Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

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

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

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

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

Primary treatment of high LDL cholesterol/atherosclerosis.

A

Lifestyle modifications:

  • Smoking reduction
  • Exercise
  • Weight control/diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

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

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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dopamine agonist
Mechanism of action
Adverse effects

A

Directly activate post-synaptic dopamine receptors

Adverse effects: Hallucinations, Orthostatic hypotension, daytime drowsiness

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Conventional Antipsychotics Mechanism of action Adverse effects
``` 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
26
Atypical Antipsychotics Mechanism of action Adverse effects
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
27
``` Phenytoin Mechanism of action Adverse effects What seizure types does it treat? Important considerations ```
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
Voltage-dependent Ca2+ channel blocker Mechanism of action Adverse effects
Block voltage-gated Ca2+ channels --> prevent release of NT and action potential propagation AEs: None
29
Glutamate antagonists Mechanism of action AEs
Block NMDA and AMPA receptors --> prevent CNS excitation | AEs: none
30
GABA potentiators
``` 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
TCAs Mechanism of action AEs
Inhibit the reuptake of NE and serotonin | AEs: Weight gain, cardiac toxicity, orthostatic hypotension, sedation, sexual dysfunction, reduced seizure threshold
32
SSRIs Mechanism of action AEs Other important things to note
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
SNRIs Mechanism of action AEs Important to note?
Inhibit the reuptake of serotonin and NE AEs: Nausea, sexual dysfunction, diastolic HTN Fast onset of action
34
MAOIs
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
Lithium Mechanism of action AEs What are the benefits of lithium?
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
Benzodiazepines Mechanism of action AEs
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
Buspirone Mechanism of action AEs
Mechanism unclear - modulate serotonergic/dopaminergic neurotransmission AEs: lightheadedness, dizziness, excitement
38
Insulin (general) Mechanism of action Adverse effects related to hypoglycemia
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
Glucagon | Mechanism of action
Promotes glycogenolysis
40
Biuguanides Mechanism of action Adverse effects
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
Sulfonylureas Mechanism of action Adverse effects
Promote insulin secretion from the pancreas Inhibit glycogenolysis 1st generation --> 2nd generation = 1000x more potent, less drug interactions AEs: pancreatic burnout, hypoglycemia
42
Meglitinides Mechanism of action AEs
Promote insulin secretion inhibit glycogenolysis AEs: less chance of hypoglycemia or pancreatic burnout
43
Glitazones
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
Alpha glucosidase inhibitors Mechanism of action Adverse effects
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
Gliptins Mechanism of action Adverse effects
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
Incretin mimetics Mechanism of action Adverse effects
Synthetic incretin analogs which promote insulin release and inhibit glucagon release AEs - hypoglycemia, pancreatitis
47
Penicillin Mechanism of action Adverse effects Indicate if broad/narrow; static or cidal
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
``` Cephalosporin Mechanism of action Adverse effects 1st gen --> 4th gen differences Indicate if broad/narrow; static or cidal ```
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
Vancomycin Mechanism of action Adverse effects Indicate if static or cidal
Inhibits cell wall synthesis by binding to precursors of cell wall synthesis and blocking transglycosylation step AEs: red person syndrome, ototoxicity Bactericidal
50
Tetracyclines Mechanism of action Adverse effects Indicate if broad/narrow; static or cidal
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
Macrolide antibiotics Mechanism of action AEs Indicate if broad/narrow; static or cidal
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
``` Oxazolidinones Mechanism of action AEs Indicate if broad/narrow; static or cidal Treatment indication ```
Bind to 50S ribosomal subunit and inhibit protein synthesis AEs: reversible myelosuppresion Bacteriostatic Narrow (gram positive) Used for MRSA or VRE only!
53
Aminoglycosides Mechanism of action AEs Indicate if broad/narrow; static or cidal
Bind to 30s ribosomal subunit and inhibit protein synthesis AEs: Irreversible ototoxicity, reversible nephrotoxicity Narrow (gram negative), bactericidal rapidly lethal to bacteria
54
Sulfonamides + Trimethoprim Mechanism of action AEs Indicate if static or cidal
Block folic acid synthesis --> prevent DNA replication AEs: photosensitivity, hypersensitivity (i.e. fever), Steven-Johnson Syndrome Bactericidal when given in combination
55
Fluoroquinolones Mechanism of action AEs Indicate if broad/narrow; static or cidal
Inhibit DNA gyrase and topoisomerase IV AEs: GI upset (nausea, vomiting, diarrhea) Broad, bactericidal
56
Isoniazid Mechanism of action AEs
Block the synthesis of mycolic acids AEs: hepatotoxicity, peripheral neuropathy used for treating TB
57
Alkylating agents - Cyclophosphamide Mechanism of action AEs Indicate if cell cycle specific or not
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
Platinum agents - cisplatin Mechanism of action AEs Indicate if cell cycle specific or not
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
Antimetabolites Mechanism of action AEs Indicate if cell cycle specific or not
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
Antitumour antibiotics - anthracycline Mechanism of action AEs
Intercalate DNA --> alter structure and inhibit DNA synthesis AEs - severe bone marrow supression, cardiotoxicity
61
Mitotic inhibitors Mechanisms of action AEs
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
Glucocorticoids Mechanism of action AEs
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
Prostate cancer treatments | Mechanisms
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
Breast cancer treatment Mechanisms of action AEs
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
Tyrosine kinase inhibitors - imatinib/Gleevec Mechanism of action AEs
Bind to tyrosine kinases and inhibit cellular proliferation --> induce apoptosis AEs: nausea, vomitting, muscle cramps, edema

Nursing Pharmacology (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions