histamine/PG COPY Flashcards
loratadine
second gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
misoprostol
PGE1 analogue
1st and 2nd trimester abortion
- Misoprostol - Methyl analog of PGE1
- Binds to PG receptors on parietal cells to inhibit acid secretion
- NSAIDs inhibit production of PG - but you can replace the PG in the stomach to stop the ulcers from forming
- Use
- Prevent NSAIDs ulcers from forming
- AE
- Diarrhea and abdominal pain
- May cause abortion by stimulating uterine contractions
- Binds to PG receptors on parietal cells to inhibit acid secretion
- Misoprostol (PGE1 derivative) - cryoprotective
Reatment of ulcer approved for the treatment of NSAID induced ulcer
Combined with mifepristone for terminating early pregnancy
nedocromil
histamine release inhibitors
- Three main things that use it
- Basophils/mast cells
- High levels in potential sites of injury (nose, mouth, feet, blood vessels)
- Cross linking of IgE on surface (via antigens) cause degranulation
- There is feedback on the H2 receptors to inhibit more release
- Released histamine
- Type 1 allergic reactions - hay fever, acute uticaria
- Inflammatory and immune modulation
- Blood vessel dialation
- Complement activation
- Cytokine release
- T cell and B cell modulation
- Brain
- Neurotransmitter function
- Enterochromaffin like cells (ECL) in stomach
- Activate acid production
- Chemical induced histamine release
- Morphine and tubocurarine
- Compound 48/80
- Drug used in the lab - it just makes the mast cells release histamine
- Mast cell injury
- Basophils/mast cells
- There is no clinical use of histamine - toxic effects overshadow clinical benefit
- How to modulate histamine clinicaly
- Phsyiologic counteraction - epinephrine
- Inhibitors of histamine release: cromolyn
- Pharamcologic blockade of histamine receptros
- Block them with antagonists
ziluteon
leukotriene inhibitor
asthma
ranitidine
H2 blocker
- H2 receptor mediated response
- CV
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Increase contractility and HR
- H2 antagonists have little effect on cardiac function - you would have to give them in really high concentrations
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Secretory tissue
- Stimulation of parietal cells - gastric acid secretion
- Ranitidine, cimetidine, nizatidine, famotidine
- CV
- Clinical uses of H2 receptor antagonists
- Reduceing gastric acid secretion
- PUD, GERD,
- Effective doses generally don’t impact
- Intesitnal secretion
- Other peripheral H2 receptor mediated effects (HR etc)
- Reduceing gastric acid secretion
CHLORPHENIRAMINE
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
clemastine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
rofecoxib
cox2 inhibitor (discontinued)
brompheniramine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
- These are all good at blocking the receptors - but the two generations are differetn in a few ways
- 2nd gen don’t cross BBB - can relieve seasonal allergies without CNS issues
- Many of the 1st gens have strong anticholinergic activity - this is primarily what cuases the CNS sedation, its also what makes some of them good at preventing motion sickness
- Duration of action: 1st gen (4-6 hours), 2nd gen (12-24 hours)
- Tox
- Sedation
- Antimuscarinic: urinary retention, blurred vision
dinoprostone
PGE2
given vaginally for abortion
can also be used to incue labor
fexofenadine
second gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
ketorolac
NSAID
azelastine
Second gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
montelukast
leukotriene inhibitor
asthma
meclizine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
desloratadine
second gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
indomethacin
NSAID
cetirizine
second gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
salicyclic acid
salicylate NSAID
cimetidine, famotidine
H2 blocker
- H2 receptor mediated response
- CV
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Increase contractility and HR
- H2 antagonists have little effect on cardiac function - you would have to give them in really high concentrations
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Secretory tissue
- Stimulation of parietal cells - gastric acid secretion
- Ranitidine, cimetidine, nizatidine, famotidine
- CV
- Clinical uses of H2 receptor antagonists
- Reduceing gastric acid secretion
- PUD, GERD,
- Effective doses generally don’t impact
- Intesitnal secretion
- Other peripheral H2 receptor mediated effects (HR etc)
- Reduceing gastric acid secretion
oxaprozin
NSAID
sulindac
NSAID
promethazine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
alprostadil
PGE1 (prostaglandin)
relaxes SM
keeps ductus arteriosis opens for neonates awating cardiac surgery
second line treatment for ED
celecoxib
COX2 inhibitor
diclofenac
NSAID
nizatidine
H2 blocker
- H2 receptor mediated response
- CV
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Increase contractility and HR
- H2 antagonists have little effect on cardiac function - you would have to give them in really high concentrations
- Higher dosese of histamine - cAMP dependent vasodilation and direct cardiac stimulation
- Secretory tissue
- Stimulation of parietal cells - gastric acid secretion
- Ranitidine, cimetidine, nizatidine, famotidine
- CV
- Clinical uses of H2 receptor antagonists
- Reduceing gastric acid secretion
- PUD, GERD,
- Effective doses generally don’t impact
- Intesitnal secretion
- Other peripheral H2 receptor mediated effects (HR etc)
- Reduceing gastric acid secretion
naproxen
NSAID
idophenpropit
H3 blocker
- H3 receptor mediated responses
- Nervous system
- Presynaptic H3 receptor activation modulates neurotransmitter release
- Metabolic effects
- Ongoing studies,
- Nervous system
cromolyn
histamine release inhibitors
- Three main things that use it
- Basophils/mast cells
- High levels in potential sites of injury (nose, mouth, feet, blood vessels)
- Cross linking of IgE on surface (via antigens) cause degranulation
- There is feedback on the H2 receptors to inhibit more release
- Released histamine
- Type 1 allergic reactions - hay fever, acute uticaria
- Inflammatory and immune modulation
- Blood vessel dialation
- Complement activation
- Cytokine release
- T cell and B cell modulation
- Brain
- Neurotransmitter function
- Enterochromaffin like cells (ECL) in stomach
- Activate acid production
- Chemical induced histamine release
- Morphine and tubocurarine
- Compound 48/80
- Drug used in the lab - it just makes the mast cells release histamine
- Mast cell injury
- Basophils/mast cells
- There is no clinical use of histamine - toxic effects overshadow clinical benefit
- How to modulate histamine clinicaly
- Phsyiologic counteraction - epinephrine
- Inhibitors of histamine release: cromolyn
- Pharamcologic blockade of histamine receptros
- Block them with antagonists
hydroxyzine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
thioperamide
H3 blocker
- H3 receptor mediated responses
- Nervous system
- Presynaptic H3 receptor activation modulates neurotransmitter release
- Metabolic effects
- Ongoing studies,
- Nervous system
dimenhydrinate
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system
Ibuprofen
NSAID
chlorbenpropit
H3 blocker
- H3 receptor mediated responses
- Nervous system
- Presynaptic H3 receptor activation modulates neurotransmitter release
- Metabolic effects
- Ongoing studies,
- Nervous system
ketoprofen
NSAID
piroxicam
NSAID
valdecoxib
cox2 inhibitor (discontinued)
aspirin
salicylate NSAID
diphenhydramine
first gen H1 blocker
- H1 receptor mediated response
- Nervous system
- Uticarial response, insect stings
- Reqpiratory neuron signaling
- CV
- Vasodilation mediated by increased NO release (very similar to how ACH cuases reaction in vascular endothelium)
- Reflex tachycardia
- Edema: increased permeability of post capillary vessels
- Bronchiolar SM
- Bronchoconstriction (particularly in asthmatic patients)
- GI smooth muscle
- Contraction of intestinal smooth emucels (high doses produce diarrhea)
- Nervous system