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- Afirah Maluin

-Alia Maliki

Q: Why ganglionic blockers are rarely used therapeutically ?
What is the primary therapeutical use of neuromuscular blocking agents?

1. Ganglionic blockers

- Not used in the treatment of chronic hypertension because of their side effects

- Used for hypertensive emergencies.

Side effects

- Prolonged neuromuscular blockade and potentiation of neuromuscular blocking agents.

- Excessive hypotension

- Constipation

- Urinary retention

- Dry mouth

2. Primary therapeutical use of neuromuscular blocking agents

- Anesthesia during surgery to relax skeletal muscle.

-Facilitate intubation in mechanical artificial ventilation.

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how physostigmine reverse an overdose of atropine

1.atropine- bind competitively & prevent Ach from binding to receptors-acts both cntrally and peripherally

2. physostigmine-inhibit AchE-stimulate cholinergic action

atropine overdose:
1. atropine molecules > Ach
2. physostigmine inhibit AchE, thus more Ach can competitively bind to receptors (Ach win yeay!)
3. atropine adverse effect is reversed!

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Fattirah Auni
Nur Haseena

How edrophonium's action differs from echothiophate

Edrophonium
🔴reversibe antichoinesterase
🔴bind to active center fof AchE
🔴Ach increase in synaptic space,increase para effect
🔴when eliminated in urine,action is lost

Echothiphate
🔴irreversible anticholinesterase
🔴organophosphate group covalently bind to active site of AchE
🔴permanent damage towards AchE
🔴Ach increase in synaptic space increase para effect
🔴to overcome,use 2-PAM (pralidoxime) to break bond btween drugs n enzyme. However,before aging only (loss of alkyl group in AchE

PRAZOSIN N ORGANIC NITRATES CAUSE FAINT AFTER WAKING UP FROM LYING DOWN

Prazosin: selective competitive alpha1 blocker receptor
Alpha1 should cause vasoconstriction,but receptor is blocked,➡vasodilation➡lower PVR➡lower BP

Organic nitrate:vascular smooth muscle relaxation

➡additive effect of drugs cause postural hypotension

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Najihah
Nabila

How does EPI cause hyperglycemic effect?

EPI- direct acting agonist
-stimulate B2 receptor which cause increase glycogenolysis in liver and release of glucagon
-stimulate a2 receptor which cause decrease release of insulin

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What is the advantage of using nadolol over pilocarpine in treating glaucoma?

Nadolol not affect pupil size thus not change focus

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Afifnephrine
Fakhrulamine

How does the body overcome the irreversible adrenergic block by phenoxybenzamine?

- Synthesize new adrenoceptor but take time,a day or longer

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Question 19 : Why dose of epinephrine need to be reduced in patient with hyperthyroidism?

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Question 19 : Why dose of epinephrine need to be reduced in patient with hyperthyroidism?

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Arisa Rashidi
Fariesya Husain

Function of Epinephrine:
1)beta-1:
Enhance CV action thru
♢iincrease HR
♢increase heart contractility
2)beta-2:
Vasodilation of skeletal muscle vasculature
3)alpha-1:
Vasoconstriction smooth muscle vasculature

Pt with hyperthyroidism
》Hypersensitive response to sympathomimetic drugs
》in beta-1 receptor: increase risk to medical complications such as hypertension, cardiac arrhythmia and congestive heart failure
》in beta-2: tremors, promotes growth and differentiation in thyroid cells
》in alpha-1&2: no significant response or alteration from both receptors in pt with hyperthyroidism.

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Q14 : why there is a slight decrease in DBP upon EPI IV injection?

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Q14 : why there is a slight decrease in DBP upon EPI IV injection?

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Ans : Epinephrine - act at adrenergic receptor on effector organs without interacting with presynaptic neuron.
Adrenoceptors have 3 general response:
1. Alpha 1: vasoconstrictions
2. Beta 1: cardiac stimulation
3. Beta 2: vasodilation
Why? Epinephrine stimulates beta 2 receptors on skeletal muscle causing vasodilation. So slight decrease in DBP bcs less blood return to heart

-Nadi & Nisah

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Najihah
Nabila

How does epinephrine cause hyperglycemic effect?

EPI - direct-acting agonist
-stimulate B2 receptor which cause increase glycogenolysis in liver and release of glucagon
-stimulate a2 receptor which cause decrease release of  insulin

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Q18: How can epinephrine be useful during anaphylactic shock?

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Q18: How can epinephrine be useful during anaphylactic shock?

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A: - Anaphylactic is hypersensitivity or allergic reaction with symptom of shortness of breath due to bronchostriction.
- Function of epinephrine:
1. bronchodilation
2. inhibit release of histamine from mast cell hence preventing allergic reaction.

Asyura
Aina

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Question 7➡Echochiophate bind irreversibly to acetylcholinesterase (AChE). What medication can be use to reactive the enzyme.How does it reactive it.

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Question 7➡Echochiophate bind irreversibly to acetylcholinesterase (AChE). What medication can be use to reactive the enzyme.How does it reactive it.

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Anis Amira
Faqihah Adlina

Echothiophate:
1)Covalently bind via its phosphate group at active site of AChE
2)So the enzyme permanently inactive

Answer:
Pralidoxime (2-PAM)
How?
👍It displace phosphate group of organophosphate➡ regenerate the enzyme
👍BUT the lost of an alkyl group which is call aging make it imposible for chemical reactivator to break bond between remaining drug and enzyme.
👍So pralidoxime need to be given before aging of alkylated enzyme occur

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Q16: Why albuterol, a b2 selective agent is more preferable than isoproterenol, a non selective beta agonist for treating asthma?

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Q16: Why albuterol, a b2 selective agent is more preferable than isoproterenol, a non selective beta agonist for treating asthma?

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A:
- Albuterol is more preferable than isoproterenol in treating asthma.
- Both are direct acting adrenergic agonist drug.
- Albuterol is a b2 selective agent that affect b2 receptor ONLY at bronchi leading to bronchodilation.
- Isoproterenol is a non selective beta agonist that affect b1 receptor at the heart leading increased contractility, HR and CO. While action on b2 receptor causes bronchodilation.
- Hence albuterol is used to avoid unwanted effect to the heart and to primarily treat asthma.

INSYIRAH KAMARULZAMAN
NURFARHANA MOHD YUSOFF

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Question 12

Nina
Fath

What are the predominant adrenergic receptor on heart, skeletal muscle, blood vessels and bronchi?

Answer:
•heart: beta 1
•skeletal muscle: beta 2
•blood vessel: alpha 1
•bronchi: beta 2

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Mawaddah Munirah

Razan Hayani

Sarah Nadia

1. How does bethanecol helps in treating megacolon & postpartum atonic urinary bladder infection?

📄Ans:

- bethanecol is a cholinergic agonist

- bethanecol major action = smooth ms bladder & git 💩

- activate muscarinic rcptr : 1. ⬆intestinal motility & tone (megacolon) 2. stimulate detrusor ms of urinary bladder -> urination🚾

2. How pilocarpine is useful in treating xerostomia 🚱 & Sjogren syndrome?

📄Ans:

- pilocarpine is a cholinergic agonist, it exhibits muscarinic activity

- it stimulates secretion of tears👀, saliva👅 & sweat💦 -> therefore it reduces the effect of xerostomia & Sjogren syndrome

27. Why epinephrine dose need to be reduced in patient with hyperthyroidism?

📄Ans:

- hyperthyroidism ⬆ production of adrenergic rcptr on vasculature (alpha & beta)

- high dose of epinephrine will cause over excitation of CVS 💓 (d/t hypersensitive response)

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Hafiz & faiz
Why patient receiving digoxin have risk of developing cardiac arrythymias when given epinephrine

Answer:
Epinephrine: positive inotrophic and chronotropic agent, act directly to the B1 receptor of cadiac muscle, hence it increase cardiac contractility

Digoxin: inhibit Na/K-ATPase pump, Na/K gradient, Na/Ca exchanger  non-function, so Ca level increase intracellularly, cardiac contractility increase

Combimation of both drugs cause double effect of positive inotroph, later contribute to cardiac arrythimias(irregular rythm of heart contraction)

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how does alpha n beta receptors differ in terms of affinity toward EPI, NE and isoproterenol?

👉🏿alpha receptor: has highest affinity towards EPI.
ie: EPI>NE>isoproterenol

👉🏿beta receptor: has highest affinity towards isoproterenol.
i.e: isoproterenol>EPI>NE

🌚nisak & hajar

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Fithriah
Fadzilah

How can a beta agonist help in patient with cardiac arrest?

Answer :
β-agonists mimic the actions of sympathetic adrenergic stimulation acting through β-adrenoceptors. The effect of β-agonists is cardiac stimulation (increased heart rate, contractility, CO). Cardiac rhythm in patients with cardiac arrest will be restored.

Mechanism of action :
Beta-agonists bind to beta-adrenoceptors located in cardiac tissue. Beta-adrenoceptors are coupled to G-proteins, which activate adenylyl cyclase to form cAMP from ATP. Increased cAMP activates a cAMP-dependent protein kinase (PK-A) that phosphorylates L-type calcium channels, which causes increased calcium entry into the cells. Increased calcium entry during action potentials leads to enhanced release of calcium by the sarcoplasmic reticulum in the  heart, these actions increase heart contractility. So heart rate and cardiac output will increase.

Example of beta agonist :
- Epinephrine
- Dobutamine
- Dopamine
- Isoproterenol

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Arina Balqis binti Hassan@Zakaria
Nur Syazwani binti Mohd Ramle

What are the common therapeutic uses of ipratropium and darifenacin?

1. Both drugs are muscarinic antagonist - inhibit cholinergic effect.
2. Ipratropium is used as bronchodilator for maintenance ttreatment of bronchospasm associated with COPD. Ipratropium is a derivative of atropine so they have the greatest inhibitory effects on bronchiol tissue.
3. Darifenacin - to treat overactiveoveractive bladder.

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AttiyaH
Fadhlin

What are the adverse effects of cholinergic stimulation?

1. Profused sweating
2. Increased salivation
3.diarrhea
4.flushing
5. Bronchospasm
6.decreased BP
7. Abdominal pain
8. Excessive urination

-

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Nazmi (^^,)
Bazli

Major therapeutic use of:
-Mirabegron
-Oxymetazoline
-Phenylephrine
-Clonidine
-Dobutamine
Dopamine
-Albuterol
-Salmeterol

Therapeutic use of these drugs:

1⃣dopamine(🅰1+🅱1)

i- cardiogenic+septic shock

ii- enhances perfusion to kidney and splanchnic area

iii- hypotension and severe heart failure

2⃣dobutamine(🅱1)

i- acute HF

ii- inotropic support after cardiac surgery

3⃣oxymetazoline(🅰1+🅰2)

i- nasal spray decongestion

ii- opthalmic drops for relief of redness of eyes

4⃣phenylephrine(🅰1)

i- nasal and oral decongestant

ii- opthalmic solution for mydriasis

5⃣clonidine(🅰2)

i- HPT

6⃣albuterol(🅱2)

i- short acting  bronchodilators (inhaler) -asthma

7⃣salmeterol(🅱2)

i- long acting bronchodilator

>12hrs

8⃣mirabegron(🅱3)

i- overactive bladder

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Siti Zulaiha bt Ahmad Sabri
Siti NurSyafiqah bt Razi

What medication can be used to reverse pilocarpine poisoning? Explain briefly.

Ans:
Poisoning cause exaggeration of parasympathetic effect which are profuse sweating (diaphoresis) and salivation.
In order to encounter the effects, atropine is administered at dose that can cross BBB.
Atropine is cholinergic antagonist which is selective muscarinic receptor blocker. Greatest inhibitory effects of atropine are on secretion of sweat & saliva.

🐆🐇

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Question 22 (Why dose of EPI needs to be reduced in hyperthyroid patient?)

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Question 22 (Why dose of EPI needs to be reduced in hyperthyroid patient?)

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Ahmad
Amarul

Hyperthyroidism - increase production of adrenergic receptors in vasculature.

Epinephrine - binds with alpha1-adrenergic receptor causing vasoconstriction

Effect: increase adrenergic receptor and increase EPI leading to blood vessel constriction which will increase peripheral resistance, increase in blood pressure and eventually leads to hypertension. That's why dose of EPI needs to be reduced.

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Nurliyana
Sharifah amirah

Q: How does alpha2 receptor activator function as a feedback inhibition of noradrenergic neurotransmission?

A: High stimulation of adrenergic nerve
~more NE released
~ some NE circles back, bind to a2 receptor at presynaptic
~ reduce production cAMP ~ inhibit further release of NE (feedback inhibition)