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Pharm SJSM > Block 2 (Sympathomimetics) > Flashcards

Block 2 (Sympathomimetics) Flashcards

1
Q

In the eye which receptors have which effect?

a1
a2
B2

A

a1= Mydriasis & distant accommodation

a2= Reduces aqueous humor production

B2= Increases aqueous humor production

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2
Q

In the blood vessels which receptors have which effect?

a1
a2
B2

A

a1:
Vascular smooth muscle contraction of arterioles to increase peripheral resistance increasing afterload
&
Vasoconstriction causing more venous return & increased preload

a2:
Increased platelet aggregation

B2:
Peripheral vasodilation to decrease peripheral vascular resistance reducing afterload

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3
Q

In the Heart which receptors have which effect?

B1

A

B1:
Increased HR/Contractility & AV nodal conduction

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4
Q

In the Bronchi which receptors have which effect?

B2

A

B2:
Bronchodilation

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5
Q

In the GiT which receptors have which effect?

B2

A

B2:
Decreased peristalsis

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6
Q

In the Liver which receptors have which effect?

a1

A

a1:
Increased glycogenolysis & Gluconeogenesis

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7
Q

In the pancreas which receptors have which effect?

a2
B2

A

a2:
Decrease insulin release

B2:
Increase insulin release

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8
Q

In the Kidneys which receptors have which effect?

B1

A

B1:
Increase the release of renin

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9
Q

In the Bladder which receptors have which effect?

a1
B2
B3

A

a1:
Urinary retention (relaxation)

B2 & B3:
Detrusor relaxation (urine retention)

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10
Q

In the female reproductive organs which receptors have which effect?

B2

A

B2:
Decreased uterine tone (tocolysis)

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11
Q

In the male reproductive organs which receptors have which effect?

a1

A

a1:
Ejaculation from the vas deferens

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12
Q

In the skeletal muscles which receptors have which effect?

B2
B3

A

B2:
Contraction & Glycogenolysis

B3:
Thermogenesis

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13
Q

In the Adipose tissue which receptors have which effect?

a1
B1-B3

A

a1:
Decreased lipolysis

B1-B3:
Increased lipolysis

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14
Q

What are the actions of IV adrenaline on BP:

A

An initial rise then fall in BP (aka Dale’s vasomotor reversal)

Acts on a1, B1, & B2 receptors (effect is dosage dependent)

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15
Q

What are the actions of Noradrenaline on BP:

Systole
Diastole
Mean BP

A

Sys: Increased
Dia: Increased
Mean: Increased

Poor B2 activity instead it has a1, a2, & B1 activity

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16
Q

What are the actions of Isoprenaline on BP:

Systole
Diastole
Mean BP

A

Sys: Increased
Dia: Decreased
Mean: Decreased or unchanged

has very little a activity instead it has B1 & B2 activity only

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17
Q

Describe the following for a1 receptors:

Which pathway does it activate?

What type of effects does it have?

What are its agonists vs antagonist?

A

Path:
a1 activates Gq to increase phospholipase C resulting in increased IP3, DAG, & Ca2+

Effects:
Sympathetic constriction of BV

1) Increase stroke volume (artery & vein constriction causes increased after & preload respectively)

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Mydriasis (contract pupillae dilator)

4) Gi & bladder sphincter contraction (reduce peristalsis & urination)

5) Glycogenolysis (to up glucose)

6) Reduce renin/RAAS

7) Reduce aqueous humor production

Agonist: Norepinephrine & epinephrine

Antagonist: Phentolamine

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18
Q

Path:
activates Gq to increase phospholipase C resulting in increased IP3, DAG, & Ca2+

Effects:
Sympathetic constriction of BV

1) Increase stroke volume (artery & vein constriction causes increased after & preload respectively)

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Mydriasis (contract pupillae dilator)

4) Gi & bladder sphincter contraction (reduce peristalsis & urination)

5) Glycogenolysis (to up glucose)

6) Reduce renin/RAAS

7) Reduce aqueous humor production

Agonist: Norepinephrine & epinephrine

Antagonist: Phentolamine

This describes which adrenergic receptor?

A

alpha 1

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19
Q

Describe the following for a2 receptors:

Which pathway does it activate?

What type of effects does it have?

A

Path:
a2 activates Gi which inhibits adenylate cyclase to reduce cAMP

Effects:
Anti-sympathetic
1) Constricting the lungs
2) Anti-insulin
3) Pro platelet aggregation

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20
Q

Path:
activates Gi which inhibits adenylate cyclase to reduce cAMP & prevent norepinephrine release from the neuron

Effects:
Anti-sympathetic
1) Constricting the lungs
2) Anti-insulin
3) Pro platelet aggregation

Describes which receptor?

A

alpha 2

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21
Q

Describe the following for B1 receptors:

Which pathway does it activate?

What type of effects does it have?

What is it’s agonist vs antagonist?

A

Path:
B1 activates Gs to increase adenylate cyclase causing more cAMP to increase release of norepinephrine

Effects:
Sympathetic

1) Increased HR, SV, Contractility

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Higher renin/RAAS

4) Increases aqueous humor secretion

Agonists: Epinephrine

Antagonist: drugs ending in lol (propranolol or metraprolol)

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22
Q

Path:
activates Gs to increase adenylate cyclase causing more cAMP to increase release of norepinephrine

Effects:
Sympathetic

1) Increased HR, SV, Contractility

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Higher renin/RAAS

4) Increases aqueous humor secretion

Agonists: Epinephrine

Antagonist: drugs ending in lol (propranolol or metraprolol)

Describes which receptor?

A

Beta 1 receptor

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23
Q

Describe the following for B2 receptors:

Which pathway does it activate?

What type of effects does it have?

A

Path:
activates Gs path which activates adenylate cyclase increased cAMP resulting in inhibited myosin light chain kinase causing relaxation

Effects:
Tocolytic effects aka RELAXATION
1) Bronchodilation
2) Vasodilation causing lower diastolic BP
3) Hypokalemia (it moves K+ into SM)
4) Increased aqueous humor production

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24
Q

Path:
activates Gs path which activates adenylate cyclase increased cAMP resulting in inhibited myosin light chain kinase causing relaxation

Effects:
Tocolytic effects aka RELAXATION
1) Bronchodilation
2) Vasodilation causing lower diastolic BP
3) Hypokalemia (it moves K+ into SM)
4) Increased aqueous humor production

Describes which receptor?

A

Beta 2 receptor

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25
Q

Describe the following for B3 receptors:

Which pathway does it activate?

What type of effects does it have?

A

Path:
activates Gs path which activates adenylate cyclase increased cAMP

Effects:
1) lipolysis

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26
Q

Path:
activates Gs path which activates adenylate cyclase increased cAMP

Effects:
1) lipolysis

describes which receptor?

A

Beta 3 receptor

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27
Q

Phenylephrine
Metaraminol
Mephentermine
Midodrine
Methoxamine

Are all examples of which receptor agonists?

What are the clinical uses?

A

alpha 1 agonists
(acts on Gq path to increase phospholipase C resulting in more IP3, DAG, & Ca2+ to increase heart contractility)

Clinical uses:
1) Hypotension (vasoconstriction to increase resistance & BP)

2) Nasal decongestion (vasoconstriction reduces mucus production)

3) Mydriatic (constricts pupillae dilator muscles)

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28
Q

alpha 1 agonists
(acts on Gq path to increase phospholipase C resulting in more IP3, DAG, & Ca2+ to increase heart contractility)

Clinical uses:
1) Hypotension (vasoconstriction to increase resistance & BP)

2) Nasal decongestion (vasoconstriction reduces mucus production)

3) Mydriatic (constricts pupillae dilator muscles)

List the 5 alpha-1 agonists

A

Phenylephrine
Metaraminol
Mephentermine
Midodrine
Methoxamine

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29
Q

Apraclonidine
Clonidine
Brimonidine
Dexmedetomidine
Guanfacine
Guanabenz
Methyldopa
Tizanidine

Are all examples of which receptor agonists?

What are the clinical uses?

A

alpha 2 receptor agonists (Act via the Gi path to inhibit adenylate cyclase to reduce cAMP & inhibit myosin light chain kinase causing constriction of the lungs

Clinical uses:

1) Hypertension (Clonidine, Guanfacine, Gauanabenz, Methyldopa, & Tizanidine)

2) Glaucoma (Apraclonidine & Brimonidine)

3) Spasticity (Tizanidine)

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30
Q

alpha 2 receptor agonists (Act via the Gi path to inhibit adenylate cyclase to reduce cAMP & inhibit myosin light chain kinase causing constriction of the lungs

Clinical uses:

1) Hypertension (Clonidine, Guanfacine, Gauanabenz, Methyldopa, & Tizanidine)

2) Glaucoma (Apraclonidine & Brimonidine)

3) Spasticity (Tizanidine)

List 8 a2 agonists

A

Apraclonidine
Clonidine
Brimonidine
Dexmedetomidine
Guanfacine
Guanabenz
Methyldopa
Tizanidine

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31
Q

Isoproterenol
Albuterol
Terbutaline
Dobutamine
Formoterol
Metaproterenol
Salmeterol

Are all examples of which receptor agonists?
- Which ones are B1/B2, B2, & B1

What are the clinical uses?

What are the side effects?
- B1/B2
- B2
- B3

A

Beta-1 agonists (that act on the Gs path to increase adenylate cyclase & increase cAMP to cause dilation in blood vessels)

B1/B2: Isoproterenol

B2: Albuterol, Terbutaline, & Metaproterenol

B1: Dobutamine

Clinical uses:

1) Asthma & Tocolysis (stop pre-birth) via B2 agonists

2) Bradycardia, Heart block (AV node), & Asthma via B1/b2 agonists

3) Acute CHF via B1 agonist

Side effects:
B1: Tachycardia

B2: Anxiety, Tremor, Restlessness, & Palpations

B1/B2: Tachycardia, Hypotension, Headache, Flushing

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32
Q

Epinephrine
Norepinephrine
Dopamine

Are all examples of which receptor type

A

Mixed receptor

Epi: a1/2 & B1/2

Norepi: a1/2 & B1

Dopa: D1, B1, & a1

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33
Q

Phentolamine (reversible)
Prazosin
Terazosin
Doxazocin
Tamsulosin

Are all which type of receptor antagonists?

A

alpha 1 antagonists

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34
Q

Phenoxybenzamine (irreversible)
Yohimbine
Mirtazapine

Are all which type of receptor antagonists?

A

alpha 2 antagonists

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35
Q

Describe the reflex response of a1 agonists:

HR
Contractility
Systemic vascular resistance

A

BP: reduced

Contractility: reduced

Systemic vascular resistance: increased

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36
Q

Describe the reflex response of a2 agonists:

HR
Contractility
Systemic vascular resistance

A

HR: reduced

Contractility: unaffected

Systemic vascular resistance: reduced

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37
Q

Describe the reflex response of a2 antagonists:

HR
Contractility
Systemic vascular resistance

A

HR: Increased

Contractility: unaffected

Systemic vascular resistance: reduced

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38
Q

Describe the reflex response of a1/2 antagonists:

HR
Contractility
Systemic vascular resistance

A

HR: increased

Contractility: unaffected

Systemic vascular resistance: reduced

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39
Q

Describe the reflex response of B1 agonists:

HR
Contractility
Systemic vascular resistance

A

HR: increased

Contractility: increased

Systemic vascular resistance: reduced

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40
Q

Describe the reflex response of B1 antagonists:

HR
Contractility
Systemic vascular resistance

A

HR: reduced

Contractility: reduced

Systemic vascular resistance: unaffected

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41
Q

Describe the reflex response of Norepinephrine (mixed agonist) (a1>B1>B2)

BP
HR
Renal blood flow

A

BP: increased

HR: unchanged/reduced

Renal blood flow: reduced

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42
Q

Describe the reflex response of Phenylephrine (a1 agonist)

BP
HR
Renal blood flow

A

BP: increased

HR: reduced

Renal blood flow: reduced

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43
Q

Describe the reflex response of Dobutamine (B agonist with a higher affinity for B1)

BP
HR
Renal blood flow

A

BP: unchanged/reduced

HR: increased

Renal blood flow: unchaged

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44
Q

Describe the reflex response of Dopamine (mixed agonist)

Low vs high dose

BP
HR
Renal blood flow

A

Low dose (D1>B1>a1)

BP: unchanged/reduced

HR: increased

Renal blood flow: increased

High dose (a1>B1>D1)

BP: increased

HR: unchanged

Renal blood flow: reduced

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45
Q

Describe the reflex response of Epinephrine (mixed agonist)

Low vs high dose

BP
HR
Renal blood flow

A

Low dose (B1>B2>a1)

BP: unchanged/reduced

HR: increased

Renal blood flow: unchanged

High dose (a1>B2>B1)

BP: increased

HR: unchanged

Renal blood flow: reduced

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46
Q

Describe the reflex response of Isoproterenol (B agonist with equal effects on B1 & B2)

BP
HR
Renal blood flow

A

BP: unchanged/reduced

HR: increased

Renal blood flow: unchanged

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47
Q

Describe the following for Epinephrine:

What is the drug type?

What is its MOA?

What are the effects of the drug?

What are the clinical uses?

A

Drug type:
A mixed agonist that favors B2 receptors

MOA:
Because it selectively targets B receptors in activated the Gs pathway to increase adenylate cyclase & cAMP resulting in more release of Norepinephrine

Effects:
1) Increased BP
2) Increased HR
3) Increased CO

Clinical uses:
1) Anaphylaxis
2) Cardiac arrest
3) Septic shock
4) Post bypass hypotension
5) Asthma
6) Open-angle glaucoma

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48
Q

Drug type:
A mixed agonist that favors B2 receptors

MOA:
Because it selectively targets B receptors in activated the Gs pathway to increase adenylate cyclase & cAMP resulting in more release of Norepinephrine

Effects:
1) Increased BP
2) Increased HR
3) Increased CO

Clinical uses:
1) Anaphylaxis
2) Cardiac arrest
3) Septic shock
4) Post bypass hypotension
5) Asthma
6) Open-angle glaucoma

Describes which drug?

A

Epinephrine

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49
Q

Describe the following for Dobutamine:

What is the drug type?

What is the MOA?

What are the effects of the drug?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
A direct-acting & selective B1 agonist (sympathomimetic)

MOA:
Because it selectively targets B receptors in activated the Gs pathway to increase adenylate cyclase & cAMP resulting in more release of Norepinephrine

Effects:
1) Increased CO without effecting the HR

Clinical uses:
1) Heart failure
2) Cardiogenic shock
3) Cardiac stress testing

Adverse effects:
1) Hypertension
2) Tachycardia
3) PVC’s
4) Arrythmias

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50
Q

Drug type:
A direct-acting & selective B1 agonist (sympathomimetic)

MOA:
Because it selectively targets B receptors in activated the Gs pathway to increase adenylate cyclase & cAMP resulting in more release of Norepinephrine

Effects:
1) Increased CO without effecting the HR

Clinical uses:
1) Heart failure
2) Cardiogenic shock
3) Cardiac stress testing

Adverse effects:
1) Hypertension
2) Tachycardia
3) PVC’s
4) Arrythmias

Describes which drug?

A

Dobutamine

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51
Q

Describe the following Albuterol:

What is the drug type?

What is the MOA?

What are the effects of the drug?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
B2 agonist (short-acting)

MOA:
It activates Gs path to activate adenylate cyclase & cAMP resulting in more release of norepinephrine to bind to B2 receptors & dilate bonchi

Effect:
1) Bronchodilation

Clinical uses:
1) Acute exacerbation & prophylaxis of exercise-induced asthma

Adverse effects:
1) Tremor
2) Arrythmia
3) Tolerance/Tachyphylaxis

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52
Q

Drug type:
B2 agonist (short-acting)

MOA:
It activates Gs path to activate adenylate cyclase & cAMP resulting in more release of norepinephrine to bind to B2 receptors & dilate bonchi

Effect:
1) Bronchodilation

Clinical uses:
1) Acute exacerbation & prophylaxis of exercise-induced asthma

Adverse effects:
1) Tremor
2) Arrythmia
3) Tolerance/Tachyphylaxis

Describes which drug?

A

Albuterol

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53
Q

Describes the following for Salbutamol:

What is the drug type?

What is the MOA?

What are its effects?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
B2 agonists (short acting)

MOA:
It activated Gs pathway to increase adenylate cyclase & cAMP to cause more release of Norepinephrine to bind to B2 receptors in the lungs (dilation)

Effects:
1) Bronchodilation

Clinical uses:
1) Asthma prophylaxis

Adverse effects:
1) Tremor
2) Arrythmia
3) Tolerance/Tachyphylaxis

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54
Q

Drug type:
B2 agonists (short acting)

MOA:
It activated Gs pathway to increase adenylate cyclase & cAMP to cause more release of Norepinephrine to bind to B2 receptors in the lungs (dilation)

Effects:
1) Bronchodilation

Clinical uses:
1) Asthma prophylaxis

Adverse effects:
1) Tremor
2) Arrythmia
3) Tolerance/Tachyphylaxis

Describes which drug?

A

Salbutamol

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55
Q

What drug types can be used to treat hyperkalemia?

A

Insulin + glucose
Calcium gluconate
B2 agonists

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56
Q

Insulin + glucose
Calcium gluconate
B2 agonists

Are all used to treat what condition?

A

Hyperkalemia

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57
Q

Describe the following for Isoproterenol:

What is the drug type?

What is the MOA?

What are its effects?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
B agonist that targets B1 & B2 receptors equally

MOA:
It activates Gs to increase adenylate cyclase & cAMP resulting in more norepinephrine release to bind to B receptors (dilation)

Effects:
1) Increased cardiac output
2) Increased heart rate
3) Reduced BP

Clinical uses:
1) Bradycardia
2) Heart block (AV)
3) Cardiac arrest

Adverse effects:
1) Tachycardia
2) Arrythmia

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58
Q

Drug type:
B agonist that targets B1 & B2 receptors equally

MOA:
It activates Gs to increase adenylate cyclase & cAMP resulting in more norepinephrine release to bind to B receptors (dilation)

Effects:
1) Increased cardiac output
2) Increased heart rate
3) Reduced BP

Clinical uses:
1) Bradycardia
2) Heart block (AV)
3) Cardiac arrest

Adverse effects:
1) Tachycardia
2) Arrythmia

Describes which drug?

A

Isoproterenol

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59
Q

What are the adverse effects of alpha 1 agonists?

A

1) Hypertension
2) Reflex bradycardia
3) Urine retention
4) Ischemia & necrosis (fingers/toes)
5) Rebound congestion
6) Piloerection

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60
Q

1) Hypertension
2) Reflex bradycardia
3) Urine retention
4) Ischemia & necrosis (fingers/toes)
5) Rebound congestion
6) Piloerection

Are all adverse side effects of which drug type?

A

alpha 1 agonists

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61
Q

What is Albuterol used to treat?

A

It’s a B agonist targeted more towards B2 to treat Asthma

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62
Q

What is Salmeterol used to treat?

A

It’s a B agonist targeted more towards B2 to treat COPD

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63
Q

What is Terbutaline used to treat?

A

It’s a B agonist targeted more towards B2 to treat preterm labor with a tocolytic effect

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64
Q

Albuterol, Salmeterol, Formoterol, & Terbutaline are all used to treat which condition?

A

Hyperkalemia (B agonists pull K+ from blood into smooth muscle)

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1
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2
3
4
5
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65
Q

What are the adverse effects of B2 agonists?

A

1) Tremor
2) Agitation
3) Insomnia
4) Diaphoresis
5) Hypotension
6) Reflex tachycardia
7) Hyperglycemia
8) Hypokalemia

66
Q

1) Tremor
2) Agitation
3) Insomnia
4) Diaphoresis
5) Hypotension
6) Reflex tachycardia
7) Hyperglycemia
8) Hypokalemia

Describe adverse side effects of which drug type?

A

B2 agonists

67
Q

Describe the following for dopamine:

What is the drug type?

What is the effect of the drug at:
- low doses
- intermediate doses
- high doses

What are the clinical uses?

What are the adverse effects?

A

Drug type:
A mixed agonist that targets D1, B1, & a1 agonists at different doses

Effects of Low doses (D1):
Vasodilation in kidney causing
1) Increased RBF
2) Increase GFR
3) Increased Na secretion

Effects at med (B1) & high (a1) doses:
Cardio effects
1) Increased BP
2) Increased HR
3) Increased CO

Clinical uses:
1) Renal failure associated with shock (low dose)
2) Unstable bradycardia (low dose)

2) Heart failure
4) Cardiogenic shock

Adverse effects:
1) Nausea/vomiting
2) Tachycardia
3) Angina pain
4) Arrythmias
5) Headache
6) Hypertension

68
Q

Drug type:
A mixed agonist that targets D1, B1, & a1 agonists at different doses

Effects of Low doses (D1):
Vasodilation in kidney causing
1) Increased RBF
2) Increase GFR
3) Increased Na secretion

Effects at med (B1) & high (a1) doses:
Cardio effects
1) Increased BP
2) Increased HR
3) Increased CO

Clinical uses:
1) Renal failure associated with shock (low dose)
2) Unstable bradycardia (low dose)

2) Heart failure
4) Cardiogenic shock

Adverse effects:
1) Nausea/vomiting
2) Tachycardia
3) Angina pain
4) Arrythmias
5) Headache
6) Hypertension

Describes which drug?

A

Dopamine

69
Q

Describe the following for Fenoldopam:

What is the drug type?

What is the MOA?

What are the effects of the drug?

What are the clinical uses?

A

Drug type:
A selective D1 agonist

MOA:
It activates Gs path to increase adenylate cyclase & cAMP to increase norepinephrine release resulting in vasodilation

Effects:
1) Reduced BP (vasodilation)
2) Increased CO
3) Increased HR

Clinical uses:
1) Hypertensive crisis
2) post-op hypertension

70
Q

Drug type:
A selective D1 agonist

MOA:
It activates Gs path to increase adenylate cyclase & cAMP to increase norepinephrine release resulting in vasodilation

Effects:
1) Reduced BP (vasodilation)
2) Increased CO
3) Increased HR

Clinical uses:
1) Hypertensive crisis
2) post-op hypertension

Describes which drug?

A

Fenoldopam

71
Q

Describe the following for methyldopa:

What is the drug type?

What is the MOA?

What are the effects of the drug?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
a2 agonist

MOA:
activates the Gi pathway to inhibit adenylate cyclase & cAMP causing less norepinephrine release resulting in constriction of blood vessels & lungs

Effects:
1) Reduced BP

Clinical uses:
1) Hypertension (safe in pregnancy!)

Adverse effects:
1) Autoimmune hemolytic anemia (+ve Coombs test)
2) SLE-like syndrome
3) Hyperprolactinemia

72
Q

Drug type:
a2 agonist

MOA:
activates the Gi pathway to inhibit adenylate cyclase & cAMP causing less norepinephrine release resulting in constriction of blood vessels & lungs

Effects:
1) Reduced BP

Clinical uses:
1) Hypertension (safe in pregnancy!)

Adverse effects:
1) Autoimmune hemolytic anemia (+ve Coombs test)
2) SLE-like syndrome
3) Hyperprolactinemia

Describes which drug?

A

Alpha-methyldopa

73
Q

What are the adverse effects of alpha-2 agonists?

A

1) Miosis
2) Dry mouth
3) Bradycardia & hypotension
4) CNS & Resp depression
5) Rebound hypertension

74
Q

1) Miosis
2) Dry mouth
3) Bradycardia & hypotension
4) CNS & Resp depression
5) Rebound hypertension

Describes the adverse effects of which drug type?

A

alpha-2 agonists

75
Q

Describe the following for Oxymetazoline:

What is the drug type?

What is the MOA?

What are the effects?

What are the clinical uses?

A

Drug type:
alpha agonists that mostly act on a1 receptors

MOA:
It acts on Gq to increase phospholipase C causing an increase in IP3, DAG, & Ca2+ (Cardiac & blood vessel contraction)

Effects:
1) May increase BP

Clinical uses:
1) Epistaxis
2) Rhinitis
3) Sinusitis
4) Rosacea
(vasoconstriction results in less mucus production & redness in skin/mucus membranes)

76
Q

Drug type:
alpha agonists that mostly act on a1 receptors

MOA:
It acts on Gq to increase phospholipase C causing an increase in IP3, DAG, & Ca2+ (Cardiac & blood vessel contraction)

Effects:
1) May increase BP

Clinical uses:
1) Epistaxis
2) Rhinitis
3) Sinusitis
4) Rosacea
(vasoconstriction results in less mucus production & redness in skin/mucus membranes)

Describes which drug?

A

Oxymetazoline

77
Q

Describe the following for phenylephrine:

What is the drug type?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
alpha agonist that targets alpha-1 receptors

MOA:
Activated Gq pathway to increase phospholipase C to increase IP3, DAG, & Ca2+ resulting in vasoconstriction (heart & BV)

Effects:
1) Increased BP
2) Reduced HR
3) No change or reduced CO

Clinical uses:
1) Hypotension
2) Nasal congestion (reduce hyperemia & mucosal edema)
3) Allergic conjunctivitis

Adverse effects:
1) Tolerance (less efficacious)
2) Atrophic rhinitis
3) Rebound hyperemia
4) Anosmia (loss of smell)
5) Nasal perforation

78
Q

Drug type:
alpha agonist that targets alpha-1 receptors

MOA:
Activated Gq pathway to increase phospholipase C to increase IP3, DAG, & Ca2+ resulting in vasoconstriction (heart & BV)

Effects:
1) Increased BP
2) Reduced HR
3) No change or reduced CO

Clinical uses:
1) Hypotension
2) Nasal congestion (reduce hyperemia & mucosal edema)
3) Allergic conjunctivitis

Adverse effects:
1) Tolerance (less efficacious)
2) Atrophic rhinitis
3) Rebound hyperemia
4) Anosmia (loss of smell)
5) Nasal perforation

Describes which drug?

A

phenylephrine

79
Q

Describe the following for mirabegron:

What is the drug type?

What is the MOA?

What are the effects?

What are the clinical uses

A

Drug type:
B3 agonist

MOA:
activates the Gs path to increase adenylate cyclase & cAMP resulting in more norepinephrine release

Effects:
1) increase BP

Clinical uses:
1) Urinary urgency/incontinence (overactive bladder)

80
Q

Drug type:
B3 agonist

MOA:
activates the Gs path to increase adenylate cyclase & cAMP resulting in more norepinephrine release

Effects:
1) increase BP

Clinical uses:
1) Urinary urgency/incontinence (overactive bladder)

Describes which drug?

A

Mirabegron

81
Q

List the alpha & beta agonist releasers

A

Tyramine
Amphetamines
Ephedrine

82
Q

Describe the following for Amphetamines:

What is the drug type?
- MOA

What are the effects?

What are the clinical uses?

A

Drug type/MOA:
An indirect-acting adrenergic receptor agonist that increases the release of norepinephrine & has a long duration of action

Effects:
1) Alertness
2) Euphoria
3) Increased attention span
4) Less need for sleep
5) Talkative
6) Improved academic performance

Clinical uses:
1) Narcolepsy
2) ADHD
3) Obesity

Adverse effects:
1) Tolerance

83
Q

What are the signs of amphetamine toxicity?

  • Central vs peripheral
A

Central toxicity:
Euphoria
Excitement
Confusion
Delirium
Hallucinations
Acute psychosis
Mydriasis

Peripheral:
Palpitations
Arrythmia
Vascular collapse

84
Q

Drug type/MOA:
An indirect-acting adrenergic receptor agonist that increases the release of norepinephrine & has a long duration of action

Effects:
1) Alertness
2) Euphoria
3) Increased attention span
4) Less need for sleep
5) Talkative
6) Improved academic performance

Clinical uses:
1) Narcolepsy
2) ADHD
3) Obesity

Adverse effects:
1) Tolerance

Describes which drug?

A

Amphetamines

85
Q

Central toxicity:
Euphoria
Excitement
Confusion
Delirium
Hallucinations
Acute psychosis
Mydriasis

Peripheral:
Palpitations
Arrythmia
Vascular collapse

Describes the toxicity of which drug?

A

amphetamines

86
Q

For the development of new drug procedure an experimental medication produces the hemodynamic response curve shown below
This new drug is most similar to which of the following substances?

A. Norepinephrine
B.lsoproterenol
C.Clonidine
D.Labetalol
E.Phenylephrine

A

B.lsoproterenol

87
Q

A 62-year-old male with suspected bacterial pneumonia is admitted to the hospital and given ceftriaxone and azithromycin for treatment. Soon after the first dose of ceftriaxone, he complains of difficulty breathing, lightheadedness and abdominal cramps, His current blood pressure is 70/50 mmHg, while his heart rate is 120/min. Physical examination reveals a diffuse maculopapular rash. Which of the following drugs should be administered next to this patient?

A.Corticosteroids
B.Epinephrine
C.Norepinephrine
D.Dobutamine
E. Diphenhydramine

A

B.Epinephrine

88
Q

Q 253
A medical student is conducting a pharmacology experiment. He infuses Drug X intravenously over different dose ranges and measures several important hemodynamic parameters. Graphs plotting the recorded measurements of renal blood flow and cardiac output change with increasing doses of Drug X are shown below.
Which of the following drug is most likely to be used in the experiment?

A.Epinephrine
B.Phenylephrine
C.Dopamine
D.Edrophonium
E.Esmolol

A

C.Dopamine

89
Q

Q 255
A 38-year-old man comes to the office with complaints of a 2-week history of nasal congestion. He has used a topical decongestant every few hours since his symptoms began. He experienced relief for almost 1 week, but then his nasal congestion returned. The patient has a history of allergic rhinitis and has had episodes of rhinorrhea in the past, but none of them lasted longer than a few days. He denies fever, throat pain, headaches, cough, and lymph node enlargement. Aside from his allergic rhinitis, the patient has no other medical problems. Physical examination shows nasal mucosa that appears edematous and red with a few areas of punctate bleeding. The remainder of the examination reveals no abnormalities. Which of the following is the most appropriate next step in the management of this patient?
A. Stop the decongestant
B. Switch to ephedrine
C. Add oral corticosteroids
D. Add antihistamines
E. Start antibiotics

A

A. Stop the decongestant

90
Q

Q 271
A new drug that is used to treat hypertensive emergencies causes arteriolar dilation. It also promotes natriuresis and increases renal perfusion. The drug described above is most similar with which of the following agents?
A.Diazoxide
B.Nitroprusside
C.Hydralazine
D.Esmolol
E.Nicardipine
F.Fenoldopam

A

F.Fenoldopam

91
Q

Q 272
An 75-year-old man is transferred to the hospital from a nursing home for altered mental status and fever. Upon arrival, the patient is admitted directly to the intensive care unit with a presumptive diagnosis of septic shock. Antibiotic therapy is initiated. The patient is unable to provide any history,but his caretakers state that he has been having non-specific symptoms,including fever,for the past few days. The patient has a history of cardiovascular disease,diverticulitis,and dementia. His blood pressure is 60/40 mm Hg despite aggressive intravenous hydration. Norepinephrine is administered in response to the patient’s hypotension.Which of the following cellular changes occurs directly in response to norepinephrine therapy?
A.cAMP increase in vascular smooth muscle cells
B.DAG decrease in vascular smooth muscle cells
C.cAMP increase in cardiac muscle cells
D.cAMP decrease in bronchial smooth muscle cells
E. IP3 increase in cardiac muscle cells

A

C.cAMP increase in cardiac muscle cells

92
Q

Describe the following for Tamsulosin:

What drug type is it?

What is its MOA?

What are its adverse effects?

What are its clinical uses?

A

Drug type:
Selective a1 & B1 blockers

MOA:
They inhibit the a1/B1 receptors causing smooth muscle relaxation in the bladder neck & prostate (free the pee!) to reduce obstruction

Adverse effects:
1) 1st dose hypotension, syncope, & headache

Clinical uses:
1) BPH

93
Q

Drug type:
Selective a1 & B1 blockers

MOA:
They inhibit the a1/B1 receptors causing smooth muscle relaxation in the bladder neck & prostate (free the pee!) to reduce obstruction

Adverse effects:
1) 1st dose hypotension, syncope, & headache

Clinical uses:
1) BPH

Describes which drug?

A

Tamsulosin

94
Q

Describe the following for cocaine:

What drug type is it?

What is its MOA?

What are its adverse effects?

What are its clinical uses?

A

Drug type/MOA
An indirect sympathomimetic (Norepi reuptake inhibitor) that increases the available norepi to bind a1 receptors

Adverse effects:
1) Very addictive
2) HTN
3) Arrythmias
4) Seizures
5) avoid giving with B-blockers or else you get unopposed a1 activation

Clinical uses:
1) Vasoconstriction
2) Local anesthesia

95
Q

Drug type/MOA
An indirect sympathomimetic (Norepi reuptake inhibitor) that increases the available norepi to bind a1 receptors

Adverse effects:
1) Very addictive
2) HTN
3) Arrythmias
4) Seizures
5) avoid giving with B-blockers or else you get unopposed a1 activation

Clinical uses:
1) Vasoconstriction
2) Local anesthesia

Describes which drug?

A

Cocaine

96
Q

Which drugs can be used to effectively treat BPH?

A

Tamsulosin
Selective B1 blockers (-azosin)

97
Q

Describe the following for Selective B1 blockers (azosins):

What is its MOA?

What are its adverse effects?

What are its clinical uses?

A

MOA:
A competitive antagonist that inhibits B1 receptors causing smooth muscle relaxation in the prostate & blood vessels

Adverse effects:
1) Ist does hypotension, syncope, & headache

Clinical uses:
1) BPH
2) Hypertension

98
Q

MOA:
A competitive antagonist that inhibits B1 receptors causing smooth muscle relaxation in the prostate & blood vessels

Adverse effects:
1) Ist does hypotension, syncope, & headache

Clinical uses:
1) BPH
2) Hypertension

Describes which type of drugs?

A

Selective B1 blockers (azosins)

99
Q

Describe the following for clonidine:

What is the drug type?

What is its MOA?

What are the effects?

What are its clinical uses?

What are the adverse effects?

A

Drug type:
A sympathomimetic a2 agonist (at the presynaptic terminals)

MOA:
It stimulates prejunctional receptors in the CNS to decrease the sympathetic outflow

Effects:
1) Reduce total peripheral resistance (lower BP)
2) Lower HR

Clinical uses:
1) Hypertensive urgency
2) ADHD
3) Tourette’s
4) Opioid withdrawal (symptom control)

Adverse effects:
1) CNS & Resp depression
2) Miosis
3) Bradycardia
4) Rebound HTN when drug use is stopped suddenly

100
Q

Drug type:
A sympathomimetic a2 agonist (at the presynaptic terminals)

MOA:
It stimulates prejunctional receptors in the CNS to decrease the sympathetic outflow

Effects:
1) Reduce total peripheral resistance (lower BP)
2) Lower HR

Clinical uses:
1) Hypertensive urgency
2) ADHD
3) Tourette’s
4) Opioid withdrawal (symptom control)

Adverse effects:
1) CNS & Resp depression
2) Miosis
3) Bradycardia
4) Rebound HTN when drug use is stopped suddenly

Describes which drug?

A

Clonidine

101
Q

Describe the following for a1 receptors:

What is the pathway it activates?

What are its effects?

Name a selective agonist

Name a selective antagonist

A

A1= “activate”

Path:
Gq pathway to increase IP3, DAG, Ca2+

Effects:
Constricts blood vessels, sphincters, smooth muscle, & organs
1) Increase stroke volume (artery & vein constriction causes increased after & preload respectively)

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Mydriasis (contract pupillae dilator)

4) Gi & bladder sphincter contraction (reduce peristalsis & urination)

5) Glycogenolysis (to up glucose)

6) Reduce renin/RAAS

7) Reduce aqueous humor production

Selective agonist:
Prazosin

Selective antagonist:
Phenylephrine

102
Q

Path:
Gq pathway to increase IP3, DAG, Ca2+

Effects:
Constricts blood vessels, sphincters, smooth muscle, & organs
1) Increase stroke volume (artery & vein constriction causes increased after & preload respectively)

2) Increased cardiac output (aka higher systolic & diastolic BP)

3) Mydriasis (contract pupillae dilator)

4) Gi & bladder sphincter contraction (reduce peristalsis & urination)

5) Glycogenolysis (to up glucose)

6) Reduce renin/RAAS

7) Reduce aqueous humor production

Selective agonist:
Prazosin

Selective antagonist:
Phenylephrine

Describes which receptor type?

A

Alpha 1 receptor

103
Q

Describe the following for a2 receptors:

What is the pathway it activates?

What are its effects?

Name a selective & non-selective agonist

Name a selective & non-selective antagonist

A

Path:
activates the Gi pathway to inhibit adenylate cyclase & reduce cAMP at prejunctional nerve endings

Effects:
Inhibits norepinephrine release, dilation/inhibition of blood vessels, glands, organs, & smooth muscle
1) Reduce sympathetic outflow
2) Reduce insulin secretion (pancreas)
3) Increase platelet aggregation
4) Certain blood vessel/SM constriction (bronchodilation)
5) Urine retention (Bladder sphincter contraction)

Selective agonist: Clonidine
Non selective agonist: Yohimbine

Selective antagonist: Isoprenaline
Non-selective antagonist: Phentolamine

104
Q

Path:
activates the Gi pathway to inhibit adenylate cyclase & reduce cAMP at prejunctional nerve endings

Effects:
Inhibits norepinephrine release, dilation/inhibition of blood vessels, glands, organs, & smooth muscle
1) Reduce sympathetic outflow
2) Reduce insulin secretion (pancreas)
3) Increase platelet aggregation
4) Certain blood vessel/SM constriction (bronchodilation)
5) Urine retention (Bladder sphincter contraction)

Selective agonist: Clonidine
Non selective agonist: Yohimbine

Selective antagonist: Isoprenaline
Non-selective antagonist: Phentolamine

Describes which receptor type?

A

Alpha 2 receptor

105
Q

Describe the following for B1 receptors:

What is the pathway it activates?

What are its effects?

Name a selective & non-selective agonist

Name a selective & non-selective antagonist

A

Path:
It activates the Gs path to increase adenylate cyclase & raise cAMP levels which takes effect in the heart & kidneys

Effects:
Increased Ca2+ in the heart & kidneys
1) Higher HR (SA node)
2) More conduction velocity (AV node)
3) More contractility
4) Higher BP (via more renin from JG cells)

Selective agonist: Dobutamine
Non-selective agonist: Isoprenaline

Selective antagonist: Metoprolol, atenolol (lols)
Non-selective antagonists: Propranolol

106
Q

Path:
It activates the Gs path to increase adenylate cyclase & raise cAMP levels which takes effect in the heart & kidneys

Effects:
Increased Ca2+ in the heart & kidneys
1) Higher HR (SA node)
2) More conduction velocity (AV node)
3) More contractility
4) Higher BP (via more renin from JG cells)

Selective agonist: Dobutamine
Non-selective agonist: Isoprenaline

Selective antagonist: Metoprolol, atenolol (lols)
Non-selective antagonists: Propranolol

Describes which receptor?

A

Beta 1 receptor

107
Q

Describe the following for B2 receptors:

What is the pathway it activates?

What are its effects?

Name a selective & non-selective agonist

Name a selective antagonist

A

Path:
Activates the Gs path to increase adenylate cyclase & raise cAMP levels to act on the lungs, blood vessels, smooth muscles, glands, & organs

Effects:
Causes dilation/relaxation
1) Bronchodilation
2) Relaxed uterus
3) Vasodilation
4) Less digestion (relaxed Gi SM)
5) Increased glucagon release (liver)
6) Urine retention (relaxed detrusor)
7) Increased aqueous humor production

Selective agonists: Salbutamol & Terbutaline

Non-selective agonists: Isoprenaline

Selective antagonists: a-methyl propranolol

108
Q

Path:
Activates the Gs path to increase adenylate cyclase & raise cAMP levels to act on the lungs, blood vessels, smooth muscles, glands, & organs

Effects:
Causes dilation/relaxation
1) Bronchodilation
2) Relaxed uterus
3) Vasodilation
4) Less digestion (relaxed Gi SM)
5) Increased glucagon release (liver)
6) Urine retention (relaxed detrusor)
7) Increased aqueous humor production

Selective agonists: Salbutamol & Terbutaline

Non-selective agonists: Isoprenaline

Selective antagonists: a-methyl propranolol

Describes which receptor?

A

Beta 2 receptor

109
Q

Describe the following for B3 receptors:

What is the pathway it activates?

What are its effects?

Name a selective agonist

A

Path:
Activates the Gs path to increase adenylate cyclase & raise cAMP levels to act on adipose tissue

Effects:
1) More lipolysis

Selective agonist: Mirabegron

110
Q

Path:
Activates the Gs path to increase adenylate cyclase & raise cAMP levels to act on adipose tissue

Effects:
1) More lipolysis

Selective agonist: Mirabegron

Describes which receptor?

A

Beta 3 receptor

111
Q

Describe the following for Timolol:

What is the drug type?

What is its MOA?

What is its effect?

A

Drug type:
B-blocker

MOA:
Blocks norepinephrine’s action at the ciliary epithelium without causing pupil or vision changes

Effects:
1) Reduced aqueous humor production (blocks B2 receptors)

112
Q

Drug type:
B-blocker

MOA:
Blocks norepinephrine’s action at the ciliary epithelium without causing pupil or vision changes

Effects:
1) Reduced aqueous humor production (blocks B2 receptors)

Describes which drug?

A

Timolol

113
Q

Describe the following for prazosin:

What is the drug type?

What is its clinical use?

What is an adverse effect?

A

drug type:
Selective alpha-1 antagonist (a1 blocker)

Clinical use:
1) Hypertension

Adverse effect:
Orthostatic hypotension

114
Q

drug type:
Selective alpha-1 antagonist (a1 blocker)

Clinical use:
1) Hypertension

Adverse effect:
Orthostatic hypotension

Describes which drug?

A

Prazosin

115
Q

Describe the following for Doxazosin & Terazosin:

What are the drug types?

What are they clinically used for?

What are the adverse effects?

A

Drug types:
Selective alpha-1 antagonists

Clinical uses:
1) BPH
2) Atrial HTN

Adverse effect:
1) Orthostatic hypotension

116
Q

Drug types:
Selective alpha-1 antagonists

Clinical uses:
1) BPH
2) Atrial HTN

Adverse effect:
1) Orthostatic hypotension

Describes which 2 drugs?

A

Doxazosin & Terazosin

117
Q

Describe the following for Tamsulosin, Alfuzosin, & Silodosin:

What are the drug types?

What are they clinically used for?

What are the adverse effects?

A

Drug type:
Alpha-1 antagonists

Clinical use:
1) BPH

Adverse effects:
1) Intraoperative floppy iris syndrome

118
Q

Drug type:
Alpha-1 antagonists

Clinical use:
1) BPH

Adverse effects:
1) Intraoperative floppy iris syndrome

Describes which 3 drugs?

A

Tamsulosin, Alfuzosin, & Silodosin

119
Q

Which type of drug would you use to treat angina pectoris & why?

A

Beta blockers to reduce HR, contractility & O2 consumption of the heart (less damage)

120
Q

Which type of drug would you use to treat Glaucoma & why?

A

A Beta blocker like timolol to reduce aqueous humor production

121
Q

Which type of drug would you use to treat Heart failure & why?

A

Beta blockers like Bisoprolol, Carvedilol, Metoprolol to reduce neurohormonal stress & deleterious remodeling

“B-blockers Curb Mortality”

122
Q

Which type of drug would you use to treat Hypertension & why?

A

B-blockers to reduce CO & BP to lessen the stress on the heart

123
Q

Which type of drug would you use to treat Hypertrophic obstructive cardiomyopathy & why?

A

Beta blockers to reduce HR & increase filling time to relieve the obstruction

124
Q

Which type of drug would you use to treat Hyperthyroidism/thyroid storm & why?

A

A beta blocker like propranolol to control the symptoms (i.e reduce HR in racing heart & tremors)

125
Q

Which type of drug would you use to treat Myocardial infarction & why?

A

A beta blocker to reduce HR & O2 demand (short term ischemia control) & reduce mortality

126
Q

Which type of drug would you use to treat Supraventricular tachycardia & why?

A

Beta blockers like metoprolol & esmolol to reduce AV nodal conduction to slow HR & reduce contractility

127
Q

Which type of drug would you use to treat Variceal bleeding & why?

A

Beta blockers like nadolol, propranolol, & carvedilol to reduce hepatic venous pressure gradient (dilating the hepatic veins) to reduce portal hypertension

128
Q

What are some of the major side effects of most beta blockers?

A

1) Erectile dysfunction (vasodilation)
2) Bradycardia, AV block, & HR
3) Seizures & sleep alterations
4) Dyslipidemia (metoprolol)
5) Masked hypoglycemia
6) Asthma/COPD exacerbation

129
Q

1) Erectile dysfunction (vasodilation)
2) Bradycardia, AV block, & HR
3) Seizures & sleep alterations
4) Dyslipidemia (metoprolol)
5) Masked hypoglycemia
6) Asthma/COPD exacerbation

Are adverse effects of which drug type (receptor type)

A

Beta blockers

130
Q

Why should you avoid Beta-blockers & cocaine?

A

Because it will result in unopposed alpha 1 activity

131
Q

Acebutolol
Atenolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol

Are all examples of which type of drug?

A

Selective B1 antagonists

132
Q

List 6 Selective B1 antagonists

A

Acebutolol
Atenolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol

133
Q

Nadolol
Pindolol
Propranolol
Timolol

Are all examples of which type of drug?

A

B1 non-selective antagonists

134
Q

List 4 B1 non-selective antagonists

A

Nadolol
Pindolol
Propranolol
Timolol

135
Q

Carvedilol
Labetalol

Are examples of which type of drug?

A

Non-selective A/B antagonists

136
Q

list 2 Non-selective A/B antagonists

A

Carvedilol
Labetalol

137
Q

Nebivolol is what type of drug?

A

A B1/B3 blocker that increases nitric oxide

138
Q

Describe the following for Atenolol:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Selective B1 antagonist (antiarrhythmic drug)

MOA:
It reduces SA & AV nodal conduction by reducing adenylate cyclase, cAMP, & Ca2+ levels which can suppress abnormal pacemaker currents with a reduced slope phase 4

Clinical use:
1) Supraventricular tachycardia (control ventricular rate for A fib & atrial flutter)

Adverse effects:
1) Impotence
2) Asthma/COPD exacerbation
3) Bradycardia
4) AV block
5) Heart failure
6) Sedation
7) Masked hypoglycemia

139
Q

Drug type:
Selective B1 antagonist (antiarrhythmic drug)

MOA:
It reduces SA & AV nodal conduction by reducing adenylate cyclase, cAMP, & Ca2+ levels which can suppress abnormal pacemaker currents with a reduced slope phase 4

Clinical use:
1) Supraventricular tachycardia (control ventricular rate for A fib & atrial flutter)

Adverse effects:
1) Impotence
2) Asthma/COPD exacerbation
3) Bradycardia
4) AV block
5) Heart failure
6) Sedation
7) Masked hypoglycemia

Describes which drug?

A

Atenolol

140
Q

How would you treat a pheochromocytoma & why?

A

Use an irreversible alpha antagonist, then use a beta-blocker before resecting the tumor.

“A before B to avoid a hypertensive crisis”

Phenoxybenzamine for pheochromocytoma

141
Q

What are the cardiac effects meaning the cases you can use a B1 antagonist (aka a B1 blockade)

A

1) HTN
2) Classical angina
3) MI
4) Supraventricular arrythmias
5) Chronic CHF
6) Hypertrophic obstructive cardiomyopathy
7) Emergency symptoms of Tetralogy of Fallot
8) MVP

142
Q

1) HTN
2) Classical angina
3) MI
4) Supraventricular arrythmias
5) Chronic CHF
6) Hypertrophic obstructive cardiomyopathy
7) Emergency symptoms of Tetralogy of Fallot
8) MVP

Are all examples of scenarios that you can use which drug type? (receptor type)

A

B1 antagonists

143
Q

What are the cardiac effects meaning the cases you can use a B2 antagonist (aka a B2 blockade)

A

1) Pheochromocytoma (after an irreversible alpha antagonist)
2) Hyperthyroidism
3) Performance anxiety
4) Tremors
5) Akathisia
6) Migraine prophylaxis
7) Glaucoma (timolol & betaxolol)
8) Alcohol & opioid withdrawal
9) Portal HTN bleeding prophylaxis

144
Q

1) Pheochromocytoma (after an irreversible alpha antagonist)
2) Hyperthyroidism
3) Performance anxiety
4) Tremors
5) Akathisia
6) Migraine prophylaxis
7) Glaucoma (timolol & betaxolol)
8) Alcohol & opioid withdrawal
9) Portal HTN bleeding prophylaxis

Are all examples of scenarios that you can use which drug type? (receptor type)

A

B2 antagonist (aka a B2 blockade)

145
Q

What are the Adverse effects if thiazide diuretics?

A

Hypokalemia and metabolic alkalosis
Hyponatremia
Hypercalcemia
Hyperglycemia
Hyperlipidemia
Hyperuricemia
Allergic reactions (sulfonamide hypersensitivity)

146
Q

Hypokalemia and metabolic alkalosis
Hyponatremia
Hypercalcemia
Hyperglycemia
Hyperlipidemia
Hyperuricemia
Allergic reactions (sulfonamide hypersensitivity)

Are all adverse effects of which diuretic?

A

Thiazide diuretics

147
Q

What are the adverse side effects of Loop diuretics?

A

“GO PANDA”: Gout, Ototoxicity, low Potassium, Allergy, Nephritis, Dehydration, Alkalosis.

148
Q

“GO PANDA”: Gout, Ototoxicity, low Potassium, Allergy, Nephritis, Dehydration, Alkalosis.

A

What are the adverse side effects of Loop diuretics?

149
Q

Which conditions would you use loop diuretics?

A

Hypertension
Edema
Cardiac (acute and congestive heart failure, peripheral edema, lung edema)
Renal (nephrotic syndrome)
Hepatic (liver cirrhosis)
Hypercalcemia

150
Q

Hypertension
Edema
Cardiac (acute and congestive heart failure, peripheral edema, lung edema)
Renal (nephrotic syndrome)
Hepatic (liver cirrhosis)
Hypercalcemia

Are all conditions that you would use which type of diuretic?

A

Loop diuretics

151
Q

Hypertension
edema secondary to congestive heart failure; cirrhosis
Prevention of calcium kidney stones, idiopathic hypercalciuria
Osteoporosis
Nephrogenic diabetes insipidus

Are all conditions that you would use which type of diuretic?

A

Thiazide diuretic

152
Q

What are the adverse effects of Thiazide diuretics

A

Hypertension
edema secondary to congestive heart failure; cirrhosis
Prevention of calcium kidney stones, idiopathic hypercalciuria
Osteoporosis
Nephrogenic diabetes insipidus

153
Q

-hyperkalemia; metabolic acidosis, can lead to cardiac arrhythmias
Spironolactone-specific side effects: endocrine disturbances
Men: antiandrogenic effects (e.g., gynecomastia, erectile dysfunction)
Women: amenorrhea

Are the adverse effects of which diuretics?

A

K+ sparring diuretics

154
Q

What are the adverse effects of K+ Sparring diuretics?

A

hyperkalemia; metabolic acidosis, can lead to cardiac arrhythmias
Spironolactone-specific side effects: endocrine disturbances
Men: antiandrogenic effects (e.g., gynecomastia, erectile dysfunction)
Women: amenorrhea

155
Q

What are the conditions you would use a K+ sparring diuretic with?

A

Hypertension
Ascites/edema due to congestive heart failure, nephrotic syndrome, or cirrhosis of the liver (mainly spironolactone)
Hyperaldosteronism (Conn syndrome)
Nephrogenic diabetes insipidus (amiloride)
Hypokalemia
Hyperandrogenic states, e.g., polycystic ovary syndrome (spironolactone)

156
Q

Hypertension
Ascites/edema due to congestive heart failure, nephrotic syndrome, or cirrhosis of the liver (mainly spironolactone)
Hyperaldosteronism (Conn syndrome)
Nephrogenic diabetes insipidus (amiloride)
Hypokalemia
Hyperandrogenic states, e.g., polycystic ovary syndrome (spironolactone)

Are conditions that you would use which type of diuretic?

A

K+ sparring

157
Q

What are the adverse effects of carbonic anhydrase inhibitor type diuretics

A

Hyperammonemia with paresthesias
Proximal renal tubular acidosis → hyperchloremic, nonanion gap metabolic acidosis
Hypokalemia
Sulfonamide hypersensitivity
Calcium phosphate stone formation (alkaline urine promotes precipitation)

158
Q

Hyperammonemia with paresthesias
Proximal renal tubular acidosis → hyperchloremic, nonanion gap metabolic acidosis
Hypokalemia
Sulfonamide hypersensitivity
Calcium phosphate stone formation (alkaline urine promotes precipitation)

Are all adverse effects of which type of diuretic?

A

Carbonic anhydrase inhibitors

159
Q

Acute glaucoma
Altitude sickness (counteracts respiratory alkalosis)
Idiopathic intracranial hypertension
Metabolic alkalosis

Are all conditions that you would use which type of diuretic?

A

Carbonic anhydrase inhibitor

160
Q

Which conditions would you use a carbonic anhydrase inhibitor?

A

Acute glaucoma
Altitude sickness (counteracts respiratory alkalosis)
Idiopathic intracranial hypertension
Metabolic alkalosis

Pharm SJSM (23 decks)

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