Pharm Drugs Pa School 3D Sem Test 1

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GASTRIC ACIDITY CONTROLLED BY

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Gastrin (endocrine), Ach (neural), Histamine (paracrine) – stimulate gastric acid through membrane receptors that ultimately activate proton pump in parietal cells

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drugs reduce gastric acidity

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gastric antacids
H2 antagonists
PPI

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ranitidine

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 H2block– longer acting 5-10x more potent then cimetidine, no p450
 competitive antagonist of H2 receptor on parietal cells, block meal stimulating and basal secretion of gastric acid by histamine and gastrin,

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 Can cause gynacomastia bc of weak androgen affect

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cimetidine

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famotidine

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 H2block – 20-160x more than cimetidine, 3-20x more than ranitidine, no p450
 competitive antagonist of H2 receptor on parietal cells, block meal stimulating and basal secretion of gastric acid by histamine and gastrin

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H2 b
ORAL
 urine excretion but 30% in liver
 Drug interactions by inhibiting p450 system

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cimetidine

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drug interactions of cimetidine

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 INCREASED level of warfarin, diazepam, phenytoin, quinidine, carbamazepine, theophylline, imiparamine

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major agent to reduce gastric acid

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PPI

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PPI,  INTERFEARS WITH LIVER METABLOLISM OF WARFARIN PHENYTOIN DIAZAPAM AND CYCLOSPORIN

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4. Omeprazole

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what does 4. Omeprazole innterfear with

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PPI,  INTERFEARS WITH LIVER METABLOLISM OF WARFARIN PHENYTOIN DIAZAPAM AND CYCLOSPORIN

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 Bind irreversibly to ATP H+/K+ pump “proton pump” in parietal cells

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PPI

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PPI  Prodrugs, need enteric coating

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lonsaprozole omeprozole

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rxn with • TETRACYCLINE

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antacids

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antacids can be what

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aloH caOH mgOH

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action of antacids

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weak bases neutralize acid

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fastest way to neutralize stomach ph

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antacids

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 Mucosal protective agent –gets stuck to damaged mucosa
 Aluminum hydroxide and sulfonated sucrose bind membrane proteins forming a gel with mucous that protects the cells from acid and pepsin
 NEEDS ACIDIC ENVIRONMENT SO DON’T USE WITH H2B, antiacids, and PPI’s!

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sulfacrate

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pg2 analog

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misoprostol

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 Weak bases that chemically neutralize stomach acid.

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antacids

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 AlOH, MgOH, CaOH

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antacids

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antacids constipation

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aloh

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antacid neural effects

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mgoh and aloh

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antacids diarhea

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mgoh

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caoh

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tums .. possibly reverse cuz ca activates acid pump

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 Prodrugs, need enteric coating

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lansoprazole omeprazole ppi

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 Mucosal protective agent –gets stuck to damaged mucosa

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sucralfate

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8. Misoprostol (prostaglandins

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stimulate release of bicarbonate from epithilal cells and neutralize acid from parietal cells.

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 NEEDS ACIDIC ENVIRONMENT SO DON’T USE WITH H2B, antiacids, and PPI’s!

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sulfacrate

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avoid during pregnancy

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misoprostol mucosal protective agent

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 Active metabolite Mesalamine, treats UC and Crohns

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sulfazasine

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 Aluminum hydroxide and sulfonated sucrose bind membrane proteins forming a gel with mucous that protects the cells from acid and pepsin

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sulfacrate mucosal protective agent

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 Monococall antibody to TNF alpha treats UC and Crohns

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infizimab

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mucosal protective drugs

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misoprostol sulfacrate

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 Prokinetic drug

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metoclopromide

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increases gastric emptying

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prokinetic drug

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 Mech blocks presynaptic Dopa receptors promoting release of Ach, which increase GI tone and motility

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metoclopromide prokinetic drug

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• GI reflux
• Diabetic gastroparesis
• Intractable hiccup
• Also has antiemetic effects

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metoproclomide

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• CNS effects common – drowsiness, extrapyramidal effx, seizures
• Contraindicated for pts with seizures, mechanical obstruction of GI, GI hemorrhage
• Pheochromocytoma –adrenaline secreting tumor blocking can raise BP

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metoproclomide

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 Retains water in intestinal tract, increases mass and peristalsis

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psyllium

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12. Psyllium

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bulk forming

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13. Docusate sodium

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surfactant

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 Mineral oil and glycerin suppositories, when you don’t want patient to strain

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docusate sodium

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14. Bisacodyl –

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stimulat secretory laxitive

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 Acts on interstinal mucosa to stimulate fluid secretion, increase peristalsis
 Pre-operatively for GI surgery
• --- abdominal cramping electrolyte and fluid depletion
• Limited to short term constipation

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bisacodyl

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diphenozylate

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 Meperidine analog opiod
 Activate GI opioid receptors to decarease ACH increasing peristalisis

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loperimide

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 Meperidine analog opiod
 Activate GI opioid receptors to decarease ACH increasing peristalisis

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 Antienemic
 PO or IV 4hr1/2 life

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ondansetron

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 Meperidine analog opiod
 Activate GI opioid receptors to decarease ACH increasing peristalisis

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loperamide and diphenozylate

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 Antienemic
 Higher affinity and longer duration IV 40 hr ½ life

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palonosetron

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antienemics

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ondansetron and palonosetron
palonosetron is better longer half life

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 Neurokinin one antagonist NK1-
 Used with Ondansetron to block nausea from chemo agents
 Substance P/NK is released from vagal afferents and activaes NK1 and emesis

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apripetant

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 Cannabinoid antiemetics
 ORAL THC
 Second line drug

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dronabinol

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local anasthetic

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Lidocaine - amide

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local anathetic

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cocaine ester

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Determines lifetime and degradation of the LA

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link ester or amide

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Group-Promotes tissue absorption and membrane penetration

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aromatic group

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Promotes interaction with the drug target, but also limits absorption.

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amino group

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a concern for inflamed tissue and for repeated administration

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reversable + charge of amino group

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inhibition of catecholamine uptake

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cocaine

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All other LAs can be enhanced by co-administration of a vasoconstrictor, such as

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epi

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LA favorable at what ph? binds to sodium channel

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LOW protanated

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pKA of LA?

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8-9

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LA fav for crossing mem non protenated

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HIGH PH

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Consequences of LA protonation

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poor absorption by inflamed tissue

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Choice of correct LA with desired duration for first application is important.
BC

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buffer capacity goes up with multiple application

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LA rapidly degraded in blood

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ester - cocaine

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LAs survive the circulation, but are degraded by detoxifying systems of the liver.

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amide- lidocaine

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Patients with liver dysfunction may have weakened detoxification.
when coadministered with.. LA

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amide

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nerve fibers that fire more frequently and more sensitive to LA because

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LA bind to channels that are intermediate or open muscles are slowered opening channels and remaind longer in closed position

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7 ways to apply LA

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Topical
Infiltration
Intravenous
Field block
Nerve block
Spinal
Epidural

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topical - affective on normal skin? why

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no. not good enough penetration

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LA must have good penetration properties (i.e. the more lipophilic the better

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topical LA

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Cocaine- its vasoconstriction action allows use by itself
Other LAs-apply with a vasoconstrictor

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topical LA

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Injection of LA directly into target tissue at desired site of action

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infiltration anasthesia

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infiltraion cant be use with vasoconstrictor where?

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end arteries. can cause hypoxia

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Not good for procedures involving large areas, or if duration of procedure may require multiple applications, due to systemic toxicity caused by too much drug.

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infiltration .. only little areas

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biers block

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IV LA

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Intravenous Anesthesia (Bier’s Block)

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used for limbs, close off limb, inject in to veins
Used to anesthetize a limb
After limiting circulation with a pressure cuff or tourniquet, LA (amides only!) injected directly into vein.
Procedures up to 45 min
Danger of premature release of bolus of LA, causing systemic toxicity.

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Field Block Anesthesia

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For large cutaneous areas (limbs, scalp, abdomen)

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Targets the nerve areas that serve the field of interest. Need to understand neuroanatomy of area
Covers a much larger area, but technically similar to infiltration anesthesia

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field block anasthesia

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Injection of LA into region of large peripheral nerve bundles or plexuses. Many anatomical regions can be anesthetized. Example: brachial plexus for shoulder.

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nerve block anasthesia

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Anesthetizes large areas (internal or surface)
Affects both sensory (pain) and motor fibers
Inject near nerve bundle, not in!
Technically similar to infiltration anesthesia (dependent upon dosage, lipophilicity, vasoconstriction)

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nerve block anasethia

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Application of LA into the spinal fluid in the spinal canal, below the terminus of the spinal cord near the L2 vertebra.
Can target the spinal cord and spinal roots
Highly effective for lower abdomen, pelvis, and legs

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spinal anasthesia

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where insert in lumbar puncture

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2-3 or 3-4

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Injection into the epidural space at multiple positions along spinal column
Infusion catheters can be used for well-regulated, long duration anesthesia even with short-acting LAs
Requires monitoring of infusion devise and tubing
Especially useful if length of procedure cannot be controlled or determined (example: labor and delivery)
Vasoconstrictors improve duration, and decrease systemic toxicity

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Epidural Anesthesia

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toxicities of LAS

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Direct neurotoxicity at site of application
Systemic toxicity after dispersal from site of application by absorption or accidental vascular injection. Exacerbated by excessive dose.
Toxicity due to a metabolic by-product

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CNS mild tox LAS

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sleepiness, lightheadedness, visual/auditory disturbances, restlessness

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CNS LAST more seroius efx

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More serious: convulsions, CNS depression, death

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avoidance for LAS

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minimal effective dose, single dose, avoid intravascular injection, avoid highly perfused tissue, premedicate to raise seizure threshold

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Tx for LAS tox

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oxygen and anxiolytic drugs

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CV tox from LAS

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From direct effects on cardiac tissue, and indirect effects on autonomic nerves that control cardiac function
Severe symptoms (cardiac failure and death) are rare, usually from excessive LA doses

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Smuscle effects LAS

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Inhibition of bowel and intestinal function, esp. with epidural and spinal anesthesia

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resp inhibition from LAS

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Inhibition of respiration from excessive doses, or misapplication, of LA

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HEME TOX FOR LAS

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Primarily due to high doses of prilocaine, which is metabolized to O-toluidine. This is an oxidizer that converts hemoglobin to methemoglobin
Concern if there is reduced pulmonary or cardiac function

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allergic rxns LAS

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Mainly seen with esters, which are metabolized to para-aminobenzoic acid derivatives

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induction agent MOST COMMON
 Maintenance of anesthesia sedation. Rapid onset and waking. VERY SHORT action. Antienemic good post op.
 Respiratory depression and hypotension. No analgesia

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Propofol

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Benzodiazepine Anxiolytics – (
- Sedation prior to anesesia, control seizures,
- Antegrade amnesia reversed with Flumazenil
- Very short acting Water soluble * not fat
- Resp depression

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Midozalem

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General Anesthetics Parenteral Anesthetics Opioid
- intraoperative , post op anesthesia
- actis on pre syn Ca channels nad post syn K channels
- 100x more potent then Morphine
- Least side efx 1.-2 hr life

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Fentanyl

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Cholinergic antagonist Nicotinic antagonist Depolarizing neuromuscular
Blocker
- Emergent intubations, rapid sequence induction
- Rapid onset 15 sec, risk of hyper K, MH

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succynylcholine

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General Anesthetics Parenteral anesthetics Opioid
- Intraoperative postop anesthesia
- Acts on pre syn Ca channels and post syn K channels
- Most side efx
- Longest acting 4-5 hrs

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Morphine

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General Anesthetics Inhalational Anesthetics Halogenated Gasses
- ether used for induction and maintenance of general anesthesia
- fast onset offset, least irritant to mucous membranes
-

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sevoflurane

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 Most affective against Parkinsons

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levodopa

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 Converted by decarboxylase or COMT and only small amt gets to brain
• Need to use Carbidopa which prevents L-Dopa conversion to Dopa in periphery so only L-dop can move in to CNS and be converted in CNS

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levodopa

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given with levodopa to block peripheral COMT

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carbidopa

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• Dyskinesias – occur after 5-7 yrs use because dose dependant, think wave chart are SEEN IN WHAT DRUG

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levodopa

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DOPAMINE AGONIST
 Pointless to give in late stages because dopa synthesis and degradation don’t work.
 Don’t have to be converted to active metabolites but cause more psychosis
 Induces liver problems. Not so popular.
 D2 reeptor agonist, and D1 antagonist with lower incidence of therapeutic response fluctuations


ERGOT

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Bromocriptine

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DOPAMINE AGONIST
 Pointless to give in late stages because dopa synthesis and degradation don’t work.
 Don’t have to be converted to active metabolites but cause more psychosis
 Nonergot
 Bind to D3, D2, and D4, do NOT BIND to D1, 5
 Side effects: nausea, somnolence, postural hypotension, edema, confusions, hallucinations, failure to control impulses


PARKINSONS AND RESTLESS LEGS

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Prompipexole and Ropinerol

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MAO inhibitor
 DOPA  MAOB. Serotonin and norepi by MOA.A
 Selective irreversible inhibitor of MAOB. Prolongs action of Dopamine.
 Enhances effects of L-Dopa and may reduce end of dose and on off phenomena
 Given with LDOPA when LDOPA reponse deteriorates
 Cant be taken with SSRIs with interactions toxic

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Selegeline

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– COMPT INHIBITOR
 Peripheral and central competitive inhibitor of COMPT
 EXPLOSIVE DIARRHEA!!haha
 Only prescribed for pple who don’t respond to Entacapone bc of hepatotoxicity

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Tocapone

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COMPT INHIBITOR
 ONLY PERIPHERAL competitive inhibitor of COMPT
• Extend bioavailability of L-DOPA

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entocopone

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ANTICHOLINERGIC
 is an anticholinergic drug principally used for the treatment of:
 Drug-induced parkinsonism, akathisia and acute dystonia;
 Benzatropine antagonises the effect of acetylcholine, decreasing the imbalance between the neurotransmitters acetylcholine and dopamine

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Benztropine

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ANTICHOLINERGIC
 Better tolerated by elderly, may improve tremor and rididity no bradykinesia.
 Cause drowsiness, delucions, mood changes, dry mouth, blurred vision.
 PD patients develop dementia and memory loss due to loss of cholingergic activity and anticholinergics may excacerbate effects
 USED EARLY IN PD alone or with MAOs Selegiline
 Used where neuroleptic parkinsons in order to reduce psychosis

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diphenhydramine

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SPASMOLYTIC (ms, cp)
 Agonist of GABA B. it’s a dimer G protein with 2 domains. Lets K out, hyperpolarizes the membrane there fore harder to get activated
 Expressed in spinal cord,
 For MS, ALS, trauma spinal injury
• Weakness, drowsyness, low seizure threshhold

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Balcofen

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SPASMOLYTIC
 Relaxes muscles reducing Ca release from SR Ca come out from rianidine channels
 Acute to treat Malignant Hyperthermia in anethisea and chronic for MS and CP


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SPASMOLYTIC
 Relaxes muscles reducing Ca release from SR Ca come out from rianidine channels
 Acute to treat Malignant Hyperthermia in anethisea and chronic for MS and CP


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for HUNTINTONS DZ (aggression dementia, rigidity, apathy… degeneration of GABAergic neurons in basal ganglia. GABA and Ach reduced, Dopa same or elevated.
 Dopamine antagonist help while dopa agonist worsens
 Anti-psychotic blocks Dopa receptors as dz progresses effects lessen bc dopa receptors are lost
 Replaced by new ani-psychotics

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Haloperidol

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Use : Partial and generalized tonic-clonic seizures (first line)

Site of action : Voltage-gated Na+ channels

Characteristics : A drug of choice for partial seizures. Some concern over possibility of aplastic anemia and agranulocytosis.

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Carbamazepine

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Use : Partial and generalized tonic-clonic seizures; status epilepticus

Site of action : Voltage-gated Na+ channels

Characteristics : A drug of choice for partial seizures, and also one of the most effective for generalized tonic-clonic seizures. Side effects include diplopia and ataxia, potentially dangerous rashes, hirsutism, and gingival hyperplasia

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Phenytoin

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Use : Partial and generalized tonin-clonic seizures (second line)

Site of action : GABA-A receptor (increases duration of channel opening)

Characteristics : Second line due to sedation, toxicity, development of tolerance

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Phenybarbital

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Use : Absence, partial, and generalized seizures

Site of action : Voltage-gated Na+ channels ; T-type Ca2+ channels ( at higher concentration)

Characteristics : Drug of choice if absence patient also experience generalized tonic-clonic seizures concomitantly. Slight potential for fatal hepatotoxicity.

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Valproic acid

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Use : Refractory partial seizures

Site of action : Voltage-gated Na+ channels

Characteristics : Adjunct drug but also used as monotherapy. May cause serious, sometimes dangerous rash.

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Lamotregine

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Use : Partial ( and probably generalized ) seizures, Usually as adjunct

Site of action : Voltage-gated Na+ channels; T-type Ca2+ channels

Characteristics : fewer drug interactions than many other drugs

Risk : Kidney stones; patients with sulfa-drug allergies

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Zonisamide

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Use : Partial ( and probably generalized ) seizures, Usually as adjunct

Site of action : Voltage-gated Na+ channels; T-type Ca2+ channels

Characteristics : fewer drug interactions than many other drugs

Risk : Kidney stones; patients with sulfa-drug allergies

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zonisamide

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Use : Absence and myoclonic seizures in children

Site of action : GABA-A receptors ( increases frequency of channel opening)

Characteristics : Development of tolerance limits usage

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Clonazapam

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Use : Status epilepticus (used i.v.)

Site of action : GABA-A receptors ( increases frequency of channel opening)

Characteristics : Sedation and tolerance

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diazapam, lorazapam

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Use : Partial and secondarily generalized seizures

Site of action : GABA-transaminase (irreversible inhibitor)

Characteristics : pronounced risk of visual field defects and psychiatric disturbances.

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vigabatrin

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Use : Refractory partial seizures (including secondarily generalized seizures)

Site of action : Poorly understood (may enhance GABA release, but likely to work in another manner).

Characteristics : Excreted unchanged by kidneys. Few side effect or drug interactions; hence, generally well tolerated. Most prevalent use is for neuropathic pain.

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gabapentin

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Use : Partial seizures ( over 12 years old), usually as adjunct. Not often perscribed

Site of action : GABA reuptake inhibitor

Characteristics :takes several weeks to titrate to therapeutic dose; potential for serious adverse effects, especially increased seizure activity

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Tiagabine

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Use : Partial seizures in adults; Lennox-Gastaut syndrome (LGS) in children

Site of action : Voltage-gated Na+ channels; Antagonism of glutamate receptors

Characteristics : Second line due to risk of aplastic anemia and hepatotoxicity

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Felbamate

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Use : FDA approved for monotheraphy for partial or primary generalized tonic-clonic seizures (10 years above). Adjunct for refractory partial seizures or Lennox-Gastaut syndrome (2 years above)

Site of action : Voltage-gated Na+, Ca2+ channels; Glutamate receptor (antagonist); others?

Characteristics : Risk of kidney stones; possible cognitive effects; diminished vision; and others. Advantage is broad range of efficacy

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Topiramate

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Use : Absence seizures

Site of action : T-type Ca2+ channels

Characteristics : Remains first-choice anti-absence drug due to greater safety than valproic acid.

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ethosuximide

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Use : Adjunct for refractory adult partial seizures, promising as monotherapy for both partial and generalized seizures.

Site of action : Binds to SV2A protein in synaptic vesicle membranes

Characteristics : reasonably safe; a hot new drug that is predicted to eventually rival carbamazepine and valproic acid.

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leveteracitam

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Use : Absense seizures

Site of action : T-type Ca2+ channels

Characteristics : Now in limited use due to prevalence of ethosuximide ( and valproic acid)

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trimethadione