exam 3 Flashcards
autacoids
-local hormones produced locally by one group of cells that exert effects on other types of cells in the same region. Histamine
histamine
-autacoid
-derived from amino acid histidine
- 2 major pools(mast cells and non mast cell tissue)
-distinct methods of storage and release
- released by degranulation
-histamine receptor blockade only PARTIALLY antagonizes degranulation
-h1 reception leads to vasodilation, capillary permeability, bronchial smooth muscle contraction, and pain/itching on neurotransmission
-h2 reception stimulates gastric acid secretion
diphenhydramine
-1st generation h1 antagonist
-unionized at physiological pH, so it can cause sedation
-benadryl
-prevents action rather than reversing it
-not usually effective as a sole agent in managing allergy or anaphylaxis
-used in allergy
loratadine
-claritin
-2nd generation h1 antagonist
- ionized at physiological pH so less sedation because less enter cns
-preferrable
-
famotidine
-h2 antagonist
-Pepcid
- inhibit gastric acid secretion
-inhibits gastric mucosa which is released from ecl cells
-used in ulcers, gerd
-not a lot of adverse effects
omeprazole
-proton pump inhibitor
-binds irreversibly and inactivates proton pump
-blocks acid secretion until more pumps are synthesized
-half life of 1 hour but affects acid for 2-3 days
-may mask symptoms of grastric cancer
ondansetron
-antiemetic
-5-ht3 (serotonin) receptor antagonist
-causes headaches and gi distress
metoclopramide
-antiemetic
-dopamine receptor antagonist
-causes movement disorders
heparin
-injectable anticoagulant
-present with histamine mast cell granules
- not a single substance
-activates anti thrombin III by conformational change increasing its affinity for serine proteases
- to inhibit thrombin it must bind to antithrombin III and thrombin
-also inhibits factor Xa, but only needs to bind to antithrombin III to do so due to low molecular weight heparins
-can cause hemorrhage, give protamine sulfate to antagonize heparin
warfarin
-anticoagulant
- vitamin k antagonist
- most important oral anticoagulant
-careful balance between too much and too little
-decreases availability of functional clotting factors II VII IX and X
-can cause hemorrhage
enoxaparin
-lmw heparin
- longer half life than full heparin
- only inhibits factor Xa
-routine monitoring is not usually required and dosing is less frequent
diazepam
-benzodiazepine
-anticonvulsant
-valium
-enhances GABAa receptors
-more gaba mediated chloride influx
-highly lipophilic
-enters cns rapidly
-helpful for active seizures (status epilepticus)
-increases efficacy of endogenous gaba on gaba a
-same amound of gaba will have greater inhibitory effect when diazepam is bound
-neuronal inhibition is net effect
-effective in stabilization therapy(active seizures)
-short term use
phenobarbitol
-anticonvulsant
-barbiturate
-enhances GABAa receptors
-more gaba mediated chloride influx
-activity at doses that do not produce anesthesia and sedation
-same as diazepam, but binds on gaba a receptors that are distinct from benzo sites
-does not enter as rapidly as benzos so it is second line drug
-induces cyp450
carbamazepine
-na channel inhibitor
-effective in most seizures except absence seizures
-maintenance therapy
-binds preferentially to inactivated sodium channels
ethosuximide
-ca channel inhibitor
monoamine theory
-states that depression is solely caused by deficient monoaminergic transmission (ne and serotonin)
-this theory does not explain everything, depression can be caused by neurodegeneration of hippocampus and weak responses of plasma cortisol to exogenous steroid administration
-monoamine uptake inhibition produces beneficial effect after 2 weeks
-moa is downregulation of beta and a2 adrenergic receptors and 5ht2(serotonin) receptors. We dont know how this relates to therapeutic effect
fluoxetine
-ssri (monoamine uptake inhibitor)
-antidepressant
-5-ht receptor
-most common
-minimal anticholinergic side effects
-less dangerous in overdose
-effective in mild and moderate depression
-also for anxiety
-well absorbed, acts for 24-96 hours
-therapeutic effects develop in 2-4 weeks
-can cause nausea diarrhea weight gain loss insomnia and sexual dysfunction but may decrease with time. also drug interactions
- less common side effect is aggression
-do not use on children, low efficacy, more excitement and insomnia, suicidal ideation
amitriptyline
-antidepressant
-tricyclic antidepressant (monoamine uptake inhibitor)
-vary in ne and serotonin reuptake
-far from ideal
-structurally similar to phenothiazines, so it was supposed to be an antipsychotic
-blocks uptake of amines by nerve terminals
-competitive binding for amine transporter
-less effect on dopamine
- affect muscarinic acetylcholine receptors, histamine receptors, and 5ht
-side effects galore: sedation confusion motor incoordination(usually wears off in 1-2 weeks), anticholinergic (dry mouth blurry vision constipation urine retention), antiadrenergic (postural hypotension), some cardiac effects
-alcohol anesthetic and antihypertensive interaction can lead to death
-easy to od
venlafaxine
-nsri (monoamine uptake inhibitor)
-antidepressant
-some serotonin selectivity
-major depression indication
bupropion
-antidepressant
-nri
-ne and dopamine reuptake inhibition
-can be used as an add on for ssris
-not a ton of weight gain or sexual dysfunction
-increased seizure risk
moclobemide (mao-a)
-antidepressant
-mao inhibitor
-monoamine ixidase is associated with mitochondria within nerve terminals, it also inactivates endogenous amines and ingested amines
-mao a has a substrate preference for 5ht
-reversible and selective for mao a
-rapid and sustained increase in serotonin >ne>dopamine
-transmitter release in response to nerve activity is not increased
-euphoria and excitement
-hypotension cns stimulation and anticholinergic
lithium
-antidepressant
-bipolar disorder indication
-narrow therapeutic window and long duration of action
-toxic cns effects, diapetes insipidus and renal failure
-hard to adjust dose
- unclear mechanism, inhibition of inositol monophosphatase to block pi pathway and inhibition of kinases
-varying cellular selectivity
-renal elimination, so interaction with diuretics can be toxic
-toxicity involves nausea diarrhea tremor polyuria renal tubular damage hypothyroidism weight gain hair loss
cheese effect
with some mao inhibitors, eating cheese can fuck you up leading to hypertension headache and even hemorrhage. This is because cheese has tyramine
positive vs negative symptoms of schizophrenia
-positive: delusions hallucinations wild thoughts word salad catatonia
-negative: social withdrawal, flattening of emotions anhedonia(inability to experience pleasure)
chlorpromazine
-1st gen antipsychotic
-typical
-d2 dopamine blockade in the mesolimbic pathway
-relieve positive symptoms
-some preference for d2 over d1
olanzapine
-2nd gen antipsychotic
-atypical
-less unwanted motor side effects
-can improve negative and positive symptoms
-highly selective for d2
-can minimize the social withdrawal and emotional bluntness
overall antipsychotic side effects
-reduce motor activity
-catalepsy (immobility while the patient is concious)
-apathy
-few emotions
-drowsiness
-no loss in intellectual function
-active dystonia (involuntary movements that be reversed by stopping treatment, face grimacing and things like that) and tardive dyskinesia(develops after months or years, irreversible, also a motor function thing but very debilitating, worsens when treatment is stopped)
-increased prolactin bc of decreased d2 which can lead to breast swelling and lactation
-anticholinergic
tacrine
-ace inhibitor for alzheimer’s
-enhance cholinergic transmission
-short half life, multiple doses a day
-not cns selective
-sludge side effects (diarrhea nausea)
- hepatotoxicity
-modest improvements in memory and cognition in 40% of patients
rivastigmine
-ace inhibitor for alzheimers
-newer drug
-limited efficacy but more effective in improving quality of life
-cns selective, so less side effects
-longer half life
levodopa
-dopamine precursor for parkinsons
-often combined with carbidopa and entacapone
-well absorbed
-short half life
-converted to dopamine in the periphery, peripheral dopamine stinks and causes side effects(this is where carbidopa is helpful)
-cns takes it up
-side effects include dyskinesia(involuntary movement that develops within 2 years), this causes the on off effect which can lead to patients feeling stuck on the off
-things like nausea, anorexia, hypotension, confusion, schizo stuff go away
carbidopa
-dopa decarboxylase inhibitor for parkinsons
-used with levodopa in order to reduce the dose needed ten fold and diminish side effects
-cant cross bbb so it effects only peripherally
selegiline
-mao b7 inhibitor for alzheimers
- lacks unwanted peripheral effects of non selective mao inhibitors used in depression
- no cheese effect
-protects dopamine from extraneuronal degradation
-combo with levodopa is effective
-metabolized to amphetamine so it can cause excitemnt anxiety and insomnia
thiopental
-injectable anesthetic
-barbiturate
increases gaba receptor activity
-the goal is to blow through stage 2
-no analgesia
-short acting (20 min)
-decrease blood flow, respiratory depression muclse relaxation
-mostly replaced by propofol
- short half life, unconsciousness in 30 sec, peak concentrtion in 1 min, redistribution, return of coniousness in 5-10min
propofol
-injectable anesthetic
-increases gaba receptor activity
-blow through stage 2
-newer
- no analgesia
- milk of anesthesia
-similar effects of thiopental
ketamine
-injectable anesthetic
-nmda receptor antagonist
- blow through stage 2
-no sleep just dissociation
-significant analgesia
-widely used for vets
-also used in painful er procedures or war zones
-prevents signaling by the excitatory neurotransmitter glutamate
-also has effect on poioid receptors, monoaminergic receptors, muscarinic and voltage gated ca channels
-actually increases blodd flow and tone in cns and cardiovascular
-apneustic breathing, rapid breath and then breath holding
-little muscle relaxation
- delerium can cause anxiety and thrashing, sometimes combined with a benzo
halothane
-inhaled anesthetic
-favors a predictable and rapid adjustment
-accurate and controlled
-have to get the blood gas partition coefficient to measure the solubility of drug
-also have to get the oil and gas partition coefficient bc it correlates with potency
-this all gives you minimum alveolar concentration which is like an ec50 but for inhaled anesthetics
-reversible generalized cns depression—amnesia analgesia unconciousenss and imobility
- not sure about mechanisms but maybe membrane lipid/protein related
-decreases co tpr, ventilation(higher co2), muscle function, and liver and kidney toxicity
-mac is inversely related to potency
lidocaine
-local anethetic
-reversible
-no loss conciousness or alteration of cns
- works like a sodium channel blocker
-potency is directly related to lipophilicy
-action is dependent on placement concentration and ph
- pain/temp>proprioception>motor function
-neurotoxicity and cardiotoxicity from the decrease in everything. minimized by injecting epi
general opioid shit
-mu kappa and delta receptors that have their own endogenous opioids
-analgesia, diarrhea, sedation, antitussive( cough)
-most of these suckers are mu and those ones cause analgesia
morphine
-opioid
-opiate(derived from opium)
-minimal cardio effects if dosed properly, but can cause hypotension
-increases myocardial perfucion through coronary vasodilation
-short half life
methadone
-opioid
-treats dependence of other mu agonists like heroin
heroin
-opioid
naloxone
-opioid antagonist
-narcan
insulin
-hypoglycemic
- b cells nside of islets of langerhans in pancreas secrete insulin
-more carbs more insulin
-postprandial (after meal) busrt of insulin
- postabsorptive reduce insulin
-helps convert glucose and shit into storage
-therapy for type 1 diabetes
-has to be iv or subc
-can cause hypoglycemia, this causes sweating confusionhunger that stuff, eat a candy bar
glucagon
-hypoglycemic
-increases blood glucose from pancreas
-more carbs less glucagon
-released in response to low blood glucose
-stimulates insulin which inhibits glucagon to create negative feedback
- can treat hypoglycemia, but can cause it in diabetics
glyburide
-sulfonylurea hypoglycemic
-on its own or with insulin
-stimulate insulin secretion from beta cells
-enhance beta cell activity
- reduce glucagon release
-few interactions and good potency
-type 2 diabetes
metformin
-biguanide hypoglycemic
- type 2 indication
- with or without insulin
- decreases blood glucose
-does not promote lipogenesis
-hypoglycemia with interactions
exenatide
-glucagon like peptide agonist
- glp 1 receptor agonist aka mmis incretin
-type 2 diabetic indication
- byetta
-subq, within 60 min before first and last meal
-causes proliferative effects in the pancreas which is bad bc diabetes is associated with pacreatitis
-studies have not shown this
-increase insulin secretion after eating in order to lower postprandial blood sugar
-suppress glucagon release after eating to prevent liver from over producing glucose and revent hyperglycemia
- slow gastric emptying to decrease the rate of glucose absorption
Describe an effective pharmacological approach for eradicating H. pylori in the treatment of gastric
ulcers. Hint: several types of drugs will be involved.
-h pylori is a bacteria that causes gastric mucosa
-causes a bunch of duodendal and gastric ulcers
- long term acid suppression is necessary, and will come back if meds are stopped
-nothing eradicates it
-often times you wanna do antibiotics and acid suppression therapy
-omeprazole amoxicillin and clarithromycin or omeprazole metronidazole tetracycline and bismuth subsalicylate
stages of anesthesia
-induction: slight analgesia, warmth tingling relaxation
-excitement/delerium: vomiting and irregular breathingpt becomes unconcious
-anesthesia: unconciosu regular breathing
-respiratory paralysis severe cns depression
