EXAM 2 BROWN Flashcards
(216 cards)
1
Q
What are the 11 steps of neurotransmission?
A
- transmitter synthesized and stored in vesicles
- AP invades presynaptic terminal
- Depolarization - opens voltage gated Ca++ channels
- influx of Ca++
- Ca++ causes vesicle fusion with pre-synaptic membrane
- NT released (exocytosis)
- NT binds to receptors
- Opening or closing of post-synaptic channels
- Post-synaptic potential changes
- Removal of NT (glial uptake or enzymatic degradation)
- retrieval of vesicular membrane from plasma membrane
2
Q
What can modulate the production of NT?
A
L-DOPA (dopamine precursor) used in human parkinson patients
3
Q
What can modulate NT release by blocking depolarization
A
local anesthetics, toxins (tetrodotoxin)
4
Q
What can modulate NT release by blocking calcium entry
A
calcium channel blockers, venom of the marine cone snail and some snake toxins
5
Q
What can modulate NT release by blocking vesicle release
A
botulinum and tetanus toxins
6
Q
Botulinum toxin mechanism
A
hits NMJ and blocks ACh release
flaccid paralysis
7
Q
Tatanus toxin mechanism
A
inhibuts inhibitory transmission (glycine and GABA)
rigid paralysis
8
Q
What can modulate termination of the NT effect
A
AChE inhibitors! they prolong the actions of ACh
Prozac (blocks serotonin reuptake)
succinylcholine (causes prolonged action of the nAChR)
9
Q
Define NT Auto-regulation
A
NT regulates its own release
10
Q
Define NT cross-regulation
A
another NT or hormone regulates release of NT
11
Q
Give examples of NT cross-regulators
A
Xylazine, Cisapride, and metoclopramide
12
Q
Why are co-transmitters important?
A
Even if you block the effect of one transmitter, if there is a co-transmitter, you are not blocking ALL of the effects of that nerve stimulation.
13
Q
define synergism
A
Synergy is when two compounds given together have a much larger effect than when either is given alone.
This can occur physiologically when two NTs have synergistic effects, between a NT and drug as well as between 2 drugs.
14
Q
define hypersensitivity
A
Chronic under stimulation by denervation (especially of muscle) or drug antagonism (e.g., beta blockers) can cause postsynaptic
hypersensitivity (oppsite of denensitization)
15
Q
Why is cross-regulation important?
A
some drugs act at these presynaptic receptors to alter (generally inhibit) another transmitter’s release and actions.
16
Q
PNS cell bodies of preganglionic fibers lie where?
A
in the brain stem and sacral section of the spinal cord
17
Q
PNS cell bodies of postganglionic fibers lie where?
A
within the target end-organ
18
Q
SNS cell bodies of preganglionic fibers lie where?
A
the lateral horn of the grey matter of the spinal cord
19
Q
SNS cell bodies of postganglionic fibers lie where?
A
within ganglia (away from the target end-organ)
20
Q
What 2 plexuses make up the ENS?
A
Myenteric and Submucosal
21
Q
What does the Myenteric Plexus do?
A
controls muscle tone, rhythmic contractions, and peristaltic waves
22
Q
What does the Submucosal Plexus do?
A
controls secretion, absorption, and some localized contractions
23
Q
ENS is innervated by PNS, SNS or both?
A
both
24
Q
A
25
Which divison of the ANS uses ACh as the preganglionic NT?
Both PNS and SNS
26
Post-ganglionic cells are activated by which type of receptor?
nAChR
27
Which divison of the ANS uses ACh as the postganglionic NT?
PNS
28
Postglanglionic NT of the PNS activates what type of receptor?
ACh activated mAChR
29
what type of receptors are mAChR?
GPCRs
30
Odd numbered mAChRs are usually **exitatory/inhibtory**
excitatory
31
Odd numbered mAChRs: M1 found where
primarily neuronal
32
Odd numbered mAChRs: M3 found where
primarily found on glands and smooth muscle
33
Mechanism of odd numbered mAChRs
activate PLC/DAG/IP3/Ca++ pathways
34
Even numbered mAChRs are usually **excitatory/inhibitory**
inhibitory
35
Even numbered mAChR mechanism
decrease cAMP formation and activate K+
36
even numbered mAChR: M2 found where?
cardiac
37
Which division of the ANS uses NE as the postganglionic NT?
SNS
38
SNS NT activates what type of receptors?
NE activates adrenergic receptors
39
adrenergic receptors are what type of receptor
GPCR
40
mechanism of α1-adrenergic receptors
activate PLC/DAG/IP3/Ca++
41
α1-adrenergic receptors tend to be **excitatory/inhibitory**
excitatory
42
mechanism of α2-adrenergic receptors
decrease cAMP and activate K+
43
α2-adrenergic receptors tend to me **excitatory/inhibitory**
inhibitory
44
mechanism of β-adrenergic receptors
increase cAMP
45
β-adrenergic receptors tend to be **excitatory/inhibitory**
excitatory
46
what type of receptor is activated by BOTH SNS and PNS in sweat glands?
mAChr
47
What is the one execption of post-ganglionic NT release in SNS?
post-ganglionic fibers innvervating sweat glands are cholinergic! (release ACh)
48
when the adrenal medulla is activated, what NT does it release?
Epinephrine
49
What is the significance of co-release of serotonin, ATP, or NO?
if you block the actions of the primary ANS NT (ACh and NE) there will still be a small effect when the ANS is activated due to the action of the co-transmitters
50
SNS effect on HR
increase
51
PNS effect on HR
decrease
52
SNS effect on GI tract
inhibits motility
53
PNS effect on GI tract
increase motility and digestion
54
SNS effect on pupils
dilate
55
PNS effect on pupils
contract
56
SNS effect on bronchi
dilate
57
PNS effect on bronchi
contract
58
SNS effect on bladder
relaxes bladder, constricts sphincter
59
PNS effect on bladder
constricts bladder, relaxes sphincter
60
Most vasculature is innervated by **PNS/SNS**
SNS
61
Eye is predominately innervated by **PNS/SNS**
PNS
62
Somatic Efferent NS: where do the cell bodies lie?
anterior horn of the spinal cord grey matter
63
Somatic Efferent NS: site of contact between the motor neuron and the muscle
NMJ
64
Somatic Efferent NS: motor neurons use what NT?
ACh
65
Somatic Efferent NS: NT activates what receptor type?
ACh activates muscle-type nAChR
66
Somatic Efferent NS: function
movement
67
how is ACh synthesized?
from Choline and acetyl CoA via choline acetly transferase (CAT)
68
ACh acts on what type of receptor?
neuronal nicotonic acetlycholine receptors (nAChR)
69
neuronal nicotonic acetlycholine receptors (nAChR) are what type of receptor
ligand-gated
70
muscarinic agonists will mimic what?
the effects of activating the PNS
71
What do muscarinic antagonists do? What does the size of effect depend on?
block the effects of activation of PNS. Size of effect depends on the tone of the PNS
72
define cholinergic
ACh-like effects without distinction of anatomical sites
73
define parasympathomimetic
describes an ACh-like effect on PNS targets
74
define muscarinic
drugs that affect muscarinic receptors
75
define nicotinic
drugs that affect nicotinic receptors
76
Whar target organs do you find mAChRs on?
1. non-vascular smooth mucle
2. glands
3. heart
4. eye
5. CNS
77
Name 2 muscarinic agonist drugs
1. Bethanechol
2. Pilocarpine
78
# Rx
Bethanechol Chloride:
Utilized to enhance bladder contractility (muscarinic agonist)
79
# Rx
Pilocarpine:
Used to treat various eye conditions, particularly glaucoma. In addition, can be used to manage dry mouth. (muscarinic agonist)
80
Cholinergic Toxicity Effects
**DUMBSLED**
Diarrhea
Urination
Miosis
Bradycardia
Salivation
Lacrimation
Emesis
Dyspnea
81
What drug can be used to reverse cholinergic toxicity symptoms?
Atropine (a muscarinic antagonist)
82
Name 3 Muscarinic Antagonists
1. Atropine
2. Glycopyrrolate
3. Tropicamide
83
# Rx
Atropine:
Prototypical muscarinic antagonist, enters CNS
84
# Rx
Glycopyrrolate:
muscarinic antagonist. Systemically longer acting than atropine. No CNS actions (doesn't cross BBB)
85
# Rx
Tropicamide:
A medication used to dilate the pupil. Muscarinic antagonist
86
Effects of muscarinic antagonists: smooth muscle
RELAXATION OF SM. MUSCLE
1. Inhibition of GI motility
2. Relaxation of other smooth muscles: bronchi, bladder, biliary
3. Eye (Pupil dilates (mydriasis) & unresponsive to light. Ciliary muscle is paralyzed (cycloplegia) and near vision is impaired)
87
Effects of muscarinic antagonists: secretions
decreased secretions (salivary, lacrimal, bronchial, and sweat)
88
Effects of muscarinic antagonists: cardiovascular
low dose atropine vs "normal" dose atropine
Low doses of atropine: bradycardia
Normal doses: modest tachycardia
89
Why do low doses of atropine cause bradycardia?
atropine has a higher affinity for presynaptic mAChRs, so blocking them will increase ACh relese and increase PNS vagal tone on the heart
90
Effects of muscarinic antagonists: CNS
if the compound can cross the BBB: excitation, increase body temp, anti-nausea
91
6 clinical uses of muscarinic antagonists
1. Antispasmodics – visceral smooth muscle relaxation
2. Bronchodilation
3. Preanesthetic during surgeries
4. Reduce vagal tone on heart
5. Eye exams and surgery
6. Cholinergic toxicity
92
muscarinic antagonist OD or toxicity symptoms
1. Tachycardia
2. Photophobia (dilated pupils)
3. Dry mouth
4. Ileus and constipation
5. Urine retention
6. Elevated temperature
7. CNS stimulation
8. Disorientation and restlessness
93
What is the difference in mechanism of action between depolarizing and non-depolarizing neuromuscular blockers?
Non-depolarizing blockers compete with ACh for binding at the receptor and depolarizing blockers are agonists for the muscle-type nAChR
94
Name 2 non-depolarizing neuromusclular blockers
1. atracurium
2. Tubocurarine (Curare)
95
# Rx
Tubocurarine (Curare)
A competitive antagonist of the nicotinic acetylcholine receptor at the neuromuscular junction. When tubocurarine is administered, it leads to muscle relaxation and flaccid paralysis.
Non-depolarizing neuromuscular blocker
96
# Rx
atracurium
A non-depolarizing block with competitive antagonism; no receptor activation, minimal histamine release; cholinesterase inhibitors reverse overdose.
97
Name a depoliarizing neuromuscular blocker
Succinylcholine
98
# Rx
Succinylcholine
Causes a depolarizing block that activates the receptor and then inactivates it; initial muscle contraction possible; AChE inhibitors worsen block (prolonging succinylcholine action).
99
What is Phase 1 of a depolarizing neuromuscular blocker
Depolarizing phase; receptor is activated
leading to depolarization and fasciculation (twitching).
Fasciculations are not always present in anesthetized animals.
100
What is Phase 2 of a depolarizing neuromuscular blocker
Non-depolarizing phase (desensitized
phase): the muscle is re-polarized but cannot contract in response to ACh
101
Therapeutic uses of NMJ Blocking agents
Skeletal muscle relaxation for procedures during surgeries (less anesthetic required)
102
Overdoses of NMJ Blockers results in death due to
paralysis of the diaphragm
103
What form of NMJ blockers can you use to reverse the block?
ONLY in non-depolarizing blockers
104
Key consideration for NMJ blockers and pain relief
The compounds paralyze but DO NOT provide pain relief
105
Name 4 AChE inhibitors
PEND
1. Physostigmine
2. Enrophonium
3. Neostigmine
4. Demecarium
106
# Rx
Neostigmine
AChE Inhibitor - Does not cross the blood-brain barrier. Use for paralytic ileus, atony of the urinary bladder, myasthenia gravis.
107
# Rx
Endrophonium
AChE Inhibitor - Does not cross the BBB; short-acting; used for diagnostic
purposes. Use for myasthenia gravis
108
# Rx
Demecarium
AChE inhibitor - A medication that has been used in the past for the treatment of glaucoma.
109
# Rx
Physostigmine
AChE inhibitor - crosses BBB. Use for paralytic ileus
110
name 2 insecticides that are AChE Inhibitors
Carbamate type
Organophosphate type
111
# Insecticide
Carbamate-type AChE inhibitors
Reversible insecticides (e.g., carbaryl)
112
# Insecticide
Organophosphate-type AChE inhibitors:
irreversible unless treated early with pralidoxime (2-PAM).
113
AChE inhibitor effects
increase ACh concentrations - will cause a combo of nicotinic (primarily muscle-type nAChR) and muscarinic effects
114
AChE inhibitors primary effects of therapeutic concentrations
DUMBSLED
Diarrhea
Urination
Miosis
Bradycardia
Salivation
Lacrimation
Emesis
Dyspnea
115
AChE Inhibitors action at the NMJ
enhancement of ACh action - augmented and/or prolonged muscle contraction. High doses lead to paralysis via depolarizing block
116
AChE inhibitors CNS effects
excitation, convulsions, depression, unconsciousness
117
Adverse effects of AChE Inhibitors
Like muscarinic agonists but with additional muscle twitching and weakness and less blood pressure effects due to no PNS innervation of blood vessels.
Miosis, bradycardia, muscle twitching and weakness, bronchoconstriction and increased secretions, diarrhea
118
AChE Inhibitors and muscarinic agonists: use extreme caution with
1. urinary obstruction
2. intestinal obstruction
3. asthma or bronchoconstriction
4. pneumonia
5. cardiac arrhythmias
119
AChE inhibitors: can reverse muscarinic effects of an OD with
atropine
120
DA, NE, and Epi are synthesized from what precursor?
Tyrosine
121
NE and/or Epi work on which recpetors?
α1, α2, β1 and β2
122
Termination of NE and Epi is primarily by
**reuptake**
123
What are the catecholamines
DA, NE, and Epi
124
Breakdown/metabolism of catecholamine main enzymes
monoamine oxidase (MAO) and catechol-O-transferase (COMT)
125
Endogenous adrenergic agonists: Epinephrine activates which receptors?
all adrenergic receptors (alpha-1 = alpha-2 < beta-1 = beta-2)
126
Endogenous adrenergic agonist: Epinephrine. Higher affinity for which receptors
higher affinity for beta receptors than alpha receptors
127
Endogenous adrenergic agonists: epinephrine cardiovascular effects
beta-1 action on the heart
(stimulatory to cardiomyocytes and AV node. Positive ionotropic and chronotropic actions - increases in CO)
beta-2 action on the blood vessels - vasodilation (decreases BP) - low concentrations
alpha-1 action on blood vessels - vasoconstriction (increases BP) - high concentrations
128
Endogenous adrenergic agonists: epinephrine smooth muscle effects - bronchi
dilate (Beta-2)
constrict (alpha-1)
129
Endogenous adrenergic agonists: epinephrine smooth muscle effects - uterus
relaxation (beta-2)
contraction (alpha-1)
dominant effect depends on species and whether pregnant
130
Endogenous adrenergic agonists: epinephrine smooth muscle effects - urinary bladder
urinary retention
relaxtion of bladder (beta)
trigone and sphincter contract (alpha)
131
Endogenous adrenergic agonists: epinephrine smooth muscle effects - eye
mydriasis
contract radial muscle and pilomotor muscles (alpha)
132
Endogenous adrenergic agonists: epinephrine metabolic effects
BG and FFA increase
isulin secretion inhibited (alpha-2)
133
Endogenous adrenergic agonists: epinephrine cardiovascular - why at high doses do you get refelx bradycardia?
Baroreflex: rapid negative feedback loop that causes a decrease in HR to decrease BP to normal
134
Epinephrine therapeutic uses
1. treat allergic reactions
2. reduce bronchospasm
3. local vasoconstriction
4. cardiac arrest
135
Epinephrine adverse effects
1. increased potential for arrhthymias
2. excessive vasoconstriction will cause hypotension - can lead to tissue necrosis
136
NE activates which receptors?
alpha-1, alpha-2, beta-1
NOT beta-2
137
NE is released from **PNS/SNS** terminals
SNS
138
NE has a **long/short** half life
very short
139
NE effects: Cardiovascular
1. increase BP (alpha-1)
2. slow HR (β-1activation accelerates heart but baroreceptor reflex slows heart (vagal activation)
140
Does NE cause relaxation in bronchi? why or why not?
No - no Beta-2!
141
DA acts on which receptors
primarily DA, some Beta-1
142
at high doses, DA stimulates release of ? via activation of which receptor?
NE (alpha-1)
143
DA cardiovascular effects
1. increased HR (Beta-1) - greater effect to increase contractility than NE or Epi!
2. better perfusion of systems during shock (DA receptor activation)
3. little change to BP with low doses
4. increase BP with high doses (alpha-1)
144
DA CNS effects
required for the initiation of movement!
145
DA therapeutic uses
acute heart failure
146
DA adverse effects
can cause tachycardia and ventricular arrhythmias
DA can cause tissue necrosis (leakage from vein with IV injection)
nausea and vomiting
BP changes can be dangerous
147
Dobutamine - receptors?
synthetic adrenergic agonist - primarily activates beta (B1 > B2)
can activate alpha at higher doses
148
Dobutamine effects
stimulates the heart (B1) increased HR and force
149
Dobutmaine therapeutic uses
heart failure (SHORT TERM ER SITCH)
150
Dobutmaine adverse effects
1. increased potential for arrhthmias (less of a problem than Epi)
2. tachycardia and increased O2 consumption
151
Examples of selective beta-2 agonists
terbutaline
152
selective beta-2 agonists: effects
1. bronchodilation
2. short-term decrease in BP
153
selective beta-2 agonists: therapeutic uses
1. Bronchial dilation
2. Bronchospasm, asthma, cough
154
selective beta-2 agonists: adverse effects
1. tachycardia (Due to heart action via β1 activation (remember “relative selectivity”) and baroreceptor feedback from β2 dilation of vasculature
2. BP changes
155
caution with selective beta-2 agonists
Patients can become refractory to the bronchodilatory effects of β2 agonists due to desensitization and downregulation of the receptors.
156
# Rx
Terbutaline
Highly effective bronchial dilator with β2 selectivity. (selective B2 agonist)
157
# Rx
Clenbuterol
β2-selective; used in horses; banned in food animals (even off-label).
158
# Rx
Phenylephrine
α1agonist
constricts smooth muscles
159
# Rx
Xylazine:
α2-selective; decreases sympathetic outflow; used in analgesia.
160
# Rx
Clonidine
α2-selective; can be used for sedation, analgesia, management of hypertension, and for behavioral issues, such as hyperactivity or aggression.
161
Non-selective β-adrenergic Antagonists (β-blockers) mechanism
Non-selective reversible block of β1 and β2 receptors
162
β-blockers: cardiac effect
Reduces sympathetic tone (decreases HR and contractility)
Reduces propensity for arrhythmias
163
β-blockers: vascular effects
1. transient increase BP (β2)
2. prolonged decrease in BP (β1 block decreases renin release from kidney)
164
β-blockers: pulmonary effects
normally very little. in asthmatics or COPD, β2 block can be fatal
165
β-blockers: metabolic effects
1. Reduces the capacity of liver to release glucose in response to hypoglycemia
2. Increased heart rate associated with hypoglycemia also blocked
166
β-blockers: eye effects
reduces ocular fluid
167
β-blockers therapeutic effects
antiarrhythmic
opthamology - reduced ocular pressure (glaucoma)
168
β-blockers: adverse effects
1. Negative inotropic effects and decrease cardiac output
2. Broncoconstriction
3. Reduced ability to respond to hypoglycemic challenge
4. Watch out for rebound hypertension and tachycardia once drug is stopped
169
Selective block of β1-adrenergic receptor examples
Metoprolol, atenolol, esmolol (short-acting)
170
Selective block of β1-adrenergic receptor: effects
All the cardiac effects of the non-selective agents w/o effects in lungs! (No Beta-2)
171
Selective block of β1-adrenergic receptor: therapeutic uses
1. Supraventricular tachycardia
2. Hypertension
3. HCM in cats
172
Selective block of β1-adrenergic receptor: adverse effects
1. Cardiac depression
2. Unusual tiredness/weakness
3. Confusion (blurred vision, dizziness)
4. Reduced ability to respond to hyperglycemia
5. Still watch out for rebound hypertension and tachycardia upon discontinuation
173
α- adrenergic Antagonists:
examples
Prazosin and acepromazine (reversible block)
Phenoxybenzamine (irreversible block)
174
α- adrenergic Antagonists: cardiovascular effects
relaxes vascular smooth muscle (decreased BP and can get reflex tachycardia)
175
α- adrenergic Antagonists: vascular smooth muscle effects
1.Relaxes urethral smooth muscle
2.Blocks pupil dilation and lid retraction of eye
176
α- adrenergic Antagonists: therapeutic uses
1. Hypertonus of the urethral sphincter
2. Reduces vasoconstriction
177
α- adrenergic Antagonists: adverse effects
**1. vasodilation and hypotension
2. reflex tachycardia**
3. nasal congestion
4. diarrhea (horses)
5. inhibits ejaculation
6. increase in itraocular pressure
7. blocks pupil dilation and lid retraction
178
α-2 adrenergic Antagonists: examples
Yohimbine and atipamezole
179
# Rx
Yohimbine
Reversible α2-selective block; reverses α2-agonist anesthetics (e.g., xylazine).
180
# Rx
Phenoxybenzamine:
α1 block ; It is primarily used for the management of certain medical conditions related to the autonomic nervous system.
Phenoxybenzamine works by blocking the effects of NE and Epi on alpha-adrenergic receptors, leading to vasodilation and a decrease in BP.
181
what is the Frank Starling law of the heart?
As preload increases, the myofiber is stretched, enhancing the contractile
state of the muscle; CO is thus increased
182
what is the Frank Starling law of the heart influenced by?
SNS and PNS stimulation
SNS increases the force of contraction
PNS lows the heart rate
183
CARDIOVASCULAR EFFECTS OF EPHINEPHRINE AND ADRENERGIC DRUGS:
B-1 action
Positive inotropic and chronotropic effects on the heart:
1. Increases force of contraction
2. Increase heart rate
184
CARDIOVASCULAR EFFECTS OF EPHINEPHRINE AND ADRENERGIC DRUGS:
B-2 action
Relaxes coronary and skeletal arteries:
1. Decrease in peripheral resistance
185
CARDIOVASCULAR EFFECTS OF EPHINEPHRINE AND ADRENERGIC DRUGS:
a1 action
Constricts arteries to skin and viscera:
1. Increase in peripheral resistance
186
Baroreceptor Reflex
activated by and increase in MAP due to stretch receptors
1. Increases afferent nerve discharge to CNS
2. Decreases SNS and increase PNS
3. Decreases heart rate and decreases peripheral resistance
4. Resulting in a decrease in blood pressure
187
M2 receptor activation: cardiac effects
decrease HR and force
188
M3 receptor activation effects
vasodialtion (via NO)
189
Histamine is released from what cells?
mast cells and neurons
190
endogenous opioids can be released from ?
neurons, pituitary gland, and immune cells
191
serotonin can be released from ?
1. released from platelets (hormone)
2. in intestinal enterochromaffin cells (paracrine)
3. released by neurons (neurotransmitter)
192
histamine is **hydrophobic/hydrophilic**
hydrophilic
193
what signals can release histamine from mast cells and basophils?
trauma, physical insult (heat, cold, x-rays), some drugs (morphine and d-tubocurarine), and immune-mediated
194
symptoms of an allergic reaction
1. Constriction of smooth muscle (bronchi)
2. Increased capillary permeability and edema formation
3. Decrease blood pressure
195
H1 receptors are associated with
allergic inflammation
196
H2 receptors are associated with
gastric acid secretion
197
H3 receptors are associated with
neurotransmission
198
H4 receptors are associated with
immunomodulation
199
Contraction of bronchi in most species
(H1 or H2)
H1
200
Contraction of bronchi in rabbits
(H1 or H2)
H2 > H1
201
contraction of uterus and ileum
(H1 or H2)
H1
202
local tissue reaction: swelling
H1 or H2
primarily H1
203
itch and pain
H1 or H2
H1
204
cardiovascular (usually decrease in BP)
H1 or H2
both
205
cardiovascular: cardiac stimulation
H1 or H2
H2
206
Antihistamines act on which H receptor
H1
207
antihistamine peripheral effects
1. relax contacted smooth muscle (bronchial and intestinal)
2. inhibit pruritis and pain sensation
3. inhibit formation of edema
208
antihistamine CNS effects
if crosses BBB, sedation and anti-emetic
209
which type of antihistamine crosses the BBB
1st gen or 2nd gen?
1st gen
210
examples of 1st generation antihistamines
benadryl (diphenhydramine)
chlorpheniramine
pyrilamine
dramamine (dimenhydramine)
211
examples of 2nd gen antihistamines
claritan (ioratidine)
Allegra (fexofenadine)
212
antihistamines adverse effects
1. CNS depression
2. paradoxical CNS excitation (esp at high doses)
3. anti-muscarinic effects (esp 1st gen)
213
examples of H2 antagonists
ranitidine (zantac)
famotidine (pepcid)
214
H2 antagonist effects
decrease basal gastric acid that is produced by histamine, food, gastrin, and vagal activation
215
H2 antagonist therapeuic uses
treat/prevent gastric, abomasal, and duodenal ulcers.
gastritis
216
H2 antihistamines adverse effects
uncommon -
1. anti-adrogenic
2. decreased reproductice performance
3. CNS effetcs
4. bacterial overgrowth in stomach
