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154 Cards in this Set
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Types of Parasympathetic receptors?
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Nn: Cell bodies
Nm: Skeletal muscle M1-3: Muscarinic |
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Difference of actions in epinephrine and norepinephrine ?
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Beta-2 receptors actions
(NE has no activity on b-2) |
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Dopamine : Peripheral effects?
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Vasodilation in mesenteric and renal capillaries
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Secretion production : (sweating etc) is almost always d/t _____ receptor stimulation?
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Muscarinic
**ALWAYS ASSOCIATED WITH MUSCARINIC EFFECTS** |
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Autonomic effects on pupillary control?
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Muscarinic effects:
1. Miosis 2. Accomodation (near) Adrenergic effects: 1. Mydriasis **No effect on accomodation** |
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Pupil size : associated muscles involved
Accomodation: muscles involved |
1. Pupil size:
i. Miosis: Sphincter(muscarinic) ii. Mydriasis: Radial(a1 adrenergic) 2. Accomodation: i Ciliary muscles(thru suspensory ligaments) Contraction increases convexity of lens for near vision (muscarinic only) |
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Muscarinic innervation of organs?
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All M3 except-
GI glands: M1 Heart : M2 ("In your heart: Aim to : Be the One" M2 B1: Receptors in heart) PANS organs(M3): 1. Eyes 2. Lungs 3. GIT(except glands) 4. Bladder 5. Sphincters 6. Glands(swat, salivary) 7. Blood vessels |
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Heart is innervated by ____ muscarinic receptor
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M2
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Muscarinic effect on bladder?
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1. Detrussor muscle contraction
2. Sphincter relaxation RESULTS IN--> 1. Voiding 2. Urinary incontinence |
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GI sphincters: Muscarinic effects?
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Relaxation
EXCEPT? |
Lower esophageal : contracts
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Types of Parasympathetic receptors?
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Nn: Cell bodies
Nm: Skeletal muscle M1-3: Muscarinic |
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Difference of actions in epinephrine and norepinephrine ?
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alpha-2 receptors actions
(NE has no activity on a-2) |
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Dopamine : Peripheral effects?
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Vasodilation in mesenteric and renal capillaries
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Secretion production : (sweating etc) is almost always d/t _____ receptor stimulation?
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Muscarinic
**ALWAYS ASSOCIATED WITH MUSCARINIC EFFECTS** |
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Autonomic effects on pupillary control?
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Muscarinic effects:
1. Miosis 2. Accomodation (near) Adrenergic effects: 1. Mydriasis **No effect on accomodation** |
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Pupil size : associated muscles involved
Accomodation: muscles involved |
1. Pupil size:
i. Miosis: Sphincter(muscarinic) ii. Mydriasis: Radial(a1 adrenergic) 2. Accomodation: i Ciliary muscles(thru suspensory ligaments) Contraction increases convexity of lens for near vision (muscarinic only) |
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Muscarinic innervation of organs?
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All M3 except-
GI glands: M1 Heart : M2 ("In your heart: Aim to : Be the One" M2 B1: Receptors in heart) PANS organs(M3): 1. Eyes 2. Lungs 3. GIT(except glands) 4. Bladder 5. Sphincters 6. Glands(swat, salivary) 7. Blood vessels |
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Heart is innervated by ____ muscarinic receptor
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M2
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Muscarinic effect on bladder?
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1. Detrussor muscle contraction
2. Sphincter relaxation RESULTS IN--> 1. Voiding 2. Urinary incontinence |
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Sphincters: Muscarinic effects?
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Relaxation
EXCEPT? |
Lower esophageal : contracts
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Muscarinic effects on blood vessels?
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Dilation
Mechanism? |
NO/endothelium derived relaxing factor
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Muscarinic effects in GI?
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Stomach:
Increased motility--> cramps Intestine: i. Diarrhea ii. Involuntary defecation |
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Nicotinic receptor stimulation: effects?
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1. Secretion of epinephrine and NE
2. Stimulation--> twitch and hyperactivity of muscles |
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M1 receptors are ____ coupled
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Gq coupled
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M2 receptors are ____ coupled
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Gi coupled
(Mi2) |
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Nn and Nm receptors are ___ coupled
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Not coupled
(No 2nd messenger) |
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M3 receptors are ____coupled
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Gq
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M1, M2 and M3 receptors: Molecular responses?
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M1:
M3: Gq coupling--> Increased phospholipase C--> Increased Ca; IP3 and DAG M2: Gi coupling-->Decreased |
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Nn and Nm: Molecular responses?
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Direct opening of Na/K channels
(No 2nd messengers) |
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"Cholinomimetics"/Muscarinic agonists: Name em?
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1. Ach
2. Bethanechol 3. Methacholine 4. Pilocarpine |
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Muscarinic agonist/s with M>N?
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Methacholine
(Methacholine has M>n) |
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Muscarinic agonist/s with M and N activity?
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Ach
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Muscarinic agonists with M activity only?
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1. Bethanechol
2. Pilocarpine (No nicotinic activity) |
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Muscarinic agonist used in:
1. Paralytic ileus 2. Glaucoma 3. Dx of asthma 4. Urinary retention 5. Xerostomia? |
1. Paralytic ileus: Bethanechol
2. Glaucoma: Pilocarpine 3. Dx of asthma: Methacholine 4. Urinary retention: Bethanechol 5. Xerostomia: Pilocarpine |
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The only muscarinic agonist hydrolyzed by AChEsterase?
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Ach :P
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Ach has no clinical use: Why?
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Short T1/2
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Blood vessels are predominantly innervated by ____(SANS/PANS)
GIT is predominantly innervated by ____(SANS/PANS) |
Blood vessels: SANS
GIT: PANS |
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Nicotinic receptor stimulation: effect on adrenal medulla?
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Release of NE and E
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_____(Nn/Nm) receptors innervate the adrenal medulla?
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Nn
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_____(Nn/Nm) receptors innervated the neuromuscular junction?
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Nm
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Acetyl cholinesterase inhibitors: Name em.
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1. Edrophonium
2. Physostigmine 3. Neostigmine 4. Pyridostigmine 5. Donepezil 6. Tacrine 7. Organophosphates |
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Short acting AChE inhibitor?
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Edrophonium
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Edrophonium use?
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Differentiate myasthenia from cholinergic crisis
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AChE inhibitors used in glaucoma?
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1. Physostigmine
2. Echothiphate (organophosphate) |
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AChE inhibitor used in atropine overdose?
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1. Physostigmine
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AChE inhibitor used in myasthenia gravis?
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1. Neostigmine
2. Pyridostigmine Why? |
Quarternary amines (with NH+. therefore no CNS entry)
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AchE inhibitor used in alzheimer's disease?
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1. Donepezil
2. Tacrine Why? |
Lipid solubility therefore CNS entry
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AchE used in paralytic ileum/urinary retention?
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1. Neostigmine
2. Pyridostigmine |
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AchE inhibitors used in non depolarizing blocks?
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1. Neostigmine
2. Pyridostigmine |
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Parathion/malathion? Metabolism?
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Long acting AChE inhibitors
Parathion/malathion---P450--->Paraoxon/Malaoxon---P450--->Inactive compunds Why are the actions more specific for insects and not humans? |
Because in humans the 1st step is slow and 2nd is fast
In insects the 1st step is fast and 2nd is slow |
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Physostigmine: uses?
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1. Atropine overdose
2. Glaucoma |
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Neostigmine/pyridostigmine: uses?
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1. Paralytic ileus/urinary retention
2. Myasthenia gravis 3. Reversal of NM block (non-depolarizing) |
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Sarin?
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AChE inhibitor: Organophopshate used as a nerve gas
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Alzheimer's disease: loss of ACh in _____nucleus?
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Meynert's
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Organosphosphate used in glaucoma?
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Echothiophate
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AChE inhibitors: toxicity?
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A. Muscarinic:
1. Diarrhea 2. Urination 3. Miosis 4. Bradycardia 5. Bronchoconstriction 6. Excitation 7. Lacrimation 8. Salivation 9. Sweating ("Urination Defecation Lacrimation Salivation") B. Nicotinic effects: 1. Skeletal muscle excitation---> 2. Paralysis 3. CNS stimulation |
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AChE toxicity: management?
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1. Atropine
2. AChE regeneration: Pralidoxime (2-PAM) (Pralidoxime is a TIME dependent management) |
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2-PAM: MOA?
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2-PAM has affinity for the phosphate bound to AChE
2-PAM binds to and removes phosphate group from AChE(thereby regenerating it) |
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Why is 2-PAM considered a time dependent management?
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1. Due to AGING(if not treated within time limit)
2. AChE undergoes irreversible aging with organophosphate rendering 3. AChE-organophosphate complex irreversible (even with 2-PAM) |
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Chronic organosphosphate(such as from insecticide) poisoning: effects?
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1. Peripheral neuropathy
Mechanism? |
Due to slow/chronic accumulation of organophosphates in myelin-->
(organophosphates are highly lipid soluble) Hapten formation---> Immune reaction---> Demyelination---> Peripheral neuropathy |
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Ganglion blocking agents? Uses?
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1. Mecamylamine
2. Hexamethonium Uses: None (previously used as hypertensives- 50 yrs ago) |
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Ganglion blocking effects on:
1. Arterioles 2. Veins 3. Heart 4. Iris 5. Ciliary muscles 6. GIT 7. Bladder 8. Salivary glands 9. Sweat glands |
1. Arterioles: (SANS) Vasodilation (hypotension)
2. Veins: (SANS) Dilation (Decreased venous return--> decreased CO) 3. Heart: (PANS) Tachycardia 4. Iris: (PANS) Mydriasis 5. Ciliary muscles: (PANS) Cycloplegia 6. GIT: (PANS) Constipation 7. Bladder: (PANS) Urinary retention 8. Salivary glands: (PANS) Xerostomia 9. Sweat glands: (SANS) Anhydrosis |
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Hemicholinium: MOA?
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Inhibits uptake of choline
(Normally choline taken up for formation of acetyl choline along with Acetyl CoA) |
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Botulinus toxin: MOA?
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Degrades synaptobrevin(required for exocytosis of ACh from vesicles)-->
Inhibits release of Ach from vesicles. Another toxin with similar MOA? |
Tetanospasmin
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Cofactor for tyrosine hydroxylase?
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Vit C
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How do you detect dopaminergic neurons in the CNS?
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Detecting AB against tyrosine B hydroxylase
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Drug that inhibits tyrosine hydroxylase?
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Methyl-p-tyrosine
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MAO-b inhibitors: MOA?
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1. Act by inhibiting degradation of NE
2. Increasing the mobile NE pool |
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NE releasers?
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1. Tyramine
2. Ephedrine 3. Amphetamines |
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Interaction between NE releaser and MAO-inhibitors?
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Increased sympathetic stimulation.
(MAO inhibitor increases NE mobile pool and delays degradation + Releasers release NE from presynaptic nerve terminals) |
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זֶרַע
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seed, offspring, descendants
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Adrenergic alpha 2 stimulation: effects?
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1. Prejunctional receptors-->decreased NE release
2. Platelet aggregation 3. Panreas--> Decreased insulin Adrenergic alpha-2 agonists C/Is? |
Alpha 2 agonists C/I in:
1. Thrombotic states (may also increase incidence of MI/stroke in hypertensive pts due to platelet aggregation effect of alpha-2) 2. Diabetics(alpha-2 decreases insulin stimulation) 3. Depressed pts taking TCAs (TCAs decrease a/htn effect of alpha-2 agonists) |
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Adrenergic beta 1 stimulation: effects?
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Heart: increased HR, contractility and conduction---->
Increased automaticity and myocardial oxygen demand Kidney: Increased renin release |
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Adrenergic beta 2 stimulation: effects?
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1. Blood vessels: vasodilation
2. Bronchiles: Dilation 3. Uterus: Relaxation 4. Skeletal muscles: Glycogenolysisc("TREMORS") 5. Liver: Glycogenolysis 6. Pancreas: Increased insulin release |
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Cofactor for tyrosine hydroxylase?
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Vit C
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How do you detect dopaminergic neurons in the CNS?
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Detecting AB against tyrosine B hydroxylase
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Drug that inhibits tyrosine hydroxylase?
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Methyl-p-tyrosine
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MAO-b inhibitors: MOA?
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1. Act by inhibiting degradation of NE
2. Increasing the mobile NE pool |
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NE releasers?
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1. Tyramine
2. Ephedrine 3. |
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Interaction between NE releaser and MAO-inhibitors?
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Increased sympathetic stimulation.
(MAO inhibitor increases NE mobile pool and delays degradation + Releasers release NE from presynaptic nerve terminals) |
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Adrenergic apha 1 stimulation: effects?
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1. Eyes: Mydriasis
2. Arterioles: Constriction 3. Veins: Constriction 4. Bladder: Urinary retention 5. Sex organs: Emission/ejaculation 6. Liver: Glycogenolysis stimulatn 7. Kidney: Renin release |
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Adrenergic alpha 2 stimulation: effects?
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1. Prejunctional receptors-->decreased NE release
2. Platelet aggregation 3. Panreas--> Decreased insulin Adrenergic alpha-2 agonists C/Is? |
Alpha 2 agonists C/I in:
1. Thrombotic states (may also increase incidence of MI/stroke in hypertensive pts due to platelet aggregation effect of alpha-2) 2. Diabetics(alpha-2 decreases insulin stimulation) 3. Depressed pts taking TCAs (TCAs decrease a/htn effect of alpha-2 agonists) |
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Adrenergic beta 1 stimulation: effects?
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Heart: increased HR, contractility and conduction---->
Increased automaticity and myocardial oxygen demand Kidney: Increased renin release |
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Adrenergic beta 2 stimulation: effects?
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1. Blood vessels: vasodilation
2. Bronchiles: Dilation 3. Uterus: Relaxation 4. Skeletal muscles: Glycogenolysisc("TREMORS") 5. Liver: Glycogenolysis 6. Pancreas: Increased insulin release |
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Adrenergic D1 effects in periphery?
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Affects blood vessels:
1. Renal 2. Coronaries 3. Mesenteric Results in VASODILATION |
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Relative sensitivies of alpha-1 and beta-1?
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1. Beta-1 more sensitive than alpha-1
2. At lower doses: beta predominates alpha 2. At higher doses: alpha predominates beta |
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Fenoldopam?
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Dopaminergic agonist used in severe hypertension
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Receptor stimulation at different levels of dopamine?
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#1: D1
#2: B1 #3: A1 |
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Metabolism of NE?
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In prejunctional nerve terminal: MAO-A
In synapse: COMT |
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How is NE effect terminated?
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Terminated by:
1. Reuptake (Re-uptake transport system) 2. Alpha-2 stimulation (-ve feedback by NE itself) 3. Metabolism by MAO-A in PREJUNCTIONAL NERVE ENDING or 4. Metabolism by COMT in the SYNAPSE |
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Rate limiting step in NE synthesis? Enzyme involved?
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Conversion of tyrosine----tyrosine hydroxylase(vit c)---> DOPA
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Dopamine synthesized in presynaptic nerve terminal is metabolized to NE in______ with the help of ____enzyme
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Metabolized to NE in "storage vesicles"
with the help of "dopamine-b-hydroxylase" |
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Mechanism of events leading to release of NE from storage vesicles?
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Presynaptic nerve terminal depolarization---> Ca channel opening-->Influx of Ca--> fusion of granular membranes with presynaptic membrane--> Exocytosis into neuro-effector jn
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Molecular effects of-
1. Alpha-1 2. Alpha-2 3. Beta-1 4. Beta-2 5. D1 stimulation? |
1. Alpha-1: Gq--Phospholipase C--->IP3, DAG, Ca increase
2. Alpha-2: Gi---> Decreased cAMP 3. Beta-1: Gs-->Increased cAMP 4. Beta-2: Gs-->Increased cAMP 5. D1: Gs-->Increased cAMP |
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Alpha-1 stimulation: effect observed on tracing?
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1. Vasoconstriction
2. Bradycardia |
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Alpha-1 agonist: Name em?
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1. Phenylephrine
2. Methoxamine |
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Adrenergic agonist used in nasal congestion?
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Phenylephrine
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Adrenergic agonist used for ophthalmic examination?
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Phenylephrine
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Adrenergic drug used in paroxysmal atrial tachycardia?
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Methoxamine
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B-agonist effect observed on tracing?
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Decreased diastolic pressure
1. Decreased MAP 2. Systolic pressure remains constant(due to b-1 stimulation) 3. Tachycardia |
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B-1 agonists: Name em?
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Dobutamine
(B1>B2) |
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B-1 and B-2 agonists: Name em?
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Isoproterenol
(B1=B2) |
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B-agonist used in acuteCHF?
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Dobutamine
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Selective B-2 agonists?
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1. Salmeterol
2. Albuterol 3. Terbutaline 4. Ritodrine |
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Alpha-1 stimulation: effect observed on tracing?
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1. Vasoconstriction
2. Bradycardia |
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Alpha-1 agonist: Name em?
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1. Phenylephrine
2. Methoxamine |
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Adrenergic agonist used in nasal congestion?
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Phenylephrine
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Adrenergic agonist used for ophthalmic examination?
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Phenylephrine
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Adrenergic drug used in paroxysmal atrial tachycardia?
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Methoxamine
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B-agonist effect observed on tracing?
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Decreased diastolic pressure
1. Decreased MAP 2. Systolic pressure remains constant(due to b-1 stimulation) 3. Tachycardia |
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B-1 agonists: Name em?
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Dobutamine
(B1>B2) |
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B-1 and B-2 agonists: Name em?
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Isoproterenol
(B1=B2) |
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B-agonist used in acuteCHF?
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Dobutamine
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Selective B-2 agonists?
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1. Salmeterol
2. Albuterol 3. Terbutaline 4. Ritodrine |
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B-agonist used in premature labor?
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Ritodrine
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B-agonists used in asthma?
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1. Albuterol
2. Salmeterol 3. Terbutaline |
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B-agonist used in heart block?
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Isoproterenol
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B-agonist used in brady-arrhythmias?
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Isoproterenol
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Adrenergic agonists used in arrhythmias?
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1. Isoproterenol: Bradyarrhythmias/heart block
2. Methoxamine: Paroxysmal atrial tachycardia |
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Norepinehrine: Effect on pulse/BP tracing?
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1. Increased MAP
2. Increased systolic BP 3, Increased diastolic BP 4. Increased HR |
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Epinephrine: Effect on pulse/BP tracing?
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Low dose:
1. Decreased MAP 2. Systolic BP: (almost same) 3. Decreased diastolic BP 4. Increased HR Medium dose: 1. No effect on MAP 2. Increased systolic BP 3. Decreased diastolic BP 4. Increased HR High dose: 1. Increased MAP 2. Increase systolic BP 3. Increased diastolic BP 4. Increased HR---> followed by reflex bradycardia Why is such a dose dependent pattern observed? |
Due to increased sensitivity of beta receptors as against alpha receptors:
At low dose beta>alpha At mod dose beta=alpa At high dose beta<alpha nuff said? |
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High dose epinephrine pulse/BP tracing emulates the pulse/BP tracing of _____drug?
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Alpha-1 agonist:
(Although no effect on HR observed initially---> followed by reflex bradycardia) |
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Differentiate between norepinephrine and high dose epinephrine?
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In presence of an alpha blocker ---> Hypotension in epinephrine---> Due to unmasking of beta receptors
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Norepinephrine/epinephrine: uses?
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1. Cardiac arrest
2. With local anesthetics 3. Hypotension 4. Anaphylaxis(epinephrine) |
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Adrenergic agonists used in cold medication?
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1. Ephedrine(NE releaser)
2. Phenylephrine (alpha1 agonist) |
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Amphetamine: Name one?
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Methylphenidate
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Medication used in ADHD?
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Amphetamine: Methylphenidate
The other one use? |
Narcolepsy
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Adrenergic re-uptake inhibitors?
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1. TCAs
2. Cocaine |
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Tyramine and MAO inhibitor: drug interaction?
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Tyramine gets metabolized by MAO in liver and gut--> increased levels of tyramine in system
MAO-A: prime location? MAO-B: prime location? |
MAO-A: Liver
MAO-B: Brain |
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Indirect acting adrenergic agonists: Name em?
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1. Tyramine
2. Amphetamines 3. Ephedrine 4. TCAs 5. Cocaine |
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Alpha antagonists: Cardiovascular effects?
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Decreased TPR--> Decreased mean BP--> reflex tachycardia + Reflex salt retention
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DOC in pheochromocytoma?
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Phenoxybenzamine
Why this drug specifically? |
Phenoxybenzamine:
It is a non-competitive alpha-1 blocker. In pheochromocytoma: excess release of epinephrine-->hypertension If competitive blocker given (phentolamine) excess epinephrine would remove phentolamine from alpha receptor. |
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Alpha receptor antagonists: main uses?
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1. Hypertension (alpha-1)
2. Pheochromocytoma 3. BPH |
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Non selective alpha blockers?
Alpha-1 selective blockers? Alpha-2 selective blockers? |
Non selective-
Competitive: Phentolamine Non competitive- Phenoxybenzamine Alpha-1 selective: 1. Prazosin 2. Doxazosin 3. Tamsulosin 4. Terazosin Alpha-2 selective: 1. Yohimbine 2. Mirtazapine |
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B-1 blockade effects?
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1. Decreased HR, contractility, velocity
2. Decreased renin 3. Decreased aqeous humor production |
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B-2 blockade effects?
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1. Bronchospasm
2. Vasospasm 3. Blocks glycogenolysis 4. Blocks gluconeogenesis 5. Increased LDLs/TGs |
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B-1 selective blockers?
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1. Acebutalol
2. Atenolol 3. Esmolol 4. Metoprolol (All b-blockers that have initials from A to M) |
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Non selective B-blockers?
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1. Propanolol
2. Pindolol 3. Timolol |
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B-blocker with maximum sedation?
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Propanolol
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B-blocker with no sedation?
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Atenolol
why does it have minimal sedantory effect? |
Since it is water soluble it does not cross the blood brain barrier. Therefore no CNS sedation.
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B-blockers with intrinsic sympathomimetic activity? What does this indicate?
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1. Acebutalol
2. Pindolol Indicates that these are partial agonists Advantage of using partial agonists? |
Have minimal effect blood lipid profile and other side effects. (Aka ceiling effect)
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B-blockers that do not affect blood lipid profile?
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1. Acebutalol
2. Pindolol |
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B-blockers used as class
___ antiarrhytmics. Name em. |
1. Class II
1. Esmolol 2. Acebutalol 3. Propanolol |
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All B-blockers can be used for?
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1. Angina
2. HTN 3. Post-MI |
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B-blocker used in glaucoma?
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Timolol (mainly open angle)
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B-blocker used in thyrotoxicosis?
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Propanolol
MOA? |
Propanolol has peripheral de-iodinase inhibition property
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B-blocker used for essential tremors?
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Propanolol
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B-blocker used for migraines?
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Propanolol
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B-blocker used for performance anxiety?
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Propanolol
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Combined alpha-1 and Beta blocking activity?
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Labetolol
Carvedilol |
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Carvedilol/labetolol: use?
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CHF
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B-blocker that also has K+ channel blocking activity?
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Sotalol: used as class III antiarrhythmic
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Autonomic drug C/I in angle closure glaucoma?
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1. Antimuscarinic drugs
2. Alpha-1 agonist |
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Drugs used to rx:
Angle closure glaucoma? Open angle glaucoma? |
Angle closure: Mannitol/carbonic anydrase inhibitor
Open angle: AchE inhibitors: Pilocarpine/echothiphate: Increase flow through canal of schlemm(M activation-->ciliary muscle contraction) 2. Timolol: b-blocker--> decreases aqeous formation |
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