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exam 3 Flashcards

1
Q

autacoids

A

-local hormones produced locally by one group of cells that exert effects on other types of cells in the same region. Histamine

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2
Q

histamine

A

-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

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3
Q

diphenhydramine

A

-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

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4
Q

loratadine

A

-claritin
-2nd generation h1 antagonist
- ionized at physiological pH so less sedation because less enter cns
-preferrable
-

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5
Q

famotidine

A

-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

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6
Q

omeprazole

A

-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

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7
Q

ondansetron

A

-antiemetic
-5-ht3 (serotonin) receptor antagonist
-causes headaches and gi distress

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8
Q

metoclopramide

A

-antiemetic
-dopamine receptor antagonist
-causes movement disorders

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9
Q

heparin

A

-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

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10
Q

warfarin

A

-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

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11
Q

enoxaparin

A

-lmw heparin
- longer half life than full heparin
- only inhibits factor Xa
-routine monitoring is not usually required and dosing is less frequent

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12
Q

diazepam

A

-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

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13
Q

phenobarbitol

A

-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

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14
Q

carbamazepine

A

-na channel inhibitor
-effective in most seizures except absence seizures
-maintenance therapy
-binds preferentially to inactivated sodium channels

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15
Q

ethosuximide

A

-ca channel inhibitor

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16
Q

monoamine theory

A

-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

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17
Q

fluoxetine

A

-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

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18
Q

amitriptyline

A

-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

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19
Q

venlafaxine

A

-nsri (monoamine uptake inhibitor)
-antidepressant
-some serotonin selectivity
-major depression indication

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20
Q

bupropion

A

-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

21
Q

moclobemide (mao-a)

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

22
Q

lithium

A

-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

23
Q

cheese effect

A

with some mao inhibitors, eating cheese can fuck you up leading to hypertension headache and even hemorrhage. This is because cheese has tyramine

24
Q

positive vs negative symptoms of schizophrenia

A

-positive: delusions hallucinations wild thoughts word salad catatonia
-negative: social withdrawal, flattening of emotions anhedonia(inability to experience pleasure)

25
chlorpromazine
-1st gen antipsychotic -typical -d2 dopamine blockade in the mesolimbic pathway -relieve positive symptoms -some preference for d2 over d1
26
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
27
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
28
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
29
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
30
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
31
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
32
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
33
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
34
propofol
-injectable anesthetic -increases gaba receptor activity -blow through stage 2 -newer - no analgesia - milk of anesthesia -similar effects of thiopental
35
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
36
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
37
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
38
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
39
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
40
methadone
-opioid -treats dependence of other mu agonists like heroin
41
heroin
-opioid
42
naloxone
-opioid antagonist -narcan
43
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
44
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
45
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
46
metformin
-biguanide hypoglycemic - type 2 indication - with or without insulin - decreases blood glucose -does not promote lipogenesis -hypoglycemia with interactions
47
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
48
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
49
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

BMS 450 (3 decks)

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