PHARMACOLOGY (INHOUSE REVIEW)  Anaphylactic Shock Bronchospasm Give

DAY 1 EPINEPHRINE ASAP

5 R’s (BASIC) Best bronchodilator

 Right patient
 Right drug  Measure VS (BP, pulse, RR)
 Right time  Cut off: do not give if less than systolic 90
 Right dose  Cannot maintain perfusion anymore
 Right route  HR- less than 60
 RR- less than 12
1. RIGHT PATIENT
 2 PATIENT IDENTIFIERS SAFETY ISSUES
 Ask name Medications Adjustment
 If patient has the same name with the  Adults- (based on weight (mg/kg body weight)
other patient, ask the birthday  Pediatric Clients (still give a low dose because no
matter how big they are they still have immature
2. RIGHT DRUG organs)
 Order, confirm with another nurse if needed.  Geriatric Considerations- low dose because
 Avoid using abbreviations organs are already degenerating
 Ex: No MSO4, MgSO4
Drugs can be toxic to certain organs
3. RIGHT DOSE  HEPATOTOXIC- monitor liver enzymes (ALT,
 Dosage & solutions, computations AST, bilirubin)
 No OD/ QID  ALT- better parameter
 20gtts/ml (10,15,20)  NEPHROTOXIC- BUN & Creatinine
 BUN- 18-20 mg/dL
4. RIGHT ROUTE  Crea- 0.6-1.2 mg/dL
 Oral, Parenteral/ Topical  OTOTOXIC
 IV fastest route  Monitor for 8th cranial nerve damage- tinnitus,
 Certain drugs that you cannot give in a particular vertigo
route
Ex: Emergency DKA IV regular insulin *Neutrophil – 40-75%

NGT- how to give medication? Do not mix with feeding MEDICATION INTERACTION
 Give the medication before feeding Drug-food interactions- can result in toxicity (therapeutic
failure)
 Do not crush meds that are ENTERIC coated, Impact of food on drug absorption
SUSTAINED release, EXTENDED release  Food delays absorption
Ex: EC ASA, MSO4 SR  Food interferes w/ absorption except of GI
*Enteric coated for protection against gastric irritant
irritation  Empty/full stomach, w/ or w/o food
*SE- action is prolonged
 That is why morphine can cause resp. depression Impact of food on drug toxicity
*ER- slow effect  Ex: MAO inhibitors & tyramine rich foods

5. RIGHT TIME Impact of food on drug action

 Give 30 MINUTES before & after the scheduled  Ex: Vit K can reduce effects of Warfarin
time  IRON- best absorbed w/ EMPTY STOMACH
 Specific time for specific meds  Take it- w/ food
 STAT- atleast WITHIN 30 Minutes
TCAs, SSRIs, MAOIs
ISCHEMIC- lack of blood supply
INFARCTION- absence of blood supply HYPERTENSIVE CRISIS

2 that occludes blood vessels Foods not allowed: aged cheese, mozzarella, preserved
 FATS meat (bacon, tocino, salami), bananas, chocolate
 BLOOD CLOTS Foods allowed: FRESH CHEESE COTTAGE cheese
CREAM cheese
LIVER- produces cholesterol between 10pm & 2am in the
morning Vit K- green leafy vegetables- spinach, kangkong
 STATINS- Simvastatin, Atorvastatin
 Given at bedtime, because there are no DRUG-DRUG INTERACTION
cholesterol produced in the morning Combination of Drugs- compatible/not, (addictive,
antagonistic, counteracts, potentiating) boosts/strengthens
STEROIDS are produced in the morning between 4am drug
until 8am  Includes herbal medications
 2nd surge : 1pm-5pm  Creation of unique response
 Ends with “sone”  Drugs combined in IV solution can form
 One in morning, one in afternoon precipitate (crystallization)

GUIDELINES: HERBAL MEDICINES

 Assess for allergies- Mild/Severe S- ambong
A-kapulko
N-iyog-niyogan  Needs Iron- pregnant, children, adolescents,
T- saang Gubat menstruating women, alcoholics (alcohol
A-mpalaya interferes w/ the absorption of iron)
L- agundi  Food decreases absorption but can cause GI
U- lasimang Bato DISCOMFORT, so take it with food
G- arlic  Liquid preparations- take with straw
B- ayabas  Vit C- increases absorption (oral)
Y- erba Buena  Administer IM preparation by Z-track method
 Irritates & stains the skin
MANNITOL should be incorporated w/ NSS  SE: black stools
 Not dextrose will CRYSTALLIZE  FeSO4 (black). Ferrous gluconate (green)

VITAMIN & MINERAL REPLACEMENT AUTONOMIC NERVOUS SYSTEM

FAT SOLUBLE VITAMINS
 Needs bile to be able to absorb these vitamins Sympathetic/ Parasympathetic/
 Excessive amounts can lead to toxicity ADRENERGIC CHOLINERGIC
 Vit A,D,K
Whenever you are: Acetylcholine
WATER SOLUBLE VITAMINS Stressed (AcH)
 Can be excreted out of our body Excited
 Vit C & B vitamins Stimulated Effects: (opposite)

*those with hepatitis & liver cirrhosis- has Vit A,D,K Body stimulates SNS HR, BP
deficiency because there are no bile produced Diarrhea
Epi, NE, Dopamine Diuresis
A- eyes, skin Pupil Constriction
D- bones excessive intake can lead to (Adrenaline) (myotic)
K- clotting Salivation
HYPERVITAMINOSIS Effects:
A,D,K BP- Vasoconstiction
HR- Myocadial O2
Hypercalcemia demand
Peristalsis preservation
Kidney Stones UO/urination skill

RENAL FAILURE Constricts blood

Vessels
VITAMIN C *Also GI & GU are not an impt
 Aids in the absorption of iron & conversion of folic Organ
acid
 Excessive doses can cause GI upset & diarrhea Decreases blood supply

ANTI-ANEMIC DRUGS *Brain & Heart impt organ

B vitamins Dry mouth
 Megaloblastic anemia- (Folic acid/ Vit B12) Dilates pupils
B vitamins Dilates bronchioles
 needed for DNA synthesis, blood production &
nervous system development  All hormones & chemicals/ drug will not work
not unless there is 2 things
Folic Acid  Chemicals & receptors
 green leafy vegetables (half-cooked- vitamins
destroyed by heat) 4 RECEPTORS IN SNS
 can affect development of CNS in 1st trimester RECEPTORS
 Baby can develop neural tube defects SPINA Epinephrine A1- vasoconstriction
bifida Norepinephrine A2- vasodilation
 400mcg/day Dopamine B1- -- HR
B2- -- bronchodilation
Vitamin B12- Cyanocobalamin (for shock)
 Essential for DNA synthesis, normal hematopoiesis Also, uterine relaxation
& nerve development (for premature labor)
 Source: meat products
 Deficiency- PERNICIOUS ANEMIA Agonist- stimulates
 Prone to vegetarians Antagonist- blockers
 Lack of INTRINSIC FACTOR- produced by
stomach. Ex: GASTRECTOMY α & β ADRENERGIC AGONISTS
 Drugs stimulating both α & β receptors
PERNICIOUS ANEMIA- given IM cyanocobalamin  Promotes breakdown of CHO- hyperglycemia
 Once every month for the rest of your life  EPINEPHRINE- used for treatment of shock,
bronchospasm
IRON  Glaucoma ( decrease IOP/ dilates pupils)
 For Hgb regeneration  NOREPINEPHRINE- for shock, cardiac arrest
 DOPAMINE (Inotropin)- DOC for shock
 Low dose- vasodilation
  High dose- vasoconstriction- HR & BP  Dyspnea

 Increases renal perfusion ( UO) NURSING CONSIDERATIONS

 HYPERGLYCEMIA is normal for people who take  give medications on time
epinephrine  Myasthenic Crisis (UNDERDOSE) & Cholinegic
Crisis (OVERDOSE)
α SPECIFIC ADRENERGIC AGONIST  If the symptoms get worst- Cholinergic crisis
 Binds only to α receptors  If the symptoms become good- Myasthenic crisis
 Stimulates only α1- PHENYLEPHRINE (Neozep)  To differentiate: TENSILON
 α1- causes vasoconstriction, therefore  Have a standby antidote at the bedside
contraindicated if there is hypertension  Anti-cholinergic drug- ATROPINE SO4
 Phenylephrine (neosynephrine)- IV for shock &
arrhythmias ANTICHOLINERGICS
 Almost same as SNS not same drugs but same
 CLONIDINE (Catapres), ALDOMET (Methyldopa) effects
 Regulates release of NE- specific to α2- BP
 Anti-hypertensives  Dry secretions (pre-operative)
 Atropine
*we don’t give if BP is greater than 120 may cause
V.Tach  Decrease peristalsis

β SPECIFIC ADRENERGIC AGONISTS  Hyoscine (Buscopan)

 Both β1 & β2 -prevent motion sickness
 ISOPROTERENOL HCl (Isuprel)- bronchodilator  Scopolamine
but HR- can cause severe TACHYCARDIA - HR
 METAPROTERENOL (Alupent)  Atropine given in ER for severely bradycardic
 When the patient says “My heart feels racing”- it is patients
NORMAL  SE: dry mouth, constipation, blurred vision & avoid
in glaucoma
 β2 only- FEWER SE
 SALBUTAMOL (Ventolin)- safest NEURO
 TERBUTALINE/ Bricanyl (uterine relaxation) PARKINSON’S DISEASE- a degenerative disorder
 dose may stimulate β1 receptors  Dopamine, AcH
 Given inhalation- faster effect  Destruction of substantia nigra (decrease
 Bronchodilator/ uterine relaxation dopamine)
 SE: tremors, restlessness, nervousness The one that produces Dopa
w/c is located at the basal ganglia
ADRENERGIC BLOCKER Basal ganglia- important for voluntary muscle control
 BP Problem: Motor
 α1 receptor antagonist-- BP
 α blockers- “zosins” (terazosin) Cardinal Signs: TRB
 Beta blockers- “olols”  Tremors, Rigidity, Bradykinesia
 β1- HR
 β2- Bronchoconstriction LEVODOPA – precursor of dopamine
 CI: ASTHMA L-dopa dopamine

Slow HR- beta blockers Receptors in the

Decrease IOP- Timoptic -brain
-heart 1% left- need a big dose
CHOLINERGICS -GI
 AcH (Myasthenia Gravis- Lack AcH) -GU
 EDROPHONIUM (Tensilon)- Short Acting AcH  Levidopa/Carbidopa (Sinemet)- allows more L-
 5-20 minutes- get better at 5s & get back dopa to be converted in the brain
at 20 mins  Substance na papalit sa dopa
 Diagnostic drug
 NEOSTIGMINE (Prostigmine) Dopamine agonists
 Pyrodistigmine  Bromocriptine (Parlodel), Amantadine
 Long Acting (Symmetrel)
 Promote peristalsis & urinary retention  Stimulates production of dopamine
 Betanechol (Urecholine)
MAOI’s
PNS  Selegeline (Elpedryl)
AcH- chemical important for skeletal muscle contraction  MAO- enzyme that promotes breakdown of Epi,
NE & Dopa w/ MAOI it stops/ inhibits the
Myasthenia Gravis- MUSCLE WEAKNESS- main breakdown
problem
Anticholinergics
Respi- diaphragm  Benztropine (Cogentin), Dipenhydramine
(Benadryl)
Lack of AcH difficulty of breathing  Stops AcH
 Ptosis- drooping of eyelids
 Dysphagia- easily aspirate, difficulty chewing OPEN ANGLE GLAUCOMA
 Diplopia
  Blockage/ obstruction of the TRABECULAR  SE: HEAD ACHE (major SE), hypotension,
MESHWORK (problem) tolerance
 Slows damage of the aqueous humor w/c  If the patient complained of HA, give paracetamol
increases IOP  Remove during night time
 If hairy, DON’T SHAVE, clip the hair or use
VOLUME=PRESSURE depilatory creams or find a spot that don’t have
much hair like arms
Pathophysiology  If you use the same site- TOLERANCE
 If transdermal- wipe off first before you apply a
Aqueous humor patch because if you don’t there will be an additive
effect
Produced by ciliary body  Don’t give with erectile dysfunction drugs
(VIAGRA)
Posterior chamber
NTG & Viagra
Anterior chamber Systemic Vasodilation + Vasodilates penis SHOCK

Trabecular meshwork Antidote: EPINEPHRINE

(Canal of schlemm)
*in NCLEX, after 3 doses of NTG and chest pain is not
relieved, do not bring the patient to hospital, instead
call 911

ANTI-ANGINALS
Beta blockers
 Decrease production of IO fluid  Atenolol, metoprolol, propranolol, nadolol
 Beta blockers  Block beta receptors
 Timolol  Decrease the heart rate
 Carbonic Anhydrase Inhibitors  Anti-anginals, antihypertensives
 ACETAZOLAMIDE (Diamox)
-diuretics Calcium Channel Blockers
 Ca- electrolyte important for muscle contraction
 Decrease outflow of IO fluid (miotic)  VND- Very Nice Drugs
 Cholinergics  Verapamil, Nifedipine (Amlodipine), Diltiazem
 Pilocarpine  treat angina, decrease BP
NC: caution patient about diminished vision in dimly lit  withhold if systolic BP <90, PR <60
Areas
MI (Heart Attack)
Other management: Blood clot
 Laser Trabeculoplasty- lasers applied to Cholesterol plaque
trabecular meshwork to open
Necrosis
CLOSED ANGLE GLAUCOMA (Brain- less than 10 mins)
 Medical emergency
 Narrow the angle formed by the cornea & More than 10mins, irreversible brain damage
the iris narrows, preventing the aqueous
humor from draining out of the eye. CPR w/in 4-6 minutes
 *The more dilated the pupils, the more
obstructed it becomes, the more angle MONA
gonna close
MSO4 O2 NTG Aspirin
CARDIOVASCULAR
Anticoagulants
ANGINA- no necrosis & w/ normal cardiac enzymes  PREVENTS new clots from forming
 Chest pain relieved by NTG lasts only in less than
15 minutes HEPARIN, Enoxaparin (Lovenox): PTT, APTT
MI- elevated cardiac enzymes w/ necrosis Antidote: Protamine SO4
Route: SQ/IV
CARDIAC MEDICATIONS
 Angina WARFARIN (Coumadin): PT, INR
 Nitrates, Calcium Channel Blockers, Beta Antidote: Vitamin K
Blockers Route: ORAL
 Increase blood supply, reduce cardiac workload SE: bleeding, avoid green leafy vegetables and monitor for
(reduce HR) bleeding

NITRATES Thrombolytics (potent drugs)

 Vasodilator HR O2 demand  DISSOLVE CLOTS
 Isosorbide Mononitrate/ Dinitrates  Alteplase (t-pA), streptokinase, urokinase
 Myocardial O2 needs  AE: Bleeding
 Dilate large coronary arteries
 SL x 3doses/q 5min MI: must be given w/in 4-6 hours of infarct
 Dark glass containers; cool storage CVA: must be given w/in 3-4 hours of episode
 Wash, DO NOT TOUCH CONTROL TIME: PT: 10-15 s
Therapeutic Time: 1.5-2 x CV (control value)
NC:
Ex: 10 x 1.5 = 15-20s  Watch for bradycardia
 Have ATROPINE at bedside
Most important question: What time/ when did the  Monitor VS & ECG
symptoms start?  Cardiac Arrest- give Epinephrine, if Vfib don’t
give anymore.
Signs of Stroke
F- ace drooping If Heart Block- pacemaker
A- rm weakness If Bradycardia- Atropine SO4
S- peech slurred
T- ongue weakness CHF- Congestive Heart Failure
Cardiac Glycoside (DIGITALIS-DIGOXIN)
Properties of Heart  Slows & strengthens heart
 AUTOMATICITY  Increase blood supply to organs
 Intrinsic pacemaker in SA node  Long acting
 CONDUCTIVITY  Toxicity: 0.5-2.0 ng/mL
 Able to travel from one point to another
 CONTRACTILITY BANDAV = (bradycardia. Anorexia, N/V, diarrhea, visual
illusions)
P wave atrial <0.11s GI
depolarization
PR interval time it takes for 0.12-0.20s Visual illusions: YELLOW GREEN HALOS
impulse to go
down from SA  Check K+ levels: prone to toxicity
to AV node  SE: bradycardia, don’t give if <60bpm
QRS complex QRS complex 0.04-0.12s  Antidote: DIGIBIND
QT interval total time for 0.42-0.43s  + inotropic= force of contraction/ squeezing
ventricular
ability
depolarization
 HYPOKALEMIA- predisposes digoxin toxicity
& repolarization
T wave ventricular  K- 3.5-5.0 mg/dL
repolarization
DIURETICS
2 potent diuretics: CAI’s & Osmotic Diuretics

5 TYPES:

1. CAI’s- Acetazolamide (Diamox)- glaucoma

 If drops, apply to lower conjunctival sac, press the
nasolacrimal duct to prevent systemic absorption, 5
mins apart
2. Osmotic Diuretics-
 MANNITOL- decrease ICP
1st Degree Heart Block 3. Loop Diuretics
-prolonged PR interval  FUROSEMIDE (Lasix)- best for CHF, fast acting
 Rebound Hypertension
4. Thiazides
 HYDROCHLOROTHIAZIDE- best for HTN
 SE: Hyperglycemia
5. K+ sparing
Cardiac arrhythmias/ if HR too slow/too fast  SPIRINOLACTONE (Aldactone)
 Monitor for orthostatic hypotension
Impaired tissue perfusion
*the closer to glomerulus, the more potent the drug
Normal Sinus rhythm
-HR: 60-100bpm Volume

110-Sinus Tachycardia BP BP

When you wake up- sinus bradycardia *(body does not want abrupt
Decrease in BP so it Vasoconstriction
VENTRICULAR TACHYCARDIA Compensates)- Loop diuretics
-most dangerous rhythm
RAAS
VTach leads to Vfib
Defibrillate: VTach & Vfib, never defibrillate Asystole Renin AI AII
ACE
Decreases HR: (Ace Inhibitors)
QUINIDINE: Atrial
LIDOCAINE: Ventricular Best technique to detect effectiveness of DIURETICS:
Bretylium  Weigh the client daily
Adenosine
Amiodarone (cordarone) ANTI HYPERTENSIVES
  PHENYLEPHRINE (Neozep, Decolgen)
CENTRAL ACTING VASODILATORS
α2 agonists Hydralazine (Apresoline) TOPICAL NASAL DECONGESTANTS
Clonidine, Aldomet NTG (Nipride)  Both adrenergics & steroids
 Prompt onset
 Potent
α BLOCKERS ACE INHIBITORS  Sustained use over several days causes
“zosins” Captopril (Capoten) REBOUND CONGESTION, making the condition
Doxazosin (Cordura) Enalapril (Vasotec) worse
Prazosin (Minipress) (produces dry cough)
Rhinitis Medicamentosa- (extended medicine use)
Ex: Nasal sprays
BETA BLOCKERS CA CHANNEL BLOCKERS
“olol” Amlodipine (Norvasc) NURSING IMPLICATIONS
Propanolol (Inderal) Felodipine (Plendil)  Decongestants may cause
Atenolol  HYPERTENSION, palpitations & CNS stimulation.
Avoid in patients with these conditions
ARBs  Patients should avoid caffeine & caffeine
(ANGIOTENSIN II RECEPTOR BLOCKERS) containing products
“sartan”  Monitor for cardiac dysrhythmias
Losartan  Monitor blood glucose levels
Telmisartan
ANTITUSSIVES
ANTILIPEMIC AGENTS  PURE FORM- MORPHINE, codeine
 Cholyestyramine (Questran)  Opioids- came from plant opium w/c is CNS
 Reduces absorption of fats from GIT-stops bile depressants
 Atorvastatin (Lipitor)  Suppress cough reflex & respirations
 Simvastatin (Zocor)  Reduces peristalsis
 Lovastatin (Mevacor)  Respiratory Depression
 Reduces production of cholesterol by the liver  *avoid activities requiring mental alertness
 Give at night  Ex: ROBITUSSIN w/ codeine (Robitussin AC)
 Check liver enzymes  Long term SE of Opioids: reduces peristalsis
 There will be steatorrhea (oily, foul smelling, causing CONSTIPATION
presence of fat in feces & Vit ADK deficiency)
 Target is BILE NON OPIOID
 Orlistat (Lesofat)  DEXTROMETHORPHAN (Vicks formula 44,
Robitussin-DM)
RESPIRATORY (COPD)
BRONCHODILATORS EXPECTORANTS
 STEROIDS- anti-inflammatory  Drugs that aid in the expectoration (removal of
 MUCOLYTICS/EXPECTORANTS mucus)
 ANTIBIOTICS (secondary infections)  Reduce viscosity of secretions
 Disintegrate & thin secretions
INFLAMMATION  Final result: thinner mucus that is easier to remove
Causes Vasodilation  GUAIFENESSIN (Robitussin)
Injury
BLOOD MUCOLYTICS
 ACETYLCYSTEINE (Flumucil, Mucomyst)
IC  Antidote for Tylenol (acetaminophen)
Mast cell overdose
Chemical mediators, cap.  CARBOCYSTEINE (Solmux), BISOLVON
Histamine, bradykinin, permeabi-
Leukotriene, prostaglandin lity COPD- BRONCHODILATORS
*All bronchodilators causes tachycardia except
Salbutamol

IT IV XANTHINE- Aminophylline (IV), Theophylline (Oral)

Edema α & β agonists- Epinephrine (α1, β1 & β2)
*we have semi permeable Isoproterenol (β1 & β2), Salbutamol (β2)
Membrane
LONG TERM STEROIDS
SIGNS OF INFLAMMATION  Inhaled Steroids
 Callor (heat)  Rinse mouth with water after use (prevent
 Rubor (redness) oral thrush)
 Dolor (pain)  Anti-Leukotriene
 Tumor (edema)  Montelukast (Singulair)
 Functio Laesa  Mast Cell Stabilizers
 Cromolyn Na (Intal)
ORAL DECONGESTANTS  AE: Bronchospasm
 vasoconstriction
 prolonged decongestant effects but delayed onset BRONCHITIS
 No rebound congestion  Air is trapped in alveoli, air goes in & does not go
 Exclusively adrenergics out
  CO2 yields carbonic acid= RESP. ACIDOSIS

EMPHYSEMA
 Alveoli w/ trapped air (bullae)
 If bullae erupts (cause pneumothorax)

ASTHMA
 Bronchoconstriction

Xanthines- caffeine--- bronchodilator

INHALERS
 1-2 in away from mouth
 MDI & spacers
 Hold breath for 5 to 10s

-6-9 months steroids- anti-inflammatory,

immunosuppressants

Oral thrush (candidiasis)

Normal flora die in mouth

TB TREATMENT

R- eddish orange secretions, hepatotoxic

I- pyridoxine (B6) to prevent peripheral neuropathy,
paresthesia, LFT
 gold standard for TB
P- raises uric acid (gout), monitor LFT
E- optic neuritis
S- ototoxic, nephrotoxic

LFT- Liver Function Test

*If exposed to person w/ TB take prophylactic tx 1-3 mos
*once on med 2-3 weeks, chances of communicability is
lessen

RIPE (Oral) S (IM/IV)