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Crrab2 > Trachte drugs > Flashcards

Trachte drugs Flashcards

1
Q

What are the major loop diuretics?

A

Lasix (furosemide)
Bumetanide
Ethacrynic acid

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2
Q

If you have a sulfa allergy can you take Lasix?

A

No

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3
Q

What should you take if you have a sulfa allergy for a loop diuretic?

A

Bumetanide

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4
Q

What is a common side effect of long term Loop diuretic use? what should you give to compensate?

A

Hypomagnesium (We are blocking NKCC here which makes the interstium very positive and paracellularly pushes 20% of Mg through)

Give Mg2+

Hypocalcemia is rare

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5
Q

What does low salt in the interstium lead to?

A

Increase in Cox 2

-Which increases prostaglandins, increases RPF and GFR, which potentiates the drug

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6
Q

What are loop diuretics good to treat?

A
  1. Pulmonary edema
  2. Edema
  3. Hyperkale
  4. Acute renal failure
  5. Anion overdoes with Bromide, flouride and iodide
  6. Acute HF
  7. Ascites
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7
Q

What are the 5 common AE of loop diuretics?

A
  1. Hypokale (Na gets exchanged for K in the collecting duct)
  2. Hearing loss
  3. Lasix (allergy can lead to Acute interstitial nephritis)
  4. Hyperurecemia
  5. Contraction Alkalosis
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8
Q

What stimulates ADH secretion?

A

Increased osmolarity

Decreased volume

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9
Q

Why would we get hyperuricemia in loop diuretic pts?

A

Cauese hypovolumic state

  • induces ADH secretion
  • Cause upregulation of UT1 which leads to increase absorption of Urea!
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10
Q

What causes contract alkalosis in pts whom are on a loop diuretic?

A

Multifold:

  1. Increase in RAAS–> increase aldosterone which upregulates K+/H+ anti-porter in the alpha intercalated cell in the collecting duct
  2. Increased RAAS–> increased AgII leads to increase in Na+/H+ anti-porter in the PCT

both lead to increased H+ in the filtrate. Leading to an alkalosis.

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11
Q

What are the major Thiazide diuretics? What is their MOA?

A
  1. Chlorithalidone
  2. Hydrochlorothiazide
  3. Metalazone
  • block NCC channel in DCT
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12
Q

What are some of the major uses of thiazides?

A
  1. HTN–> 1st line
  2. HF–> adjunctive treatment with 1st line Loopers
  3. Nephrolithiasis by Hypercalcemia
  4. Nephrogenic diabetes insipidus
  5. Osteoporosis
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13
Q

How do thiazides lead to hypercalemia?

A

There is an Na/Ca antiporter on the basolateral side of the endothelial cells. This is driven by concentration gradients.

  • Since Thiazides block Na into cell this increase the pump
  • Ca is going out of the cell and Na is coming in
  • Increasing the pump thus decreases the intracellular Ca which leads to a greater conc. gradient
  • Ca flows faster down the TRPV5 channel into the cell
  • leads to hypercalcemia
  • treats calcium related stones
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14
Q

Can one with a sulfa allergy take thiazides?

A

No

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15
Q

What are some major AE of Thiazides?

A
  1. Hyperglycemia
  2. Hyperuricemia
  3. Hypokale
  4. Hyperlipidemia–> 5-15% increase in LDL’s
  5. Hyponatremia
  6. allergic rxns
  7. Contraction alkalosis
  8. Lithium pt monitored
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16
Q

What causes the hyperglycemia in Thiazide use?

A
  • There are potassium pumps on Beta-Cells in the pancreas
  • When these are closed–> leads to more positive membrane potential inside cell which depolarizes and causes Calcium channels to open
  • Calcium rushes and cause insulin vesicle release
  • Sulfonyureas inhibit Potassium pumps
  • Increases K+ intracellular
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17
Q

What are the 2 mechanisms of Potassium sparing diuretics?

A
  1. Inhibit aldosterone receptors

2. Inhibit Na exchange for K and H in the cortical collecting duct

18
Q

What are the aldosterone inhibitors?

A
  1. Spironolactone (aldactone

2. Eplerenone (inspra)

19
Q

What are the Na exchange inhibitors potassium sparring diuretics?

A
  1. Amiloride (Midamor)

2. Triamterene (Dyrenium)

20
Q

What is Amiloride used to treat

A

Li+ induced nephrogenic diabetes insipitus

21
Q

What is the MOA of Potassium sparing diuretics?

A

Blocks absorption of Na in the collecting duct for the exchange of K+

22
Q

Where does aldosterone bind and what are its affects?

A

Intracellular SRE

  1. Increase K+ excretion
  2. Increase Na+ resorption
  3. Increase H+ excretion
  4. Upregulates Na/K ATPase of basolateral membrane
23
Q

What is the MOA of Elperenone?

A

Mineralcorticol receptor antagonist

24
Q

what is the MOA of Amlodipine?

A

inhibits ENAC thus decreases Na resorption

25
Q

What is the MOA of Triamterene?

A

Blocks ENAC

26
Q

What is the MOA of spironolactone?

A

Antagonist of the mineralcorticoid receptor

- blocks 17 alpha-hydroxylase which is the enzyme used to make testosterone from cholesterol

27
Q

what are potassium sparing diuretics used for?

A
  1. HF
  2. Prevents myocardial remodeling
  3. Liddle’s syndrome
  4. Hyperaldosteronism 1st and 2nd degree
28
Q

If spironolactone blocks 17 a-hydroxylase what are some of its SE’s?

A
  1. Gynecomastia
  2. Impotence and decrease libido
  3. Polycystic ovarian syndrome
29
Q

What are the general AE’s of K sparing diuretics?

A
  1. Hyperkale
  2. Hyperchloremic metabolic acidosis
  3. Gynecomastia
  4. Acute renal failure
  5. Kidney stones
  6. Type 4 renal tubular acidosis
30
Q

What is the synthetic version of vasopressin? What is it used for?

A

Desmopressin

  1. Diabetes insipidus
  2. Bedwetting
31
Q

What is Desmopressins MOA?

A

G protein coupled receptor in the collecting duct that recruits Aquaporins
- Leads to downstream induction of CREB-P a transcription factor that promotes the mRNA transcription and protein translation of Aquaporins

32
Q

What is Covaptan?

A

Non-selective ADH antagonist that can be used to treat syndromes of inappropriate ADH secretion

33
Q

What is Demococycline?

A

a tetracycline- 30s inhibitor

- however has some ADH antagonistic affects

34
Q

What class drug is Mannitol and how does it work?

A

Osmotic diuretic

- Its not reabsorbed and keeps filtrate osmolality high which keeps water in the tubule

35
Q

What is Mannitol used to treat?

A

Intracranial pressure

Increased intraocular pressure

36
Q

What are some AE’s of Mannitol?

A
  1. Pulmonary edema
  2. Extracellular volume expansion
  3. Dehydration, hyperkale and hypernatremia
  4. Hyponatremia with renal impairment
37
Q

Above what level will glucose start spilling into the urine?

A

240 mg/dL

38
Q

What is the MOA of SGLT-2 blockers?

A

Block glucose resorption in the PCT

39
Q

What can SGLT-2 blockers be used for?

A
  1. Treat DM

2. Weight loss

40
Q

What are some AE’s of SGLT-2 blockers?

A
  1. Ketoacidosis
  2. UTI’s
  3. Yeast infections
  4. Hypoglycemia
41
Q

What are some examples of SGLT-2 blockers?

A
  1. Canigliflozin (Invokana)
  2. Dapagliflozin (Farziga)
  3. Gliflozin

increases flow and some zin to urine

Crrab2 (14 decks)

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