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Pharmacology > drugs only module 15-17 > Flashcards

drugs only module 15-17 Flashcards

1
Q

short duration-rapid acting insulin

A

3 types of insulin: Insulin lispro, insulin aspart, insulin glulisine

  • admin in assoc with meals to control postprandial rise in glucose
  • sub q (may be admin IV if necessary)
  • CLEAR
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2
Q

short duration-slower acting insulin

A

type: unmodified human insulin
injected before meals to control postprandial rises in glucose or infused to provide basal control of blood glucose
sub q or (rarely) IM
following injection - the molecules form small aggregates or dimers which slows absorption
-CLEAR

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3
Q

intermediate duration insulin

A

2 types: neutral protamine hormone (NPH) insulin and insulin detemir
onset of action delayed, so not to be used at meal time
injected 1-2x/day to control blood glucose between meals & in the evening
why delayed? NPH- is insulin conjugated to protamine (lg protein) - makes less soluble which delays absorption
insulin detemir - the molecules bind strongly to each other which delays absorption
subq
NPH - CLOUDY
Detemir - CLEAR

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4
Q

Long acting insulin

A 
type: insulin glargine
main advantage: long duration of action
subq 1x/day at bedtime
long duration d/t low solubility at physiological pH - when it's injected it forms microprecipitates that slowly dissolve & therefore release it in small amts over an extended time
CLEAR
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5
Q

biguanides

A 
oral antidiabetic (type II)
often the drug of choice
lower blood glucose 3 ways:
increase sensitivity and number of insulin receptors
decrease hepatic gluconeogenesis
reduce intestinal glucose absorption

*major advantage - don’t increase insulin levels, so pose no risk of hypoglycemia

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6
Q

adverse effects of biguanides?

A

nausea
decreased appetite
diarrhea
decreased absorption of vit B12 and folic acid
lactic acidosis rare but serious (mortality in 50% of pt.s who get it)

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7
Q

sulfonylureas

A

oral antidiabetic (type II)

act primarily by stimulating release of insulin from the pancreas
inhibits glycogenolysis (breakdown of glycogen to glucose)
1st & 2nd generations
2nd generation more potent (1000x) & cause fewer drug interactions

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8
Q

adverse effects of sulfonylureas?

A

hypoglycemia

prolonged use may cause pancreatic burnout - reduced capacity to synth insulin

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9
Q

meglitinides

A

oral antidiabetic (type II)
same mech of action as sulfonylureas but differ in that they:
short half-life so effective for tx postprandial rise in glucose
less likely to cause hypoglycemia
less likely to cause pancreatic burnout

*didn’t list adverse effects

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10
Q

Glitazonnes

A

oral antidiabetic (type II)
act by increasing insulin sensitivity in target tissues and decreasing hepatic gluconeogenesis
activate PPAR gamma receptor which is an intracellular receptor
increased number of receptors = increased sensitivity
also activate PPAR alpha which increase HDL and decrease triglycerides

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11
Q

adverse effects glitazones?

A

fluid retention/edema (shouldn’t be used with heart failure)
headache
myalgia (muscle pain)

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12
Q

Alpha-glucosidase inhibitors

A

oral antidiabetic (type II)
Alpha-glucosidase is an enzyme which breaks down complex carbs into monosaccharides in the intestine
This inhibits those enzymes therefore decreasing complex carb metabolism
Reduces rise in postprandial blood glucose

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13
Q

adverse effects of Alpha-glucosidase inhibitors?

A 
flatulence
cramps
abdominal distention
diarrhea
decreased iron absorption
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14
Q

Gliptins

A

oral antidiabetic (type II)
inhibit enzyme dipeptidyl peptidase 4 (DPP-4)
DPP-4 breaks down incretin hormones GLP-1 and GIP
these hormones are released from GI tract after meal and cause increased release of insulin & decreased release of glucagon
by inhibiting DPP-4, more incretin hormones reach pancreas therefore causing increased insulin release & suppression of glucagon release

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15
Q

adverse effects of gliptins?

A

no known major adverse effects

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16
Q

Incretin mimetics

A

subq injected antidiabetic (type II)
synthetic incretin analogs that mimic actions of incretin hormones
cause increase in insulin release & decrease in glucagon release
used as adjunct to biguanides or sulfonylureas

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17
Q

adverse effects of incretin mimetics

A

hypoglycemia

pancreatitis

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18
Q

what is the mechanism of action generally for penicillins?

A

inhibit transpeptidases & activate autolysins
result: disrupt synth of cell wall & promote cell wall destruction
the bacteria take up excess water & die (lyse)
*bactericidal
*only effective against bacteria actively growing & dividing
*much more effective against gram+ d/t no outer membrane

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19
Q

what are the classes of peniciillins?

A

narrow spectrum
narrow spectrum penicillase resistant
broad spectrum
extended spectrum

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20
Q

what are the features of narrow spectrum penicillins?

A

gram+
must be admin IV or IM (as destructed by gastric acid)
safe
drug allergy primary adverse effect

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21
Q

narrow spectrum penicillase resistant penicillins

A

altered side chain - not sucsceptible to effects of beta lactamase enzymes (eg. penicillase)
tx staphylococci that produce penicillase
not effective for abscesses/penetrating into bone
MRSA is resistant to this

22
Q

broad spectrum penicillins

A

effective for both gram+ and gram-
ability to penetrate outer membrane of gram-
susceptible to effects of beta lactamases

23
Q

extended spectrum penicillins

A

effective for both gram+ and gram-
effective tx Pseudomonas aeruginosa (resistant to all other penicillins)
susceptible to effects of beta lactamases

24
Q

cephalosporins

A

same mech of action as penicillins
batericidal
4 generations - moving from 1st to 4th - increased activity against gram neg,, increased resistance to effects of beta lactamases, increased ability to penetrate cerebrospinal fluid
*allergy most freq adverse effect
*suitable alternative for pt.s allergic to penicillin

25
Q

vancomycin

A

potentially toxic and reserved to tx serious infections such as those caused by MRSA
it binds to presursors of cell wall synth to block transglycosylation step
*may cause ototoxicity (hearing loss)
*rapid infusion may cause ‘red person syndrome’ - flushing, rash, itching, hypotension

26
Q

tetracyclines

A

protein synth inhibitors
bind to ribsomes and prevent addition of amino acids to peptide chain
*broad spectrum antibiotics, bacteriostatic
adverse effects: GI irritation, photosensitivity, susceptible to superinfection

27
Q

macrolide antibiotics

A

protein synth inhibitors
bind to ribsomes and block addition of amino acids to peptide chain
*broad spectrum antibiotics, bacteriostatic
adverse effects: GI upset, QT interval prolongation

28
Q

oxazolidinones

A

protein synth inhibitors
bind to ribsomes and inhibit protein synth
*narrow spectrum - only against gram +, bacteriostatic
effective tx MRSA, VRE - this antibiotic should be reserved for these bacteria
adverse effects: reversible myelosuppression (bone marrow toxicity)

29
Q

aminoglycosides

A

protein synth inhibitors
bind to ribsomes and prevent protein synth
*narrow spectrum - only against gram neg., bactericidal
rapidly lethal to bacteria & mechanism of lethality unknown
adverse effects: ototoxicity, reversible nephrotoxicity

30
Q

sulfonamides and trimethoprim

A

bacteria synth their own folic acid to incrop into DNA
these drugs block the synth of folic acid at different stages
often given in combination
*batericidal
adverse effect: hypersensitivity reaction such as fever and photosensitivity, and small risk of hypersensitivity reaction called Stevens-Johnson Syndrome

31
Q

fluoroquinolones

A

inhibit DNA replication by inhibiting two enzymes: DNA gyrase and topoisomerase IV
*broad spectrum, bactericidal
adverse effects: GI symptoms (nausea, vomiting, diarrhea)

32
Q

Isoniazid

A

tx of TB exclusively
inhibits synth of mycolic acid, a component unique to the cellwall of TB causing bacteria named M. tuberculosis
adverse effects: peripheral neuropathy and hepatotoxicity

33
Q

what are the major classes of anti-cancer drugs?

A
  1. cytotoxic agents

2. hormonal and other agents

34
Q

what are the different types of cytotozix agents?

A 
alkylating agents
platinum compounds
antimetabolites
antitumour antibiotics
mitotic inhibitors
35
Q

cyclophosphamide

A

alkylating agent
transfer alkyl group
cross-bridges between nitrogen and guanine
result: miscoding, breaking of DNA, inhibition of DNA replication
*cell-cycle non-specific

cyclophosphamide is a prodrug

36
Q

cisplatin

A

platinum compound
cross-bridges by binding to guanine, inhibit DNA replication
*cell-cycle non-specific
cisplatin extremely nephrotoxic, ototoxic, emetogenic (causes worse N/V than other drugs)

37
Q

antimetabolites

A

inhibit particular enzymes or prevent DNA replication

*phase specific - S-phase

38
Q

what are the 3 subclasses of antimetabolites?

A

folic acid analogs - block conversion of folate to its active forms
purine analogs - inhibit synth of DNA and RNA
pyrimidine analogs - inhibit synth of DNA and RNA

39
Q

anthracyclines

A

antitumour antibiotic
kill cancer cells - intercalating
*poorly absorbed so given IV
anthracyclines - can cause severe bone marrow suppression and are cardiotoxic

40
Q

mitotic inhibitors

A

act during cell cycle to inhibit mitosis and prevent cell division
2 classes - vinca alkaloids & taxanes

41
Q

Vinca alkaloids

A

derives from periwinkle plant
block mitosis during metaphase
bind to protein tubulin, a major component of the microtubule - this disrupts the org of microtubules during cell division and leads to inappropriate distribution of chromosomes and eventually cell death

42
Q

Taxanes

A

act in late G2 phase just prior to mitosis

stabilized microtubule bundles and prevent cell division

43
Q

glucocorticoids

A

hormonal agent
used as adjunct to other agnets in cancers derived from lymphoid tissue
directly toxic to lymphoid tissue
side effects long term use: osteoporosis, adrenal insufficiency, susceptibility to infection, GI ulceration, electrolyte disturbance, growth retardation
*can help manage complications of other drugs including reduction of N/V, pain, and improves appetite

44
Q

GnRH agonist

A

drug to tx prostate cancer, as primary goal is androgen deprivation
GnRH agonists cause a transient increase in testosterone production in the testes, so cancer symptoms may increase at the start of therapy
over time, testosterone synth and release is decreased

45
Q

Androgen Receptor antagonists

A

drug to tx prostate cancer, as primary goal is androgen deprivation
used in combo with GnRH agonist or castration
blocks androgen receptors in tumour cells

46
Q

what is the primary goal of breast cancer pharmacological therapy and what are the 3 classes?

A

primary goal is estrogen deprivation

1) anti-estrogens
2) aromatase inhibitors
3) Trastuzumab

47
Q

Tamoxifen

A

most commonly prescribed drug for breast cancer
partial estrogen receptor agonist
(minimally activates the receptor and blocks endogenous estrogen from binding)

48
Q

aromatase inhibitors

A

inhibit the conversion of androgens to estrogen, decreasing the amt of estrogen avail to the breast cancer cells
*note - these drugs don’t block the ovarian estrogen synth, therefore only useful in postmenopausal women

49
Q

Trastuzumab

A

some pt.s have increased number of HER2 receptors
it’s a transmembrane receptor that helps regulate cell growth
tumours with HER2 have especially aggressive tumour growth
Trastuzumab is an atibody that binds to the HER2 receptors & revents cell proliferation
*administered IV
adverse effect: cardiotoxicity

50
Q

Imatinib (Gleevec)

A

tyrosine kinase inhibitor - tyrosine kinases can activate gene transcription and/or DNA synth

Imatinib -inhibition of cellular proliferation and cell death via apoptosis
-adverse effects: N/V, edema, muscle cramps

51
Q

explain how tyrosine kinase inhibitors work

A

imatinib mimics ATP
kinase normally binds ATP & uses phosphate from the ATP and transfers it to the substrate. The substrate changes its shape and signals cell proliferation

imatinib binds to the kinase preventing ATP from binding therefore ultimately preventing cell growth

Pharmacology (7 decks)

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