Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS 450 > exam 3 > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

loratadine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ondansetron

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

metoclopramide

A

-antiemetic
-dopamine receptor antagonist
-causes movement disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

carbamazepine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ethosuximide

A

-ca channel inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

venlafaxine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

chlorpromazine

A

-1st gen antipsychotic
-typical
-d2 dopamine blockade in the mesolimbic pathway
-relieve positive symptoms
-some preference for d2 over d1

26
Q

olanzapine

A

-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
Q

overall antipsychotic side effects

A

-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
Q

tacrine

A

-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
Q

rivastigmine

A

-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
Q

levodopa

A

-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
Q

carbidopa

A

-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
Q

selegiline

A

-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
Q

thiopental

A

-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
Q

propofol

A

-injectable anesthetic
-increases gaba receptor activity
-blow through stage 2
-newer
- no analgesia
- milk of anesthesia
-similar effects of thiopental

35
Q

ketamine

A

-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
Q

halothane

A

-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
Q

lidocaine

A

-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
Q

general opioid shit

A

-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
Q

morphine

A

-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
Q

methadone

A

-opioid
-treats dependence of other mu agonists like heroin

41
Q

heroin

A

-opioid

42
Q

naloxone

A

-opioid antagonist
-narcan

43
Q

insulin

A

-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
Q

glucagon

A

-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
Q

glyburide

A

-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
Q

metformin

A

-biguanide hypoglycemic
- type 2 indication
- with or without insulin
- decreases blood glucose
-does not promote lipogenesis
-hypoglycemia with interactions

47
Q

exenatide

A

-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
Q

Describe an effective pharmacological approach for eradicating H. pylori in the treatment of gastric
ulcers. Hint: several types of drugs will be involved.

A

-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
Q

stages of anesthesia

A

-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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions