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Nursing Pharmacology > Modules 12-17 - Mechanisms, Adverse effects and important considerations > Flashcards

Modules 12-17 - Mechanisms, Adverse effects and important considerations Flashcards

1
Q

Statins:
Mechanism of action including overall therapeutic benefit
Main difference between the two statins.
Adverse effects

A

Inhibit HMG-CoA reductase.
Increases hepatic LDL receptors.
Decreases plasma LDL

1) increase HDL
2) Decrease LDL
3) Decrease TGs

Atorvastatin (Lipitor) vs. Rosuvastatin (Crestor)
Rosuvastatin is not greatly metabolized and caution must be exercised when prescribing to Asian patients

Adverse effects:
Myopathy
Hepatotoxicity
Rhabdomyolysis (can lead to cardiac dysrhythmias)
Teratogenic
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2
Q 
Nicotinic Acid/Niacin
Vitamin name?
Mechanism of action
Therapeutic benefit
Adverse effects
A

Vitamin B3

Inhibits hepatic VLDL secretion –> less LDL in plasma as a result
Increased HDL + decreased LDL

Skin rash, Hepatotoxicity, hyperglycemia, Facial flushing, Increased levels of uric acid

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3
Q

Bile acid sequestrants
Mechanism of action
Adverse effects

A

Positively charged molecules that bind to bile acids (negatively charged) and prevent intestinal absorption of bile acids.
This causes a need for cholesterol for bile acid synthesis. Thus, there are increased hepatic LDL receptors, and less plasma LDL

Bloating, Constipation, Decreased absorption (thiazide diuretics, certain antibiotics, warfarin, digoxin)

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4
Q

Cholesterol absorption inhibitors
Combination pill
Mechanism of action
Adverse effects

A

Combination pill - statin + cholesterol absorption inhibitor - called vytorin [simvastatin + ezetimibe (Zetia)]

Binds to and inhibits intestinal cholesterol transporter, NPC1L1. This decreases cholesterol absorption –> decreased plasma LDL + increased hepatic cholesterol synthesis

No major adverse effects

Often used in combination with statins

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5
Q

Fibrates
Mechanism of action
Overall therapeutic benefit
Adverse effects

A

Activates PPAR-alpha:

1) Increased lipoprotein lipase synthesis
2) Decreased apolipoprotein CIII (lipoprotein lipase inhibitor)
3) Increased apolipoprotein a1, a2 (transport of lipids to the liver)

Decreased TGs and increased HDL

Increased risk of gallstones, myopathy, hepatotoxicity

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6
Q

Pathogenesis of atherosclerosis

A

Endothelial cell injury (smoking, hemodynamic factors, immune reaction, elevated blood lipids, HTN)
LDL cholesterol invades the sub-endothelial space
LDL becomes oxidized, and recruits monocytes
Monocytes become macrophages and engulf the oxidized LDL
Macrophages enlarge and become vacuolated = Foam cells
As foam cells accumulate, a fatty streak appears
As the fatty streak grows, platelet adhesion, smooth muscle migration and collagen synthesis occurs –> fibrous cap

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7
Q

Primary treatment of high LDL cholesterol/atherosclerosis.

A

Lifestyle modifications:

  • Smoking reduction
  • Exercise
  • Weight control/diet
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8
Q

Loop Diuretics
Mechanism of Action
Adverse effects
Usual indication

A

Work at the ascending Loop of Henle to reduce Na+/Cl- reabsorption (with the unfortunate side effect of causing reduced potassium reabsorption)
This promotes sodium-chloride, and thus water excretion, decreasing BP (through a decrease in blood volume)

Adverse effects: Hypokalemia, Hyponatremia, Hypotension, Dehydration

Used in severe fluid overload cases - i.e. edema, severe renal failure, severe HTN (not responding to other diuretics)

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9
Q

Thiazide diuretics
Mechanism of action
Adverse effects\

A

Blocks Na+/Cl- reabsorption in the distal tubule –> decreased water reasborption –> decreased BP

Adverse effects: Hyponetremia, Hypokalemia, Dehydration

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10
Q

Potassium sparing diuretics/Aldosterone antagonists
Mechanism of action
Adverse effects
Important contraindication

A

Inhibit aldosterone receptors in the collecting duct –> decreased sodium reabsorption = decreased potassium excretion –> water excretion –> decreased BP

Adverse effects: hyperkalemia

DO NOT use with ACEIs or ARBs

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11
Q

Beta Blockers
Mechanism of Action - differentiate between 1st and 2nd generation

Adverse effects

Suffix

A

Block beta 1 receptors in the heart (Decreased CO and BP) and in the juxtaglomerular cells (decreased renin production = decreased PVR).
1st generation beta blockers also block beta 2 receptors in the lungs

Adverse effects:
2nd generation (selective): Bradycardia, rebound HTN, cardiac failure (rare), decreased CO
1st generation (non-selective) - additional AEs include bronchoconstriction and inhibition of glycogenolysis

“olol” - e.g. metaprolol

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12
Q

ACEIs
Mechanism of action
Adverse effects
Suffix

A

Inhibit ACE in the lungs –> reduction of angiotensin II production –> reduction of aldosterone (decreased Na+ reasborption), ADH (decreased water reabsorption) and decreased PVR (angiotensin II no longer binds to AT1 on smooth muscle)
Inhibition of bradykin breakdown (vasodilation)

Overall: decreased blood volume = decreased CO, and decreased PVR

Adverse effects:
-Angiotensin II: 1st dose hypotension, hyperkalemia (DO NOT USE WITH POTASSIUM SPARING DIURETICS)

Bradykinin: Persistent cough, angioedema

Suffix: “ipril” - e.g. Ramipril

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13
Q 
ARBs
Mechanism of action
Therapeutic benefit
Adverse effects
suffix
A

Block the angiotensin II receptor (AT1) on smooth muscle (decreased PVR), and inhibit aldosterone synthesis (decreased Na+/H20 reabsorption)

Decreased blood volume (decreased CO) and decreased PVR

Adverse effects: Angioedema
(DO NOT USE WITH ALDOSTERONE ANTAGONISTS)

Suffix: “sartan” - e.g. eprosartan

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14
Q

DRIs
Mechanism of action
Adverse effects

A

Bind to and inhibit renin (rate limiting step in RAAS = affect whole pathway)

Adverse effects: Hyperkalemia, angioedema, diarrhea, persistent cough

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15
Q 
Calcium Channel Blockers
Difference between the two types
Mechanism of action
Adverse effects
Suffix
A

Dihydropyridine - only blocks calcium channels in smooth muscle at therapeutic doses
Non-dihydropyridine - blocks both cardiac and smooth muscle calcium channels

Mechanism: Inhibition of calcium uptake reduces tone/contraction of smooth/cardiac muscle - decreasing PVR and CO

Suffix - “dipine”

Adverse effects:
-Dihydropyridine: headache, dizziness, skin rash, flushing, peripheral edema, reflex tachycardia

  • Non-dihydropyridine” compromised cardiac function, dizziness, constipation, flushing, edema, headache
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16
Q

Centrally acting alpha 2 agonists
Mechanism of action
Adverse effects

A

Bind to and activate alpha 2 receptors in the brain stem –> decreased sympathetic outflow to smooth muscle and to the heart (decreased CO and PVR)

Adverse effects:
- drowsiness, dry mouth, rebound HTN

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17
Q

L-DOPA
Mechanism of action
Therapeutic benefit
Adverse effects

A 
Inactive molecule that is actively transported across the BBB, then decarboxylated to become dopamine
Increases available dopamine
Often administered with carbidopa - inhibits peripheral metabolism
Vitamin B6 (pyridoxine) speeds up the reaction (L-DOPA to dopamine)

Nausea, vomiting, Dyskinesia, cardiac dysrhythmia, orthostatic hypotension, psychosis

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18
Q

Dopamine agonist
Mechanism of action
Adverse effects

A

Directly activate post-synaptic dopamine receptors

Adverse effects: Hallucinations, Orthostatic hypotension, daytime drowsiness

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19
Q

Dopamine releasers
Mechanism of action
Adverse effects

A

Stimulate dopamine release from pre-synapatic nerve terminals
Block NMDA receptors (reduce dyskinesia side effect of L-DOPA - i.e. used in combination)
Block dopamine reuptake

Adverse effects: Nausea, vomitting, dizziness, Lethargy, Anticholinergic effects

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20
Q

Catecholamine-O-Methyltransferase inhibitor (COMT)
Mechanism of action
Adverse effects

A

Inhibits COMT, thus reducing methylation (and inhibition) of L-DOPA –> allows a greater drug fraction to reach the site of action

AEs: Hallucinations, vivid dreaming, nausea, orthostatic hypotension

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21
Q

MAOB inhibitor
Mechanism of action
Adverse effects

A

Inhibit Monoamine oxidase B and thus oxidative metabolism of L-DOPA and dopamine –> more conversion to dopamine in the brain + more dopamine available in nerve terminals to be released

AEs: Insomnia, orthostatic hypotension, dizziness

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22
Q

Anticholinergic drugs
Mechanism of action
Adverse effects

A

Block binding of Ach –> decreases urinary incontinence, salivation and diaphoresis
AEs: dry mouth, constipation, blurred vision, urinary retention, tachycardia

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23
Q

Cholinesterase inhibitors
Mechanism of action
Adverse effects

A

Inhibit cholinesterases and thus the metabolism of ACh –> more remains in the synaptic cleft

AEs: Diarrhea, Insomnia, Vomiting, nausea

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24
Q

NMDA receptor antagonists
Mechanism of action
Adverse effects

A

Block the NMDA receptor, decreasing calcium influx into the post-synaptic neuron –> prevents degradation of neurons

AEs: No Major Drug Adverse effects

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25
Q

Conventional Antipsychotics
Mechanism of action
Adverse effects

A 
Block D2 (dopamine) receptors in the mesolimbic area of the brain
Also block NE, histamine and ACh receptors

AEs: Anticholinergic effects, sedation, skin rash, fever, orthostatic hypotension, EPS

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26
Q

Atypical Antipsychotics
Mechanism of action
Adverse effects

A

Mainly block 5-HT1a and 5-HT2a receptors, and D2 receptors (minimally)

Adverse effects:
Type 2 diabetes risk, weight gain, sedation, orthostatic hypotension, anticholinergic effects

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27
Q 
Phenytoin
Mechanism of action
Adverse effects
What seizure types does it treat?
Important considerations
A

Sodium channel blocker –> increases the length of the refractory state in neurons, prevent rapid firing of neurons

AEs: skin rash, sedation, gingival hyperplasia, teratogenic

Treats all seizure but absence

Non-linear kinetics; narrow therapeutic range

28
Q

Voltage-dependent Ca2+ channel blocker
Mechanism of action
Adverse effects

A

Block voltage-gated Ca2+ channels –> prevent release of NT and action potential propagation

AEs: None

29
Q

Glutamate antagonists
Mechanism of action
AEs

A

Block NMDA and AMPA receptors –> prevent CNS excitation

AEs: none

30
Q

GABA potentiators

A 
Stimulate GABA release
Enhance GABA binding to its receptor
Stimulate GABA reuptake
Inhibit GABA metabolism
All of which promote Cl- entry and hyperpolarization of neurons

AEs: none

31
Q

TCAs
Mechanism of action
AEs

A

Inhibit the reuptake of NE and serotonin

AEs: Weight gain, cardiac toxicity, orthostatic hypotension, sedation, sexual dysfunction, reduced seizure threshold

32
Q

SSRIs
Mechanism of action
AEs
Other important things to note

A

Inhibit reuptake of serotonin

AEs: Serotonin syndrome, weight gain, insomnia, sexual dysfunction

Lower propensity to give sides (compared to TCAs); primary treatment for depression

33
Q

SNRIs
Mechanism of action
AEs
Important to note?

A

Inhibit the reuptake of serotonin and NE
AEs: Nausea, sexual dysfunction, diastolic HTN
Fast onset of action

34
Q

MAOIs

A

Inhibit MAO-A and B –> decreased metabolism of serotonin, NE, dopamine
acts within the pre-synaptic nerve terminal to allow more of these NTs to be released

AEs: Agitation, anxiety, Insomnia, Orthostatic hypotension, HTN crisis

35
Q

Lithium
Mechanism of action
AEs
What are the benefits of lithium?

A

Mechanism of action is unclear but thought to alter uptake and release of glutamate and block binding of serotonin

AEs - only present with diuretics (affect salt balance) - GI upset, Tremors, sedation, hypotension

Relieve manic/depressive symptoms
Do not worsen manic/depressive symptoms and do not affect rate of cycling
Prevent recurrence of manic/depressive symptoms

36
Q

Benzodiazepines
Mechanism of action
AEs

A

Bind to a different site on the GABA receptor (i.e. not an agonist) and potentiate the effects of GABA –> Cl- uptake and CNS depression

AEs: CNS depression, Respiratory depression, anterograde amnesia, tolerance, withdrawal, teratogenic

37
Q

Buspirone
Mechanism of action
AEs

A

Mechanism unclear - modulate serotonergic/dopaminergic neurotransmission

AEs: lightheadedness, dizziness, excitement

38
Q

Insulin (general)
Mechanism of action
Adverse effects related to hypoglycemia

A

Promotes the uptake of glucose in the liver, and formation of glycogen
Promotes fatty acid synthesis and TG synthesis in adipose tissue
Promotes amino acid uptake and protein synthesis, as well as glycogen synthesis, in muscle cells

Rapid decrease: tachycardia, palpitations, sweating, nervousness

Gradual decrease: headache, confusion, drowsiness, fatigue

Severe decrease: coma, convulsions, death

39
Q

Glucagon

Mechanism of action

A

Promotes glycogenolysis

40
Q

Biuguanides
Mechanism of action
Adverse effects

A

Increase sensitivity to insulin and the number of insulin receptors
Decrease hepatic gluconeogenesis
Decrease intestinal glucose absorptoin

AEs:
Nausea, decreased appetite, decreased absorption of folate and vitamin B12, lactic acidsosis

41
Q

Sulfonylureas
Mechanism of action
Adverse effects

A

Promote insulin secretion from the pancreas
Inhibit glycogenolysis
1st generation –> 2nd generation = 1000x more potent, less drug interactions

AEs: pancreatic burnout, hypoglycemia

42
Q

Meglitinides
Mechanism of action
AEs

A

Promote insulin secretion
inhibit glycogenolysis

AEs: less chance of hypoglycemia or pancreatic burnout

43
Q

Glitazones

A

Activate PPAR-gamma –> promotes transcription of genes controlling carbohydrate metabolism –> increased number of glucose transporters –> increased insulin sensitivity

Activates PPAR-alpha too –> decreased TGs and increased HDL

AEs
Edema, fluid retention, headache and myalgia

44
Q

Alpha glucosidase inhibitors
Mechanism of action
Adverse effects

A

Inhibits enzyme important in digestion of complex carbs to simple carbs, thereby decreasing intestinal absorption of glucose

AEs: abdominal distention, cramps, flatulence, diarrhea, decreased absorption of iron

45
Q

Gliptins
Mechanism of action
Adverse effects

A

Inhibit DPP-4 –> thus get increased release of incretin hormones (GLP-1 and GIP) after meals from the intestine which stimulate release of insulin and decrease glucagon release

AEs - none

46
Q

Incretin mimetics
Mechanism of action
Adverse effects

A

Synthetic incretin analogs which promote insulin release and inhibit glucagon release

AEs - hypoglycemia, pancreatitis

47
Q

Penicillin
Mechanism of action
Adverse effects
Indicate if broad/narrow; static or cidal

A

Binds to PBPs –> activates autolysins, which degrade the cell wall (peptidoglycan), and inhibits transpeptidases (which promote cross bridge formation)

AEs: allergy
Narrow spectrum (gram positive) and bactericidal
Exception is broad spectrum penicillin - can penetrate outer membrane of gram negatives

48
Q 
Cephalosporin
Mechanism of action
Adverse effects
1st gen --> 4th gen differences
Indicate if broad/narrow; static or cidal
A

Inhibit transpeptidases, activate autolysins
1st–>4th - higher penetrance into CSF, more resistant to penicillinase (beta lactamase) and more effective against gram negative bacteria
Narrow –> broad (i.e. 4th generation is more broad than 1st)
Bactericidal

49
Q

Vancomycin
Mechanism of action
Adverse effects
Indicate if static or cidal

A

Inhibits cell wall synthesis by binding to precursors of cell wall synthesis and blocking transglycosylation step

AEs: red person syndrome, ototoxicity
Bactericidal

50
Q

Tetracyclines
Mechanism of action
Adverse effects
Indicate if broad/narrow; static or cidal

A

Bind to the 30S ribosomal subunit of bacteria and prevent addition of amino acids to the peptide chain

AEs: GI upset, photosensitivity, susceptibility to superinfection

Bacteriostatic, broad

51
Q

Macrolide antibiotics
Mechanism of action
AEs
Indicate if broad/narrow; static or cidal

A

Bind to 50S ribosomal subunit and prevent addition of amino acids to the lengthening peptide chain

AEs: GI upset, QT interval prolongation
Bacteriostatic, broad

52
Q 
Oxazolidinones
Mechanism of action
AEs
Indicate if broad/narrow; static or cidal
Treatment indication
A

Bind to 50S ribosomal subunit and inhibit protein synthesis

AEs: reversible myelosuppresion
Bacteriostatic
Narrow (gram positive)
Used for MRSA or VRE only!

53
Q

Aminoglycosides
Mechanism of action
AEs
Indicate if broad/narrow; static or cidal

A

Bind to 30s ribosomal subunit and inhibit protein synthesis

AEs: Irreversible ototoxicity, reversible nephrotoxicity
Narrow (gram negative), bactericidal
rapidly lethal to bacteria

54
Q

Sulfonamides + Trimethoprim
Mechanism of action
AEs
Indicate if static or cidal

A

Block folic acid synthesis –> prevent DNA replication
AEs: photosensitivity, hypersensitivity (i.e. fever), Steven-Johnson Syndrome
Bactericidal when given in combination

55
Q

Fluoroquinolones
Mechanism of action
AEs
Indicate if broad/narrow; static or cidal

A

Inhibit DNA gyrase and topoisomerase IV
AEs: GI upset (nausea, vomiting, diarrhea)
Broad, bactericidal

56
Q

Isoniazid
Mechanism of action
AEs

A

Block the synthesis of mycolic acids
AEs: hepatotoxicity, peripheral neuropathy
used for treating TB

57
Q

Alkylating agents - Cyclophosphamide
Mechanism of action
AEs
Indicate if cell cycle specific or not

A

Pro-drug activated by the liver - Forms cross bridges between guanine nucleotides, breaking DNA and inhibiting DNA replication

AEs - none
Cell cycle phase non specific

58
Q

Platinum agents - cisplatin
Mechanism of action
AEs
Indicate if cell cycle specific or not

A

Forms cross bridges between guanine nucleotides, causing DNA mismatches/breaking and stopping DNA replication

AEs: ototoxicity, nausea, vomiting (emetogenic), nephrotoxicity
Cell cycle phase non-specific

59
Q

Antimetabolites
Mechanism of action
AEs
Indicate if cell cycle specific or not

A

Inhibit enzymes or prevent DNA replication
Folic acid analogs - prevent folate conversion to folic acid
Purine/pyrimidine analogs - cause DNA replication arrest

AEs - none

Cell cycle phase specific - mostly S phase

60
Q

Antitumour antibiotics - anthracycline
Mechanism of action
AEs

A

Intercalate DNA –> alter structure and inhibit DNA synthesis

AEs - severe bone marrow supression, cardiotoxicity

61
Q

Mitotic inhibitors
Mechanisms of action
AEs

A

Vinca alkaloids - bind to tubulin and destabilize MT bundles, causing inapprorpiate chromosome segregation, and cell death (metaphase)
Taxanes - (late G2) bind to and stabilize MTs to prevent replication

AEs - none
Cell cycle phase specific (obviously)

62
Q

Glucocorticoids
Mechanism of action
AEs

A

Toxic to lymphoid tissue; used as adjunct to other chemotherapy to reduce Nausea dn vomitting, pain and lack of appetite

AEs - adrenal insufficiency, osteoporosis, susceptibility to infection, electrolyte imbalance, GI ulceration, growth retardation

63
Q

Prostate cancer treatments

Mechanisms

A

GnRH agonists - promote test release from testes, which negatively feedback to the prostate, decreasing GnRH synthesis and release, and thus androgen levels
Castration removes test synthesis from testes
Androgen receptor antagonists - block androgen binding in the prostate - decreased response (combined with either of the above)

64
Q

Breast cancer treatment
Mechanisms of action
AEs

A

Tamoxifen - partial receptor agonist - minimally activates receptor and prevents endogenous estrogen from binding
Aromatase inhibitors - prevent conversion of androgens to estrogen (only effective in post-menopausal women since ovarian production of estradiol is not stopped)
Trastuzumab - monoclonal antibody which binds to HER2 and inhibits its replicative effects

AEs - Trastuzumab - cardiotoxicity

65
Q

Tyrosine kinase inhibitors - imatinib/Gleevec
Mechanism of action
AEs

A

Bind to tyrosine kinases and inhibit cellular proliferation –> induce apoptosis

AEs: nausea, vomitting, muscle cramps, edema

Nursing Pharmacology (30 decks)

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