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N550 Pharm > Cancer, CAD, CHF > Flashcards

Cancer, CAD, CHF Flashcards

1
Q

What are the 6 hallmarks of cancer?

A

Sustaining proliferative signaling, resisting cell death, inducing angiogenesis, enabling replicative immortality, activating invasion and metastasis, evading growth suppressors

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2
Q

Are telomerase up or down- regulated in cancer?

A

UPregulated, these are the enzymes that maintain telomeres, which lets the cell keep living

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3
Q

What is p53?

A

Tumor suppressor gene that prevents damaged cells from proliferating; turned off in cancer cells

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4
Q

Proto-oncogenes vs. oncogenes?

A

Proto-oncogenes have regular function in the cell relating to proliferation and differentiation
When over-expressed, they can become oncogenes, the cancerous version of this cell

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5
Q

What is the two-hit hypothesis?

A

Describes why tumor suppressor genes become insufficient to prevent cancer
Both alleles for a tumor suppressor gene must be mutated in order for a gene to lose function (germline and somatic)

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6
Q

How does Methotrexate work?

A

Methotrexate has a higher affinity for DHFR (dehydrate reductase) compared to FH2, preventing reduction to FH4
Note: A cell needs folate for replication and it is reduced to FH2 then FH4 to produce nucleosides

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7
Q

What is doxorubicin?

A

Cytotoxic antibiotic that indirectly inhibits topoisomerase II
Top II relaxes DNA coil and breaks the strand for replication
Doxorubicin prevents the DNA strand from being put back together, inhibiting DNA replication

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8
Q

What is cyclophosphamide?

A

Alkylating agent that prevents replication of DNA by attaching alkyl groups to guanines which causes guanines to crosslink, sticking DNA so it can’t uncoil and can’t replicate

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9
Q

What is vincristine?

A

Interferes with mitosis by binding to microtubule dimers, preventing polymerization (pulling apart) of dimers, this arrests the cell in metaphase

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10
Q

What is tamoxifen?

A

Treats estrogen receptor positive breast cancer by antagonizing at the estrogen receptor, preventing cell proliferation

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11
Q

What are monoclonal antibodies 2 functions?

A
  1. block growth signals

2. stop new blood vessels from forming

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12
Q

How does Cetuximab work?

A

Blocks growth signals

Cetuximab binds to mutated growth factor receptor and prevents its downstream signaling (proliferation)

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13
Q

Because Cetuximab only prevents DOWNSTREAM signaling, in what case would it not be effective?

A

When hyper-proliferation is caused by something other than mutated external growth factor receptor

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14
Q

How does Bevacizumab (Avastin) work?

A

Anti-angiogenic
Monoclonal antibody that blocks angiogenesis
Inhibits vascular endothelial growth factor A

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15
Q

How do tyrosine kinase inhibitors work? Example: Gleevec (imantinib)

A

Prevent phosphorylation of the tyrosine kinase target
Tyrosine kinase is an enzyme that removes a phosphate group from ATP and attaches it to a tyrosine amino acid which starts a signaling cascade leading to cell proliferation

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16
Q

What is BCR-Abl?

A

A fusion gene of the philadelphia chromosome/translocation (chromosome 22 is long, 9 is short, they easily translocate, associated with CML)
It contains a portion that codes for tyrosine kinase. When it is mutated, tyrosine kinase is always on.

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17
Q

At rest, coronary blood flow is ___mL/min/100g which is ___% cardiac output. ___% oxygen extracted from myocardial tissue beds

A

70mL/min/100g
5% CO
70% oxygen, very high!

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18
Q

With intense exercise, coronary blood flow increases ____ fold (supply) and demand increases ____ fold

A

Supply by 2-4 fold

Demand by 4-7 fold! This includes preload, HR, contractility

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19
Q

What equation describes perfusion pressure to the LV?

A

DBP - LVEDP

So someone with diastolic dysfunction has trouble with perfusion! Remember, coronary arteries fill during DIASTOLE

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20
Q

The incidence of myocardial ischemia in surgery is highly related to what?

A

HIGH HR (over 110)

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21
Q

What increases myocardial oxygen supply? What increases demand?

A

Supply: hemoglobin conc, O2 sats, bradycardia, inc DBP, low preload, dec contractility
Demand: tachycardia, high afterload, high preload, inc contractility

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22
Q

What is the HR goal with CAD patient? What meds are used, what is contraindicated/cautioned?

A

Slow
B-blockers, Ca channel blockers used
Caution with isoproterenol, dobutamine, ketamine, pancuronium

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23
Q

What is the preload goal with CAD patient? What meds are used, what is CI/cautioned?

A

Low-normal
Nitroglycerine, diuretics used
Caution with volume overload

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24
Q

What is the afterload goal with CAD patient? What meds are used, what is CI/cautioned?

A

High-normal
Phenylephrine used
Caution with nitroprusside and high-dose volatile agents

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25
Q

What is the contractility goal with CAD patient? What meds are used, what is CI/cautioned?

A

Normal-decreased
B-blockers, Ca channel blockers, and high-dose volatile agents used
Caution with epi and dopamine

26
Q

Nitrates MOA? Name some

A

Nitrates release nitric oxide after metabolism(a healthy person releases this from the endothelium, someone with atherosclerosis has plaque covering the endothelium leading to less release). NO inc cGMP, discourages Ca influx/contraction, inc protein kinase G
Relax venous capacitance vessels and coronary arteries to DEC preload and wall tension (DEC supply, INC demand), DEC afterload, stops coronary spasm
Nitroglycerine, isosorbide dinitrate (isordil), isosorbide mononitrate (imdur)

27
Q

Nitroglycerine metabolism? E1/2t?

A

90% degraded by liver, inactive metabolites
E1/2t IV 1.5 min!
Sublingual and transdermal bypass liver and first pass metabolism

28
Q

Nitroglycerine adverse effects?

A

Headache (cerebral vasodilation)
Postural hypotension, fainting
Methemoglobinemia (high doses, liver disease)

29
Q

What can help with nitrate tolerance?

A

With nitrate tolerance, efficacy starts to decrease and they gain tolerance to adverse effects
Nitrate-free intervals help, remove patch at night

30
Q

Nitrate drug interactions? Treatment?

A

Silfenafil (viagra), tadalafil (cialis), and vardenafil (levitra) are phosphodiesterase inhibitors that break down cGMP, adding to the effect of nitrates causing a life-threatening hypotensive effect
Treat with phenylephrine

31
Q

Beta antagonists- What do they do? Supply/demand?

A

Provide a good O2 supply-demand balance
Used in preventing angina, improves long-term survival in CAD
Decrease demand by decreasing CO (esp with activity)
Improve diastolic filling time (inc supply), decrease HR and contractility

32
Q

Side effects of beta blockers?

A

Depression, insomnia, mask hypoglycemic s/s in DM, exercise intolerance, bronchospasm in asthma
DO NOT discontinue suddenly, they will upregulate receptors, dangerous

33
Q

How to Ca channel blockers work? What are the 4 effects?

A

Bind to A1 subunit of the L-type Ca channel so the channel will not repond to depolarization stimuli

  1. SA node chonotropy, dec HR
  2. AV node dromotropic effect, dec HR
  3. Cardiac muscle inotropy, dec contractility
  4. Coronary vascular dilation, Artery dilation
34
Q

Dihydropyridines vs. non-dihydropyridine Ca channel blockers?

A

Dihydropyridines are more selective for Ca channels in vessels, which may cause more reflex tachycardia
Non-dihydropyridines are more selective for Ca channels in the heart, DON’T give these with beta-blockers

35
Q

Dihydropyridines vs. non-dihydropyridine Ca channel blockers, list specific drugs in the two classes.

A

Dihydropyridines: amlodipine (norvasc), nifedipine (procardia, adalat), nicardipine (cardene)
Non-dihydropyridines: verapamil, diltiazem

36
Q

Why are CAD patients on aspirin?

A

Antiplatelet activity is very important to prevent platelets from forming thrombi
Irreversible inhibition of pro-aggregate TxA2

37
Q

How does treatment of a NSTEMI differ from a STEMI?

A

NSTEMI treatment: antianginal drugs, heparin/aspirin, GPIIb/IIIa antagonists, clopidogrel (plavix)
STEMI treatment: surgery and thrombolytics (streptokinase, alteplase/tPA)

38
Q

What is clopidogrel (plavix) and how does it work?

A

Antiplatelet that works as a irreversible platelet ADP-receptor antagonist
Good option for coronary syndrome patients with ASA allergy, reduces recurrent coronary events

39
Q

What do GPIIb/IIIa inhibitors reduce risk of? Name a few.

A

Reduce risk of MI in pt with unstable angina
Reduce risk of recurrent MI with NSTEMI
Abciximab (ReoPro), eptifibatide (integrilin), tirofiban (aggrastat)

40
Q

Treatment of stable angina vs. unstable angina vs. variant angina

A

Stable: nitrates, b-blockers, Ca channel blockers
Unstable: nitrates, b-blockers, Ca channel blockers, ASA/plavix, heparin/thrombolytics, GIIb/IIIa inhibitor
Variant: nitrates, Ca channel blockers

41
Q

What diseases are systolic dysfunction seen in? Diastolic dysfunction?

A 
Systolic dysfunction (EF <40%): CAD and nonischemic cardiomyopathy (HTN, valve disease, ETOH, thyroid disease, drugs)
Diastolic dysfunction: cardiomyopathies, ischemia (incomplete relaxation of LV)
42
Q

What are the three goals of drug therapy in heart failure? Which drugs help reach these goals?

A
  1. Reduce preload: diuretics, aldosterone antagonists, venodilators (nitroglycerine)
  2. Reduce afterload: ACEI, B-blockers, vasodilators
  3. Increase inotropy: cardiac glycosides, sympathomimetic amines, phosphodiesterase inhibitors (milrinone)
43
Q

What do loop diuretics do? Name some

A

Inhibit Na-K-Cl co-transporter in the loop of Henle, increasing excretion of Na, K, and H2O (also inhibit reabsorption of Ca, Mg)
Furosemide, bumetanide, torsemide

44
Q

What diuretics work on the distal tubule?

A

These increase Na excretion, but not as much as loop diuretics
Thiazides, metolazone (zaroxolyn), K-sparing (spironolactone, eplerenone)

45
Q

How does spironolactone work?

A

K-sparing diuretic that is a competitive antagonist at the aldosterone receptor
Dec K/Na exchange at distal tubule
30% mortality!!!
If given with ACEI, monitor K, both dec excretion of K

46
Q

Spironolactone (aldactone) AE?

A

Gynecomasta, impotence

Also inhibits androgen and mineralocorticoid receptors

47
Q

How does nitroglycerine work?

A

Ventilator that increases venous capacitance, reducing venous return
Dec myocardial O2 demand
Alleviate ischemia, improves diastole, improves LV compliance
Reduces preload (use caution)

48
Q

How do ACEI work?

A

Reverse vasoconstriction and volume retention cause by RAA activation
Reduce afterload which increases SV, increases GFR, increases natriuresis and diuresis
Reverses aldosterone-related volume retention, decreases preload

49
Q

How do ARBs work?

A

Similar to ACEI with less side effects but also less effective
Less preload reduction

50
Q

How are B-blockers helpful in CHF?

A

Inhibit renin release, stop cytotoxic signaling of catecholamines, prevent ACS
Not used in acute decompensated heart failure

51
Q

When are hydralazine and isosorbide dinatrate indicated in CHF?

A

When pt doesn’t tolerate ACEI
Mortality benefit in african americans
Used together, hydralazine is an arterial dilator and isosorbide dinitrate is a venodilator

52
Q

What does digoxin do?

A

Na-K adenosine triphosphate inhibitor
Decreases HR, preload, afterload, conduction velocity, renal absorption of Na, SNS outflow (vagal effect)
Increased AV refractory period, PSNS outflow

53
Q

Digoxin therapeutic levels? Onset of action? E1/2t? How excreted?

A

0.5-1.2 ng/mL (narrow TI)
Onset 30-60 min
E1/2t 36 hours

54
Q

Digoxin AE? Antidote?

A

AE: hypoK, AV block, ventricular ectopy
Antidote: digoxin immune Fab (digibind, digifab)

55
Q

Digoxin interactions?

A

B-blockers increase AV block, dec contractility
CCB dec contractility
Antibiotics inc absorption
Verapamil, quinidine, amiodarone increase digoxin levels by affection Vd or renal clearance

56
Q

How does dobutamine help with CHF?

A

B1 stimulation increases cardiac contractility

B2 stimulation causes arterial vasodilation and reduced afterload

57
Q

How do phosphodiesterase inhibitors work? What effects do they have on the heart?

A

Inhibit degradation of cAMP and cGMP in cardiac myocytes and vascular smooth muscle (art/veno-dilation), “inodilators”
Inc contractility (inc intracellular Ca), inc demand, helps B-blocker overdose
Dec preload and afterload, improve diastole relaxation by removing Ca after action potential
Mild bronchodilation

58
Q

What does Amrinone do?

A

Inc CO and LV EF
Dec LVEDP and pulm wedge pressures
HR inc, BP dec

59
Q

Amrinone E1/2t, dose, onset, DOA, excretion?

A 
E1/2t 6h
0.5-1.5 mg/kg IV or 2-10 mcg/kg/min
Max dose 10 mg/kg in a day
Onset 5 min
DOA 2 hours
Renal excretion, unchanged
60
Q

Amrinone AE?

A

Hypotension and thrombocytopenia mainly
Arrhythmias
Wide TI so toxicity is unlikely

61
Q

How does Milrinone compare to Amrinone?

A

Milrinone has less tachycardia and thrombocytopenia which is popular post CPB and to manage acute HF

62
Q

Milrinone dose, E1/2t, exretion?

A

50 mcg/kg IV or gtt at 0.5 mcg/kg/min
E1/2t 3 hours
80% excreted unchanged by kidneys
Wide TI, toxicity unlikely

N550 Pharm (14 decks)

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