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(D) Pharmacology > T3- CV Part 2 > Flashcards

T3- CV Part 2 Flashcards

1
Q

What are the 5 functional zones of nephron?

A

Proximal Convoluted Tubule
Descending Loop of Henle
Ascending Loop of Henle
Distal Convoluted Tubule
Collecting Tubule and Duct

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2
Q

What generally happens in the proximal convoluted tubule?

A

most of filtered Na+, Sodium bicarb, potassium, water, and glucose/amino acids are reabsorbed.

Organic acids are also secreted.

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3
Q

What generally happens in the descending loop of Henle?

A

Loop passes into the kidney’s medulla.
Water is extracted by osmotic forces found in the hypertonic medullary interstitium.
Osmolarity increases, aka salt concentration increases by 3x.

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4
Q

What generally happens in the ascending loop of Henle?

A

25% of NaCl is reabsorbed without water following, aka the diluting segment.

Location of the Na/K/2Cl cotransporter, so K returns to the cell.

Mg and Ca are reabsorbed via paracellular pathway.

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5
Q

What generally happens in the distal convoluted tubule?

A

10% of filtered NaCl is reabsorbed via thiazide-sensitive Na/Cl cotransporter.

Ca reabsorbed via Na/Ca exchanger, which is regulated via parathyroid hormone.

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6
Q

What generally happens in the collecting tubule?

A

Only responsible for 2-5% of NaCl reabsorption by the kidney.

Final site of NaCl reabsorption.

Site at which mineralcorticoids work.

Important site of K secretion by the kidney and where nearly all diuretic-induced changes in K balance occur!!!!

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7
Q

What cells does aldosterone work on in the kidneys?

A

Principal cells.

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8
Q

What kind of transporter does the principal cell have?

A

Na/K, generally pumping Na back into the blood, and K back into the urine.

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9
Q

What happens if a diuretic increases Na+ delivery to the collecting duct?

A

More potassium shifts of out the blood, so your urine concentration of K is much higher.

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10
Q

What are the water channels in principal cells called?

A

Aquaporins.

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11
Q

What hormone regulates aquaporins?

A

ADH/Vasopressin.

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12
Q

What does ADH do to an aquaporin?

A

Makes cells permeable to water, concentrating the urine.

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13
Q

Where do loop diuretics work on in the kidney?

A

Ascending loop

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14
Q

Why do we like loop diuretics?

A

They have the highest efficacy in diuretic effect, aka you take more, the more effect. They are sometimes known as high-ceiling diuretics.

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15
Q

What are the 3 loop diuretics?

A

Furosemide (Lasix)
Torsemide
Bumetanide (Bumex)

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16
Q

What is the MOA of a loop diuretic?

A

inhibition of Na/K/2Cl pump.
This causes a significant increase in the amount of sodium in the urine and therefore water in the urine.

Increased urinary Ca and Mg, but most Ca is reabsorbed later.

Can increase renal blood flow by increasing prostaglandin production.

Note: NSAIDs can reduce effect.

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17
Q

What is the PK of a loop diuretic?

A

2-8 hours, either orally or paraenterally
Rapid onset, even with renal insufficiency.
2-8 hours, (lasix = six hours)
Secreted into urine via organic acid system.

The most potent is bumetanide, following by torsemide and furosemide.

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18
Q

What are the indications for a loop diuretic?

A

Reducing edema, both peripheral and central.

Combined with water, it is good for hypercalcemia patients.

Also can treat hyperkalemia.

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19
Q

What are some contraindications for a loop diuretic?

A

Black Box Warning: Leads to profound diuresis with water and electrolyte depletion.

Hypersensitivity to sulfonamides.

Ototoxicity with hearing loss/vertigo, seen mainly when combined with other ototoxic drugs.

Hypovolemia, hypokalemia, hypomagnesemia.

Hyperuricemia

Pregnancy C

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20
Q

What kind of patients should not use loop diuretics?

A

People on other ototoxic drugs like aminogylcosides.
People with gout or high uric acid levels.

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21
Q

What are the thiazide drugs we learned?

A

Chlorothiazide (Diuril)
Chlorthalidone
Hydrochlorothiazide (HCTZ, most common)
Indapamide
Metolazone (most potent, inpatient only)

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22
Q

What are thiazide drugs a derivative of?

A

Sulfonamides.

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23
Q

What part of the kidney does a thiazide drug work on?

A

Distal convoluted tubule.

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24
Q

What is the MOA of a thiazide drug?

A

Decreases Na+ reabsorption, keeping more water in the urine. (done via inhibition of Na/Cl transporter)

Increases K+ loss in urine.

Loss of Mg

Decreases urinary excretion of Ca, so serum Ca increases.

Reduces peripheral vascular resistance.

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25
Q

What is the PK of a thiazide drug?

A

Equal max effect, potency varies.

Oral

Exceptions:
Chlorothiazide has low lipid solubility, so it requires high dosages AND can be given parenterally.

Chlorthalidone has a half life of 50-60 hours, longest duration.

Metolazone is most potent, can be used in renal failure.

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26
Q

What are thiazide drugs also known as?

A

Low ceiling drugs. They have a max effect, unlike the loop diuretics, which are high ceiling.

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27
Q

Which thiazide can be given in renal failure?

A

Metolazone, the most potent.

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28
Q

Which thiazide would I use if I just wanted to give one dose every few days?

A

Chlorthalidone

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29
Q

Which thiazide would I use if I wanted to use the most common?

A

Hydrochlorothiazide, HCTZ.

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30
Q

Which thiazide would I use if I wanted an IV administration one?

A

Chlorothiazide.

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31
Q

How long does it take a thiazide to reach max/stable BP reduction?

A

1-3 weeks.

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32
Q

What system do thiazide drugs compete with in excretion? Implications?

A

Organic acid secretion, which means uric acid can build up.

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33
Q

Can thiazides be given while pregnant?

A

No, Category D.

34
Q

What are the clinical indications for a thiazide drug?

A

HTN (recommended first-line, mild to moderate reduction)

Edema dt HF (loops are first, but thiazides can be added for extra diuresis, should be administered 30 mins before a loop)

Hypercalciuria (pts that commonly have kidney stones made of calcium oxalate)

Diabetes Insipidus (Can change urine composition and make the pt urinate less)

35
Q

What are the contraindications for a thiazide drug?

A

Hypersensitivity to sulfonamides (derivative)

Hypokalemia (most common adverse effect)
This is dt the fact it increases K+ excretion.

Hyponatremia (Loss of Na because it makes you pee a lot, which causes ADH to activate to dilute your serum)

Hypovolemia (can lead to orthostatic hypotension or lightheadedness)

Hyperuricemia (competes with organic acid secretion)

Hypercalcemia

Hyperglycemia (most frequent with thiazides over all other BP meds)
Can worsen glucose control of pts with DM.

36
Q

Where do the K-sparing diuretics work in the kidney?

A

Collecting tubule

37
Q

What are the two classes of K-sparing diuretics?

A

Aldosterone antagonists:
Spironolactone
Eplerenone

Sodium channel blockers:
Amiloride
Triamterene (Dyrenium)

38
Q

What do we typically use the sodium channel blockers for?

A

HTN (not used often as a diuretic)

Combined with other diuretics due to their K-sparing ability.

39
Q

What can sodium channel blockers cause?

A

Hyperuricemia, hyperkalemia.

Therefore, avoided in people with renal dysfunction or hyperkalemia.

40
Q

What part of the kidney do carbonic anhydrase inhibitors work on?

A

Proximal convoluted tubule.

41
Q

What are the carbonic anhydrase inhibitors we learned about?

A

Acetazolamide
Methazolamide
Brinzolamide (Azopt) **
Dorzolamide **

All end in -zolamide
** are topical formulations only

42
Q

What is the PK of a carbonic anhydrase inhibitor?

A

Good oral absorption.
Exception: Acetazolamide can be given parenterally for 5-10 minute onset.

Increase in urine pH due to loss of bicarb. This exists for 30 minutes, maxes out at 2 hours, and persists for 12 hours after a single dose.
Exception: Methazolamide is absorbed slower, so onset is 2-4 hours, maxed at 10-18 hours, with a HL of 14 days.

Excretion occurs in secretion of proximal tubule segment S2, so renal insufficiency requires dosage adjustments.

43
Q

Which carbonic anhydrase inhibitor would I give for a quick onset?

A

Acetazolamide parenterally.

44
Q

What will happen to my pt’s pH after I given them a carbonic anhydrase inhibitor?

A

Slight increase in urine pH.
Slight decrease in pt’s blood pH

Loss of bicarb = loss of base, so base leaves the blood and goes into the urine.

45
Q

At maximal efficacy, how much of my bicarb in the PCT is not being reabsorbed?

A

85%

46
Q

What happens to the diuretic efficacy of acetazolamide over time?

A

Decreases as the nephron adjusts.

Enhanced bicarb depletion leads to enhanced NaCl reabsorption.

47
Q

What are the clinical indications for carbonic anhydrase inhibitors?

A

Glaucoma (topical formulations)

Altitude sickness (decreases blood and brain pH, increase ventilation to counter the mountain sickness)

48
Q

What are the adverse effects of carbonic anhydrase inhibitors?

A

Hyperchloremic metabolic acidosis (increase urine pH = loss of bicarb = decreased blood pH)

Renal stones

Hypokalemia (increased Na delivery to other parts of the kidney makes K get secreted more)

49
Q

What are the contraindications of carbonic anhydrase inhibitors?

A

Sulfonamide hypersensitivity

Cirrhosis (dt decreased urinary excretion of NH4)

Pregancy category C

50
Q

What diuretics are sulfa derivatives?

A

Carbonic anhydrase inhibitors
Loop diuretics
Thiazide diuretics

51
Q

What are the 2 general classes of calcium channel blockers and the drugs we learned? (CCBs)

A

Non-DHPs:
Verapamil (diphenylalkylamine, AKA Calan SR, Verelan)
Diltiazem (Benzothiazepine, AKA cardizem, cartia XT)

DHPs:
Amlodipine (Norvasc, Katerzia)
Clevidipine (Cleviprex)
Felodipine
Isradipine
Nicardipine (Cardene IV)
Nifedipine (Procardia XL)
Nisoldipine (Sular)

Note: All DHP CCBs end in -dipine

52
Q

What is the MOA of a CCB in the heart?

A

Decreased HR (reflex tachy can occur with nifedipine)

Decreased AV conduction

Decreased contractility

53
Q

What is the MOA of a CCB in the peripheral vessels?

A

Blocks L type calcium channels, which prevents vessel constriction by the smooth muscle.

54
Q

What is the different MOA for the 3 types of CCBs?

A

For the Non-DHPs:

Verapamil is the least selective, having effects on both cardiac and smooth muscle.

Diltiazem is more selective, but still has effects on both. It has a reduced inotropic effect on the heart (Does not affect the contractility much)

For the DHPs:
Much more selective for vascular smooth muscle.
Excellent choice for HTN
Low drug-drug interactions!

55
Q

What is the PK for most CCBs?

A

Short HLs, EXCEPT amlodipine
Most agents have SR formulations for daily oral dosing.
Well-absorbed, tolerated pretty well.

56
Q

What are the clinical indications for CCBs?

A

Verapamil (diphenylalkylamine) and Diltiazem (benzothiazepine) have the same uses:

HTN/angina sometimes
Good for HR control in tachyarrhythmias

DHPs:

Better choice for HTN, some angina relief. NOT USED FOR Tachyarrhythmias.

57
Q

What are the adverse effects of CCBs?

A

For the Non-DHPs:
Avoid in bradycardia, and systolic HF

For the DHPs:
Avoid in hypotensive pts
Peripheral edema and flushing are common side effects.
Gingival hyperplasia may also occur, not as common.

Note:
For systolic HF, Non-DHPs are absolutely contraindicated. DHPs are not as heavily contraindicated.

58
Q

What are the 3 types of beta blockers and their examples? (BB)

A

Cardioselective BB (B1 selective) aka MANBABE
Metoprolol - lopressor, toprol XL
Atenolol - tenormin
Nebivolol - bystolic
Betaxolol
Acebutolol (with ISA)
Bisoprolol
Esmolol - brevibloc

Nonselective BB (B1 & B2)
Propranolol - inderal XL
Nadolol - Corgard
Pindolol (with ISA)
Timolol
Sotalol (betapace, antiarrhythmic)

Mixed Alpha/Beta
Carvedilol - Coreg
Labetalol

Note:
All Beta only blockers end in olol. The 3 special ones (sotalol, carvedilol, and labetalol) do different things.

59
Q

What does ISA mean in terms of BBs? Which BBs have ISA and what does it do?

A

ISA stands for intrinsic sympathomimetic activity.
This means that while the BB itself lowers HR, the ISA portion can increase HR. It is similar to an agonist-antagonist relationship.

Acebutolol (cardioselective)
Pindolol (non-cardioselective)

60
Q

Name all the Cardioselective BBs.

A

MANBABE

Metoprolol
Atenolol
Nebivolol
Betaxolol
Acebutolol
Bisoprolol
Esmolol

61
Q

Name all the non-cardioselective BBs.

A

Propranolol
Nadolol
Pindolol
Timolol
Sotalol

62
Q

Name all the mixed alpha/beta blockers.

A

Carvedilol
Labetalol

63
Q

What is the MOA of a cardioselective BB?

A

Decreased HR, contractility, workload, and AV node conduction.

64
Q

What is the MOA of a non-selective BB?

A

In addition to all the effects of a cardioselective BB, can also cause bronchoconstriction and peripheral vasoconstriction.

65
Q

What is the MOA of a mixed alpha/beta blocker?

A

On top of all the non-selective and cardioselective BB MOAs, it can also vasodilate and decreased peripheral vascular resistance.

66
Q

Which BBs are hepatically cleared and long-acting?

A

Carvedilol, labetalol, metoprolol, propranolol.

Clear my liver permanently

67
Q

Which BBs are renally cleared and short-acting?

A

Acebutolol, atenolol, sotalol, pindolol.

ASAP

68
Q

Which BBs have mixed hepatic and renal clearance?

A

Bisoprolol and nebivolol.

Needs Both

69
Q

What are the clinical indications for BBs?

A

Used for first-line HTN IF PT HAS THESE CONDITIONS:
Post-MI, stable ischemic heart disease, CHF, cardiac arrhythmias.

HTN crisis: labetalol is first-line for pregnancy

CHF: Bisoprolol, carvedilol, metoprolol succinate

Glaucoma: Ophthalmic timolol, betaxolol

Migraine prophylaxis/essential tremors: Propranolol

70
Q

What BB is best used for a pregnancy induced HTN crisis?

A

Labetalol

71
Q

What BBs can be used for CHF?

A

Bisoprolol, carvedilol, and Metoprolol succinate.

72
Q

Which BBs are used for glaucoma?

A

Topical timolol, betaxolol.

73
Q

Bonus: What are all the drugs used for glaucoma that we learned about?

A

Topical timolol, betaxolol, brinzolamide and dorzolamide.

BBs and carbonic anhydrase inhibitors.

74
Q

What are the adverse effects of a BB?

A

Contraindicated in bradycardia, severe AV blocks, SSS (Sick sinus syndrome) if no PM implant, cardiogenic shock, and caution in COPD/asthma.

Can cause:
Bradycardia/hypotension
Mask hypoglycemic conditions (aka tachy and tremors, which get masked by non-selectives)

Hyperkalemia, Hypertriglyceridemia

DO NOT STOP ABRUPTLY! (Rebound HTN and tachy)

75
Q

Lecture Q1:
A 1-month follow-up with a patient started on a new BP medication presents with hypokalemia. What medication were they probably started on?

A

A thiazide medication.

First-line antiHTN medication with a side effect of hypokalemia, due to excess K excretion in the urine.

76
Q

Lecture Q2:
TL is a 50 yo pt with CHF. What kind of meds should be avoided?

A

Non-DHP CCBs, specifically verapamil.

Verapamil reduces a heart’s contractility, which is already generally weaker in CHF.

77
Q

Lecture Q3:
What kind of agents can lead to gout attacks?

A

Anything that competes with the organic acid secretion system in urine.

This includes:
Loop diuretics
Thiazides
Sodium channel blockers

78
Q

Lecture Q4:
A pt present with rapid HR dt AFib and HTN. What kind of medication would be most beneficial to manage both disorders in this pt?

A

Diltiazem.

Diltiazem is indicated in pts with tachyarrythmias and has antiHTN properties due to it being a non-DHP CCB.

79
Q

Lecture Q5:
A pt has a hx of SJS (steven johnson syndrome) with sulfa abx. What kind of meds should this pt avoid?

A

Loop diuretics
Thiazides
Carbonic anhydrase inhibitors

80
Q

Lecture Q6:
What medications should be avoided in a pt with asthma?

A

Non-selective BBs.

(D) Pharmacology (18 decks)

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