicity (many diuretics cause hypokalemia)--additionally
What is the formula for blood pressure?
- arterial pressure = CO x peripheral resistance
- CO is determined by HR, contractility, BV, venous return
- Resistance is determined by arteriolar constriction
For antihypertensives to work, what must they do?
- Either decrease CO (HR, contractility/SV, BV, or venous return)
OR/AND
decrease peripheral resistance
Which systems in the body help to regulate blood pressure?
- Stimulation of sympathetic baroreceptor B1 and A1
- Renin Angiotensin Aldosterone system (angiotensin 2 = vasoconstrictor; aldosterone = retention of NaCl and secretion/excretion of K)
- Renal regulation of blood volume (reabsorption of NaCl and water,
What are the five stages of hypertension?
Normal: <120/<80
Elevated: 120-129/<80
HTN Stage 1: 130-139/80-89
HTN Stage 2: >140/>90
HTN Stage 3: >180/>120
What are the nonpharmacologic approaches to treating HTN?
- Weight reduction
- DASH eating plan
- Restrict dietary sodium
- Increase physical activity
- Moderation of alcohol
- Stop smoking
What is a special consideration regarding pregnant women and antihypertensives?
Preeclampsia and eclampsia as well as fetal drug exposure
What are predictable side effects of antihypertensives?
- Orthostatic hypotension with dizziness and syncope
- Reflex tachycardia in non-sympatholytic drugs
- Compensatory Na and H2O retention with associated peripheral edema in non-diuretic drugs
- Rebound HTN and HTN crisis with abrupt drug withdrawal
What is the treatment BP goal across antihypertensive medications?
- <130/<80
Hydrochlorothiazide - mechanism of action
- Diuretic
- Blocks sodium reabsorption in the early convoluted tubule --> decreased volume
- Decreases resistance (unknown mechanism)
Hydrochlorothiazide - what is it for
- Hypertension (regardless of age, race, or diabetes mellitus)
Hydrochlorothiazide - side effects
- Hypokalemia
- Hypercholesterolemia
- Hypertriglyceridemia
- Hyperuricemia
- Altered fat metabolism (increase LDL/TG, decrease HDL)
- Hyperglycemia
- Dehydration/hypovolemia
- Hypotension
Hydrochlorothiazide - nursing considerations
- HCTZ is a less powerful diuretic than furosemide; does not work if pt. GFR <15-20
- HCTZ is often combines with other antihypertensives in a single pill to simplify treatment
Lisinopril - mechanism of action
- Inhibits angiotensin converting enzyme (blocks angiotenin II and decreases aldosterone secretion
- This above two things lead to vasodilation and secretion/excretion of Na/H2O and reabsorption of potassium (net effect is decreased BP)
- Also increases b
Lisinopril - what is it for?
- Lowers blood pressure (antihypertensive); especially good for patients with CKD
- Can be used for HF, as it blocks aldosterone (which leads to cardiac remodeling and vascular fibrosis)
Lisinopril - nursing considerations
- Therapy starts with ACE-I (lisinopril); if ineffective, switch to ARB (valsartan)
- ACE-Is are not as effective for African Americans
Lisinopril - side effects
- Hyperkalemia
- Hypovolemia
- Fetal injury
- Cough
- Angioedema (rare)
Valsartan - mechanism of action
- Angiotensin receptor blocker-->inhibits angiotensin II and aldosterone, leading to vasodilation and secretion/excretion of Na/H2O and reabsorption of K. The net effect is decreased BP
Valsartan - what is it for?
- HTN, especially in pt. with CKD; not as effective for African Americans
- HF b/c it prevents cardiac remodeling and vascular fibrosis
Valsartan - side effects
- Hyperkalemia
- Hypovolemia
- Fetal injury
- Cough
- Angioedema (rare)
Valsartan - nursing considerations
- For HTN, pt. typically started on an ACE-I and then switched to ARB (valsartan) if the ACE-I was problematic
Nifedipine - mechanism of action
- Block calcium channels in vascular smooth muscle, resulting in vasodilation of peripheral arteries (decreases resistance --> decreased BP) and coronary arteries (increases blood flow)
Nifedipine - what is it for?
- Primarily indicated for HTN, especially beneficial for African Americans
- Secondary indication is angina pectoris
Nifedipine - side effects
- Flushing
- Dizziness
- Headache
- Tachycardia
- Peripheral edema
Nifedipine - contraindications
- Use with caution if pt. has hypotension, sick sinus syndrome, and second or third degree AV block
Nifedipine - nursing consideration
- Give beta blocker to prevent reflex tachycardia
What are the two important second-line drugs used to treat HTN?
- Metoprolol (beta blocker (targets B1 receptors on heart); decreases HR and contractility, which will lower BP. Not first line for HTN, but very useful for HF)
- Hydralazine (direct acting and powerful vasodilator by an unknown mechanism; ideal for emerg
Which antihypertensives are best for African Americans?
- CCBs
- Diuretics
Which antihypertensives are best for white people?
- All work relatively the same
Furosemide - what does it do?
- Blocks reabsorption of Na/Cl and H2O at the ascending loop of Henle
Furosemide - what is it for?
- Used to treat HTN and fluid overload/edema
- Effective for patients that have low glomerular filtration (<15-20mls/min)
Furosemide - side/adverse effects
- Hypokalemia
- Dehydration/hypovolemia
- Hypotension
- Hyponatremia
- Hyperglycemia
- Hyperuricemia
- Altered fat metabolism (increased LDLs, TGs; decreased HDLs)
- Ototoxicity (hearing loss), especially when paired with "mycin" antibiotics
Furosemide - nursing considerations
- Can be paired with spironolactone to offset hypokalemia
- Effective in patients with low glomerular filtration
What are the primary indications for diuretics?
- Fluid overload/edema
- HTN
- Congestive HF
What are general side/adverse effects of diuretics?
- Hypovolemia and dehydration
- Na/Cl depletion (hyponatremia)
- Hyperkalemia
What are general nursing considerations for diuretics?
- Important to assess pt. fluid volume (1000ml = 1L = 1kg = 2.2lb) and physical changes (mucus mebranes, edema, skin tugur)
- Check orthostatic vital signs and postural changes due to hypotension
- Dose in the morning to prevent nocurtia (nocturia is a le
Spironolactone - what does it do?
- Inhibits aldosterone at the late distal tubule, resulting in mild sodium and water excretion and substantial potassium reabsorption
- Blocks aldosterone receptors on the heart and blood vessels
Spironolactone - what is it for?
- Primary indication is to reduce morbidity and mortality in pt. with congestive heart failure (by blocking aldosterone receptors on the heart and blood vessels; prevents cardiac remodeling and vascular fibrosis); it is one of the first drugs given to pat
Spironolactone - side effects
- Hyperkalemia
- Unpredictable effects given it's chemical structure being similar to the structure of estrogen and testosterone
Mannitol - what does it do?
- Mannitol is a form of non reabsorbed sugar that gets added to filtrate; water is pulled into the tubule by osmotic gradient, leading to significant diuresis
Mannitol - what is it for?
- Powerful diuretic; primary indication is to protect kidneys during low flow states
- Secondary indication is to treat intracranial HTN and increased intraocular pressure
Mannitol - nursing considerations
- Vascular osmotic effect precedes renal diuretic effect; therefore, mannitol is contraindicated in heart failure
Mannitol - side effects
- Can cause edema (d/t vascular osmotic effect; veins become overfull, increasing hydrostatic pressure and pushing fluid into interstitial space)
- Hypovolemia/dehydration
- Headache, nausea, vomiting, fluid and electrolyte imbalances
What are the primary components of blood clots?
- Fibrin strands
- Platelets
What is the main concern regarding use of anti-platelets, anticoagulants, and thrombolytics?
- Bleeding
What is the main target for anti-platelet drugs and why?
- Glyocoprotein IIb/IIIb receptor. This is because the GIIb/IIIb receptor, when activated, allows platelets to stick together by using fibrinogen as a tether
What is the sequential pathway by which GIIa/IIIa is activated?
Arachidonic acid --> (cyclooxygenase-->) Thromboxane A2 --> GIIa/IIIa activation
Aspirin - mechanism of action
- Aspirin blocks cyclooxygenase (COX), which prevents the activation of GIIa/IIIa
Aspirin - what is it for?
- Arterial atherosclerotic disease, because it prevents platelet aggregation near atherosclerotic lesions
- Secondary indications: reduce fever (antipyretic) and pain (analgesic) by inhibiting prostaglandins
Aspirin - how is it dosed?
- Anti-platelet effect = 81-325mg/day
- Antipyretic/analgesic = 325-640mg/4hrs
Aspirin - nursing considerations
- Aspirin irreversibly binds to platelets; use must be discontinued 7-10 days before any invasive procedure
- Aspirin blocks production of prostaglandins E2 and I2, which protect the gastric mucosa. Lack of these prostaglandins leads to gastric ulceration
Aspirin - side effects
- Damage to gastric mucosa (due to inhibition of prostaglandins E2 and I2)
- Bleeding/bruising
- Salicylism (Tinnitus)
Aspirin - contraindications
- Should not be given to children under 12; could develop Reye's syndrome (inflammation of brain and liver) if they have a viral infection while taking aspirin (only exception is Kawasaki disease)
What type of drug class do ticlopidine and clopidogrel fall into?
- These drugs are antiplatelets
Clotting factors are activated by which two pathways? Where do these two pathways join? What happens then?
- Intrinsic and common
- Pathways merge at clotting factor Xa, at which point, thrombin converts fibrinogen to fibrin to form thef strands of the mature clot
How does the body fight against clots?
- Plasminogen is converted to plasmin, which destroys the fibrin strands of the clot
Heparin - what does it do?
- Activates thrombin III, which inactivates activated clotting factors in the common and intrinsic pathways
Heparin - what is it for?
- Two main indications:
1. Acute thromboembolic disorders (IV administration; bleeding times closely monitored)
--- Acute MI
--- Ischemich thrombotic or embolic stroke
--- DCT and/or PE
2. Post-operative prophylaxis against formation of DVT (SQ administra
Heparin - nursing considerations
- Protein bound, does not cross placenta, so good for pregnant women
- Extremely important to follow bleeding times when administered via IV. Lab test is Activated Partial Thromboplastin Time (aPTT): normal - 40s, therapeutic - 60-80s, overtreatment = >80
Heparin - side effects
- Bleeding (10%)
- Heparin induced thrombocytopenia (<5%)
What is the difference between heparin and enoxaparin?
- Enoxaparin is the low molecular weight alternative; it is easier to administer and does not require bleeding tests
Warfarin - how does it work?
- Inactivates hepatic vitamin K dependent clotting factors VII, IX, and X, as well as prothrombin
Warfarin - what is it for?
- Used as a long-term prophylaxis/treatment of thromboembolic disorders, including
--- Venous thrombus and PE
--- Artificial anatomic structures that arte thrombogenic (valves, joints)
--- Atrial fibrillation (prevents stasis of blood in atria)
Warfarin - nursing considerations
- Oral administration only
- Takes up to three days to start working; usually started alongside heparin (heparin is discontinued once warfarin takes effect)
- Protein bound and crosses the placenta (bad for pregnant patients--it is a terotagen)
- Laborato
What are dabigatran and apixaban used for? How do they work?
- Both drugs are oral replacements for warfarin
- Clotting tests are not needed to monitor effectiveness
- Fewer drug interactions than warfarin
- Expensive
- Dabigatran MOA = thrombin inhibition
- Apixaban MOA = clotting factor Xa inhibition
What are thrombolytics used for?
- Used to reestablish blood flow in emergency thrombotic situations when time is essential, including:
--- Acute MI
--- Cerebrovascular (ischemic) accident
- They work by activating plasmin
What are some general nursing considerations when using thrombolytics?
- There is a high risk of bleeding, so use is reserved for specialty areas
- Timely clot degradation and tissue reperfusion will prevent tissue necrosis (MI = best outcome if given w/i 2hr, will not work after 12hr) (Ischemic stroke = must administer with
Alteplase - what does it do?
- Alteplase is a synthetically derived tissue plasminogen activator (tPA) that converts plasminogen to plasmin, which dissolves fibrin in clots
Alteplase - what is it used for?
- Used during life-threatening clotting situations (acute MI, acute ischemic stroke, massive PE, declotting a central line)
Alteplase - nursing considerations
- IV therapy only; rapid onset and short half life
- Must use early to prevent tissue necrosis (MI = 2hr-12hr, Ischemic stroke = 3-4.5hr)
What are other names for the parasympathetic nervous system?
- Cholinergic
- Muscarinic
What is another name for the sympathetic nervous system?
- Adrenergic
What are the functions of the parasympathetic nervous system (AKA cholinergic, AKA muscarinic)?
- Rest, digestion, secretion
What is the neurotransmitter associated with the parasympathetic nervous system?
- Acetylcholine
Which receptors are used in the parasympathetic nervous system?
- Muscarinic
What are the target organs of the parasympathetic nervous system?
- Eyes, heart, lungs, bladder, GI tract, sweat glands, sex organs
What are the functions of the sympathetic nervous system (AKA adrenergic)?
- Fight and flight
Which neurotransmitters are associated with the sympathetic nervous system?
- Epinephrine, norepinephine, and dopamine
Which receptors are used in the sympathetic nervous system
- Alpha1 (eyes, peripheral arteries and veins, prostate and bladder, male sex organs)
- Beta1 (heart, kidney)
- Beta2 (arterioles of heart, lung, and skeletal muscles; bronchi, liver, uterus)
Albuterol - mechanism of action
- Selective beta2 agonist
Atropine - mechanism of action
- Non-selective muscarinic antagonist (blocks effects of the parasympathetic nervous system; mimics effects of the sympathetic nervous system)
Bethanechol - what does it do?
- Agonizes muscarinic receptors of the urinary system, specifically the detrusor, trigone, and urinary sphincter
Bethanechol - what is it for?
- Empties the bladder; indicated for urinary retention (to check for effectiveness, scan bladder--it should be empty)
Bethanechol - side effects
- It is not selective for the urinary system, so it can have broader effects, such as: bradycardia-->hypotension; salivation, diarrhea; bronchoconstriction and airway secretions
Bethanechol - nursing considerations
- Contraindicated in pt. with urinary stones/tumors, intestinal tumors/obstruction, and recent bowel surgery (fragile surgical site)
- Have facilities readily availabel
- Notify provider of excess muscarinic activity
Pyridostigmine - what does it do?
- Cholinesterase inhibitor (prevents the breakdown of ACh at the NMJ)
Pyridostigmine - what is it for?
- Indicated for patients with Myasthenia Gravis (MG), which destroys ACh receptors at the NMJ. Particularly affects the eyes/mouth (95%) and head (60%)
- Pyridostigmine saturates the NMJ with ACh, ensuring all available ACh receptors are fully agonized, w
Pyridostigmine - side/adverse effects
- Myasthenic crisis (undertreatment): severe muscle weakness (ptosis, difficulty chewing and swallowing); treat by giving more pyridostigmine
- Cholinergic crisis (overtreatment): severe muscle weakness & issues with rest, digestion, and secretions (decre
Pyridostigmine - nursing considerations
- Before administering, assess pt. ability to swallow; if unable to swallow, give paternally
- Pt. should make determination of dosage adjustments based on symptoms
Epinephrine - what does it do?
- Non-selective adrenergic agonist (a1, b1, b2)
- Effects/side effects are predictable based on MOA
Epinephrine - what is it for?
- Many indications based on MOA (a1 = raise BP, control superficial bleeding, delay absorption of local anesthetic; mydriasis); (b1 = increase HR, increase cardiac responsiveness to defibrillation); (b2 = bronchodilation)
- Drug of choice for anaphylaxis,
Epinephine - side/adverse effects
- Hypertension
- Extravasation and necrosis
- Light intolerance/photophobia
- Tachycardia
- Increased myocardial oxygen demand
- Hyperglycemia
What do the following drugs have in common? Epinephrine, norepinephrine; isoproterenol; dopamine; dobutamine; phenylephrine; albuterol
- All of these drugs are adrenergic agonists
--- Epinephrine = a1, b1, b2
--- Norepinephrine = a1, b1
--- Isoproterenol = b1, b2
--- Dopamine = a1, b1
--- Dobutamine = b1
--- Phenylephrine = a1
--- Albuterol = b2
Metoprolol - what does it do?
- Antagonizes cardiac b1 receptors, which leads to: reduced HR, reduced force of contraction; reduced conduction speed
- Some non-cardiac effects: reduced renin angiotensin aldosterone (RAA); reduced glycogenolysis
Metoprolol - what is it for?
- Tachycardia
- Ischemic heart disease: angina and acute coronary syndromes (because it reduces myocardial oxygen demand by reducing BP, HR, and contractility)
- Heart failure (reduces the work of the heart)
Metoprolol - side/adverse effects
- Bradycardia and conduction block
- Hypotension
- Hypoglycemia (metoprolol also blocks b2 receptors)--can lead to hypoglycemic unawareness (decreased fight or flight response)
Metoprolol - nursing considerations (including when to administer/hold and goals)
- Hold for BP <90/60 or HR <50
- Desired outcome = HR >50 and less than 70-80, BP at goal (<130/<80); plus relief of chest pain or angina symptoms and decreased progression of HF
What do propanolol, metoprolol, and carvedilol all have in common?
- These drugs are all beta blockers (propanolol blocks b1 and b2; metoprolol blocks b1 and b2; carvedilol blocks a1 and b1)
What do neostigmine, pyridostigmine, and rivastigmine all have in common?
- They are all cholinesterase inhibitors
What do "phrine" and "terol" drugs have in common?
- They are adrenergic agonists ("terol" = b2 agonist; "phrine" = various adrenergic receptor agonists)
What do "azosin" and "olol/ilol/alol" drugs have in common?
- They are all adrenergic antagonists ("azosin" = a1 antagonist; "olol/ilol/alol" = b1 nonselective antagonists)