Block 2 (Sympathomimetics) Flashcards

(160 cards)

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
Describe the following for B3 receptors: Which pathway does it activate? What type of effects does it have?
Path: activates Gs path which activates adenylate cyclase increased cAMP Effects: 1) lipolysis
26
Path: activates Gs path which activates adenylate cyclase increased cAMP Effects: 1) lipolysis describes which receptor?
Beta 3 receptor
27
Phenylephrine Metaraminol Mephentermine Midodrine Methoxamine Are all examples of which receptor agonists? What are the clinical uses?
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)
28
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
Phenylephrine Metaraminol Mephentermine Midodrine Methoxamine
29
Apraclonidine Clonidine Brimonidine Dexmedetomidine Guanfacine Guanabenz Methyldopa Tizanidine Are all examples of which receptor agonists? What are the clinical uses?
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)
30
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
Apraclonidine Clonidine Brimonidine Dexmedetomidine Guanfacine Guanabenz Methyldopa Tizanidine
31
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
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
32
Epinephrine Norepinephrine Dopamine Are all examples of which receptor type
Mixed receptor Epi: a1/2 & B1/2 Norepi: a1/2 & B1 Dopa: D1, B1, & a1
33
Phentolamine (reversible) Prazosin Terazosin Doxazocin Tamsulosin Are all which type of receptor antagonists?
alpha 1 antagonists
34
Phenoxybenzamine (irreversible) Yohimbine Mirtazapine Are all which type of receptor antagonists?
alpha 2 antagonists
35
Describe the reflex response of a1 agonists: HR Contractility Systemic vascular resistance
BP: reduced Contractility: reduced Systemic vascular resistance: increased
36
Describe the reflex response of a2 agonists: HR Contractility Systemic vascular resistance
HR: reduced Contractility: unaffected Systemic vascular resistance: reduced
37
Describe the reflex response of a2 antagonists: HR Contractility Systemic vascular resistance
HR: Increased Contractility: unaffected Systemic vascular resistance: reduced
38
Describe the reflex response of a1/2 antagonists: HR Contractility Systemic vascular resistance
HR: increased Contractility: unaffected Systemic vascular resistance: reduced
39
Describe the reflex response of B1 agonists: HR Contractility Systemic vascular resistance
HR: increased Contractility: increased Systemic vascular resistance: reduced
40
Describe the reflex response of B1 antagonists: HR Contractility Systemic vascular resistance
HR: reduced Contractility: reduced Systemic vascular resistance: unaffected
41
Describe the reflex response of Norepinephrine (mixed agonist) (a1>B1>B2) BP HR Renal blood flow
BP: increased HR: unchanged/reduced Renal blood flow: reduced
42
Describe the reflex response of Phenylephrine (a1 agonist) BP HR Renal blood flow
BP: increased HR: reduced Renal blood flow: reduced
43
Describe the reflex response of Dobutamine (B agonist with a higher affinity for B1) BP HR Renal blood flow
BP: unchanged/reduced HR: increased Renal blood flow: unchaged
44
Describe the reflex response of Dopamine (mixed agonist) Low vs high dose BP HR Renal blood flow
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
45
Describe the reflex response of Epinephrine (mixed agonist) Low vs high dose BP HR Renal blood flow
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
46
Describe the reflex response of Isoproterenol (B agonist with equal effects on B1 & B2) BP HR Renal blood flow
BP: unchanged/reduced HR: increased Renal blood flow: unchanged
47
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?
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
48
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?
Epinephrine
49
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?
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
50
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?
Dobutamine
51
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?
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
52
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?
Albuterol
53
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?
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
54
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?
Salbutamol
55
What drug types can be used to treat hyperkalemia?
Insulin + glucose Calcium gluconate B2 agonists
56
Insulin + glucose Calcium gluconate B2 agonists Are all used to treat what condition?
Hyperkalemia
57
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?
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
58
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?
Isoproterenol
59
What are the adverse effects of alpha 1 agonists?
1) Hypertension 2) Reflex bradycardia 3) Urine retention 4) Ischemia & necrosis (fingers/toes) 5) Rebound congestion 6) Piloerection
60
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?
alpha 1 agonists
61
What is Albuterol used to treat?
It's a B agonist targeted more towards B2 to treat Asthma
62
What is Salmeterol used to treat?
It's a B agonist targeted more towards B2 to treat COPD
63
What is Terbutaline used to treat?
It's a B agonist targeted more towards B2 to treat preterm labor with a tocolytic effect
64
Albuterol, Salmeterol, Formoterol, & Terbutaline are all used to treat which condition?
Hyperkalemia (B agonists pull K+ from blood into smooth muscle)
65
What are the adverse effects of B2 agonists?
1) Tremor 2) Agitation 3) Insomnia 4) Diaphoresis 5) Hypotension 6) Reflex tachycardia 7) Hyperglycemia 8) Hypokalemia
66
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?
B2 agonists
67
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?
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
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?
Dopamine
69
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?
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
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?
Fenoldopam
71
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?
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
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?
Alpha-methyldopa
73
What are the adverse effects of alpha-2 agonists?
1) Miosis 2) Dry mouth 3) Bradycardia & hypotension 4) CNS & Resp depression 5) Rebound hypertension
74
1) Miosis 2) Dry mouth 3) Bradycardia & hypotension 4) CNS & Resp depression 5) Rebound hypertension Describes the adverse effects of which drug type?
alpha-2 agonists
75
Describe the following for Oxymetazoline: What is the drug type? What is the MOA? What are the effects? What are the clinical uses?
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
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?
Oxymetazoline
77
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?
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
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?
phenylephrine
79
Describe the following for mirabegron: What is the drug type? What is the MOA? What are the effects? What are the clinical uses
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
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?
Mirabegron
81
List the alpha & beta agonist releasers
Tyramine Amphetamines Ephedrine
82
Describe the following for Amphetamines: What is the drug type? - MOA What are the effects? What are the clinical uses?
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
What are the signs of amphetamine toxicity? - Central vs peripheral
Central toxicity: Euphoria Excitement Confusion Delirium Hallucinations Acute psychosis Mydriasis Peripheral: Palpitations Arrythmia Vascular collapse
84
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?
Amphetamines
85
Central toxicity: Euphoria Excitement Confusion Delirium Hallucinations Acute psychosis Mydriasis Peripheral: Palpitations Arrythmia Vascular collapse Describes the toxicity of which drug?
amphetamines
86
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
B.lsoproterenol
87
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
B.Epinephrine
88
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
C.Dopamine
89
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. Stop the decongestant
90
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
F.Fenoldopam
91
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
C.cAMP increase in cardiac muscle cells
92
Describe the following for Tamsulosin: What drug type is it? What is its MOA? What are its adverse effects? What are its clinical uses?
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
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?
Tamsulosin
94
Describe the following for cocaine: What drug type is it? What is its MOA? What are its adverse effects? What are its clinical uses?
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
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?
Cocaine
96
Which drugs can be used to effectively treat BPH?
Tamsulosin Selective B1 blockers (-azosin)
97
Describe the following for Selective B1 blockers (azosins): What is its MOA? What are its adverse effects? What are its clinical uses?
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
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?
Selective B1 blockers (azosins)
99
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?
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
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?
Clonidine
101
Describe the following for a1 receptors: What is the pathway it activates? What are its effects? Name a selective agonist Name a selective antagonist
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
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?
Alpha 1 receptor
103
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
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
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?
Alpha 2 receptor
105
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
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
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?
Beta 1 receptor
107
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
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
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?
Beta 2 receptor
109
Describe the following for B3 receptors: What is the pathway it activates? What are its effects? Name a selective agonist
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
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?
Beta 3 receptor
111
Describe the following for Timolol: What is the drug type? What is its MOA? What is its effect?
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
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?
Timolol
113
Describe the following for prazosin: What is the drug type? What is its clinical use? What is an adverse effect?
drug type: Selective alpha-1 antagonist (a1 blocker) Clinical use: 1) Hypertension Adverse effect: Orthostatic hypotension
114
drug type: Selective alpha-1 antagonist (a1 blocker) Clinical use: 1) Hypertension Adverse effect: Orthostatic hypotension Describes which drug?
Prazosin
115
Describe the following for Doxazosin & Terazosin: What are the drug types? What are they clinically used for? What are the adverse effects?
Drug types: Selective alpha-1 antagonists Clinical uses: 1) BPH 2) Atrial HTN Adverse effect: 1) Orthostatic hypotension
116
Drug types: Selective alpha-1 antagonists Clinical uses: 1) BPH 2) Atrial HTN Adverse effect: 1) Orthostatic hypotension Describes which 2 drugs?
Doxazosin & Terazosin
117
Describe the following for Tamsulosin, Alfuzosin, & Silodosin: What are the drug types? What are they clinically used for? What are the adverse effects?
Drug type: Alpha-1 antagonists Clinical use: 1) BPH Adverse effects: 1) Intraoperative floppy iris syndrome
118
Drug type: Alpha-1 antagonists Clinical use: 1) BPH Adverse effects: 1) Intraoperative floppy iris syndrome Describes which 3 drugs?
Tamsulosin, Alfuzosin, & Silodosin
119
Which type of drug would you use to treat angina pectoris & why?
Beta blockers to reduce HR, contractility & O2 consumption of the heart (less damage)
120
Which type of drug would you use to treat Glaucoma & why?
A Beta blocker like timolol to reduce aqueous humor production
121
Which type of drug would you use to treat Heart failure & why?
Beta blockers like Bisoprolol, Carvedilol, Metoprolol to reduce neurohormonal stress & deleterious remodeling "B-blockers Curb Mortality"
122
Which type of drug would you use to treat Hypertension & why?
B-blockers to reduce CO & BP to lessen the stress on the heart
123
Which type of drug would you use to treat Hypertrophic obstructive cardiomyopathy & why?
Beta blockers to reduce HR & increase filling time to relieve the obstruction
124
Which type of drug would you use to treat Hyperthyroidism/thyroid storm & why?
A beta blocker like propranolol to control the symptoms (i.e reduce HR in racing heart & tremors)
125
Which type of drug would you use to treat Myocardial infarction & why?
A beta blocker to reduce HR & O2 demand (short term ischemia control) & reduce mortality
126
Which type of drug would you use to treat Supraventricular tachycardia & why?
Beta blockers like metoprolol & esmolol to reduce AV nodal conduction to slow HR & reduce contractility
127
Which type of drug would you use to treat Variceal bleeding & why?
Beta blockers like nadolol, propranolol, & carvedilol to reduce hepatic venous pressure gradient (dilating the hepatic veins) to reduce portal hypertension
128
What are some of the major side effects of most beta blockers?
1) Erectile dysfunction (vasodilation) 2) Bradycardia, AV block, & HR 3) Seizures & sleep alterations 4) Dyslipidemia (metoprolol) 5) Masked hypoglycemia 6) Asthma/COPD exacerbation
129
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)
Beta blockers
130
Why should you avoid Beta-blockers & cocaine?
Because it will result in unopposed alpha 1 activity
131
Acebutolol Atenolol Betaxolol Bisoprolol Esmolol Metoprolol Are all examples of which type of drug?
Selective B1 antagonists
132
List 6 Selective B1 antagonists
Acebutolol Atenolol Betaxolol Bisoprolol Esmolol Metoprolol
133
Nadolol Pindolol Propranolol Timolol Are all examples of which type of drug?
B1 non-selective antagonists
134
List 4 B1 non-selective antagonists
Nadolol Pindolol Propranolol Timolol
135
Carvedilol Labetalol Are examples of which type of drug?
Non-selective A/B antagonists
136
list 2 Non-selective A/B antagonists
Carvedilol Labetalol
137
Nebivolol is what type of drug?
A B1/B3 blocker that increases nitric oxide
138
Describe the following for Atenolol: What is the drug type? What is the MOA? What are the clinical uses? What are the adverse effects?
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
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?
Atenolol
140
How would you treat a pheochromocytoma & why?
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
What are the cardiac effects meaning the cases you can use a B1 antagonist (aka a B1 blockade)
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
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)
B1 antagonists
143
What are the cardiac effects meaning the cases you can use a B2 antagonist (aka a B2 blockade)
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
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)
B2 antagonist (aka a B2 blockade)
145
What are the Adverse effects if thiazide diuretics?
Hypokalemia and metabolic alkalosis Hyponatremia Hypercalcemia Hyperglycemia Hyperlipidemia Hyperuricemia Allergic reactions (sulfonamide hypersensitivity)
146
Hypokalemia and metabolic alkalosis Hyponatremia Hypercalcemia Hyperglycemia Hyperlipidemia Hyperuricemia Allergic reactions (sulfonamide hypersensitivity) Are all adverse effects of which diuretic?
Thiazide diuretics
147
What are the adverse side effects of Loop diuretics?
“GO PANDA”: Gout, Ototoxicity, low Potassium, Allergy, Nephritis, Dehydration, Alkalosis.
148
“GO PANDA”: Gout, Ototoxicity, low Potassium, Allergy, Nephritis, Dehydration, Alkalosis.
What are the adverse side effects of Loop diuretics?
149
Which conditions would you use loop diuretics?
Hypertension Edema Cardiac (acute and congestive heart failure, peripheral edema, lung edema) Renal (nephrotic syndrome) Hepatic (liver cirrhosis) Hypercalcemia
150
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?
Loop diuretics
151
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?
Thiazide diuretic
152
What are the adverse effects of Thiazide diuretics
Hypertension edema secondary to congestive heart failure; cirrhosis Prevention of calcium kidney stones, idiopathic hypercalciuria Osteoporosis Nephrogenic diabetes insipidus
153
-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?
K+ sparring diuretics
154
What are the adverse effects of K+ Sparring diuretics?
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
What are the conditions you would use a K+ sparring diuretic with?
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
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?
K+ sparring
157
What are the adverse effects of carbonic anhydrase inhibitor type diuretics
Hyperammonemia with paresthesias Proximal renal tubular acidosis → hyperchloremic, nonanion gap metabolic acidosis Hypokalemia Sulfonamide hypersensitivity Calcium phosphate stone formation (alkaline urine promotes precipitation)
158
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?
Carbonic anhydrase inhibitors
159
Acute glaucoma Altitude sickness (counteracts respiratory alkalosis) Idiopathic intracranial hypertension Metabolic alkalosis Are all conditions that you would use which type of diuretic?
Carbonic anhydrase inhibitor
160
Which conditions would you use a carbonic anhydrase inhibitor?
Acute glaucoma Altitude sickness (counteracts respiratory alkalosis) Idiopathic intracranial hypertension Metabolic alkalosis