8.

Right to refuse
Pharmacology– Study of biological 9. Right assessment
10. Right evaluation
effects of chemicals.

* All drugs are chemical and are introduced to the

body, and this will cause change.
There are different sources of drugs:
 ANIMALS – insulin – DM – pancreas of cows
and pigs.
 PLANTS – St. John’s Wort: depression
 INORGANIC COMPOUNDS – Mg, Ch, Ca, Fe
 SYNTHETIC – Insulin from E. Coli.
Branches of Pharmacology
 PHARMACODYNAMICS – DRUG’S EFFECT TO
THE BODY (e.g., Drug is introduced to
the body. In the body, there is a cell
that has a receptor that the drug will
bind to for it to produce an
effect/change in the body.)
 PHARMACOKINETICS – BODY’S REACTION
TOWARDS THE DRUG. (e.g., since the
drug is an antigen (foreign substance)
the body will react to it.)
*The following are the processes that
will move the drug in the body:
 Liberation
 Absorption
 Distribution
 Metabolism
 Excretion
Rights of Drug Administration
* First 5 are the most important
1. Right Medication
2. Right Dose
3. Right patient – 3x check the identity of
the patient– WHEN: going to get the drug,
preparing the drug, administering to the
patient.
4. Right time
5. Right route – most convenient is oral
route, least safe is IV.
6. Right documentation
7. Right client education
Pharmacodynamics – what the drugs
do to the body.
- How can a drug produce a change in the
body.
Actions of Drugs:
 Replace a missing substance (DM - Insulin)
(Hypothyroidism – T3 and T4) (Addison’s dse
– corticosteroid and mineralocorticoids)
 Increase cellular activities – (Epinephrine -
Adrenergic, Digoxin – Heart dse)
 Depress cellular activity – (-olols – beta
blockers)
 Interfere with the growth of a foreign
cells – (antibiotic, anticancer drugs)
Drugs Action maybe through:
 Receptors
 Enzymes and pumps
 Chemical interaction
 Altering metabolic processes
Drug-Receptor Interaction
e.g., Insulin. Insulin needs to transport sugar into
the cells but before that, the insulin needs to
bind to a receptor in the cells to transport sugar.
AGONISTS – stimulate
ANTAGONIST – block/against
*2 types of Antagonists:
• Competitive antagonist – binds to the
same receptor. (1 receptor = many drugs).
 Potency of an agonist is reduced
  Diazepam and Flumazenil

*Same sila makakapasok sa receptor ng cell pero

mababawasan yung potency ng isang drug.

• Non-competitive antagonist – binds to

a different receptor. (1 receptor = 1
drug)
 Prevents potency of an agonist.
 Epinephrine and Phenoxybenzamine
(adrenergic agent and an alpha
blocker)

*Yung impulse is yung message from the brain. It

*Kahit may different silang receptor,
mabblock nya yung potency ng isa.
EXAMPLE: AUTONOMIC DRUGS (ANS)
will now travel on the axon terminal where there
are neurotransmitters, then the impulse will be
transmitted from the neuron to a receptor. Since
muscle yung receptor, ACH yung bababang impulse
that will cause contraction of the muscle.

SNS PSNS

RECPETORS
SNS: ALPHA BETA

PSNS: NICOTINIC MUSCARINIC

Drug-Enzyme Interaction
(e.g., cholinesterase inhibitors. Breakdown Ach)
*After ng contraction, papasok si cholinesterase
that will breakdown ACH that causing relaxation of
the muscle.
 Drugs that interact with
cholinesterase
• Neostigmine – drug for myasthenia gravis
(-tigmine drugs)

*Impulse will travel to the axon terminal which in

turn secrete neurotransmitter (in this case 5HT or
serotonin). Serotonin will bind to a receptor in the
nerve that will cause impulse transmission.
*Neostigmine will block the action of
cholinesterase that will cause ACH to remain in
muscle receptor causing continuous contraction
of the muscle.

INHIBITING PUMPS – reuptake inhibitors

EXAMPLE: reuptake inhibitors

*After the action of serotonin, it will need to be

re-uptaken to the axon again. This is one of the
body’s ways of conserving chemical.
*After serotonin reuptake, the receptor will be
free and ready to bind to another
neurotransmitters.
Drugs that inhibit reuptake
SSRIs (Selective Serotonin Reuptake
Inhibitor)- antidepressant.
*Acc. to BIOGENIC AMINE THEORY, depression is
caused by a lack in Norepinephrine (NE), Dopamine
(Dopa), and Serotonin (5HT). So, the drugs for
depression should increase the action of the 3
mentioned chemicals. The drugs that increase the
action of those 3 chemicals are called
ANTIDEPRESSANT.
*Since na-inhibit ng SSRIs ang reuptake,hindi siya
makakabalik sa axon, bale nasa tabi-tabi lang siya
around the synapse. Hindi siya pwede sa loob ng
receptor kasi kailangan ng bagong
neurotransmitters. With that, kapag nagpaulit-ulit
yung mechanism, dadami yung serotonin sa synapse
increasing serotonin levels. Therefore, we can call
SSRIs an antidepressant.
Pharmacokinetics – response of the
body to the drugs.
1. LIBERATION
*Drug enters the body through mouth, travels to
the stomach. In the stomach, there will be the
release of an active ingredients.
2. ABSORPTION
- This time, the active ingredients from
the drugs will now be free in the blood.
- Movement of drug into the bloodstream
ROUTES OF DRUG ABSORPTION
• ENTERAL ROUTE – GIT (from mouth to
anus).
 Oral
 Rectal – fastest absorption among
enteral route because there are many
blood vessel in the rectum.
- Dosage form ng drugs if rectal is
suppository.
- How are you supposed to store
suppository drugs? Chiller (sa labas
lang ng ref).
 Nasogastric
5. ELIMINATION/EXCRETION
• PARENTERAL ROUTE
 IV – fastest absorption among
parenteral route – IV pinakafastest
absorption among all the routes.
 SQ
 IM – second fastest absorption among
parenteral route because muscles are
highly vascular.
 ID
• TRANSMUCOSAL ROUTE
 Sublingual – fastest absorption among
transmucosal route.
 Inhalation
 Topical
3. DISTRIBUTION – the drug that is in the
blood will now be transmitted to the
receptor of the target cell.
- After binding, there will be a change
or effect that will happen.
4. METABOLISM (biotransformation) - If
administering oral drugs. For example,
500mg of oral drugs. It will be liberated
and absorbed but before distribution it will
need to pass first the liver. In the liver
there is an enzyme called CYTOCHROME P450
that will breakdown the drug from 500mg
it will now be a new drug with 400mg that is
now less active/potent. This effect is called
FIRST PASS EFFECT. Now, the 400mg drugs
only will be distributed to the body.
- Also, one of the major functions of the
liver to the drug is to detoxify to lessen
the toxicity of the drug to the body.
- If the drugs was given IV 500mg, then
500mg will be distributed to the body. It
will not undergo metabolism and there will
be no First Pass Effect.
- In the case where the patient is pedia,
elderly, or with cirrhosis or liver dse, we
need to compute for the dosage to
prevent the risk for toxicity.
- Nasa target cell na yung gamot.
- Whatever not be used by the cell will be
eliminated
- Organs where elimination will take place:
(Kidney – major organ for elimination,
Feces, Lungs and Skin) – It is called
Excretion.
Pharmacokinetics
• DOSE
o Amount of drug to be administered
to the patient
• SCHEDULE
o Frequency, how many dose/s per
day. How many days/ Durations.
• RECOMMENDED DOSE
o RIGHT amount + RIGHT schedule
o Level of drug that will produce
their peak of effect
 • CRITICAL CONCENTRATION
o Level of drug in the blood which
produces a therapeutic effect

• THERAPEUTIC EFFECT
o Favorable response after a
treatment of any kind
o Healing, Cure

• LOADING DOSE • X – hour

o Initial dose, immediate response • Y – amount of the drug in the body
• HALF TIME Amoxicillin 500 mg every 8 hours for 7 days T
o Time it takes for a drug to become ½: 8 hours
half of its previously peaked level
4 half-lives to reach the effect.
o Reference of the drug for its
schedule (frequency)
• Recommended Dose (RED)– Right Dose
(amount), Right Schedule (frequency).
EXAMPLE: o If you are giving the recommended
Cefuroxime dose, you will able to reach the
Time ½ = 12 hours critical concentration.
o If you reach the critical
6am = 500 mg
concentration, you will able to have
After 12 hr, which is 6 pm = 250mg
the therapeutic effect (cure).
6am = 125 mg
6 pm = 62.5 mg o The cure will start when you reach
6am = 31.25mg the critical concentration. That’s
6 pm = 15.61mg why it is necessary to give the right
6am = 7.8mg dose, right time, right amount.
6 pm = 3.9
6am = 1.9 mg
6 pm = 0.9mg
6am =0.45mg
6 pm =0.2mg
6am =0.1mg
6 pm = something

How many days until the drug is excreted? 7

days in 500 mg.

Aspirin – Blood thinner, can’t undergo Example:

surgery the patient will be at risk for
bleeding. Defer, discontinue aspirin (5-7
days) if surgery is required.
Board Exam Question:
How much left in the body after 5 half-lives?
Marites bought prefer cheaper medicine of 250mg
na dapat 500mg = UNDERDOSE (BLUE) (Critical
Concentration and Therapeutic effect is not
reached).

= 15.61 mg
Example: • Maintenance of Elderly (PINK):
Students who forgot to take their medicine in the Continuous to have a plateau effect.
said schedule. (GREEN)
* If the patient has overdose:
 Give antidote
o Paracetamol - Acetyl
o Opioids/ Narcotics/ Morphine -
Naloxone (Narcan)
o Warfarin - Vitamin K
o Heparin - Protamine Sulfate
o Digoxin - Digibind

∗ When to take maintenance?

∗ Once they stop taking the maintenance the
therapeutic effect will definitely go down.
So if it is for hypertension there will be no
• Loading Dose – higher than the control with the hypertension. You have to
recommended dose. We give this in take it ASAP.
emergency cases. (PINK)
 First Dose (initial dose) which
gives us the immediate
Dosage Forms of Drugs
effect. Recommended dose A. Solid
will be followed after the 1. Tablet
loading dose. a. Scored
 It has a line — to be easily
divided
Example:
Remdesivir: RD 100mg OD x 5 days 1vial = 100 mg.
How many vials? = 6 to complete the 5 days.

Loading dose is given as the first dose: 200mg b. Layered

 2 or more chemicals in a tablet
All drugs can be given a loading dose, depending if
 Ex. Neozep - contains
it is emergency. Paracetamol, Phenylephrine
We can mix 2 antibiotics as long as it targets HCl, Chlorphenamine Maleate
different organ/cell in the body.
 c. Enteric-coated
 Tablets not dissolved in the
stomach but in an alkaline
environment (small intestine)
— lesser gastric irritation
 Ex. Aspirin
3. Lozenges
 solid dosage forms that are
intended to be dissolved or
disintegrated slowly in the mouth
 there are SOME that can be mixed in
juices
 Ex. Antiseptic - destroy bacteria
Anesthetic - relieve pain

B. Liquids
1. Syrup
d. Chewable  Sugar-based, clear, flavored
 Liquid forms are better  Usually for kids
absorbed 2. Suspension
 Ex. Celeen Chewables  Chemical and water will separate in
a couple of minutes
 NI: shake before administration
3. Elixir
 Contains alcohol
 It will cause drowsiness
 NI: avoid driving and operating
e. Sustained Release big machineries
 The absorption, and liberation is
delayed and not at the same time.
 The duration is longer C. Topical
1. Ointment
 Oil-based
 Intervention  For dry lesions
o If the patient cannot swallow the tablet:
 Crush the tablet then mix it to the
water, juice, or milk
 Scored, layered, chewable can be
crushed
 Do not crush enteric-coated and
sustained-release tablets, swallow it
2. Cream
whole to avoid liberation
 Water-based
 For wet lesions
2. Capsule
a. Hard gel
 Gel-capsuled with powder inside

3. Lotion (medicated)
b. Soft gel  Used if the lesion is extensive
 4. Patch
NI:
 Apply over dry and non-hairy areas
 Rotate the sites to prevent
irritation
 If the site has abundant hairs, do
not shave. TRIM IT!!
one direction from the dendrites, to the soma,
and to the axon.
 The myelin sheath will not let the impulse to
pass through the axon so it will jump
(salutatory conduction) along the nodes of
ranvier until it reaches the axon terminal. An
electrical impulse cannot cross a synapse

∗ Presynaptic nerve - before a synapse

∗ Postsynaptic nerve - after a synapse
∗ Repetitions of salutatory conduction in every
nerves the end point will be effector cell.
Effector cell can be a:
- Muscle
- Gland
- Another nerve

PHARMACOLOGY TIPS:
Remembering medications and the body
system affected…
Review the sympathetic and parasympathetic
nervous system since many medications have
actions that affect these systems.

Question:
Nervous System How can this electrical impulse which is carrying a
message be able to transmit that to the effector
cell if it cannot cross the synapse?
 When there is an impulse only up to the axon
terminal, the axon terminal will be releasing
neurotransmitters (chemicals) which will be
carrying the message and cross the synapse
binds to the receptors on the dendrites. Once
it has hit the receptors on the dendrites, the
dendrites will again form another electrical
impulse. The message will be on the electrical
a. Dendrites impulse once again. After a series of electrical
b. Soma - cell body impulse, the chemicals will be binding to the
c. Axon receptors.
d. Myelin Sheath - insulator of electricity  If the effector cell is a muscle — contraction,
e. Nodes of ranvier - axons without myelin gland — secretion of hormones, nerve —
sheath transmission of impulses
f. Schwann cell
g. Nerve ending
Neurotransmitters
 Impulse runs along the nerve which brings a  Chemicals in the body acting as “messenger”
message or information 1. Acetylcholine (ACH)
 The message should reach the end of a series  muscle contraction
— synapse  memory
 Whenever there will be an impulse, the  ↑ may cause bipolar
movement of the impulse along the neuron is  ↓ may cause Alzheimer’s Disease
2. Norepinephrine and Epinephrine (NE/E)  If a nerve produces
 Catecholamine - released during  ACTH - Cholinergic nerves
sympathetic stimulation  Epinephrine - Adrenalines
 ↑ may cause schizophrenia, mania (Adrenergic nerves — produces in
 ↓ may cause depression, ADHD adrenal medulla
 Norepinephrine - Adrenergic nerves
3. Dopamine (DOPA)  Dopamine - Dopaminergic nerve
 coordination of impulses and responses  Serotonin - Serotonergic nerve
 cognitive behaviors (thinking, learning,  Dopamine - Dopaminergic nerve
reasoning)
 ↑ may cause schizophrenia, mania
 ↓may cause depression, parkinson’s,
AUTONOMIC NERVOUS SYSTEM
ADHD Two (2) neurotransmitters:
1. Norepinephrine
4. Serotonin (5HT) 2. Acetylcholine
 For arousal and sleep
 Prevent depression
 Promotes motivation
Two (2) branches:
1. Sympathetic Nervous System
 Foods provide serotonin:
 a.k.a Adrenergic nervous system
o Chocolates
 releases norepinephrine (Adrenergic
o Banana
nerves)
 ↑ may cause schizophrenia
2. Parasympathetic Nervous System
 ↓may cause depression
 a.k.a Cholinergic
 releases acetylcholine
5. Gamma-aminobutyric Acid (GABA)
 Inhibitory neurotransmitter
 Inhibits nerve activity
 Prevents overexcitablity or stimulation
such as seizure activity
 Used for depression
 Anticonvulsant will stimulate the GABA
 ↑ TREATS SEIZURE
 Pharma 2 – Autonomic Nervous System Drugs
SYMPATHETIC = SNS = Adrenergic
AGONIST = stimulate
MIMETIC = copy / mimic / gaya gaya
EXAMPLES OF - MIMETIC:
PARASYMPATHETIC = PSNS = Cholinergic
ANTAGONIST = Block
LYTIC = block / destroy / dissolve
EXAMPLES OF - LYTIC:
● Anxiolytic - Block anxiety
(Pampakalma)
● Mucolytic - Dissolve mucus
● Thrombolytic - Dissolve Thrombus
● Tocolytic - Block Toco (Tone of
Muscles)
 EXAMPLES OF SYMPATHOMIMETIC: EXAMPLES OF SYMPATHOLYTIC:
(Symphato = SNS) (Mimetic = Copy) (Symphato = SNS) (Lytic = Block)
● Sympathomimetic to the Heart ● Sympatholytic to the Pupils
- Increase the Heart Rate - Meiosis
● Sympathomimetic to the Bronchus ● Sympatholytic to the Blood Vessels
- Increase RR and Bronchodilation - Causes Vasodilation
● Sympathomimetic to the GIT ● Sympatholytic to the Bladder
- Causes Constipation - Emptying of the urine
● Sympathomimetic to the Bladder ● Sympatholytic to the Heart
- Urinary Retention - Decrease the heart rate
● Sympathomimetic to the Blood Vessels ● Sympatholytic to the Bronchus -
- Causes Vasoconstriction Decrease RR and
● Sympathomimetic to the Blood Flow in Bronchoconstriction
Kidney
- Decrease (Do not Pee)

EXAMPLES OF PARASYMPATHOMIMETIC: EXAMPLES OF PARASYMPATHOLYTIC:

● Parasympathomimetic to the GIT ● Parasympatholytic to the Pupils
- Causes Diarrhea - Mydriasis
● Parasympathomimetic to the Blood ● Parasympatholytic to the GIT
Vessels - Causes Constipation
- Causes Vasodilation
● Parasympathomimetic to the Pupils
- Meiosis
● Parasympathomimetic to the bronchus
- Decrease RR and
Bronchoconstriction

● Adrenergic Agonist to the Heart

- Increase HR
● Cholinergic Agonist to the Blood Vessels
- Causes Vasodilation
● Adrenergic Antagonist to the GIT
- Causes Diarrhea

● MECHANISM - Anti (Block) & Cholinergic

What drug do we give to patients in the
(Parasympathetic) It will block the PSNS,
OR aside of Anesthesia?
therefore SNS will dominate. SNS will help to
● ANSWER - ATROPINE
lessen the secretion and decrease the risk
● RATIONALE - It will lessen the secretions. To
decrease the risk of aspiration of aspiration.

● CLASSIFICATION - Anticholinergic Drug


Is the commercial about DIATABS correct?
“1 Dose, 1 Hour LBM ay tapos. Diatabs have
Anticholinergic Action!”
● ANSWER - YES
● Do you expect your patient to have dryness
of the mouth if ever the patient is taking
Antipsychotics? YES. If it is SNS dominance, there
will be a decrease of secretion such as
Saliva secretion, bronchial secretion, GI
secretions

ANS drugs
● CLASSIFICATION - Anticholinergic Drug
● MECHANISM - Anti (Block) & Cholinergic
(Parasympathetic) It will block the PSNS,
1. ADRENERGIC AGONIST
therefore SNS will dominate.
a. Epinephrine - CPR, Shock
● RATIONALE - SNS effect will help to cause b. Dobutamine - CHF
constipation. c. Dopamine - CHF, Cardiogenic Shock
d. Norepinephrine - Cardiac Arrest
What drug do we use for schizophrenia?
2. ALPHA 2 ADRENERGIC AGONIST
● ANSWER - Antipsychotics / Neuroleptic a. Clonidine (Catapres)
● What are the side effects - NMS - Found in CNS neurons - to
(Neuroleptic Malignant Syndrome), Tardive decrease Epinephrine flow
Dyskinesia, - Hypertension
Pseudoparkinsonism, Akathesia,
Anticholinergic
3. BETA 1 ADRENERGIC AGONIST
a. Dobutamne
● Do you expect your patient to have diarrhea - CHF
if ever the patient is taking Antipsychotics?
4. BETA 2 ADRENERGIC AGONIST
NO. Since the patient is taking an a. Albuterol / salbutamol
Antipsychotic drug (it will have an b. Isoproterenol
anticholinergic side effect) It will cause c. Terbutaline
d. Isoxsuprine
constipation instead of diarrhea.
● NURSING CONSIDERATION - Increase oral fluid
5. BETA ADRENERGIC ANTAGONIST “olol”
intake, increase fiber in the diet a. Propranolol
b. Pindolol - Severe hypertension due to
● Do you expect your patient to have
pheochromocytoma
emptying of the bladder if ever the patient
6. BETA SPECIFIC ADRENERGIC ANTAGONIST
is taking Antipsychotics? NO. We will expect
(6 only)
Urinary Retention. a. Betaxolol
● NURSING CONSIDERATION - Before taking the b. Esmolol
during the must patient must void first and c. Atenolol
d. Metoprolol
empty their bladder first, Bladder training
e. Bisoprolol
(Go to the bathroom to urinate every 3-4 f. Acebutolol
hours), less sodium intake.
BLOOD PRESSURE = HEART RATE X STROKE Day 2: Part 2
VOLUME X TOTAL PERIPHERAL RESISTANCE
TPR = Pressure in the blood vessels
Alpha 2 Adrenergic Agonist
ALPHA 1 ADRENERGIC AGONIST
(SNS ) (SNS) (STIMULATE)
Example ALPHA 1 ADRENERGIC AGONIST:
1. PHENYLEPHRINE (SYMPATHETIC) (part of
neozep, decolgen, bioflu) - Which receptors
does phenylephrine act upon? Blood vessels.
- Decongestant
- Allergic Rhinitis = It will cause
vasoconstriction = Blood flow to the area is
decrease = decreased O2 and nutrients to
• receptor found in CNS
the cells in the area = will result to cell
• Clonidine (catapres) is an alpha 2
shrink = blood vessels are much smaller = will
adrenergic agonist
be able to breathe comfortable
- For eyes during eye exam = It will cause • Other alpha 2 drug (methyldopa)
dilation (mydriasis) • ROUTE: sublingual and oral
- Effect on the Heart = Increase HR • Clonidine used to decrease blood pressure
- SIDE EFFECT OF PHENYLEPHRINE = causes (antihypontensive drug) and has an effect
vasoconstriction = Hypertension of SNS.
- Increase TPR = Increase BP • SNS = increase heart rate
- Decrease Blood volume a. What if the heart rate increase?
2. MIDODRINE * The blood pressure will increase.
- Drug of Choice = Orthostatic Hypotension b. What is SNS in blood vessels?
* vasoconstriction
- Will cause vasoconstriction
* and if there’s vasoconstriction the TPR
- Increase TPR = increase BP
will be increase and the effect in the blood
pressure will increase.
 • SNS increase blood pressure and CLONIDINE
has SNS effect and decrease the blood
pressure.
• Alpha 2 has SNS effect, but if it stimulating
the alpha 2 the sympathetic effect there
will be decrease in NE (sympathetic)
• If the NE decrease it will weaken the SNS
effect.
• PSNS will dominate
• PNS to the heart rate will decrease and if
the heart rate decrease the blood pressure
will decrease.
• This will cause the vasoconstriction
decrease and the TPR will decrease and the
blood pressure decrease.
• If it’s alpha 2 the stimulation will opposite.
BOARD EXAM QUESTION:
Which of the following is a CENTRALLY ACTING
ANTIHYPERTENSIVE DRUG?
- ALPHA 2 adrenergic agonist (CLONIDINE)
- We can also ind alpha 2 in the pancreas.
- Pancreas produce insulin the effect in alpha
2 will release less insulin. It is alpha 2 the
stimulation will opposite so the result will be
HYPERGLYCEMIA.
o RATIONALIZE: why is there hyperglycemia?
o Is Sympathetic is fight or flight?
- Yes, we need a lot of energy and we get
our energy in glucose. That’s why if
there’s sympathetic stimulation there
will be hyperglycemia because we need
energy.
Beta 1 Adrenergic Agonist
- BETA 1 we find receptor in the heart
- DRUG: DOBUTAMINE it is synthetic dopamine.
- Used Cardiovascular Heart Failure (pagod na
ang puso)
- Sympathomimetic
- This will help the heart contract
Side effects:
1. Palpitation ( increase hr)
2. Hypertension because the HR
If it’s stimulate BETA 1
- potassium will enter the cells
(antiarrhythmic drugs)
- it will increase also the stroke volume
- Beta 1 receptor also found in kidneys this will
- increase the renin release this will effect of
renin, angiotensin and aldosterone this will cause
increase in blood pressure.
Beta 2 Adrenergic Agonist
- Beta 2 receptor found in the LUNGS and it has
effect of sympathetic that will result in
BRONCHODILATION because it has SNS effect.
- DRUGS: albuterol or salbutamol (Ventolin)
- used for patient with asthma and COPD
- SE: palpitation and tremors.
* Reason; Alam natin yung beta 2 yung receptor
niya si lungs at yung albuterol mahal niya yung
beta 2 kaso nga lang si albuterol parang may crush
siya sa beta 1 or nagbinds sa beta 1 kaso yung beta
1 receptor nasa heart kaya parang naapektuhan din
ng albutamol si heart kaya nagkakaroon ng
palpitation and tremors. SANA MAGETS NIYO
HAHAHAHA.
- Beta 2 receptors can be found also in the UTERUS.
- the effect will cause the RELAXATION of uterus.
- Other DRUG: TERBUTALINE
- used in asthma and COPD
- also, used in premature labor called as TOCOLYTIC.
* LYTIC – it means block the TOCO
 * TOCO- it means tone of the muscle in the uterus. - decrease the TPR
- that will cause relaxation - used in hypertension this will decrease BP
- Beta 2 receptors can be found also in the BLOOD
VESSELS OF HEART, LUNGS AND SKELETAL MUSCLES.
- this will cause VASODILATION. 2. DOXAZOSIN
- Beta 2 receptors can be found also in the LIVER - “two timers” loves blood vessels and urinary
this will GLYCOGENOLYSIS. bladder
* LYSIS – it means blocking the glycogen
- caused vasodilation
* GLYCOGEN – stored glucose in the liver.
If there’s breakdown in glycogen this will cause - used for HYPERTENSION
HYPERGLYCEMIA. - decrease TPR also this will decrease BP

TAKE NOTE: If it’s sympathetic we have additional

glucose in the blood because of the activation of
alpha2 and for beta 2 receptor this will cause
hyperglycemia.
- Another drug: ISOSIXPRINE it is a tocolytic.
______________________________________
Alpha Adrenergic Antagonist
3. TERAZOSIN
- loves blood vessels and urinary bladder
-emptying the bladder
- used for BPH (benign prostatic hypertrophy)
4. ALFUZOSIN
- “loyal” always bind in urinary bladder
- emptying the bladder
- used in BPH
HEALTH TEACHING: If client has hypertension
and BPH we can give doxazosin and terazosin
drugs. It has lesser side effects.

5. TAMSULOSIN
- used for BPH

Beta Adrenergic Blockers

Alpha 1 Adrenergic Antagonist (Olol)

Alpha = SNS Adrenergic = SNS ANTAGONIST = BLOCK

It will block the SNS
DRUGS: INDICATIONS:
a. HYPERTENSION- because this will decrease the
1. PRAZOSIN heart rate and will decrease the blood pressure.
- love only the blood vessels it will bind to b. ANGINA – decreased oxygen supply and increase
the blood vessels oxygen demand
GOAL: Increase oxygen supply and decrease oxygen demand.
- the effect is vasodilation
BETA blocker decreases the heart rate and the
workload of heart decrease the oxygen demand
decrease and the oxygen supply will increase. Parasympathetic Receptors
c. MI – same rationale
d. SURPAVENTRIUCULAR ARRHYTHMIA, ATRIAL FIB
e. CHF (cautious) pagod na ang puso Cholinergic Receptors
- decrease the heart rate and this will decrease
workload of the heart and the energy the heart 2 TYPES:
diverted of the contraction or increase the force MUSCARINIC
of contraction (INOTROPY) NICOTINIC
f. ANXIETY - (propranolol)
- tachycardia, tremors and palpitations. MUSCARINIC AGONIST TO PUPILS= meiosis
- this will decrease heart rate. ANTINICOTINIC TO THE BLADDER= retention
g. MIGRAINE
h. OPEN- ANGLE GLAUCOMA- (betaxol, timolol) Where can we find these receptors?

SIDE EFFECTS: CONTRAINDICATIONS: NURSING

CONSIDERATIONS:

1. Bradycardia 1. monitor heart 1. hold if the

2. Hypotension rate heart rate is less
3. Broncho 2. monitor blood than 60 bpm
constriction. pressure 2. hold if the bp
4. Hypoglycemia 3. monitor breath is less than 90/ 60
5. Impotence sounds. mmHg
4. monitor serum 3. Avoid in
glucose patient with
asthma and COPD.
4. Caution in DM
NMJ= Neuromuscular Junction
CASE: A patient 60 year old, male, non alcoholic
drinker
History: Asthma
CENTRAL NERVOUS SYSTEM DRUGS
DX: Hypertension given beta blocker.
BETA blocker is a beta 1 specific adrenergic NORMAL PROCESS
blocker. Presynaptic N. will receive impulse release of
acetylcholine acetylcholine will bind to muscle
Beta 1 Selective Adrenergic receptor muscle will contract cholinesterase
will breakdown acetylcholine muscle will relax.

Blockers Myasthenia Gravis

- BISOPROLOL, BETAXOLO

(Autoimmune Problem)
- ESMOLOL
- ACEBUTOLO, ATENOLO
- METOPROLOL
* For patient with ASTHMA and COPD (the problem in MG is the receptor)

PROPANOLOL Autoimmune there is antibodies antibodies

= tachycardia and tremors in hyperthyroidism supposed to attack antigen which are foreign
bodies

In MG antibody is not attacking the antigen but

attacking the receptor resulting in absence of
receptors
Presynaptic N. will receive impulse  release of
acetylcholine but since there is no receptor
ANTICHOLINESTERASE BLOCKS CHOLINESTERASE
there will be plenty of acetylcholine since it
doesn’t have anything to bind on there will be
no contraction of muscles hence relaxation of
muscles only (paralysis)
Note: if there are still some receptors it can
manifest as weakness and not paralysis (initial
sign=ptosis)
• NEOSTIGMINE treatment
• PYRIDOSTIGMINEtreatment
• PHYSOSTIGMINE treatment
• EDROPHONIUM CHLORIDE
(tensilon)Diagnostic
o Are they anticholinergic or
cholinergic? Ans. Cholinergic

Cholinergic=Ach
MG=DECENDING PARALYSIS Anticholinergic=anti Ach

GUILLAN BARRE SYNDROME =ASCENDING MYASTHENIA GRAVIS: DIAGNOSTIC TEST

• TENSILON TEST (ENDROPHONIUM HCL)
PARALYSIS o Temporarily strengthens muscle for
5-10 mins.
G-galing B-baba S
o Route: IV
MYASTHENIA GRAVIS
• In women, 20-40 y/o, unkown cause or
MYASTHENIC CRISIS VS. CHOLINERGIC CRISIS
idiopathic
MYASTHENIC CRISIS CHOLINERGIC CRISIS
• Autoimmune
weakness, paralysis weakness, paralysis
• Descending muscle weakness caused by under caused by overdosage
dosage of cholinergic of cholinergic drug
MYASTHENIA GRAVIS: SIGNS & SYMPTOMS drug
treatment: give
• Ptosis- check palpebral fissure treatment: give anticholinergic drugs
• Diplopia- Double vision cholinergic drugs (atropine sulfate)
• Mask-like facial expression
• Dysphagia- risk of aspiration when a cholinergic
• Weakening of laryngeal muscles when a cholinergic drug is given via IV,
• Respiratory muscle weakness drug is given via IV, the condition will
o Lead respiratory arrest there will be an worsen
o Prepare at bedside tracheostomy increase in muscle
strength NI: prepare antidote
set
(atropine) during
• Extreme muscle weakness tensilon test

NURSING PRIORITIES
• AIRWAY
• ASPIRATION/ DYSPHAGIA
• IMMOBILITY

NO CURE FOR MG SINCE IT IS AUTOIMMUNE, WE

CAN ONLY STRENGTHEN THE MUSCLE BY GIVING
ANTICHOLINESTERASE SO THERE WON’T BE
BREAKDOWN OF ACETYLCHOLINE AND THERE
WILL BE CONTRACTION OF MUSCLES.
c