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z f1: pharmacology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Sympathetic system

A

Two neurons
Short then long ganglion
Postganglion release NE and E

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2
Q

The sympathetic trunk ganglia innervates what

A

Thorax, abdomen, head, neck

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3
Q

The prevertebral ganglia innervates what

A

Organ below diaphragm

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4
Q

What is the percentage release of E and NE in sympathetic system and adrenal medulla

A

Sympathetic: 80% NE, 20% E
Adrenal Medulla: 20% NE, 80% E

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5
Q

What happens in the adrenal medulla

A

One neuron system
ACh is released by pregnaglion
Preganglion innervates chromaffin cells in medulla and release NE and E
(NE and E are hormones because they are in the circulation and not released at a synapse)

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6
Q

What are the presynaptic receptors in the sympathetic system and adrenal medulla

A

Both are nicotinic receptors (Nn)

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7
Q

For the adrenergic presynaptic receptors what do the auto receptors and hetero receptors do in respect to NE release

A

Auto receptors: inhibit and activate NE release
Hetero receptors: inhibit NE release

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8
Q

What are the two subgroups of the adrenergic receptors

A

Alpha and Beta

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9
Q

What does a2 receptor do

A

autoreceptor that inhibits of NE release

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10
Q

What does b2 receptor do

A

autoreceptor that facilitates of NE release

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11
Q

Heteroreceptors presynaptically

A

inhibit release of NE (M2, M4)
-DA receptor
-Histamine receptor
-Serotonin receptor

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12
Q

What is a1 receptor

A

Gq, PLC, increase IP3 DAG and Ca2+

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13
Q

What is a2 receptor

A

Gi, AC, decrease cAMP

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14
Q

What is b1, b2, and b3 receptor

A

Gs, AC, increase cAMP

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15
Q

E and NE in a1, a2, b1, b2, b3

A

a1: E > NE
a2: E = NE
b1: E = NE
b2: E > NE
b3: E < NE

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16
Q

Catecholamines

A

Involved in chemical transmission in the CNS and PNS
Dopamine (mesocortical neuron) -> NE (sympathetic postganglionic neurons) -> E (adrenal medulla)

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17
Q

Synthesis of catecholamines

A

hydroxylation -> decarboxylation -> hydroxylation -> methylation

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18
Q

Enzyme locations of catecholamines

A

DBM in secretory vesicles

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19
Q

Enzymes and primary product of dopaminergic neurons

A

Product: Dopamine
Little or no DBM and PNMT

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20
Q

Enzymes and primary product of adrenergic neurons

A

product: NE
Less PNMT than DBM

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21
Q

Enzymes and primary product of adrenal medulla

A

E (80%) NE (20%)
DBM and PNMT present

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22
Q

What drugs inhibit CA synthesis

A

alpha-methyltyrosine (inhibit tyrosine hydroxylase, treat pheochromocytoma)
carbidopa (increases DOPA, treatment of parkinsonism)

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23
Q

What drugs inhibit CA storage

A

reserpine (inhibit VMAT, antihypertensive drug)
tetrabenazine (inhibit VMAT, hyperkinetic disorders)

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24
Q

Inhibitor effects of VMAT mechanism

A

decrease NE storage -> decrease NE release
depletion of CA at synapse
NE accumulated in cytoplasm is degraded

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25
Q

Diffusion of CA (catecholamine action) at synapse

A

Dilution of CA at synapse
Uptake at extraneuronal sites by non-neuronal transporters

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26
Q

Reuptake of CA (catecholamine action) at synapse

A

(85% of CA)
Into nerve terminals by neuronal transporters
CA can be stored in vesicles and/or metabolized

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27
Q

Metabolism of CA (catecholamine action) at synapse

A

Following uptake and reuptake, CA undergoes enzymatic catabolism

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28
Q

Reuptake of CA: Neuronal and Non-Neuronal transporters

A

Neuronal:
-Norepinephrine transporter (NET) –neurons, adrenal medulla, liver, placenta
-Dopamine transporter (DAT) –neurons, kidney, stomach, pancreas

Non-neuronal:
-OCT1, OCT2, ENT –liver, kidney, intestine

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29
Q

NET affinity and DAT affinity

A

NET: NE > E and DA
DAT: DA > NE and E

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30
Q

DAT and NET transporters

A

block antidepressants and substance of abuse
increase NT levels at synapse
NET - Cocaine, Desipramine
DAT - Cocaine, Mazindol

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31
Q

NET transporter movement of molecules

A

Co-transporter (symport) Na+, Cl-, NE
Na+ and energy dependent, Na/K ATPase creates Na+ gradient
Binding of K+ returns the transporter to outward position

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32
Q

What are MAO (monoamine oxidase)

A

MAO-A
-Periphery: placenta and liver
-Brain: region containing catecholamines
-NE, E, DA, serotonin

MAO-B
-Periphery: platelets, lymphocytes, liver
-Brain
-DA, amines

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33
Q

What are COMT (catechol-O-methyl-transferase)

A

Largely cytoplasmic enzyme
Exception in adrenal medulla is membrane bound
Less COMT than MAO in sympathetic neurons

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34
Q

Catabolism of NE and E: MAO mechanism

A

MAO forms aldehyde (DOPGAL) then turns into an alcohol (DOPEG)

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35
Q

Catabolism of NE and E: COMT mechanism

A

COMT methylates DOPEG to form MOPEG converted to VMA

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36
Q

What is the final end product of DA metabolism

A

HVA (homovanillic acid)

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37
Q

What is another route to form VMA other than COMT main pathway

A

minor pathway in neurons
methylation of NE and E by COMT then deamination by MAO, MOPGAL formed then VMA

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38
Q

Classification of adrenergic agonists

A

Adrenergic agonists:

Directing acting -> Selective and nonselective: act directly on one or more of the adrenergic receptors
Mixed-acting: indirectly release NE and activate receptors
Indirect acting -> Releasing agents, uptake inhibitor, MOA inhibitor, COMT inhibitors: increase NE or E levels to stimulate adrenergic receptors

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39
Q

Adrenergic Effects in the eye

A

Dilation of pupils (mydriasis)
Far vision: muscle relaxation, increase ligament tension, flat lens

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40
Q

Adrenergic receptors: Iris dilator

A

radial muscle only sympathetic innervation
pupil dilation

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41
Q

Adrenergic receptors: Ciliary muscle

A

also parasympathetic innervation M3R
far vision (flat lens)

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42
Q

a1 adrenergic receptors in the eye

A

Gq
increase Ca2+
Muscle contraction

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43
Q

B2 receptors in the eye

A

Gs
Increase cAMP
myosin light chain kinase-P (inactive)
Muscle relaxation

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44
Q

Difference between radial muscle and circular muscle

A

radial muscle: pull out, dilation
circular muscle: muscle relaxation, decrease pupil size

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45
Q

Adrenergic effects on the respiratory tract

A

Bronchodilation: relax bronchial smooth muscle, decrease airway resistance

Decrease bronchial secretion

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46
Q

What kind of receptors do bronchi have

A

B2 receptors -> E has a better effect than NE

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47
Q

Short-acting beta 2 adrenergic agonists

A

Albuterol (salbutamol)
Levalbuterol (xopenex)
sulfation metabolism

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48
Q

Systemic SABA beta 2 adrenergic agonists

A

Terbutaline (brethine)
Epinephrine

sulfation metabolism

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49
Q

Long Acting beta 2 adrenergic agonists

A

Formoterol (foradil)
Salmeterol (serevent)

COMT and MAO metabolism

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50
Q

Very long acting beta 2 adrenergic agonists

A

Indacaterol (arcapta neohaler)
Arformoterol (brovana)
Olodaterol (striverdi, resoimat)
Vilanterol only in combination inhalers

Glucuronidation and O-demethylation

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51
Q

Mechanism of action of smooth muscle contraction

A

Increase intracellular Ca2+
bind to calmodulin (CaM)
activates myosin light chain kinase (MLCK)
Increase myosin ATPase activity
cross bridges slide along actin and create muscle tension

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52
Q

Combination inhalors

A

Contain long-acting inhaled B2 agonist & corticosteroid

Advair: Salmeterol and fluticasone
Symbicort: Formoterol and budesonide
Dulera: Formoterol and nometasone
Brea Ellipta: Vilanterol and fluticasone

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53
Q

Adverse effect die to excessive activation of B2 receptors

A

Muscle tremor (skeletal muscle)
Tachycardia: due to reflex effect, vasodilation, stimulation of heart
Hypokalemia
Metabolic effects

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54
Q

Adrenergic effects in the heart

A

Increase heart rate (chronotropy)
Increase rate of conduction (dromotropy)
Increase force of contraction (inotropy)

Disturb cardiac rhythm and cause arrhythmias

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55
Q

What does the AV and SA node do

A

AV increase conduction velocity
SA increase heart rate

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56
Q

Cardiac therapeutic uses of beta agonists

A

Rapid on set short duration
E: cardiac arrest
Dobutamine: increase contractility -> used for cardiac surgery, heart failure, acute myocardial infarction

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57
Q

Blood vessels are only activated by what system

A

Sympathetic (increase system, increases vasoconstriction)

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58
Q

What are the receptors in the sympathetic vessels and what do they do

A

Alpha 1: contraction caused by baroreceptors
Beta 2: relaxation, increases blood flow

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59
Q

Alpha 1 adrenergic agonist drugs to treat hypotension

A

Metadaminol
Midodrine (prodrug)

Side effects are urine retention, goose bumps, bradycardia

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60
Q

Condone alpha 2 adrenergic agonist

A

Treats hypertension and opiate withdrawal
Diagnose hypertension and pheochromocytoma

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61
Q

Postsynaptic a2 agonist Brimonidine

A

Treat glaucoma (reduce eye pressure)
Side effects: drowsiness, eye itching
Treat eye redness

Decrease fluid pressure and construction

62
Q

Difference between direct and indirect effect on glands

A

Direct: increase secretion (Refresh-eye, Glaucon-eye)

Indirect: decrease secretion (decongestant, afrain)

63
Q

Sympathetic effects in the urinary tract

A

Detrusor muscle - B2 activation, muscle relaxation

Urethral Sphincter - a1 activation, contract sphincter

Urinary retention

64
Q

Adrenergic effects in the GI tract

A

Decrease motility and GI tone
Constrict sphincters
Decrease movement

B2 receptors in smooth muscle
a1 in sphincter

65
Q

Adrenergic effects on uterine contraction

A

uterine relaxation B2
uterine contraction a1

66
Q

Ritodrine and Terbutaline receptor selectivity (uterine contraction)

A

Beta 2

67
Q

E in emergency treatment for anaphylaxis

A

Release histamine
a1 - increase vasoconstriction, increase BP, decrease mucosal edema

B2 - increase bronchodilation, decrease mediator release

68
Q

NE effects

A

Increase contractility and heart rate and vasoconstriction

Used for maintain BL in cardiogenic and septic shock

Adverse reaction: arrhythmia, anxiety, headache

69
Q

Adrenergic agonists releasing agents and uptake inhibitors

A

releasing: amphetamine, tyramine
uptake: cocaine
(increase E and NE to stimulate adrenergic receptors)

70
Q

What are indirect adrenergic agonists drugs that decrease and increase NE and E

A

Drugs that decrease NE and E re-uptake
-Cocaine
-Desipramine

Drugs that increase NE and E release
-Amphetamine
-Ephedrine
-Tyramine

71
Q

Does indirect adrenergic agonists have the same mechanism as NT release

A

no

72
Q

Mechanism of action of indirect agonists

A

-Amphetamine is transported into nerve terminal by NET -> competitively inhibit reuptake
-Drug taken in by VMAT -> exchange drug for NE
-NE increase in cytosol

73
Q

Amphetamine effects in CNS stimulant

A

wakefulness
good mood
increased motor
physical improvement
need to keep increasing dosage

74
Q

Amphetamine effects in peripheral alpha and beta actions

A

Increase BP
Increase HR -> cardiac arrhythmias
Pupil Dilation
Urinary incontinence

75
Q

Ephedrine effects

A

Mixed-acting sympathomimetic
-a and B receptors
-Increase release of NE from sympathetic neurons

Effects
-Increase HR
-Increase peripheral resistance
-Broncodilation
-Urinary retention
-CNS stimulant

76
Q

Tyramine effects (not a drug)

A

Product of tyrosine metabolism
Produced in high concentration in rich-protein foods by decarboxylation of tyrosine during fermentation
Indirect sympathomimetic action (caused by catecholamines)

77
Q

Tyramine increase NE release causing severe hypertensive response. If patient is taking MAO inhibitors, patient should avoid eating what

A

Cured meats, pickled food, cheese, wine

78
Q

Inhibitors of NE uptake: Cocaine

A

causes tachycardia and increase BP
CNS causes euphoria and excitement

79
Q

Inhibitors of NE uptake: Desipramine

A

Tricyclic antidepressent

80
Q

Inhibitors of NE uptake: Atomxetine

A

selective inhibitor with clonidine-like effect in CNS

81
Q

What do adrenergic antagonist do

A

Block the effects of NE, E and other sympathomimetic drugs by preventing their binding to adrenergic receptors

82
Q

alpha 1 receptor antagonists

A

block contraction of arterial and venous smooth muscle -> vasodilation -> decrease BP
(block contraction of visceral smooth muscle

83
Q

alpha 2 receptor antagonists

A

block regulation of sympathetic output

84
Q

beta 1 receptor antagonists

A

block cardiac receptors

85
Q

Non-selective alpha 1 antagonists

A

reversible antagonist -> Phentolamine
irreversible antagonist -> Phenoxibenzamine

86
Q

selective alpha 1 antagonists

A

“-osin” ending drugs

87
Q

Phentolamine

A

can dissociate from receptor
competitive inhibitor -> can be reversed with sufficiently high concentration of agonists
used in short-term control of hypertension
decreases BP

88
Q

Phenoxybenzamine

A

blocks alpha 1 and alpha receptors
alkylating agent
persistent effects
anti-hypertensive
decreases vasoconstriction produced by NE and E
decreases BP

89
Q

What do prazosin, terazosin, and doxazosin do (alpha 1 adrenergic antagonists)

A

used for hypertension

90
Q

What do tamsulosin, silodosin do (alpha 1 adrenergic antagonists)

A

selective for alpha 1 A
mainly for benign phosphate hyperthrophy

91
Q

Effects of alpha 1-antagonists

A

Block alpha 1 receptors in blood vessels
Block vasoconstriction produced by endogenous CA
Decrease venous return
Decrease BP

92
Q

How do alpha 1 antagonists completely reverse effects of phenylephrine but only partially reverse the effects of NE

A

NE has an extra methyl group

93
Q

Therapeutic uses of alpha 1 adrenergic antagonists

A

-Treatment of essential hypertension
-Benign prostatic hyperplasia - Tamsulosin and Silodosin
—Enlargement of prostate increased smooth muscle mass and tone in prostate
—Decrease flow of urine

94
Q

Adverse effects of alpha 1 antagonists

A

Orthostatic hypotenstion
Dizziness and headache
Syncope
Tachycardia
Miosis
Nasal stuffiness

95
Q

alpha 2 receptor antagonists

A

Block CNS receptors
Increase NE release
Increase HR and BP
(Yohimbine, Indoramin)

96
Q

Beta adrenergic antagonists

A

Antagonize effects of catecholamines
Treatment of hypertension, heart failure

97
Q

Traditional beta blockers: nonselective and selective

A

nonselective: block beta 1 and 2, propanolol
selective: block beta 1, esmolol, metoprolol

98
Q

Third generation beta blockers: nonselective and selective

A

nonselective: carvededilol, vasodilation (alpha 1)
selective: betaxolol, vasodilation

99
Q

Beta blockers with ISA activity

A

B1 > B2
selective
not used because of partial agonist activity

100
Q

Effects of beta antagonists in the heart

A

Decrease HR, rate of conduction, force of contraction, cardiac output

101
Q

Therapeutic uses of beta blockers

A

Hypertension
Angina
Cardiac arrhythmias
Glaucoma

102
Q

Adverse effects of Beta 1 adrenergic antagonists

A

hypotension
bradycardia
dizziness
fatigue
heart block

103
Q

Histamine

A

biologically active amine that functions as a NT
-mediator for allergic rxns

104
Q

Histamine metabolism

A

rapidly inactivated
excreted in urine
N-methyltransferase in most tissues (MAO)

105
Q

Histamine release: Immunologic

A

Allergic reactions
Degranulation of sensitized mast cells or basophils
(needs Ca2+)

106
Q

Histamine release: Chemical release

A

Caused by therapeutic agents
released from mast cells directly and without sensitization

107
Q

Allergin-induced histamine release

A

evokes IgE production
cell sensitization
allergen (antigen) binds to IgE
degranulation of sensitized cells

108
Q

Localized responses of histamine

A

Allergic Rhinitis (hay fever)
-rxn in conjunctivae and nasal mucosa
Asthma
-rxn in mucous membranes of bronchi
Food Allergy
-rxn in upper or lower GI can induce smooth muscle contraction and vasodilation -> vomiting and diarrhea

109
Q

Systemic Type 1 responses

A

Systemic Anaphylaxis (shock-like reaction)
-onset w/in minutes of type I reaction
-decreased BP, urination, defecation

Wide range of antigens

E used to counteract effects of mediators

110
Q

H1 Histamine Receptors

A

Gq
Phospholipase C
IP3, DAG
In Smooth muscles, heart, CNS
Increases vascular permeability at sites of inflammation

Allergies

111
Q

H2 Histamine receptors

A

Gs
Adenylyl cyclase
Increase cAMP
In gastric parietal cells, cardiac muscle, mast cells, CNS
Increase gastric acids release, cardiac stiimulation

Acid reflex

112
Q

Histamine effects in cardiac system

A

Increase HR, AV conduction, force and rate of contraction

113
Q

Histamine effects in vascular system

A

vasodilation -> smooth muscle relaxation
-decreases BP
Edema
In blood vessels

114
Q

Histamine effects at H1 receptors

A

Higher affinity for histamine
activation at low histamine concentration
vasodilation is mediated by NO production
rapid onset short duration

115
Q

Histamine effects at H2 receptors

A

Produces vasodilation
mediated by cAMP and PKA pathway
Slow onset long duration

116
Q

Histamine effects on capillaries

A

Dilation of blood vessels
increased capillary permeability in small vessels -> activation of H2 receptors
Induction of endothelial cell contraction -> capillaries become leaky
Fluid and proteins move into ECM tissue -> edema formation

117
Q

Histamine effects on bronchial smooth muscle

A

Bronchoconstriction
Increased broncho secretion
(important for asthma patients)

117
Q

Histamine effects on exocrine glands

A

Increase lacrimation, mucus secretion, salivation

117
Q

Effect of histamine on GI tract

A

H1 receptors: contraction of intestinal smooth muscle, increase motility and GI tone, increase GI movement

H2 receptors: activation of parietal cells, increase gastric acid secretion

118
Q

Flush, flare and wheal

A

Flush: red line or spot due to capillary dilation
Flare: red zone redness in the surrounding area due to arteriolar dilation
Wheals: localized edema due to education of fluid from capillaries and venules

119
Q

Clinical uses of histamine

A

Bronchial hyper-reactivity in asthmatics
Allergy skin testing

120
Q

Histamine toxicity

A

Hypotension
Headache
Tachycardia
Bronchoconstriction
Upset GI

121
Q

Histamine effects

A

Increase secretion from glands, mucus secretion, heart rate, HCl secretion, motility of GI, bronco constriction

122
Q

Histamine release inhibitors mechanism of action

A

Reduce or inhibit degranulation of mast cells -> mast cell stabilizers
Prophylactic Drugs (nasalcrone, opticrome, gastrocom, nedocromil sodium)
Poor absorption though GI

123
Q

Therapeutic uses of histamine release

A

Decrease histamine effects
Asthma - reduce level of bronchial reactivity
Allergic reactions - rhinoconjunctivatis

124
Q

Histamine receptor antagonist

A

H1 receptor antagonist
Antihistamines

H2 receptor antagonists
Treatment of gastric acid secretion

125
Q

First generation H1 blockers

A

Sedating drugs
Not for children

126
Q

Second gen H1 blockers

A

Reduce distributions into the CNS -> no sedating effect

127
Q

First gen H1 antagonist drugs

A

Diphenhydramine
Pyrilamine
Chlorpheniramine
Cyclizine

Well absorbed
Muscarinjc cholinergic responses

128
Q

Second gen H1 antagonists drugs

A

Cetirizine
Fexofenadine
Loratadine

Non sedating
Anti inflammatory effects

129
Q

Main effects of H1 antagonists

A

Decrease secretion of glands, broncoconstriction, mucus secretion, hypotension, edema, vasodilation

130
Q

H1 antagonist effects on nerve endings

A

Suppress the action of histamine on nerve endings
Suppress itching, pain, flare

131
Q

H1 antagonist effects in the CNS

A

Depression:
Slow alertness, reaction times, and somnolence
Don’t use at bedtime

Stimulation:
Uncommon
Restlessness, nervous, unable to sleep

132
Q

Adverse effects of H1 antagonists

A

Sedation
Dry mouth
Loss of appetite
Allergic response

133
Q

H1 antagonist drug interactions

A

Antibiotics
Grapefruit juice
Additive effects with CNS depression drugs

134
Q

Clinical uses of H1 antagonists

A

Allergic reactions
Motion sickness (vertigo)
Local anesthesia

135
Q

Organization of components for gastric acid secretion

A

Parietal cells secrete H+ and Cl- separately into the gastric lumen of the stomach

HCl is formed in the gastric lumen

136
Q

Acid secretion of parietal cells

A

H+ from H2CO3
Exchanged for K+
Cl- into cells for HCO3
Excess K+ removed

137
Q

Regulation of gastric acid secretion

A

ACh
Histamine
Gastrin

They activate specific receptors on the parietal cells

138
Q

Direct regulation of gastric acid

A

Bind ACh, gastrin, and histamine to receptors in surface of parietal cells
Increase cAMP and Ca2+ activate PKA
PKA phosphorylates and activates H+, K+ ATP-ase producing gastric acid

139
Q

Indirect regulation of gastric acid secretion

A

ECL cells produce and release histamine
Histamine activates H2 receptors on parietal cells producing gastric acid

140
Q

Defense mechanism of gastric acid

A

Esophageal sphincter: prevent reflex of Garrick content into esophageal

Stomach: traps bicarbonate at cell surface increase pH

Mucus production: PGs stimulate this by decreasing acid secretions, NSAIDs inhibit PG synthesis -> decreasing production

141
Q

antacids react with hydrochloric acid to form what two things

A

salt
water

141
Q

Therapeutic uses of antiacids

A

intermittent heartburn
dyspepsia

141
Q

What are the 4 gastric acid drugs

A

alka seltzer
gaviscon
maalox
tums

141
Q

H2 antagonists

A

inhibit gastric acid secretion from parietal cells

142
Q

H2 antagonist drugs

A

cimetidine
famotidine
nizatidine

143
Q

H2 antagonists: mechanism of action

A

-reduce gastric acid secretion
-competitively inhibit histamine by binding to H2R
-inhibit acid secretion stimulated by gastrin and ACh through activation of ECL cells

144
Q

PPIs

A

-most potent inhibitors of gastric acid secretion
-new pump molecules need to be synthesized to resume secretion

145
Q

What are the 4 proton pump inhibitors

A

Omeprazole
Zegrid
Esomeprazole
Lansoprazole

z f1: pharmacology (4 decks)

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