Pharm exam 3

what are the locations of the four histamine receptors and their functions

H1: Smooth muscle, endothelium, brain: bronchoconstriction, vasodilation, itching
H2: Stomach parietal cells: acid secretion
H3: CNS: Neurotransmitter modulation
H4: immune cells: chemotaxis, inflammation

What are the names and properties of 1st gen histamine blockers

diphenhydramine, chlorpheniramine, hydroxyzine.
high lipid solubility so they can cross BBB and cause sedating effects
competitively block H1 receptors

what are the names and properties of 2nd gen histamine blockers

loratadine, cetirizine, fexofenadine
low lipid solubility so can’t cross BBB
competitive inhibition with H1 receptors

what are common side of effects of H1 blockers

anticholinergic effects (dry mouth, eyes)

what is the MOA of mast cell stabilizers

they block Ca2+ influx which prevent mast cell degranulation when stops release of histamines and leukotriene

names of mast cell stabilizers

cromolyn sodium and nedocromil

what is the pathophysiology of asthma

airway hyperreactivity
mucus oversecretion
inflammation due to eosinophils and mast cells
bronchoconstriction

B2 agonists

end in -ol and work by increasing cAMP which relaxes bronchial smooth muscle

anticholinergics for respiratory

ipratropium and tiotropium
block M3 which stops constriction and mucus production

corticosteroids (respiratory)

end in -sone
stops cytokine production, inflammatory cell infiltration and increases B2 sensitivity
increase B2 sensitivity

leukotriene inhibitors

end in -kast
blocks leukotriene receptor or synthesis via LOX inhibition

what are the reproductive hormones and their functions

Estrogen: secondary sex characteristics regulates endometrial cycle
progesterone: endometrial cycle and bone health
testosterone: secondary sex characteristics, libido, energy, erythropoiesis
FSH: maturation of gametes
LH: ovulation and testosterone production

what is Anovulation and what treats it

lack of response to FSH and LH
clomiphene: blocks estrogen receptors to stop negative feedback of LH and FSH
-end in tropin: acts as FSH to grow a follicle

MOA of sildenafil and tadalafil

inhibit PDE5 which normally breaks down’ cGMP which is what causes vasodilation

GLUT receptors

GLUT 2: releases insulin. cascade is as follows: glucose enters cell, makes atp, closes K channel, opens Ca channel, insulin released
GLUT 4: insulin dependent, insulin causes it to translocate to the surface of the membrane and take up glucose

Diabetes Mellitus

increased urination and glucose in urine
type 1: autoimmune that attack beta cells
type 2: insulin resistant
symptoms: hyperglycemia, glycosuria, polyuria, polydipsia, polyphagia

what is incretin and amylin

incretin: hormone released from digestive tract after eating food and signals pancreas to release insulin
amylin: slows gastric emptying, suppresses glucagon, promotes satiety

incretin mimetics

end in -tide, semaglutide and tirzepatide
only used in type 2 because they need functional beta cells

Secretagogues

chlorpropamide and glipizide
induces insulin release by blocking potassium which depolarizes and triggers Ca influx and thus insulin release

antihyperglycemic drugs

Miglitol/Acarbose: stop glucose absorption in intestine
metformin: decreases liver glucose production
Pioglitazone/Rosiglitazone: sensitize receptors to insulin
Alogliptin/Saxagliptin: inhibit enzyme that breaks down incretin
canagliflozin/Dapagliflozin: stop sodium-glucose cotransporter (filtered glucose can’t reenter blood)

what is serotonin syndrome and its effects

Too much serotonin can lead to confusion, fever, tremors, restlessness, coma and death

SSRI’s

fluoxetine
merely stop reuptake so the cleft concentration increases

SNRI’s

duloxetine
Inhibit reuptake of both serotonin and norepinephrine

TCAs

amiltriptyline
like SNRI’s but is not selective and can block muscarinic and and histaminic receptors as well as other things

MAOIs

Phenelzine
has dietary restrictions, stops the enzyme that breaks down serotonin

SARI

trazodone
weak SNRI, associated with priapism

NDRI

bupropion
increases release of NE and DA and inhibit reuptake
reduced appetite, increased libido

Psychomotor stimulants

amphetamine
methylphenidate
dextroamphetamine
increase NE and DA, used for narcolepsy and hyperkinesis

Lithium

used to treat bipolar
similar to Na, interferes with nerve conduction and lowers excitability
SE: toxic to heart/kidneys and contraindicated with thyroid conditions

benzodiazepines

-end in am/pam
activate Cl- and decrease neuron firing, can be used to help treat anxiety

what is the main/root problem of schizophrenia

too much dopamine and serotoninw

what can happen if you block too much dopamine

you get extrapyramidal syndrome which looks a lot like parkinsons symptoms

Phenothiazines (antipsychotic class)

• end in zine

doesn’t cure psychosis but controls it
SE: AC and AH effects, Tardive dyskinesia, akathisia(must move around),

Butyrophenones (antipsychotic class)

haloperidol
more potent then phenothiazines, used in highly manic patients and for tics in tourettes

Thioxanthenes (antipsychotic class)

thiothixene
High chance of EPS less AC and AH effect

Atypical (antipsychotic class)

aripiprazole: DA and 5HT antagonist, high pot, SE: constipation, sleep troubles, anxiety
clozapine: Mod pot, low EPS but higher AC and PH, and agranulocytosis(more infection risk)
olanzapine: high pot, low EPS, effective in acute mania and bipolar.
- sedation, weight gain, postural hypotension

what does the mesolimbic pathway do

if there is a problem in this then you get psychotic symptoms

what does the nigrostriatal pathway do

if you have problems here then you get problems with movement (parkinsons)

what does SMART stand for in parkinsons

S: shuffling gait
M: mask like face
A: akinesia
R: rigidity
T: tremor

explain what happens as dopamine and Ach change in relative frequency in the basal ganglia

Parkinsons: low dopamine too much Ach
tourettes: too much dopamine too little Ach

Rasagiline

used for parkinsons
MAO-B inhibitor that stops breakdown of L-dopa and DA

Tolcapone

used for parkinsons
catechol-O-methyltransferase inhibitor
inhibits COMT and increases DA peripherally and centrally

Bromocriptine

used for parkinsons
DA receptor agonist

how can anticholinergics be useful for parkinson treatment

parkinsons is categorized by too little dopamine and too much Ach so if you decrease Ach you can bring things back into balance. also useful for EPS symptoms in antipsychotics