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NMT150 midterm > Pharm week 1-6 > Flashcards

Pharm week 1-6 Flashcards

1
Q

pharmacokinetics vs phamacodynamic

A

pharmacokinetics
ADME
absirption
distribution
metabolism
excretion

phamacodynamics
-receptor binding
-signal trasnduction
-pharmacological effects
-dose responseh

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2
Q

how are most drugs absorbed

A

passive diffusion

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3
Q

which form of drugs can pass through lipid bilayer

A

non ionized formed (no charge)

many drugs are weak acids and bases

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4
Q

where are most drugs metabolized

A

liver via enzymes

**prodrugs need to be activated by metabolism

make it more water soluble to be excreted bye kidneys

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5
Q

first pass effect

A

Drugs absorbed via the gut reach the liver via the portal vein before entering the systemic circulation

The degree to which the drug is inactivated by liver enzymes prior to entering the systemic circulation substantially alters the drug’s bioavailability

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6
Q

phase 1 vs phase 2 metabolism

A

phase 1
–>Primary goal is to introduce or open up a binding site for hydrophilic compounds to be added later by phase II mechanisms
–>Oxidative reactions by far the most common
–>Microsomal cytochrome P450 (CYP450) system

phase 2
–>Not all drugs require phase I metabolism prior to phase II but most do
–>These reactions essentially conjugate a water-soluble molecule to the spot opened up by phase 1 reactions
–>In many instances, this means conjugating something to an available hydroxyl group
–>Each phase 2 mechanism has its own enzyme that catalyzes the reactions

phase 1 is oxidative to make binding site
phase 2 is conjugation to increase solubility

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7
Q

enterohepatic circulation

A

Glucuronide conjugates are excreted in bile (fat soluble drugs)

Some commensal gut bacteria have glucuronidase enzymes which can cleave the glucuronide off the metabolite resulting in the parent drug being able to be reabsorbed

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8
Q

elimination

A

water soluble via kidney
lipid soluble via feces

Most water-soluble drug metabolites are excreted by the kidneys

Various mechanisms exist throughout the sections of the nephron

Lipid-soluble drugs are excreted in the distal tubule if they’re small enough

Lipid-soluble drug metabolites and glucuronide-conjugates are excreted by the liver into bile and are excreted in feces

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9
Q

agonist vs antagonist

A

Agonist – a substance that initiates a physiological response when combined with a receptor

Antagonist – a substance that interferes with or inhibits the physiological action of another substance

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10
Q

competitive vs allosteric

A

Competitive – used to describe when two substances use the same binding site on a receptor

Allosteric – used to describe when a substance binds to a receptor away from an active binding site but still alters the physiological effect

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11
Q

measure of safety

A

Therapeutic Index (TI)

LD50 – dose at which causes death in 50% of individual (animal)

ED50 – dose at which causes a therapeutic response in 50% of individuals (human)

TI= LD50/ED50

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12
Q

beta lactam antibitocs

A

β-lactam antibiotics are antibiotics that contain a beta-lactam ring in their chemical structure. This includes penicillin derivatives, cephalosporins

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13
Q

most common bacterial pathogens of acute otitis media

A

Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis

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14
Q

watchful waiting and who should never do it

A

Withhold antibiotic prescriptions for 48 hours in children over 6 months of age provided they have:

Nonsevere illness (mild pain and fever < 39°C)

Uncomplicated AOM (no episode in the preceding month, no acute facial nerve palsy, mastoiditis, meningitis, or labyrinthitis)

Infants under 6 weeks of age should be immediately referred to the nearest emergency department

Patients aged 6 weeks to 6 months should begin antibiotic therapy immediately

Patients with 3 or more episodes in 6 months or 4 or more within a year should begin antibiotic therapy immediately

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15
Q

how to overcome antibiotic resistance in strep pneumonia

and influenza and catarhalis

A

S. pneumoniae resistance is a result of the alteration of penicillin-binding cell wall proteins leading to decreased drug affinity

This is overcome by doubling the dose of amoxicillin

–
H. influenzae and M. catarrhalis produce beta-lactamases which confer resistance

This is overcome by using a beta-lactamase inhibitor called clavulanate

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16
Q

what is the first line therapy fro acute otitis media

A

amoxicillin

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17
Q

what are alternative for acute otitis media

A

cephalosporins !!

Cefuroxime axetil and Cefprozil
Second-generation cephalosporins have reasonable activity against H. influenzae and M. catarrhalis as they are more resistant to bacterial beta-lactamases
Less effective against S. pneumoniae Considered second-line agents

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18
Q

what is type 1 hypersensitivity to penicillin/ amoxicillin

A

macrolides –>
Azithromycin and Clarithromycin should be reserved for patients with type 1 hypersensitivity reactions to beta- lactam antibiotics

lincosamides –>Clindamycin can be used for patients with type 1 hypersensitivity reactions to beta-lactam antibiotics

It does not cover H. influenzae or M. catarrhalis

19
Q

The resistance mechanism produced by H. influenzae can be overcome by which of the following strategies?
A. Doubling the dose of amoxicillin
B. Giving amoxicillin and clavulanate together
C. Using clindamycin as an alternative to amoxicillin D. Giving cefprozil and clavulanate together

A

B. Giving amoxicillin and clavulanate together

20
Q

2 types of corticosteroids and what are the different mechanisms

A
  1. Glucocorticoids – effect carb, fat, protein metabolism + anti inflame, immunosuppress
  2. Mineralcorticoids – effect electrolytes by renal excretion
21
Q

when can get adverse effects from corticosteroids

A

too high potency or too long

systemic suppression of HPA axis

use finger tip units !

22
Q

topical drug vehicles

A
  1. Creams (least effective at penetrating skin)
  2. Gel (for hairy and oily areas)
  3. Lotion (for large and hariy areas)
  4. Ointment (thick and greasy; emollient effect, best permeability)
  5. Foam (greasy spray for hard to reach areas)
23
Q

potency for topical corticosteroids

A

Class 1 is the highest potency also called the superpotent or ultra-high class.

Class 2 – high,
Class 3 – medium-high,
Class 4/5 - medium
Class 6/7 – low potency

24
Q

which potencies for which parts of body

A

low potency on face and skin folds with thin skin

medium potency on body and scalp

high potency on palms and soles

25
Q

A high-potency topical corticosteroid would be an appropriate initial recommendation for the treatment of which of the following body areas?
A. Face B. Elbow C. Palm D. Scalp

A

C. Palm

26
Q

what are the 2 types of NSAIDs

and what are they inhibiting

A

o Non specifc COX inhibitor: acetylsalicylic acid (ASA) and ibuprofen

o COX 2 specific inhibitor: celecoxib

COX1 can increase GI bleeds
both have CVD risk

27
Q

which COX do you want to inhibit for anti inflammatory

A

the inducible COX2

because COX2 prostaglandins are inflammatory which can thus cause pain

28
Q

what are the side effects of inhibiting COX1

A

GI function; mucous secretion in stomach

ulcers and GI bleeds

29
Q

which non opioid analgesics inhibit COX 1 and have side effects of GI bleeds

A

ASA and ibuprofen

30
Q

what non opioid analgesics inhibit COX 2

A

celecoxib

31
Q

acetylsalicylic acid (ASA) is an NSAID that binds…

A

irreversible inhibition of COX vis covalent bond

non competitive inhibitor

activates COX binding site

short half life; became salicylic acid then eliminated in urine

contraindicated in kids with viral infection
GI bleeds
tinnitus

32
Q

aspirin is aka…

A

acetylsalicylic acid (an NSAID)

33
Q

what drug has an affinity for COX3

and what are its effects

A

acetaminophen (tylenol_)

 Little anti inflammatory effect
 Analgesic and antipyretic

FOR PAIN AND FEVER; not inflame

34
Q

acetaminophen (tylenol_) is absorbed where

and what are the intermediates

A

absorbed rapidly in the gut

toxic intermediates formed with CYPs

35
Q

what is a disease celecoxib can be used for

A

osteoarthritis

its a cox2 Non-steroidal anti-inflammatory drugs (NSAIDSs)

36
Q

how to help w gastroprotection when using NSAIDs

A

1.Using COX-2 selective NSAIDs

  1. Using prostaglandin analogues: misoprostol

3.Using proton pump inhibitors: omeprazole

37
Q

Which of the following NSAIDs acts through non- competitive inhibition of COX enzymes?
A. Acetaminophen
B. Acetylsalicylic acid
C. Ibuprofen
D. Celecoxib

A

B. Acetylsalicylic acid

38
Q

what are gaba derivatives? what are they used for? where do they act?

A

a. Pregabalin
b. Gabapentin
i. For soft tissue and hyperalgesic pain, neuropathic pain
ii. Act centrally

39
Q

what receptors do gaba derivatives act with

A

voltage gated calcium channel

–> dorasl horn of spinal column

NOT gaba receptors

40
Q

GABA derivatives side effects

A

sedation, GI, tremors, weight gain

cannot abruptly discontinue

41
Q

types of muscle relaxants

A

a. Antispasmodics

i. Benzodiazepines or non-benzodiazepines (methocarbamol) (work via CNS not muscle contraction fibers)

b. Antispastics (baclofen) (help with muscle rigidity)

42
Q

what is methocarbamol

A

non benzodiazepine muscle relaxant (antispasmodic)

doesnt effect muscle fiber contractions

works via CNS depressant and block reflexes, prolong refractory period

43
Q

what is baclofen

A

anti spastic muscle relaxant

GABA receptor agonist on beta subunit (on pre or post synaptic neruron) causes K+ influx and hyper polarization and decrease Ca2+ influx = reduce AP and activation of muscle

44
Q

Which of the following drugs is classified as a non- benzodiazepine antispasmodic?
A. Gabapentin
B. Baclofen
C. Pregabalin
D. Methocarbamol

A

D. Methocarbamol

NMT150 midterm (12 decks)

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