Real Final Flashcards
antimicrobial agent (AMA)
substance that kills or inhibits the growth of microorganisms such as bacteria, fungi, or protozoans
antibiotic agent
an antibacterial agent kills or inhibits the growth of bacteria
choosing antibiotics
are chosen based on type of bacteria, not strength
find the right drug not the strongest
will be able to tell if it is the “right antibiotic” within 24 hours -> people will start to look better, and WBC should be going down
ceph___ or cepf___
cephalosporins
___cillins
penicillins
actions of abx drugs *
- affect target organism’s structure, metabolism, or life cycle
- goal is to eliminate the pathogen -> bactericidal = kill bacteria, bacteriostatic = slow growth of bacteria
- may be used for prophylactic treatment of people with suppressed of compromised immune systems
important abx considerations*
- make sure pt knows to finish all abx -> if not followed, can lead to the development of drug-resistant bacteria
- do not share
- keep away from children (safety lid and lock)
- educate pt that abx will decrease oral contraceptive pills and hormonal IUD -> use a back up birth control
- teach when to take with food or when to avoid certain foods
- teach clients to wear medic-alert bracelets if allergic
- inform about side effects -> skin, teeth, tendons, ears, kidneys -> assess for renal and hepatic function (especially in elderly) = 2.2lb or 1kg per day of weight gain
- assess for persistent diarrhea in children
- tell pt. to take probiotics 1-2x/day to counter antibiotic
- monitor for hypersensitivity with first dose
- make sure pt know S+S of allergic reaction
- most antibiotics best taken on an empty stomach
penicillins
most effective against gram-positive bacteria
beta-lactamase or penicillinase is the enzyme that allows bacteria to be resistant to penicillin
new penicillins are penicillinase-resistant and there are combination drugs with beta-lactamase inhibitors
kill bacteria by disrupting their cell walls
ex. oxacillin, cloxacillin, penicillin G potassium
role of nurse with penicillins*
- assess previous drug reactions to penicillin
- assess animal products exposed to antibiotics
- avoid cephalosporins if client has history of severe penicillin allergy
- monitor for hyperkalmia and hypernatremia -> increased risk in pt with diabetes mellitus or on dialysis (kidneys)
- monitor cardiac status, including ECG changes
cephalosporins
similar in structure and function to penicillins
broad spectrum activity against gram-negative organisms
have a beta-lactam ring and are bactericidal
cross sensitivity with penicillins -> 5-10% of the population
are divided into 4 generations -> 1st and 2nd generation of cephalosporins will no cross the blood brain barrier * if treating meningitis must be a a 3rd or 4th generation
inhibits cell wall synthesis
ex. cefazolin
role of nurse with cephalosporin therapy *
assess for presence or history of bleeding disorders
-> cephalosporins may reduce prothrombin levels
assess renal and hepatic function -> especially in elderly
assess for persistent diarrhea in children
avoid alcohol -> will cause vomiting, creates an disulfiram (Antabuse) like reaction (med used to treat alcoholism, creates unpleasant side effects)
tetracyclines
broadest spectrums of any abx class -> effective against gram-positive and gram-negative organisms
treats Rocky Mountain spotted fever, peptic ulcers caused by H. pylori, and chlamydial infections
ex. doxycycline, tetracycline
role of nurse tetracycline therapy*
- tetracyclines decrease effectiveness of oral contraceptives -> use back up birth control while taking med
- increases potential for vaginal yeast infections while taking oral contraceptives and tetracylines
- use in caution in clients with impaired kidney or liver function
- take on empty stomach, increases absorption
- may cause photosensitivity -> wear SPF 100
- do not take with milk products, iron supplements, magnesium containing laxatives, or antacids (fluoros)
- watch for supra infection such as pseudomembranous colitis
acronym for tetracyclines adverse effects
tetracyclines = teeth and tan lines
teeth discolouration and photosensitivity
macrolides
safe alternative to penicillin
broad spectrum so superinfections may occur
-mycin
ex. erythromycin, clarithromycin
EES
EES = erythromycin estolate
however in vernal EES represents all macrocodes
EES interacts with the liver -> CYP
role of nurse in macrolide therapy*
- watch the liver with EES
- multiple drug-drug interactions occur with macrocodes -> CYP
- monitor -> exacerbates heart disease
- causes a metallic taste in mouth
aminoglycosides
reserved for serious systemic infections caused by aerobic gram-negative bacteria
ex. gentamycin, tobramycin
adverse effects of aminoglycosides*
- more toxic than most antibiotics
- have potential to cause serious adverse effects
-> ototoxicity - worse if given with Lasix (furosemide)
-> nephrotoxicity - worse if given with Zovirax (acyclovir)
-> neuromuscular blockage - including respiratory paralysis - last names don’t work with this family and macrolides
fluoroquinolones*
- decreased by 90% if taken with multivitamins or minerals such as calcium, magnesium, iron, or zinc (tetras 50%)
- IV is the same as taking PO, therefore easy to transition home
- don’t give to teenagers or athletes!!! risk of tendon rupture
- can cause C.diff
- QT prolongation/arrhythmias (IRR vs RRR)
ex. ciprofloxacin, levofloxacin, moxifloxacin
role of the nurse fluoroquinolone therapy*
- decreased WBC
- monitor pt with liver and renal dysfunction
- watch for liver failure
- teach that drugs may cause dizziness and lightheadedness
- advise against driving or performing hazardous tasks while taking med
**
- Norfloxacin may cause photophobia -> light hurts eyes
- teach that drug (Cipro specifically) may affect tendons especially in children
- do NOT give to athletes
- monitor for dysrhythmias
- crosses into breast milk
sulfonamides*
- widespread use had lead to increased resistance and decreased usage/prescription (Rx)
- used in a combination to treat UTIs
- anti-inflammatory properties of sulfonamide component can help with RA and ulcerative colitis
- teratogenic (birth defects)
- do not take while breastfeeding or pregnant
allergic reactions and sulphonamides*
- caution reaction to a sulfonamide abx could mean allergy to other sulfonamide meds
examples -> - diabetes mellitus sulfonylureas - glyburide (glynase, diabeta) and glimepiride (Amaryl)
- NSAIDS - celecoxib
- certain diuretics - furosemide and chlorothiazide
- IBD meds - sulfasalazine
allergy to these meds may cause sensitivity to abx -> caution with 1st dose
trimethoprim-suldamethoxazole *
a sulfonamide
aka. tmp/smz
Bactrim, Septra, Cotrimoxazole
mechanism of action = to kill bacteria by inhibiting bacterial metabolism of folic acid
primary use = broad spectrum for UTIs, pneumocystis carinii pneumonia, shigella, and bronchitis
adverse effects = skin rashes, N/V, agranulocytosis or thrombocytopenia (use cautiously with pernicious anemia), photosensitivity
role of nurse in sulfonamide therapy*
- assess for anemia or other hematological disorders (HgB and platelets)
- assess renal function, sulfonamides may increase risk for crystalluria -> encourage increased fluids
- ensure if on oral contraceptive pills that pt uses alternate form of birth control
- teach how to decrease effects of photosensitivity
- contraindicated in pt with history of hypersensitivity to sulfonamides -> can induce skin abnormality called Stevens-johnson syndrome
carbapenems
used for tx of infections known or suspected to be caused by a multi-drug resistant (MDR) bacteria
used primarily in hospitalized pt
low incidence of adverse effects
don’t interchange IV and IM
glycopeptides
- vancomycin (PO/IV)
- breaks down amino acid wall
- used to treat C-Diff
glycosamides
- clindamycin (IV only)
- can cause C. Diff
Vancomycin *
mechanism of action = bactericidal, inhibits cell wall synthesis
primary use = reserved for severe or resistant gram-positive infections, effective for MRSA infections, used to treat C. Diff
adverse effects = ototoxicity, nephrotoxicity (NOT hepatotoxic), red man syndrome, confusion/hallucinations, anaphylaxis
acquired resistance*
when antibiotics are used, they destroy sensitive bacteria
insensitive (mutated) bacteria remain
-> free from competition from bacteria that were sensitive to the drug, the mutated bacteria thrives
-> the pt now develops an infection that is resistant to conventional therapy
-> this resistant bacteria can be transmitted to others
Super bugs*
aka. antibiotic resistance organisms (ABO)
-> carbapenem-resistant enterobacterioaceae (CBO/CBE) -> PCNs and cephalosporins are useless
-> Methicillin-resistant staphylococcus-aureus (MRSA) -> will not respond to fluroquinolones, macrocodes, ahminoglycosides, or tetracyclines***
To-many-fucking-antibiotics
-> Vancomycin-resistant entoerocci (VRE)
-> vancomycin-resistant staphylococcus-aureus (VRSA or VISA)
teaching about acquired resistance*
when an organism is resistant to more than one drug = multi drug resistant
- teach pt to take full course of abx, even when they feel better
- do not save antibiotics or share with others
- antibiotics don’t treat viral infections
- over prescribing has lead to ARO
- C&S prior to treatment is preferable
C&S testing*
may reduce resistance as you will know you are using the right abx and not potentially exposing the body to an abx that is not treating the correct bacteria -> leads to increased resistance
C&S testing may take days or weeks for results and tests several abx for effectiveness
superinfections*
a secondary infections that occur when too many host flora are killed by an abx
microorganisms multiply -> more food for bad bacteria
S+S
- diarrhea (pseudomembranous colitis or c. diff)
- bladder pain and painful urination (e.coli/UTI)
- abnormal vaginal discharge (yeast - Candida)
- red rash with satellite lesions (yeast - candida)
ex. thrush, c.diff
all abx’s will cause
N/V/diarrhea
foods to avoid when on abx
Calcium, iron for tetracyclines
magnesium, aluminium
important considerations for abx*
- inform pt about side effects -> skin, teeth, tendons, ears, kidneys
- tell pts to take probiotics to counter antibiotic
- teach pt to wear medic-alert bracelets if allergic
- make sure pt knows S+S of allergic reaction
characteristics of fungal infections *
- not easily transmitted through casual contact -> they love dark, moist environments and lots of sugar
-serious fungal infections are uncommon in people with healthy immune defences
- immunocompromised pt. (DM, HIV, cancer) -> systemic fungal infections may be rapidly fatal and may experience frequent fungal infections and require aggressive pharmacotherapy
- tx may require weeks to months of therapy due to resistance.
mycosis
disease caused by a fungus infection
two classifications -> superficial and subcutaneous (topical meds), and systemic (oral meds)
amphotericin
systemic anti fungal med
for severe infections
administered over 2-6 hours -> start a second IV because fluids have to run constantly while administering amphotericin
SE = acute fever, chills, vomiting, anorexia, headache, phlebitis, potassium deficiency, electrolyte imbalance
Serious adverse effects = cardiac arrest, ototoxicity, nephrotoxicity, hepatotoxicity, anaphylaxis, dysrhythmias, blood abnormalities.
if given to quickly can lead to shock
dont give if BUN over 40mg/dL or if serum creatinine over 3mg/dL -> kidney function
azoles
antifungals
broad spectrums
can be administered PO and have good safety profile
systemic azoles have a similar spectrum to ampotericin B but less toxic and given PO
SE = N/V/diarrhea
be aware in pt with hepatic and renal impairment -> CYP
monitor serum levels
Nystatin
anti fungal -> superficial type
used for candida infections (thrush) of the vagina, skin, mouth, throat, and GI
adverse effects -> minor skin irritation and burning (topical), contact dermatitis (topical), diarrhea/N/V (PO)
contraindications -> hypersensitivity to the drug, pregnancy and lactation
Nystatin considerations*
drug interactions = unknown
treatment of overdose = symptomatic
considerations:
- Hx and assessment -> observe for improvement and report persistent infections
- avoid occlusive dressing or ointment on moist, dark areas of the body
- teach pt to avoid sharing shoes, towels, or personal objects -> especially with candida
drugs similar to nystatin*
griseofulvin -> give PO only (ineffective topically)
used to tx skin infections such as jock itch, athletes foot, and ringworm, and fungal infections of scalp, finger/toenails
reserved for cases with hair, nail, or large body surface involvement
side effects = photosensitivity, SJS, urticaria (rash), dizziness, decreased effecting of oral contraceptive pills, alcohol = disulifiram-like (Antabuse) reaction
when to check blood glucose*
- if the pt is not feeling well
- if pt is back from an exam and didn’t get breakfast
- if pt is sweating or confused
- if in doubt
- watch for hypoglycemia with beta blockers -> they mask the S+S of hypoglycemia
somogyi effect
rebound effect with hyperglycemia in the morning
overdose of insulin leads to hypoglycemia due to long acting insulins or no snack before bed
blood sugar drops while sleeping and the body releases hormones to counteract the drop
results in hyperglycemia when waking up
dawn phenomenon
hyperglycemia present in the morning
hormones are released that trigger the liver to put out glucose in predawn hours -> not enough insulin in the body to counter regulate blood sugar rise
growth hormone/ cortisol are possible factors
rapid acting insulin*
ex. lisper (Humalog), aspart (novorapid), glulisine (apidra)
onset = < 15 min -> give 0-15 min before meal
peak = 30 min to an hour -> best time to be eating
duration = 3-4 hours.
short acting insulin*
ex. regular (humulin R or novolin R)
Onset = 30 min to a hour -> give 30 min before a meal**
peak = 2-3 hours
duration = 8 hour
regular insulin is the only one that can be given IV -> to treat DKA or HHNK **
used in gestational diabetes*
adverse effects of regular (short acting) insulin *
- irritation at injection site
- lipodystrophy
- weight gain
serious adverse effect
- hypoglycemia
- rebound hyperglycemia
- hypokalemia
insulin therapy considerations*
- medicine hx -> herbs and dietary supplements, noting any meds that could alter the affects of insulin
ex. - garlic, black cohosh, bitter melon, bilberry, ginseng, rosemary, cocoa, sulfonlureas, MAOIs, steroids, alcohol, salicylates, furosemide, ACE inhibitors, thiazide diuretics
- assess alcohol intake and blood glucose levels
- ensure pt has consumed or has food to eat to prevent a hypoglycaemic reaction -> caution when sending pt off to procedures
- administer only regular insulin IV
- assess pt knowledge of insulin therapy, diet, exercise, and how they impact serum glucose levels
administering insulin*
- DO NOT administer when blood glucose levels are less than 4 mmol of if pt has signs of hypoglycemia
- rotate injection sites weekly to prevent lipodystophy
- check periodic hemoglobin A1C levels
- assess pt for S+S of long-term diabetes complications -> eyes, heart, kidneys, feet
role of nurse in insulin therapy*
- be familiar with onset, peak, and duration of prescribed insulin*
- be aware of important aspects of each specific insulin *
- not all types of insulin are compatible -> some can’t be mixed into a single syringe
- when mixing insulins clear must always be drawn up first*
- know signs and symptoms of hypoglycemia and hyperglycemia*
considerations for all oral anti diabetics meds*
- monitor BG for hypo/hyperglycemia
- check for S+S of illness or infection
- watch liver function
- assess for adherence to therapy and ability for self-care
- sulfonylureas contraindicated in women who are pregnant or breast feeding, and in people with renal or liver disease
- second generation sulfonylureas have fewer drug-drug interactions
sulfonylureas*
an oral anti diabetic med
- increase insulin release from pancreas
- increased sensitivity to insulin receptors
- decreased chance of prolonged hypoglycemia
- 10% experience decreased effectiveness after prolonger use
- most SE are minor and GI related
ex.
glipzide
glyburide
glimepiride
contraindications for sulfoylureas*
- sensitivity to sulpha drugs or thiazide diuretics
-renal or hepatic disease - if used during pregnancy, discontinue at least 1 month before delivery
sulfonylureas drug interactions*
- alcohol
- oral anticoagulants, MAOIs, probenecid, sulfonamides
- chloramphenicol, salicylates, clofibrate
- rifampin
- thiazides/sulfonamide bades drugs
- ginseng, garlic, black cohosh, juniper berries, fenugreek, coriander, dandelion root
biguanides*
- decrease glucose production by the liver
- increase insulin sensitivity at tissues
- improve glucose transport into cells
- do not promote weight gain
- usually first line treatment
- 6-12 weeks to reach therapeutic effect
- needs to be held 48 hours prior and 48 hours after a pt needs contrast dye to prevent lactic acid build up
only drug is metformin
biguanades contraindications *
- impaired renal function*
- heart failure, liver failure, history of lactic acidosis
- concurrent serious infection
- any condition that predisposes pt to hypoxeima
- anemia, diarrhea, vomiting, dehydration, fever, gastroparesis, GI obstruction
- hyperthyroidism*, pituitary insufficiency, trauma
- pregnancy and lactation
alpha 1
periphery -> decreases blood flow to fingers, toes, penis, nose
pupils
pee
alpha 2 receptors
decrease BP, HR, NE release, causes vasoconstriction (less than alpha 1 receptors), decreases insulin secretion, and causes platelet aggregation
adrenergic
an umbrella term for beta and alpha receptors
Beta 1
heart
beta 2 receptors
lungs and uterus
sympathomimetic
catecholamines
- adrenalin (epinephrine)
- noradrenalin (norepinephrine)
- dopamine
parasympathomimetic
acetylcholine
cholinergic meds
“wet as an ocean”
possible SE
- slowed HR
- decreased contractility
- drop in BP
- pupil constriction
- increased digestion
- bronchial constriction
uses for cholinergic meds*
- neurogenic bladder
- urinary retention
-BPH - glaucome
- myasthenia graves
- alzheimer’s
S+S of cholinergic toxicity*
“SLUDGE”
salivation
lacrimation (flow of tears)
urinary incontinence
diarrhea
GI cramps
emesis
physostigmine
used as an antidote for anticholinergic poisoning (atropine)
anticholinergic meds*
“dry as the desert”
possible SE= dry mouth, decreased nasal mucous, urinary retention, increased HR, bronchial dilation, pupil dilation
ex.
atropine
scopolamine
benxotropine
dicylomine
anticholinergics are to be used cautiously with the geriatric population -> especially in males with BPH and urinary retention
atropine
anticholinergic
reversal drug for cholinergic overdose
adrenergic agonists
kick the bear
nonselective adrenergic agonist = epinephrine
alpha agonist = phenylephrine
beta agonist = iosproterenol
may act directly by binding to adrenergic receptors or indirectly by increasing the amount of norepinephrine at synapses
classified as catecholamines or noncatecholamines
catecholamines*
adrenergic agonists
- short duration of action
- destroyed rapidly by MAO and COMT (comt is an enzyme in the intestinal tract that degrades catecholamines like dopamine, epinephrine, and norepinephrine)
- NO PO -> must be parenteral or inhalation due to COMT in the GI tract
- does not cross BBB
are bear drugs
noncatecholamines *
adrenergic agonists
- can be taken PO
- not destroyed as rapidly as catecholamines
- better able to enter brain and affect CNS
nonselective adrenergic agonists
activate both alpha and beta receptors and are used to treat bronchospasm, cardiac arrest, and hypotension
alpha 1 receptor agonists
generally prescribed fr nasal connection and hypotension
may be used to dilate the pupil during eye exams
alpha 2 receptor agonists
prescribed for treatment of hypertension and act through non-autonomic mechanisms
beta1 receptor agonists
HEART
critical care drugs -> epinephrine, NE, dopamine
used for heart attack, heart failure, shock
beta2 receptor agonists
lungs and uterus
- used to treat asthma
- reduce preterm labor contractions of uterus
beta 3 receptor agonists
works on adipose tissue, skeletal muscle, bladder, and gallbladder
- regulation of lipolysis and thermogenesis
- some anti-stress effects and use in overactive bladder
epinephrine
nonselective adrenergic agonist, catecholamine
fight or flight response
adverse effects
- nervousness
- tremors
- tachycardia
-dizziness
- headache
- stinging at site
serious adverse effects
- HTN
- dysrhythmias
- pulmonary edema
-cardiac arrest
epinephrine considerations *
- assess for underlying problem or preexisting conditions
- history and prognosis -> vital signs
- closely monitor resp status
- use cardiac monitor/resuscitation equipment
- monitor BP closely
- inform prescriber of changes in intake and output
- monitor for hyperglycemia (stress response increase blood sugar) -> insulin gtt
- examine ocular and nasal mucosa
- protect from light -> extreme heat and cold will denature it
- store api-pens in a dark place
of pt is on epinephrine they must be on telemetry
norepinephrine
ex. levophed -> nearly dead, life saving med
does not activate beta3 receptors
phenylephrine contraindications *
an alpha 1 agonist
is an antihypotensive and nasal decongestant
contraindications
- severe HTN
- preexisting bradycardia
- advanced CAD
- nitroglycerin
- narrow-angle glaucoma
- hyperthyroidism
- diabetes
phenylephrine overdose and considerations*
alpha 1 agonist
tx of overdose
- phentolamine
- anti-dysrhythmic drugs
considerations
- examine IV sites frequently
- advise pt to remove contact lenses
- dark eye protection after ophthalmic administration
- avoid caffeine -> with all adrenergic agonists
- contact HCP is palpitations or jittery/nervousness.
muscarinic antagonists uses *
ex. Belladonna -> natural source of alkaloids with anticholinergic activity
uses
- GI disorders such as IBS
- ophthalmic procedures
- cardiac rhythm disorders
- chemo induced diarrhea
- adjuncts to anesthesia -> decrease secretions
- asthma and COPD -> bronchodilation effects
- antidotes for poisoning or overdose
- urge incontinence (overactive bladder) -> watch with BPH
- Parkinson disease
helps with spasms -> after prostate or bladder surgery
-> after chemo diarrhea, induces spasms
cardiac selective meds
Beta 1
don’t have to worry about asthmatics -> won’t constrict airway
muscarinic antagonists adverse effects*
there is a relatively high incidence of adverse effects
ex. atropine
- urinary retention
- xerostomia (dry mouth)
- tachycardia
- CNS stimulation
- dry eyes
- photophobia
- urinary retention in BPH
anticholinergic syndrome*
aka overdose
- dry mouth, difficulty swallowing
- visual changes, blurred vision, photophobia
- agitation and hallucinations
antidote is physostigmine -> generally only administered to pt showing severe symptoms
nicotinic antagonists: neuromuscular blockers*
works at motor end plate of muscle
-> causes release of Ach to travel to receptors on skeletal muscle = muscle contraction
continuous depolarized state in which calcium does not return to its storage depots = sustained muscle contraction and then flaccid muscle and paralyzes pt necessary for certain surgical procedures
depolarizing = succinylcholine (watch for contraction to signal success, restlessness indicates no success)(used during short medical-surgical procedures)
non depolarizing = tubocararine (lasts longer, used during longer surgical procedures)
succinylcholine *
paralysis preceded by contraction
is fast acting and pt will recover quickly
muscles will be sore -> like clenching a muscle for a long time
succinylcholine uses*
- surgical anesthesia
- pseudocholinesterase
- relaxes abdominal muscles or for relaxation prior to intubation
- induces relaxation in less than 1 minute
- muscle strength returns quickly discontinuation of the drug
- pt can still feel pain and is aware of their surroundings -> use benzes and opioids
adverse effects succinylcholine*
- complete paralysis of diaphragm/intercostal muscles -> watch for respiratory paralysis
- tachycardia
- hypotension
- urinary retention
serious adverse effects
- malignant hyperthermia -> muscles rigid, skin hot
- respiratory depression
- apnea
- dysrhythmias
black box warning
- children with congenital musculoskeletal diseases at greater risk for cardiac arrest
- no way to predict which pt at risk
tubocurarine*
nicotinic antagonist
non depolarizing neuromuscular blockers (NDNBs)
tubocurarine is the prototype -> 9 others in the class
used to relax skeletal muscles during surgical procedures -> causes flaccid paralysis
does not cause sedation, analgesia, or loss of consciousness -> must use benzos, propofol, and opioids
alpha adrenergic antagonists
alpha receptors are located on smooth muscle of the heart, GI and GU systems, and the brain
blocking of alpha receptors dilates blood vessels -> decreased BP
decrease peripheral resistance and decreases preload
first dose phenomenon*
when SNS is blocked the PNS predominates -> causes hypotension, orthostatic hypotension due to decreased blood flow to the brain and may cause syncope
prevention by initial therapy given at low doses and usually given at bedtime
reflex tachycardia and nasal congestion also occur
nonselective alpha blockers
ex. phentolamine and phenoxybenzamine
activate alpha 1 and alpha 2 receptors
high incidence of side effects like hypotension (and compensatory tachycardia), N/V/diarrhea, increased urination, and erectile disfunction
selective alpha blockers
greater treatment of HTN, but never first line option
selective alpha1 blockers work on arterioles and veins
ex.
- doxazosin
- prazosin
-terazosin
selective alpha 1 blockers*
- block peripheral catecholamines
- work on arterioles -> block vasoconstriction on vascular smooth muscle (after load) which lowers BP directly
- works on veins -> block vasoconstriction which decreased venous return (preload) to hear and lowers BP indirectly
- alpha blockers can be used concurrently with other drugs like diuretics to decrease BP
relax smooth muscle of bladder (detrusor) and prostate -> increases urine flow
alpha blocker = severe HTN
therapeutic uses of selective alpha 1 blockers*
- benign prostatic hyperplasia
-> two selective agent used in BPH - alfuzosin and tamsulosin
alpha1 blockers don’t cure the condition -> surgery needed
- pheochromocytoma (small tumour of adrenal medulla -> causing irregular secretion of epi and NE) -> excessive secretion of catecholamine causes severe HTN
- HTN
-> alpha1 blockers are used to treat severe HTN - Raynauds disease
beta-adrenergic antagonists*
selective:
- block only beta1 receptors
- cardio selective
- fewer non cardiac side effects
- little effect on bronchial smooth muscle
- can safely be given to clients with asthma and COPD
nonselective:
- block beta1 and beta2 receptors
- produce more side effects than selective beta 1 antagonists
- serious side effect is bronchoconstriction -> caution in pt with COPD and asthma
therapeutic uses of beta-adrenergic antagonists*
- most therapeutic actions relate to the CV system
- slow conduction velocity through AV node -> decreased HR (chronotropic) and decreased force of contractions (inotropic)
- during stress/exercise prevents normal sympathetic stimulation to heart
- caution when administering CCBs concurrently as may potentiate heart failure
adverse effects of beta blockers*
- prevents hyperglycaemic effect of catecholamines
-> dangerous in pt with DM - cause hypoglycemia and can masks S+S of it - beta blockers decrease amount of free fatty acids available during metabolic stress
- bronchoconstriction -> cannot be used in pt with COPD, asthma
- rebound cardiac excitation may occur if beta blockers are withdrawn abruptly -> educate pt to never stop without talking to HCP first
propranolol
non-selective beta blocker
used for
- HTN
- angina pectoris
- dysrhythmias
- migrane prophylaxis
- MI prophylaxis
side effects
- N/V/D
- CNS
- bradycardia
contraindications
- bradycardia
- hypotension
- 2nd and 3rd degree heart block
- HF
- COPD/asthma
- diabetes
- reduced renal output
- cardiogenic shock
propranolol considerations**
- monitor VS q15min - q1hr
- hx and prognosis -> assess for asthma and COPD
- review lab tests for kidney, liver, hematologic, and cardiac function
- watch for ADRs in older adults and in pt with impaired renal fuction
- monitors I/O and take daily weights -> especially in HF
- educate regarding decreasing salt intake and not to stop drug suddenly
- examine pt for impaired circulation -> IRR, SOB, BLE edema
- caution when giving CCBs concurrently may potentiate HF
- watch for widening QRS segment -> immediate nursing attention
nonselective beta blocker names*
- olol
- carvedilol -> black sheep last name
- labetalol -> black sheep last name
- nadolol
- pendutolo
- pindolol
-sotalol -> watch for widening QRS complex - timolol
metoprolol
selective beta1 blocker
treats HTN
side effects
- N/V
- dizziness
- fatigue
- insomnia
- bradycardia
- dyspnea
metoprolol considerations *
- monitor BP and HR frequently during IV administration
- have baseline ECG and repeat if telemetry changes or chest pain
- monitor for symptoms of impending HF
- record I&O, daily weights, bilateral breath sounds
- take radial pulse -> don’t administer if HR <60bpm or is SBP <100 (watch for hypotension)
- do not omit, increase or decrease dose -> you can hold but let HCP know if you are
- avoid late evening doses
- watch for symptoms of depression
- watch for masked hyperthyroidism
- report visual problems, cold painful tender feet or hands
- caution with DM pt
- discontinue drug slowly due to potential rebound effect
- dont breast feed without consulting provider.
Intrinsic sympathomimetic activity (ISA
Beta blockers that exhibit mixed beta-antagonist and beta-agonist activity, characterizes a group of beta blockers that are able to stimulate beta-adrenergic receptors (agonist effect) and to oppose the stimulating effects of catecholamines (antagonist effect) in a competitive way
calcium channel blockers*
prevents contraction of peripheral arterioles
-> vasodilation and fall in BP
after load reduced
-> lower myocardial oxygen demand and less workload for heart
dilation of coronary arteries
-> more blood flow to heart
CCBs stop influx of CA into vascular smooth muscle.
calcium channel effects of heart*
myocardium effects
- reduces force of myocardial contractions (negative inotropic effect)
- reduces inwards movement of calcium during plateau phase of action potential
cardiac conduction effects
- negative chronotropic effect
- SA node generates fever action potentials
- slows automaticity
- decreases HR
dihydropyridine CCBs
are selective for vascular smooth muscle and are used to treat HTN and angina pectoris
- dipine
nifedipine
dihydropyridine CCB
selectively blocks Ca channels in vascular smooth muscle
decreases amount of Ca available for muscle contraction
nifedipine drug interaction and tx of overdose*
drug interactions
- may interact with drugs that induce or inhibit CYP3A4 (liver)
- additive effects with other antihypertensive drugs
- increased risk of congestive heart failure with beta blockers
- increased serum levels of dioxin -> bradycardia
- syncope/drop in BP with alcohol
overdose tx
- rapid-acting vasopressor such as dopamine or dobutamine
- calcium infusions
nondihydropyridine CCBs
act on both vascular smooth muscle and the myocardium
treat HTN and coronary artery disease
verapamil
nondihydropyridine CCB
antidysrhythmic, antihypertensive, chronic angina
verapamil drug interactions*
increases digoxin levels = increased risk of bradycardia
additive hypotension or bradycardia with other hypertensive drugs
3x plasma concentration of bus-irons
risk of myopathy increases significantly with statins
verapamil increases carbamazepine (tegretol) levels = neurotoxicity (ataxia) -> increase tegretol levels when D/C verapamil
grapefruit juice may increase levels -> don’t take it wit any CCB
verapamil considerations*
- monitor BP before administration of drug and 30 min to 1 jour after and just prior to next dose
- withhold drug if systolic BP <90 or symptomatic
- monitor for edema
- keep pt recumbent for at least 1hr after administration
- monitor for heart block or bradycardia with digoxin use
- monitor I/O
- monitor on telemetry continuously if giving it IV
drugs similar to verapamil*
diltaiazem
- tx of partial dysrhythmias and HTN, stable and vasospastic angina
- same profile as verapamil
- migraine prophylaxis off-label
physiology of the upper GI tract*
the stomach secretes acid, enzymes, and hormone that are essential to digestive physiology
natural defences include
- Somatostatin (inhibits gastric secretion)
- Prostaglandin E2
- bicarb ion
- mucus
prostaglandin antagonists include
- NSAIDs/ASA (damages GI mucosa directly)
- corticosteroids
PUD
peptic ulcer disease
ethology and pathogenesis of PUD*
peptic ulcer risk factors
- infection with helicobacter pylori
- close family history of PUD
- drugs -> glucocorticoids, NSAIDs, and platelet inhibitors
- blood group O
- smoking tobacco
- excessive caffeine
- psychological stress -> for a long time though to be primary cause of PUD
NSAID induced PUD risk factors
- long-term use
- advanced age
- history of ulcers
- corticosteroids -> predispose people to peptic ulcers, increased risk of perforation
- anticoagulants
- alcohol and smoking
proton pump inhibitors *
end in -prazole
block gastric acid secretion of H+, K+, and ATPase and are the drugs of choice in the therapy of PUD and GERD
activated by food intake -> take 20-30 mins before first major meal of the day
don’t effect pH levels, just amount of acid in the stomach
H2 - receptor antagonists*
H2- receptor antagonists
- Ranitidine
- cimetidine -> causes the most issues in this family, interacts with a lot of different meds
- famotidine
- nizatidine
ends in -tidine
suppresses gastric acid secretion
impacts pH levels.
H2-receptor antagonists pharmacokinetic properties*
- rapid absorption from small intestine
- 30min onset
- half life 1-4 hours
- no known effects on the fetus
- excreted primarily from kidneys
Antacids
alkaline substance that neutralize stomach acid to treat symptoms of heartburn
adverse effect of antacids*
- CONSTIPATION
- at high doses, aluminum products bind with phosphate in GI tract -> long term use can result in phosphate depletion
- high risk = malnourished people, alcoholics, renal disease
exam question:
- constipation due to meds can lead to obstruction
- be very careful with pt who are constipated
- if obstructed stop med
- firm, distended, tender, with N/V = obstruction
- only thing getting past an obstruction is watery poop
we want SNT no D
antacid contrindications*
- prolonged use with low serum phosphate
- avoid with suspected bowel obstruction
antacid drug interactions*
- don’t take with other meds -> interferes with absorption
- decreased absorption of cimetidine, fluoroquinolones, digoxin, isoniazid, chloroquine, NSAIDs, iron salts, phenytoin, tetracyclines, and thyroxine
- anticholinergic drugs increase effects of antacids
- aluminum and calcium antacids may inhibit absorption of dietary iron
antacid considerations*
- past medical history
- watch kidney lab values
- monitor for bowel changes and worsening symptoms
- hold drug and notify MRP if pt has symptoms of appendicitis, undiagnosed GI bleeding, or a suspected obstruction
pharmacotherapy for N/V*
- anticholinergic agents (scopolamine) and antihistamines (dimenhyrdrinate/diphenhydramine) are used for simple nausea, like nausea due to motion sickness
- serotonin receptor antagonists (zofran) are for chemotherapy-induced nausea and vomiting which is the primary indication for the use of antiemetic meds
exam question:
serotonin triggers nausea by being released into the gut faster than it can be digested -> antiemetic target serotonin receptors to reduce nausea
scopolamine is used for sea sickness, little white patch behind ears
can give metoclopramide, gravel, and ondansetron at the same time
ondansetron*
antiemetic
serotonin receptor antagonist
treats serious N/V, used at least 30min prior to chemotherapy and continued for several days after
off label use for cholestatic of opioid-induced pruritus
blocks serotonin receptors int he chemoreceptor trigger zone
pharmacotherapy with laxatives*
laxative -> bulk forming = Metamucil and surfactant type = docusate sodium
- promote defecation
- prevents and treats constipation
saline cathartic -> pulls water into stools (sennosides)
- implies accelerated, stronger, and more complete bowel emptying through osmosis
laxative action*
- treats simple, chronic constipation
- accelerate removal of ingested toxic substance
- accelerate removal of dead parasites
- cleanse the bowel prior to diagnostic or surgical procedures
- avoid increased colon pressure
- possible bowel perforation
- monitor for retrosternal pain
exam question:
retrosternal pain with bulk-forming laxatives
Metamucil considerations*
bulk forming laxative
- know past medical history
- assess bowel movements and GI functioning
- mid powder and granules with at LEAST 8 OUNCES of a pleasant tasting liquid immediately before and drink lots of water**
- immediately report complaints of retrosternal pain after taking drug to prescriber***
- smaller more frequent doses spaces through the day may be indicated to relieve discomfort
- monitor warfarin and digoxin levels closely
diphenoxylate with atropine *
antidiarrheal
it is a opioid
acts on smooth muscle cells of the intestine to slow peristalsis
adverse effects***
- dizziness
- lethargy, drowsiness -> may also cause dizziness
- anticholinergic effects of atropine -> anti pig, drys up poop, causes heart palpitations
diphenoxylate with atropine considerations *
- know past medical history and symptoms
- perform complete assessment of bowel movements and GI functioning -> monitor frequency and consistency of stools
- report abd distention and signs of decreased peristalsis to provider
- monitor S+S of dehydration especially in young kids
- maintain safe environment because it may cause drowsiness or dizziness
pharmacotherapy of IBD*
IBD is treated with 5-ASA agents, immunosuppressants, biologic therapies, and anti-inflammatory drugs
goals
- reduce symptoms
- keep in remission -> immunosuppressive agents
- alter progression of the disease
sulfasalazine*
agent for IBD
be aware of sulpha allergies -> sulfonamide is the basis of several drug groups
- sulfonylureas
- sulfonamide abx
- loop and thiazide diuretics.
sulfasalzine Contraindications/precaution*
- Patients with sulfonamide or salicylate
hypersensitivity - Patients with urinary obstruction
- May worsen blood dyscrasias
- Hepatic impairment
- Dehydration
- Diabetes or hypoglycemia
classifications of lipids
- triglycerides -> neutral fats, most common, major storage form of fat in body
- phospholipids -> essential to building plasma membranes
- sterols -> aka. cholesterol, best known, promotes atherosclerosis
lipoproteins
are important predictors of CV disease
HDL (high density lipoprotein)
- contains most apoprotein
LDL (low density lipoprotein)
- contains most cholesterol
HDL is better than LDL
VLDL (very low density lipoprotein)
- primary carrier of triglycerides in blood
hyperlipidemia
high levels of lipids in blood
long term consequences of being unaware of hyperlipidemia is cardiovascular disease
hypercholesterolemia
elevated blood cholesterol
cholesterol is made in the liver
dyslipidemia
abnormal levels if lipoproteins
hypertriglyceridemia
increase in triglyceride levels
patients are often asymptomatic until progression to chest pain or HTN
non-pharmacologic management of lipid levels
- maintain a healthy weight
- exercise -> 30min 3-5 days a week
- monitor blood lipid levels regularly
- dietary modification
- minimize alcohol -> especially beer
Statins
- most effective at reducing blood lipid levels
- are the recommended first line therapy
- can reduce LDL levels by 20 to 40%
- can raise HDL levels
- can lower triglyceride and VLDL levels
work by interfering with the HMG-CoA reductase, an enzyme involved with the biosynthesis of cholesterol
statin primary prevention
administering statins to pts with no history of CVD
statin secondary prevention
slowing progression and reducing mortality in pts with history of CVD
considerations with statins
are very hard on the liver
- test liver function before starting med, 6 weeks after and then every 3 to 6 months
all are given orally and tolerated well by most
no grapefruit juice (>1L)
stop if myopathies (muscle disease) occur
ARE ALL PREGNANCY CATEGORY X
statins and rhabdomyolysis*
rhabdomyolysis
- the breakdown of muscle fibres
- rare but serious adverse effect of statins
when muscles begin to breakdown, the larger muscle cells enter the blood stream and can wreck the kidneys when they filter the blood
-> in bad cases patients may need to go on dialysis or get a kidney transplant
atorvastatin (Lipitor)
antihyperlipidemic
HMG-CoA reductase inhibitor -> liver makes less cholesterol and responds by making more LDL receptors to remove cholesterol from blood
atorvastatin (Lipitor) adverse effects
- headache
- GI cramping
- diarrhea
- constipation
- rhabdomyolysis
contraindications
- pregnancy
- lactation
- caution in hepatic impairment
atorvastatin (Lipitor) drug interactions
- may increase digoxin levels (slow HR)
- may increase levels of oral contraceptive pills
- increase erythromycin levels
atorvastatin (Lipitor) considerations*
- obtain baseline lipid values
- monitor LDL cholesterol levels
- assess lipid lab tests within 2-4 weeks of initiation of therapy or change in dose
- assess for signs of rhabdomyolysis or myopathies (will look like generalized muscles pain/aches all over)
- observe for digoxin toxicity
- watch for hepatotoxicity -> teach pts about S+S of liver failure: jaundice, RUQ pain, changes in stools, and distention, bleeding/bruising
- no grapefruit juice
- NO ALCOHOL (think liver)
bile acid sequestrants
are often combined with statins to reduce LDL cholesterol levels
tend to cause more frequent adverse effects in the GI tract
can produce 20% drop in LDL levels
cholestyramine
antihyperlipidemic
bile acid sequestrant
binds to bile acids and forms insoluble complex containing cholesterol that is excreted in feces -> also lowers LDL levels by increasing LDL receptors on hepatocytes
cholestyramine adverse effects
- constipation -> increase fibre intake to prevent
- bloating
- belching
- nausea
- obstruction of GI tract
- hyperchloremic acidosis
- malabsorption syndrome
cholestyramine drug interactions
reduces effect of digoxin, penicillins, iron, thyroid med, and thiazide diuretics
increases effects of warfarin because less vitamins K is absorbed
cholestryamine (questran) considerations*
- completely dissolve powder before administration
- increase fluid intake
- assess for early signs of hypoprothrombinemia (risk of bleeding)
- monitor lab tests for therapeutic effectiveness
- consult prescriber to see if supplemental vitamins A,D and folic acid are required in long-term care
Niacin
can reduce triglycerides and LDL cholesterol levels, but adverse effects limit its usefulness
is a B- complex vitamin (B3)
produces more adverse effects than statins
causes additive effects with other drugs
decreases the production of VLDL
fibric acid
lower triglyceride levels but have little effect on LDL cholesterol -> used to treat severe hypertriglyceridemia
include:
- fenofibrate
- fenofibric acid
- gemfibrozil
gemfibrozil (Lopid)
antihyperlipidemic
fibric acid agent
second line therapy after statins
inhibits breakdown of stored fat
gemfibrozil (Lopid) adverse effects *
- abdominal cramping
- diarrhea
- nausea
- dyspepsia (indigestion)
- headache
- dizziness
- peripheral neuropathy
- diminished libido
- cholelithiasis (gall stones)
- anemia
- eosinophilia (increase in eosinophils)
- bleeding
contraindications
- gallbladder disease
- serious liver impairment
- renal impairment
gemfibrozil drug interactions*
- increased risk of myositis and rhabdomyolysis with use of statins
- increased risk of bleeding with anticoagulants
- enhanced hypoglycaemic effects with anti diabetic agents
gemfibrozil considerations*
- monitor lab tests
- consult provider if inadequate response after 3 months
- educate pt that drug will cause bloating and gas
- watch for bleeding
ezetimibe
antihyperlipidemic
only drug in its class
blocks absorption of cholesterol in intestinal lumen -> body responds by making more cholesterol
statin must be administered concurrently
renin-angiotensin-aldosterone system (RAAS)
goal of the RAAS system is to increase blood pressure and blood volume
BP drops -> SNS kicks in -> stimulates kidneys juxtaglomerular cells to release renin -> renin activates angiotensiongen within the liver to form angiotensin I-> ACE (angiotensin converting enzyme) that is found in the lungs and kidneys converts angiotensin I to angiotensin II -> angiotensin II causes vasoconstriction, increased sodium reabsorption, stimulates the leases of ADH and aldosterone
ACE inhibitors*
they are the first line agents in treatment of HTN and HF
they block the conversion of angiotensin I to angiotensin II -> because this occurs in the lung, there is potential for pt to develop a cough
decreases in BP and pulse rate
decreases release of aldosterone which reduces blood volume
they also inhibit the break down of bradykinin (it is similar to histamine)
-> accumulation of bradykinin causes several of the adverse effects of ACE inhibitors
are heart and kidney protective -> good to give to pts with HF and DM
Indications for ACE inhibitors *
- slow progression of heart failure
- lower mortality of recent acute MI
- prophylaxis for adverse cardiac events
- prevent or delay progression of renal disease and retinopathy of diabetics (can also increase the body’s sensitivity to insulin, sometime used off-label to prevent new-onset type 2 diabetes)
ACE inhibitor contraindications *
there is a low incidence of serious adverse effects
contraindicated with:
- hypotension
- renal failure
- hyperkalemia
-> caution when using ACEI with K+ sparing diuretics
-> watch K+ levels (do lab work regularly)
angioedema is the most serious
-> rapid swelling of throat, face, larynx, tongue can lead to airway obstruction
all carry black box warning regarding risk for major congenital defects.
lisinopril (prinivil, zestril) *
antihypertensive
ACE inhibitor
therapeutic effects
- heart failure
- HTN
- acute MI
MOA
- bings to and inhibits action of ACE
- decrease in serum angiotensin II reduces aldosterone, which results in less sodium and water retention
lisinopril adverse effects *
- cough
- headache
- dizziness
- orthostatic hypotension
serious:
- angioedema
- agranulocytosis
- hepatotoxicity
lisinopril contraindications*
- pregnancy category D
- angioedema
- hyperkalemia
- serious renal impairment
lisinopril considerations*
- check renal labs and K+ levels for hyperkalemia
- monitor BP before administration and 30 mins to 1 hour after
lisinopril drug interactions*
decreased antihypertensive activity and worsened renal disease with use of NSAIDs
synergistic hypotensive action with diuretics and other hypotensive
hyperkalemia with potassium supplements and potassium sparing diuretics
pregnancy category C (first semester)
Pregnancy category D (second and third trimesters)
lisinopril treatment of overdose*
normal saline or vasopressor
hemodialysis
angiotensin II receptor blockers (ARBS)
are used to treat HTN and heart failure
block angiotensin II from activating their target receptors in smooth muscle -> causing vasodilation, reduce pulse rate, and decrease BP
they also prevent aldosterone secretion and promote the excretion of Na+ and water by the kidneys
indications for ARBS*
same as ACEI
- treat HTN and HF
- some are approved to treat MI and prophylaxis of CVA
do not cause cough and angioedema is less common
Losartan (Cozaar) *
antihypertensive
ARB
therapeutic effects and uses:
- HTN
- CVA prophylaxis
- Prevention of diabetic nephropathy
- off label use for heart failure
MOA:
- selectively blocks angiotensin AT1 receptors, resulting in decreased BP
- blockade prevents cardiac remodelling and deterioration of renal function in pts with diabetes
losartan treatment of overdose
normal saline or vasopressor
the drug is not removed by hemodialysis
losartan drug interactions*
decreased antihypertensive activity with NSAIDs
additive hypotensive actions with diuretics and other hypotensive
hyperkalemia with potassium supplements and potassium-sparing diuretics
additive hypotensive effect with alcohol
losartan considerations
monitor for hypotension
monitor electrolytes, CBC, liver and renal function during therapy
aldosterone
works on the kidneys and promotes the reabsorption of water and excretion of potassium
will increase BP
aldosterone antagonists
used to treat edema and HTN
spironolactone -> K+ sparing diuretic
and
eplerenone
Angiotensin receptor neprilysin inhibitor (ARNI)
treats HF and CV disease
a combination of and ARB and a neprilysin inhibitor
neprilysin inhibitor increases vasodilatory peptides, which helps the body get rid of more sodium and open blood vessels wider
pregnant or breastfeeding people should not take ARNIs
ex. sacubitril/valsartan
bradydysrhythmias
HR less than 60 BPM
major indication for pacemakers
common bradydysrhythmias
- sinus bradycardia
- sinoartrial node dysfunction
- atrioventricular conduction block
tachydysrhythmias
HR over 100 BPM
common ones
- atrial tachycardia
- atrial flutter
- afib
- ventricular tachycardia
- ventricular fibrillation
class I dysrhythmia drugs
sodium channel blockers
act by blocking ion channels in myocardial cells
class IA dysrhythmia drugs
quinidine
disopyramide
procainamide
class IB dysrhythmia drugs
lidocaine
mexiletine
phenytoin
class 1C dysrhythmia drugs
flecainide
propafenone
Class II dysrhythmia drugs
beta blockers
class III dysrhythmia drugs
Potassium channel blockers
ex. amiodoarone
class IV dysrhythmia drugs
calcium channel blockers
pathophysiology of HF*
location of failure:
left sided failure = pulmonary edema
right sided failure = peripheral edema
type of failure:
systolic failure = decreased contractility, decreased ejection fraction
diastolic failure = decreased ventricular filling, normal ejection fraction
considerations with afib
be concerned about clots because the blood will pool and clot in the atria
when giving a med that fixes the quiver in the atria, the blood with clots will go out into the body -> could cause DVT, stroke, MI
consideration of HF*
- ensure the pt monitor for dependent bilateral lower extremity (BLE) edema -> both legs have to have edema for it to be HF
- watch for worsening SOB or new onset SOB
- evaluate the number of pillows needed to sleep at night or if the are sleeping in a recliner
- weigh themselves every day -> same time, scale, clothes: call HCP if 2lb weight gain in 1 day (textbook) , or 5lbs in 2-3 days (reality)
goals of pharmacologic management of HF
- reduce preload
- reduce systemic vascular resistance (after load reduction)
- inhibition of RAAS and vasoconstrictor mechanisms of sympathetic nervous system
ACE inhibitors and HF
ACE inhibitors are becoming more common as first line treatment for HF instead of cardiac glycosides (digoxin)
policies are changing
cardiac glycosides*
- used in treating HF before ACE inhibitors -> less common now, policies are changing
- increased contractility -> improves symptoms, but does not improve mortality
- stabilize cardiac conduction abnormalities -> water for other antiarrhythmics ** (test question)
- digitalization -> dose gradually increases until tissues become saturated with medications and symptoms of HF diminish
beta blockers for HF
can dramatically reduce hospitalizations and increase the survival of pts with heart failure
digoxin
drug for hear failure
cardiac glycoside, positive inotropic (strength of contraction) agent
indications = heart failure
digoxin adverse effects*
- general malaise
- dizziness
- headache
- N/V
- anorexia
- visual disturbances -> blurred or yellow vision or green halos
serious AE
- ventricular dysrhythmias
- AV block
- atrial dysrhythmias
- sinus bradycardia
digoxin drug interactions
can cause hyperkalemia with -> ACEI, spironolactone, potassium supplements
digoxin overdose treatment
digibind
organic nitrates *
mechanism
- relax venous muscle -> reduces preload = less work for the heart
- relax arterial muscle -> increases blood flow to myocardium
adverse effects = hypotension, headache, tolerance
nitric oxide is a cell-signalling molecule and potent vasodilator
short acting = to stop angina attack
long acting = prevent angina attacks
ex. nitroglycerin
nitroglycerin MOA*
works at vascular smooth muscle, forms nitric oxide, which trigger a cascade resulting in release of calcium ions
relaxes both arterial and venous smooth muscle = less cardiac return (less preload)
dilates coronary arteries = increases O2 to the myocardium
nitroglycerin drug interactions
NO VIAGRA with nitrates -> life threatening hypotension and CV collapse
additive hypotension with
- antihypertensives
- ethanol
- CCBs
- antidepressants
- phenothiazines
sympathomimetics antagonize action
beta-adrenergic blockers
and management of myocardial infarction*
beta-adrenergic blockers
- reduce myocardial demand -> decreases HR (negative chronotropic effect), decreases contractility (negative inotropic effect), decreases BP, counter effects of sympathetic stimulation
- reduces conduction -> prevents dysrhythmias
- therapy usually continued for rest of pts life
ACE inhibitors
and management of myocardial infarction*
ACE inhibitors
- given within 24 hours of onset MI
- prevents cardiac remodelling
- suppress dysrhythmias
- therapy usually continued for rest of pts life
- watch K+ levels and for angioedema
- check lab work for K+ and renal function
Aspirin and management of myocardial infarction*
160 to 325 mg initially and then 81 mg daily
lower dose causes less GI bleeding
thrombolitics and management of myocardial infarction*
- dissolve active clots
- only for use in early MI -> best within 30 mins, no benefit after 24 hours
- severe risk of bleeding
ex. alteplase (Activase)
how to choose anti epileptic drug and when to stop it*
choice of anti epileptic drug therapy is dependent on seizure type and characteristics, as well as
- medical history
- results of EEG and other tests
- comorbidity conditions
never stop taking medication even if feeling “better” without guidance of HCP, may cause WITHDRAWAL seizures
benzodiazepines*
- control seizures by acting in limbic, thalamic, and hypothalamic regions of the CNS
- there are limited applications -> used for seizures when other drugs are proven ineffective
- when administering by IV, resuscitation equipment should be readily available -> monitor pt closely for CV collapse and resp depression
benzodiazepine considerations*
- educate pt on S+S of resp depression and CV collapse
- assess for decrease in seizure activity
- maintain pt safety pre and post seizures -> watch for triggers
- assess for history of smoking -> may require larger doses
- assess for urinary retention
- do not mix with other drugs parenterally
hydantoins
are effective in the management of most types of seizures but have many adverse effects
phenytoin considerations*
anti epileptic drug
- shake suspension well prior to administration
- watch for extravasation with IV route
- beck blood levels regularly (like with lithium and digoxin)
- monitor CBC (for blood dyscrasia)
- watch for near changes and side effects
- monitor blood glucose in diabetics
- assess folic acid deficiency
carbamazepine contraindications*
anti epileptic drug
- hypersensitivity
- increased ocular pressure (visual disturbances)
- lupus
- cardiac/hepatic disease
- HTN
- older adults
- pregnancy category D
carbamazepine considerations
- do not administer within 14 days of MAOI
- watch lab results
- assess for CNS ADRS
- assess for GI distress
- assess VS and I/O
valproic acid drug interactions*
anti epileptic drug
gaba agonist
additive sedation with CNS depressants and alcohol
more rapid metabolism with enzyme inducing anti epileptic drugs
increased serum levels of TCAS (tricyclic antidepressants)
increased serum levels of aspirin, isoniazid, and cimetidine -> watch for bleeding
decreased absorption with cholestyramine
valproic acid considerations*
- monitor seizure activity and check serum levels
- obtain baseline platelet counts and check PT/PTT/INR regularly during therapy
- monitor for signs of hyperammonemia and bleedings
- watch liver lab work
damage caused by HTN to the body*
heart
- hypertrophy
- MI
- HF -> watch for rapid wt gain (5lbs/ 2-3 days), SOB, BLE edema
eyes
- blindness -> frequent eye checks
brain
- stroke -> assess for speech changes, dropping face, one sided weakness
kidneys
- kidney failure -> watch for protein in the urine (micro and macro albuminuria)
diuretics*
thiazide diuretic is first line treatment option for HTN
multi-drug therapy is often required
diuretics decrease blood volume and pressure
diuretics adverse effects*
- dehydration
- hyponatremia
- hypokalemia (less with potassium-sparing diuretics)
- nocturia (if taken too late in the day)
- orthostatic hypotension
types of diuretics*
thiazide and thiazide-like diuretics
- most common diuretic for HTN
- ex. hydrochlorothiazide
potassium-sparing diuretics
- triamterene, spironolactone
loop (high-ceiling) diuretics
- usually not used for HTN
- furosemide, bumetanide = K+
ACEI*
causes vasodilation by reducing angiotensin II
- decreases aldosterone effects -> increases effectiveness of diuretics
- protects the kidneys
- ex. enalapril, lisinopril, captopril
ACEI adverse effects*
- persistent cough
- postural hypotension
- hyperkalemia
- angioedema
ARBS*
inhibit effects of angiotensin II
has similar effect to ACEI
has fewer adverse effects
- hypotension
- angioedema -> rarer than with ACEI
- more expensive
- no cough
ex. losartan
beta adrenergic antagonists therapy*
aka beta blockers
nonspecific beta blockers also causes bronchoconstriction -> use with caution for pt with asthma or heart failure
beta -blocker therapy
- at low doses adverse effects are uncommon
- at higher doses, adverse effect include:
- fatigue, activity intolerance
- erectile dysfunction
- masks symptoms of hypoglycemia
- clinical depression
direct acting vasodilators*
relax arterial smooth muscle directly = decreased resistance and decreased after load
-> some drugs also affect veins such as isosorbide denigrate (long acting nitrate) = also decreased preload
ex. hydralazine, diazoxide, nitroprusside
vasodilator adverse effects*
- reflex tachycardia (HR increases in response to low BP ), and hypotension
- fluid retention -> can be minimized with beta blockers and diuretics
hydralazine *
antihypertensive
direct vasodilator
therapeutic use
- moderate to severe HTN
- hypertensive emergencies
- acute heart failure
MOA
- causes peripheral vasodilation
- decreased vascular resistance, heart rate, cardiac output
- decreased after load
- is selective for arterioles *
hydralazine considerations*
- past medical history
- monitor lab tests for antinuclear antibody titer before and during therapy
- monitor I & O
- watch for adverse effects -> HA, tachycardia, palpitation, N/V/D, orthostatic hypotension
- assess for rapid drop in BP and subsequent tachycardia (reflex tachycardia)
nitroprusside sodium
use in hypertensive emergencies
a direct vasodilator
thrombolytics *
aka. fibrinolytics -> alteplase (tPa), tenecteplase (TNK-tPa)
dissolve bonds that hold existing thrombi together
clot busters -> are only used for life-threatening illnesses
antifibrinolytics*
amniocaproic acid and tranexamic acid
inhibit the activation of plasminogen to plasmin (destroys clots) , prevent the break up of fibrin and maintain clot stability
used to prevent excessive bleeding
used to stabilize post surgical bleeds
types of anticoagulants*
parenteral
- heparin
- LMWH
- fondaparinuxn (chemically related to LMWH)
- direct thrombin inhibitors
oral
- warfarin
- dabigatran
do not actually breakdown existing clots -> prevent enlargement and formation of new ones
anticoagulant considerations*
- baseline blood tests
- monitor aPTT(tests how long it take for blood to clot) every 6 hours when adjusting dose (follow PPOs)
- monitor for signs of bleeding
- apply firm pressure for 5 mins venous and 10 mins for arterial needle sticks
- reduce risk of trauma
- keep heparin antidote readily available (protamine sulphate)
anticoagulant pt education*
- no razors, wax or use electric razor instead
- soft bristled toothbrush
- no high impact activities
- if bleeding for longer than 30 min, go to hospital
- if GIB bleed (coffee ground emesis or melena) go to hospital
warfarin
stop use 24hrs pre and post surgery
warfarin considerations*
- assess for risk of thromboemboli
- monitor PT/INR
- monitor urine, stool, liver function, and blood
- monitor risk groups for non adherence
- teach pt to avoid or eat sparingly food rich in vitamin K, such as broccoli, leafy greens
warfarin pt education*
- provide education for anticoagulants
- monitor for signs of bleeding
- apply firm pressure for 5 min venous and 10 mins for arterial needle sticks
- reduce risk of trauma
heparin*
anticoagulant
indirect thrombin inhibitor
therapeutic effects
- acute thromboembolic disorders
- DVT/PE
- unstable angina/evolving MI
- prophylaxis
MOA
- activates antithrombin III, which inhibits thrombin and to lesser extent factor Xa -> prevent the formation of clots
heparin considerations*
- baseline blood tests
- monitor aPTT every 6hrs when adjusting dose
- monitor for signs of bleeding
- apply firm pressure 5 min for venous and 10 mins for arterial needle sticks
- reduce risk of trauma
- keep heparin antidote readily available (protamine sulfate)
ADP receptor blockers*
“aka P2Y12 inhibitors
irreversibly inhibit platelet ADP receptors (for platelets life -> 8 days)
-> inhibit aggregation (decreases body’s ability to clot)
-> makes the blood less “sticky
clopidogrel = once a day, MI and stroke (irreversible)
ticlopidine = two times a day, stroke prophylaxis (reversible)”
ADP receptor blocker adverse effects*
bleeding
neutropenia/agranulocytosis
thrombotic thrombocytopenia purpura(blood clots form in small blood vessels throughout the body, leading to low platelet counts, red blood cell destruction, and potential organ dysfunction)
clopidogrel *
anti platelet agent
ADP receptor blocker
therapeutic effects
- reduce risk of CVA/MI
- reducing thrombolytic events post CVA/MI
- prevent DVT
- prevent thrombi formation in unstable angina/coronary stents
MOA
- inhibits ADP receptors on platelets and prolongs bleeding time by irreversibly inhibiting platelet aggregation
-CYP450 interaction (liver)
risk factors of thrombolytics*
risk of bleeding with thrombolytics may outweigh benefits -> watch for S+S of hemorrhagic stroke (LOC)
streptokinase (SK)/ urokinase (UK)
- older, slower, more side effects, cheap, and allergenic
- treat PE, MI, DVT
tenecteplase (TNK-tPa), alteplase (tPa)
- are newer drugs with fewer side effects
antifibrinolytics
aka hemostatics
administered via IV
stabilizes clots, prevents digestion of fibrin clot by plasmin
antifibrinolytics therapeutic effects*
- aplastic anemia
- hepatic cirrhosis
- postoperative cardiac surgery
- certain carcinomas
- hemophilia A (blod clotting disorder)
- excessive post surgical bleeds
ferrous sulfate
agent for anemia
iron supplement
ferrous sulfate adverse effects*
- N/V
- brown stains on teeth from liquid
- darkened stools
- constipation
ferrous sulfate contraindications*
hemochromatosis
PUD
regional enteritis
ulcerative colitis
ferrous sulfate considerations*
- assess vital signs for cellular hypoxia
- give on a empty stomach if possible
- if difficulty swallowing tablets or capsules, recommended a liquid formulation or a less corrosive form, such ferrous gluconate
- prevent staining of teeth -> rinse with H2O
- monitor bowel movements
- continue iron therapy for 2-3 months after normal Hgb
- mix feosol elixir with water
ferrous sulfate pt and family education*
- don’t take tablets or capsules within 1 hour of bedtime
- do not crush tablets of empty contents of capsule
- take ferrous sulfate with a full glass of water
- rinse mouth with clear water immediately after ingestion
- consume citrus fruit or tomato juice with preparations (except the elixir form)
- avoid taking drug with milk, eggs, antacids, or caffeine
- dark green or black stools are a harmless side effect
- report constipation or diarrhea
cyanocobalamin
agent for anemia
vitamin supplement
used for vitamin B12 deficiency anemia
cyanocobalamin adverse effects*
- rashes, itching, or other signs of allergy
serious AE
- sodium retention with possible worsening of HF
- anaphylaxis
- hypokalemia and potential dysrhythmias
cyanocobalamin drug interactions*
decreased absorption with
- ethanol/alcohol
- amino salicylic acid (ASA)
- omeprazole
- neomycin
- chloramphenicol
bipolar disorder*
alternates between extreme feelings of sadness and extreme mania
significantly impacts social and occupational functioning
nonpharmacologic interventions -> support groups, ECT
-> triggers include lack of sleep, excessive stress, poor nutrition
pharmacologic interventions -> highly individualized based on severity and predominant symptoms
non adherence is a serious problem
lithium
antimanic
alkali-metal ion salt
used to treat bipolar disorder
lithium increases the synthesis of serotonin
lithium adverse effects and contraindications
initial AE
- polyuria, nocturia
- N/V
- muscle weakness
long term AE
- kidney impairment
- goiter
- circulatory collapse
contraindications
- serious CV or renal impairment
- severe dehydration
- sodium depletion
precautions
- urinary retention
- older adults/ children
- CV disease
- diabetes
lithium drug interactions*
diuretics = increased risk of lithium toxicity
NSAIDs and thiazide diuretics can increase lithium levels
antithyroid drugs and drugs containing iodine cause increased hypothyroid effect
haloperidol causes increased neurotoxicity
SSRIs, MAOIs, dextromethorphan may result in serotonin syndrome
some herbal and food interactions
lithium considerations*
monitor serum levels Q1-3 days initially and 2-3 months after
assess for symptoms of bipolar disorder before and during treatment
obtain baseline thyroid, kidney, cardiac function, electrolyte levels
monitor for symptoms of lithium toxicity
assess daily for weight changes, edema, changes to skin turgor
lithium is a salt so think water levels in the body -> dehydrated increased lithium and over hydrated decreased lithium levels -> watch pts what increase exercise or are N/V/D
monitor sodium intake -> continue to take table salt to maintain osmotic hydration but don’t over do it
lithium toxicity S+S*
- Nausea/Vomiting
- Persistent diarrhea
- Coarse trembling of hands or legs.
- Frequent muscle twitching such as pronounced jerking of arms or legs.
- Blurred vision.
- Marked dizziness.
- Difficulty walking.
- Slurred speech.
- Irregular heart beat.
- Swelling of the feet or lower legs.
etiology of schizophrenia *
the precise etiology of schizophrenia remain unknown
genetic component -> 5 to 10x greater risk if first degree relative has disorder
neurotransmitter imbalance -> overactive dopaminergic pathways in basal nuclei
-> associated with dopamine type 2 (D2) receptors - antipsychotic drugs block these receptors
too much dopamine
second generation (atypical) antipsychotics have become drugs of choice for the treatment of schizophrenia
management of psychoses*
initial treatment
- first doses of antipsychotic drug may be higher than normal -> produces sedation if pt is agitated, aggressive, or posing danger to others
most drugs are provided orally
benzodiazepines (lorazepam)
-> provided IM to relax pt and may allow initial dose of antipsychotic to be reduced
acute symptoms usually resolve in 3 to 7 days
adverse effects of antipsychotic drugs*
extrapyramidal side effects
neuroleptic malignant syndrome
adverse effects on reproductive system -> major cause of nonadherance; sexual, menstrual, or breast dysfunction
extrapyramidal side effects of antipsychotic drugs*
refers to locations in the CND associated with postural and automatic movements
include:
- acute dystonia -> severe spasms of the muscles of the tongue, face, neck, or back, arching forward of trunk while legs thrust back
- akathisia -> pacing, squirming, inability to sit still
- Parkinsonism -> tremor, rigidity, shuffling gait, drooling, symptoms can’t be distinguished from true parkinsons
- tardive dyskinesia -> involuntary, unusual movements of tongue and face and lip-smoking movements
neuroleptic malignant syndrome (NMS) side effect of antipsychotic drugs*
- potentially fatal adverse reaction
- symptoms include high fever, diaphoresis, muscle rigidity, tachycardia, BP fluctuations
- without quick, aggressive treatment, condition can deteriorate to stupor or coma
- treatment includes antipyretics, electrolytes, muscle relaxants
haloperidol
antipsychotic (first-generation)
nonphenothiazine, dopamine antagonist
haloperidol adverse effects*
- anticholinergic symptoms -> blurred vision, dry eyes, glaucoma
- weight gain
- headache
- anemia
- phytotoxicity
- MOST LIKELY TO PRODUCE EPS
serious AE
- tachycardia
- cardiac arrest
- laryngospasm
- respiratory depression
- seizures
- neuroleptic malignant syndrome
- agranulocytosis/leukopenia/leukocytosis
risperidone
antipsychotic (second generation, atypical)
benzisoxazole and dopamine antagonist
risperidone considerations*
if medication causes drowsiness -> take at bedtime
watch pt for orthostatic hypotension -> rise slowly
assess for EPS/TD/ Akathesias/ NMS
educate pt for S+S of above and what to watch for and when to contact HCP
encourage sips of water or hard candies for sry mouth and anticholinergic like symptoms
avoid alcohol and caffeine
increase fluid and fibre
watch liver lab results and educate pt on S+S of liver involvement (jaundice and stool)
tell pt to report significant wt gain (5lb per week)
ensure pt knows that definite improvement may not be seen for 6-8 weeks
drugs similar to risperidone*
second generation atypical antipsychotics
- quetiapine (Seroquel)
- olanzapine (zyprexa)
- clozapine (colzaril, flazaclo)
-pine
considerations of all psych meds*
be sure to know the S+S of and which drugs cause :
- tardive dyskinesia -> Haloperidol, Fluphenazine, Risperidone
- EPS -> Haloperidol, Fluphenazine, Risperidone (high dose)
- neuroleptic malignant syndrome -> Haloperidol, Fluphenazine, Olanzapine
- serotonin syndrome -> SSRIs, MAOIs, Tramadol, MDMA, Serotonergic combos
dopamine system stabilizer considerations *
aripiprazole -> only drug in this class
- monitor for EPS symptoms or anticholinergic effects
- ensure adequate nutrition, fluid
- monitor for signs of neuroleptic malignant syndrome
- watch liver labs
provide pt education
- monitor for weight gain or changes in sexual characteristics (lactation in men)
- no alcohol use of illegal drug use
- no caffeine use
- no smoking
typical vs atypical antipsychotics
typical antipsychotics have more adverse effects compared to atypical
symptoms of anxiety disorders *
- apprehension
- worry, fear
- palpitations
- shortness of breath
- heart burn
- dry mouth
- excess sweating
high levels of anxiety or a “panic attack” can often be misconstrued as a heart attack
rule out MI first -> diagnostic tests and ECG -> then obtain a history of recent events that might trigger anxiety or that might indicate drug abuse.
diagnosing anxiety disorders*
accurate diagnosis necessary
nurse needs to take complete history to rule out
- medications that may worsen/cause anxiety symptoms
- medical conditions that may be associated with anxiety
- consider non pharmacological interventions that will reduce environmental, physical and emotional stressors prior to medications
contraindications of blood thinners
GI bleed
Hemorrhagic stroke
Trauma
Surgery
Blood disorders
benzodiazepines cautions*
are the drugs of choice for generalized anxiety disorder and short-term therapy of insomnia
- change dose gradually- do not stop abruptly
- watch for suicidal ideation
- may cause mania or psychosis
- watch in use with dysfunctional kidneys, liver, CV or pulmonary system
- use cautiously when using with the elderly
lorazepam considerations *
anti anxiety/ anti seizure agent
benzodiazepine, GABA receptor agonist
- aspirate prior to injection (IM)
- assess for paradoxical CNS excitement (unexpected increase in activity and arousal as a result of taking a medication or drug intended to have a sedative or calming effect)
- advise pt to stop smoking
- watch CBC, liver and renal function
- does the pt actually need anti anxiety meds?
- assess for S+S of overdose or abuse
- teach nonpharmacologic methods of sleep and relaxation
- assess for suicidal ideation
dont give to pregnant women
barbiturates
sedative-hypnotics
have a high dependence -> limit treatment to 14 days
overdose or withdrawal are severe
phenobarbital
barbiturate
sedative-hypnotic
anti epileptic drug
phenobarbital adverse effects *
- over sedation
- hangover effect, lethargy
- hallucinations
- blood dycrasias
- hypocalcemia
- hepatic disease
- N/V/D/C
- paradoxical excitation in children/ older adults
phenobarbital serious adverse effects*
- coma
- Steven johnson syndrome
- angioedema
- periorbital edema
- thrombophlebitis
phenobarbital considerations*
- monitor for respiratory depression
- assess pt given IV barbiturates q15 mins
- monitor for signs of blood dycrasias
- aspirate prior to injection
- monitor therapeutic concentrations of drug -> like dig, dilantin, and lithium
- teach nonpharmacologic methods of relaxation/sleep
- assess baseline hepatic and renal function and monitor during therapy
- if pt develops fever, angioedema, and body rash -> hold med and call MD
depression*
a mood disorder
- persistent disturbance in emotion that impairs ability to effectively deal with ADLs
- two primary types of mood disorders are depression and bipolar disorder
causes of depression
- environmental
- situational
- hereditary
- no longer though to be related to parenting or unresolved childhood conflicts
often coexist with other conditions
- anxiety
- substance abuse
- hypertension or arthritis
assessment of depression*
majority of persons who commit suicide have been diagnosed with major depression
three or more weeks of antidepressant therapy may be required before pts mood begins to improve
-> 6 - 8 weeks to reach maximal benefit
-> risk of attempted suicide highest the month before pharmacotherapy
nurses role
- careful monitoring of talk of suicide
- weekly or daily pt contact
- careful monitoring of medications
disadvantages of tricyclic antidepressants *
side effects
- anticholinergic effects/sympathomimetic effects
- orthostatic hypotension
- sedation -> worsened by concurrent use of other CNS depressants
- relatively high incidence of sexual dysfunction (cause of cessation)
- withdrawal symptoms if not tapered -> don’t stop suddenly
- may take 3 weeks to see effects and 6 weeks to see optimum benefits
imipramine
tricyclic antidepressant
norepinephrine reuptake inhibitor
blocks Ach receptors
imipramine contraindications *
- heart attack, heart block, dysrhythmias
- asthma, GI disorders, alcoholism, schizophrenia, bipolar disorder
- avoid use with alcohol
- seizure disorders
precautions -> due to sympathomimetic effect
- suicidal tendencies
- urinary retention
- prostatic hyperplasia
- cardiac/hepatic disease
- increased intraocular pressure
- hyperthyroidism
- Parkinson disease
imipramine considerations *
- monitor for suicidal ideation
- be sure patient swallows each dose
- encourage compliance
- monitor for urinary retention or constipation
- treat for dry mouth
selective serotonin reuptake inhibitors (SSRIs)
drugs of choice for treating depression due to low incidence of serious adverse effects
serotonin syndrome
when a pt takes multiple medications (or overdose) that causes serotonin to accumulate in neurons in CNS
-> confusion, restlessness, tremors, lack of muscle control
conservative treatment to discontinue all serotonergic drugs.
fluoxetine (prozac)
SSRI
antidepressant, anti anxiety agent
fluoxetine adverse effects*
- N/V/D/C
- anorexia
- cramping
- fluctuations in weight
- sexual dysfunction
- seizures
- poor concentration
- nightmares
- hot flashed
- palpitations
- serotonin syndrome
exam question?*
pediatric patients may experience personality disorders or hyperkinesia (extreme or excessive movement of the body, especially the muscles)
fluoxetine contraindication/precautions*
- bipolar disorder
- cardiac dysfunction
- diabetes
- seizure disorders
- carefully observe pediatric patients for hyperkinesia and personality changes/disorders***
- late pregnancy
monoamine oxidase inhibitors (MAOIs) *
- rare use
- high incidence of adverse effects
- avoid foods containing tyramine (MAO in food) -> food that have been aged or fermented (think charcuterie board)
- avoid L-tyrosine -> tyramine a component of tyrosine
- avoid caffeine
- off label use for OCD, panic disorder, social anxiety disorder, migraine prophylaxis
- potentiates (increases) effect on insulin and diabetic drugs
MAOI adverse effects*
-dizziness/orthostatic hypotension
- drowsiness/HA
- sexual dysfunction
- anorexia / diarrhea
serious AE
- hypertensive crisis -> with foods with tyramine (charcuterie board)
- dyshythmias
- SIADH like symptoms (low sodium, increased BP)
high incidence of adverse effects and high level of non-compliance
MOAI precautions and considerations*
precautions
- epilepsy
- severe, frequent headaches
- HTN
- dysrhythmias
- suicidal tendencies
considerations
- assess for suicidal ideation
- encourage compliance
- avoid foods containing tyramine -> charcuterie board
- avoid L-tyrosine -> tyramine is a component of tyrosine
- avoid caffeine
EXAM QUESTION* Alteplase (Activase) fibrinolytic is prescribed for a client with an acute myocardial infarction. Which is the priority nursing intervention for this client?
Monitor APTT.
Monitor injection sites.
Monitor level of consciousness (LOC).
Monitor PT/INR.
correct answer is monitor level of consciousness -> risk of bleeding could lead to hemorrhagic stroke
quick tricks for ferrous gluconate -> Cs and Ts
- No Calcium (or dairy)
- No Thyroid meds
- Constipates
- Causes black feces
- N&V/Take with food
quick tricks for statins
- Watch Liver:
a. Jaundice (watch enzymes)
b. No ETOH
c. Stool changes
d. RUQ Pain
e. Distension - Rhabdomyolysis
- Grapefruit Juice (don’t take it)
quick tricks thyroid meds
No Calcium (or dairy)
2. No Iron
3. No Caffeine
4. Take on an empty stomach
quick tricks for CCB and BB
- Heart Block
- Hypotension
- Bradycardia
- BB: Asthmatics, Diabetics (masks S&S
hypoglycemia), don’t stop suddenly - CCB: HF, RF & no grapefruit juice
quick tricks for bentos (5 Bs)
Blood dyscrasias (CBC)
2. Bile (Liver/No ETOH)
3. Brain (CNS depressant & interactions)
4. BP (Hypotension)
5. Bonkers (makes elderly go delirious
sometimes)
quick tricks for SSRIs 5Ss and 2Cs
Seizures
2. Suicidal ideation
3. Sexual dysfunction
4. Ø Stopping suddenly (SS)
5. See (Narrow Angle Glaucoma)
6. Cirrhosis (Liver/No ETOH)
7. CNS depressant & interactions
quick tricks for ARBs (sartans) and ACEI (prils)
RF
2. Hypotension
3. Hyperkalemia – watch K+ with K+ sparing
diuretics
4. Angioedema
5. Cough
quick tricks for flagyl (metronidazole)
- Liver
- Rust coloured urine
- Metallic taste in the mouth
quick tricks for steroids (PO/IV)
Osteoporosis
2. Poor wound healing/Risk for infections
3. Mood volatility
4. Moon Face/Buffalo Hump (Truncal obesity)
5. GI Bleed (MUST take with food)
a. Never stop suddenly
b. Hyperglycemia in Diabetics
quick tricks for opioids
LOC
2. Decreased respirations
3. N/V
4. Constipation
5. Urinary Retention
quick tricks for antibiotics
Keep out of reach of children
2. Do not share
3. No leftovers (take ALL as prescribed)
4. N/V/D
5. Watch skin, ears, kidneys – drink lots of
water
