Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Renal > Lecture 14: Diuretics + Antidiuretics > Flashcards

Lecture 14: Diuretics + Antidiuretics Flashcards

1
Q

Define diuresis and natriuresis

A

Diuresis:
Inc. in urine flow rate

Natriuresis:
Inc. excretion of Na + anions

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

List the four major classes of diuretics

A

CA inhibitors (CAIs)

Loop diuretics (LDs)

Thiazides diuretics (TZs)

K+ sparing diuretics

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

What do each class of diuretics inhibit?

A

CA inhibitors:
Inhibit H+ secretion in PT

Loop diuretics:
Inhibit NKCC2 in thick AL

Thiazide diuretics:
Inhibit NCC in DCT

K+ sparing diuretics:
Inhibit ENaC in CNT/CD

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

What is an example of carbonic anhydrase inhibitors?

A

Acetazolamide

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

What are examples of loop diuretics?

A

Furosemide

Bumetanide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are examples of thiazide diuretics?

A

Hydrochlorothiazide

Chlorthalidone

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

What are examples of K+ sparing diuretics?

A

Triamterene

Amiloride

Sprironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the max acute decrease in sodium reabsorption that can occur following administration of

CAIs
LDs
TZs
K sparing diuretics

A

Loop = 25%

Thiazides = 5-8%

CA inhibitors = 5%

K sparing = 1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism for TRIAMTERENE and AMILORIDE blocking ENaC?

How about for Spironolactone?

A

Directly block ENaC

Spironolactone: competitive inhibition of aldo binding to MR
(Very effective in patients with high aldosterone, not effective in patients with low aldo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do diuretics get into tubular fluid?

A

Enter TF mainly via tubular secretion, where OAT family transporters help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe mechanisms for natriuresis

CAIs
LDs
TZs
K-sparing

A

CAIs =
Inhibit H+ secretion in PT

LDs =
Inhibit NKCC2 in thick AL

TZs =
Inhibit NCC in DCT

K-sparing =
Inhibit ENaC in CNT/CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe mechanism for diuresis

A 
Dec. Na reabsorption 
=
More particles remaining in tubular fluid 
=
Dec. water reabsorption 
=
Inc. urine flow rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the importance of the diuretic breaking phenomenon

A

Compensatory mechanism to restore sodium balance with chronic use of diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does diuretic breaking involve?

A

Activation of symp division

Activation of RAAS

Other mechanisms
+ load dependence of sodium reabsorption
+ dec. BP = dec. pressure natriuresis
+ dec. natriuretic hormones
+ inc. expression of transporters in tubular epithelial cells
+ hypertrophy of tubular epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a consequence of even a brief period of negative Na balance?

A 
Dec. total body Na
=
Dec. ECF 
=
Dec. ECV
(The part of the ECF that can activate mechanisms to induce changes in sodium excretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the key for activating diuretic braking mechanism?

A

Dec. ECV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the effect of dec. ECV on BP?

A

Dec. ECV = dec. BP

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

What results from dec. BP after fall in ECV?

A

(1) arterial BRs = reflex inc. sympathetic tone to kidneys

(2) dec. stretch of afferent arterioles will stimulate renal BRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Besides drop in BP, what else will reduce stretch of AA in kidney?

A

Reflex inc. sympathetic tone to kidneys

By constricting AA via alpha1 stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are consequences of inc. sympathetic tone to kidneys?

A

1) constriction of AA via alpha1 receptor stimulation
2) inc. renin secretion via stimulation of beta1 receptors on granular cells
3) inc. Na reabsorption in PT by increasing NHE (Na/H exchange)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What factors following diuretic therapy will lead to increased renin secretion?

A

1) dec. stretch of AA as sensed by renal BRs
2) beta1 sympathetic stimulation
3) dec. Na delivery to macula densa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are consequences of more sodium reabsorption in PT following diuretic therapy and increased symp tone?

A

1) reduced Na dlievery to macula densa

2) dec. sodium excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is effect of inc. renin secretion on AngII?

A

Inc. renin = inc. AngII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are consequences of inc. AngII following diuretic therapy?

A

1) inc. Na reabsorption in PT by stimulating more Na/H exchange
2) stimulate AT1 receptor to inc. Aldo secretion
3) inc. Na reabsorption in DCT, CNT/CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are effects of increased aldosterone secretion?
Increased Na reabsorption in CNT/CD
26
What mechanisms contribute to reduction in sodium excretion | AKA restoration of Na balance via diuretic breaking
(1) inc. Na reabsorption in DCT, CNT/CD (From AngII) (2) inc. reabsorption in CNT/CD (From aldo) (3) inc. Na reabsorption in PT + DCT (From symp tone)
27
Where does all regulation of potassium excretion occur?
CNT/CD
28
How does inc. Na reabsorption in CNT/CD lead to increased K secretion?
``` Inc. Na reabsorption via ENaC = Inc. electrochemical gradient for K secretion = Inc. K secretion ```
29
Describe effect of CAIs, LDs, and TZs on potassium excretion
``` All inc. sodium delivery to CNT/CD by inhibiting Na reabsorption proximal to CNT/CD = Inc. Na reabsorption in CNT/CD = Inc. electrochemical gradient for K secretion = Inc. K secretion in CNT/CD = Inc. K excretion (common AE of hypokalemia) ```
30
What effect does increased flow through CNT/CD have on K?
Further enhances electrochemical gradient by washing away secreted K
31
Describe effect of K-sparing diuretics on K excretion
``` Dec. Na reabsorption in CNT/CD by inhibiting ENaC = Dec. electrochemical gradient for K secretion = Dec. K secretion in CNT/CD = Dec. K excretion (Potential AE: hyperkalemia) ```
32
What other drugs spare potassium?
ACEIs ARBs Trimethoprim (Related to triamterene)
33
How do CA inhibitors affect H+ and HCO3?
``` Dec. H+ secretion in PT by inhibiting CA = Dec. HCO3 reabsorption in PT = Inc. bicarbonate excretion ``` ``` Common adverse effect: Metabolic acidosis (which limits ability of carbonic anhydrases because if pH is low enough, they aren't needed as much!) ```
34
What is effect of LDs and TZs on H+ and HCO3?
``` Both inc. sodium delivery to CNT/CD by inhibition Na reabsorption proximal to CNT/CD = Inc. Na reabsorption in CNT/CD = Inc. electrochemical gradient for H+ secretion = Inc. H+ secretion in CNT/CD = More new HCO3 made ``` Common AE = metabolic alkalosis
35
What are effect of K-sparing diuretics on H+ and HCO3?
``` Dec. Na reabsorption in CNT/CD by inhibiting ENaC = Dec. electrochemical gradient for H+ secretion = Dec. H+ secretion in CNT/CD = Dec. HCO3 reabsorption in CNT/CD = Inc. HCO3 excretion ``` (Potential AE: metabolic acidosis)
36
What are requirements for concentrating urine mechanism?
1) ADH | 2) medullary gradient
37
What does formation and maintenance of medullary gradient require?
NaCl reabsorption in thick AL by NKCC2 | Which is the transporter that Loop diuretics block
38
What effect do loop diuretics have on concentrating mechanism?
Markedly impair concentrating mechanism by completely abolishing medullary gradient
39
What are requirements for formation of a dilute urine?
1) no ADH 2) delivery of hypo-osmotic TF to CNT/CD - have NaCl reabsorption in thick AL by NKCC2 - minor way to assure: block NaCl reabsorption by NCC in DCT
40
What effect do LDs have on diluting mechanism?
Markedly impair diluting mechanisms | Smaller impairment with thiazides
41
What is mannitol ?
Osmotic diuretic that produces both diuresis and natriuresis
42
How do osmotic diuretics work?
``` Dec. water reabsorption in PT = Dec. sodium in tubular fluid in PT = Dec. sodium reabsorption in PT ```
43
What is the maximum amount osmotic diuretics can dec. Na reabsorption ?
20%
44
What are examples of aquaretics?
ADH antagonists ("Vaptans") = most selective: Conivaptan Tolvaptan Demeclocycline Lithium
45
How do aquaretics work?
Produce diuresis ONLY Vaptans selective for V2 receptor
46
What are effects of V1A and V2 receptors?
V1A = Gq Vasoconstriction V2 = Gs Anti-diuretic effects, urea permeability
47
In what conditions does edema most commonly occur?
HF Cirrhosis Kidney disease
48
What are therapeutic uses of diuretics?
Edema ``` Non-edema: HTN Nephrolithiasis Hypercalcemia Nephrogenic diabetes insipidus ```
49
Which diuretics are used for HTN?
Thiazides
50
What is a difference between chlorthalidone and hydrochlorothiazide?
Chlorthalidone = more potent, longer duration of action in maintaining low BP throughout 24 hours
51
What is nephrolithiasis?
Kidney stones
52
Why use a thiazides for kidney stones?
Decrease calcium excretion b/c many patients with these Ca-containing kidney stones got it from inc. calcium excretion ``` Tx: Thiazide cause mild volume depletion = Inc. Na reabsorption in PT = More calcium reabsorption in PT = Dec. calcium excretion ```
53
What usually causes hypercalcemia?
Inc. PTH
54
What is a possible treatment for hypercalcemia?
Inc. calcium excretion with a loop diuretic: ``` LD inhibits NKCC2 in thick AL = Dec. lumen positive TEP in thick AL = Dec. paracellular Ca reabsorption in thick AL = Inc. calcium excretion ```
55
What is an ADH congener?
Anti-diuretic
56
What is treatment for central DI ADH deficiency?
Replace ADH with an ADH congener (antidiuretic)
57
What does nephrogenic DI mean?
Nephrons failing to respond to ADH
58
How can you treat genetic and acquired nephrogenic DI?
Genetic: Thiazides Acquired: Thiazides Amiloride
59
What kind of therapy could be recommended to a patient with severe edema due to HF?
Start patient on LD Add thiazide for more natriuresis Add K-sparing diuretic for even more natriuresis
60
What AEs could be prevented or attenuated by adding K-sparing diuretic to LD/TZ?
Hypokalemia Metabolic alkalosis
61
What is the most common use of K sparing diuretics?
In combo therapy with LD or TZ in order to: Inc. natriuresis Dec. hypokalemia Dec. metabolic alkalosis
62
What is the main instance in which K-sparing diuretics are used alone?
In patients with high aldosterone
63
What are therapeutic uses of CAIs?
Acute mountain sickness Glaucoma
64
What are osmotic diuretics used for?
To shift fluid from IC to EC compartment Cerebral edema (IC edema) Dialysis Crush injuries Glaucoma
65
What are aquaretics used for?
Syndrome of inappropriate ADH secretion (SIADH) Hypervolemic hyponatremia
66
What is SIADH?
Syndrome of inappropriate ADH secretion ADH secreted at level that is inappropriate for patient's volume and osmolality status, resulting in hyponatremia
67
What are predictable AEs from diuretics?
K+ abnormalities Acid-base disorders Ca abnormalities Hyponatremia Hypomagnesemia Hyperuricemia And others
68
What predictable AE are caused by CAIs?
Hypokalemia Metabolic acidosis Nephrolithiasis
69
What predictable AEs are caused by LDs?
Hypokalemia Metabolic alkalosis Hypocalcemia Hyponatremia Hypomagnesemia Hyperuricemia Hypovolemic, postural hypotension
70
What predicable AEs are caused by thiazides?
Hypokalemia Metabolic alkalosis Hypercalcemia Hyperuricemia Hyponatremia Hypomagnesemia Hypovolemic, postural hypotension
71
What AEs are caused by K-sparing diuretics?
Hyperkalemia Metabolic acidosis (Spironolactone: gynecomastic, ED)
72
What AEs result from mannitol?
Pulmonary edema in patients with decreased LV function
73
What AEs are not predictable?
Hyperglycemia = Thiazides, loop diuretics Hyperlipidemia = Thiazides, loop diuretics Ototoxicity = Loop diuretics Rashes, etc.... any drug!
74
In what nephron segment does Bartter's syndrome effect? What transporters/channels are abnormal?
Thick AL ``` NKCC2 ROMK Cl channels Barttin subunit CaSR ```
75
What abnormalities are characteristic of Bartter's syndrome? What drug does it mimic?
Hypokalemia Metabolic alkalosis Hypercalciuria Impaired concentrating mechanism Mimics loop diuretics
76
What nephron segment does Gitelman's syndrome affect? What transporters/channels are abnormal?
DCT NCC Cl channels (CLC-KB)
77
What abnormalities are characteristic of Gitelman's syndrome? What drug does it mimic?
Hypokalemia Metabolic alkalosis Hypocalciuria Normal concentrating mechanism Mimics thiazides
78
What nephron segment does pseudohypo-aldosteronism affect? What transporters/channels are abnormal?
CNT/CD Mineralocorticoid receptor
79
What abnormalities are characteristic of pseudo-hypoaldosteronism? What drug does it mimic?
Hyperkalemia Hypovolemic Mimics K-sparing diuretics
80
Why is synthetic ADH seldom used as an antidiuretic?
Prominent vasoconstrictor effects!
81
Name an ADH congener
Desmopressin
82
What is desmopressin used for?
Central DI | Nocturnal enuresis Bed-wetting
83
What is an advantage of desmopressin vs. synthetic ADH?
Desmopressin has minimal V1A agonist activity = minimal vasoconstriction !!!

Renal (17 decks)

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