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Renal 2 Final > Kruse Part 1 > Flashcards

Kruse Part 1 Flashcards

1
Q

Blood Pressure Equation

A

MAP=CO x TPR

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2
Q

Cardiac output

A
  • HR x SV
  • the volume of blood pumped through the heart per minute
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3
Q

BP Drug Strategies

A
  • reduce cardiac output and bp is reduced
  • reduce total peripheral resistance and bp is reduced
  • compensatory responses may include:

–reflex tachycardia (increased sympathetic activity)

–edema (increased renin activity)

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4
Q

4 major classes of antihypertensive agents

A
  • diuretics
  • agents that block the production or action of angiotensin
  • direct vasodilators
  • sympathoplegic agents (those that alter sympathetic function)
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5
Q

In the PCT, reabsorption of

A

approximately 65% of total sodium, K+ and water; 85% of NaHCO3; nearly 100% of glucose and main acids

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6
Q

NaHCO3–reabsorption in the PCT

A

-iniitated by action of the Na+/H+ exchanger (NHE3) located in luminal membrane

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7
Q

Na+/K+ ATP in basolateral membrane

A

pumps reabsorbed Na+ into the interstitium to maintain a low intracellular Na+ concentration

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8
Q

In the straight segment of the proximal tubule (late PT)

A

acid secretory systems secrete organic acids into the luminal fluid from the blood

-diuretics are delivered to the luminal side of the tubule where most of them act

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9
Q

Loop of Henle: H2O

A

-reabsorbed from the thin descending limb of the loop of Henle

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10
Q

Thin ascending limb of the loop of Henle

A

-relatively water imperbeable and is impermeable to other ions/solutes

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11
Q

Thick ascending limb of the loop of Henle

A

-reabsorbs Na+ and is impermeable to water

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12
Q

NaCl transport system in luminal membrane of thick ascending loop of Henle

A
  • Na+/K+/2Cl- cotransporter
  • establishes ion gradient in the interstitium
  • increase in K+ concentration in the cells causes back diffusion of K+ into the tubular lumen–positive electrical potential to drive reabsorption of cations (Mg2+, Ca2+) via paracellular pathway
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13
Q

Inhibition of salt transport in thick ascending limb

A

reduces the lumen-positive potential and causes an increase in urinary excretion of divalent cations in addition to NaCl

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14
Q

Distal Convoluted tubule

A
  • 10% of sodium chloride is reabsorbed
  • relatively impermeable to water; NaCl reabsorption further dilutes tubular fluid
  • NaCl is transported via a thiazide-sensitive Na+ and Cl- cotransporter

Ca2+ is passively reabsorbed by calcium channels (regulated by PTH)

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15
Q

Collecting tubule

A
  • 2-5% of NaCl reabsorption through ENaC
  • most important site of K+ secretion by the kidney and the site at which virtually all diuretic-induced changes in K+ balance occur
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16
Q

Diuretics that act upstream of the CCT will

A

increase Na+ delivery, which will enhance K+ secretion

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17
Q

Aldosterone

A

-increases the expression of both the ENaC and the basolateral Na+/K+-ATPase, leading to an increase in Na+ reabsorption and K+ secretion (which causes retention of water, an increase in blood volume, and an increase in BP)

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18
Q

H+ in Collecting Tubule

A

-secreted by proton pumps (H+-ATPases) into the lumen and increase urine acidity

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19
Q

ADH, vasopressin

A

-controls the permeability of the CCT to water by controlling the expression levles of functional aquaporin-2 water channels that insert into the apical membrane

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20
Q

Diuretics

A
  • increase the rate of urine flow and sodium excretion
  • used to adjust the volume and/or composition of body fluids in a variety of clinical situations including
  • edematous states: heart failure, kidney disease and renal failure, liver disease (cirrhosis)
  • nonedematous states: hypertension, nephrolithiasis (kidney stones), hypercalcemia, and diabetes insipidus
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21
Q

In the absence of ADH, the CCT (and collecting duct) is

A

impermeable to water and dilute urine is produced

-alcohol decreases ADH release and increases urine production

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22
Q

Diuretics molecular targets

A
  • specific membrane transport proteins
  • enzymes
  • hormone receptors
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23
Q

Loop diuretics target

A

sodium/potassium/chloride cotransporter

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24
Q

Thiazide diuretics target

A

sodium/chloride cotransporter

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25
Q

K+-sparing diuretics target

A

sodium channels

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26
Q

Changes in urinary electrolytes and body pH with carbonic anhydrase inhibitors

A
  • increased NaHCO3 in urine
  • decreased body pH
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27
Q

Changes in urinary electrolytes and body pH with loop agents

A

increased NaCl in urine

increased body pH

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28
Q

Changes in urinary electrolytes and body pH with thiazides

A
  • increased NaCl but not as much as loop agents
  • increased body pH
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29
Q

Changes in urinary electrolytes and body pH with loop agents plus thiazides

A
  • very increased NaCl in urine
  • increased K+ in urine
  • increased body pH
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30
Q

Changes in urinary electrolytes and body pH with K+ sparing agents

A
  • K+ is lost in urine with all diuretics except these
  • body pH decreased
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31
Q

Carbonic Anhydrase inhibitors act on

A

-Na/H (NHE3), carbonic anhydrase in the PCT

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32
Q

Loop diuretics act on

A

Na/K/2Cl cotransporter in thick ascending limb

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33
Q

Thiazides act on

A

Na/Cl transporter in Distal convoluted tubule

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34
Q

K+ sparing diuretics act on

A

ENaC channels in cortical collecting tubule

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35
Q

vasopressin antagonist act on

A

aquaporins in medullary collecting duct

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36
Q

carbonic anhydrase inhibitors include

A
  • acetazolamide
  • brinzolamide
  • dorzolamide
  • methazolamide
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37
Q

Loop diuretics include

A
  • bumetanide
  • ethacrynic acid
  • furosomide
  • torsemide
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38
Q

Thiazide diuretics include

A
  • bendroglumethiazide
  • chlorothiazide
  • hydrochlorithiazide
  • indapamide
  • methylclothiazide
  • metolazone
  • polythiazide
  • trichlormethiazide
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39
Q

K+ sparing diuretics include

A
  • aldosterone agonists: eplerenone and spironolactone
  • epithelial sodium channel inhibitors: amiloride; triamterene
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40
Q

Carbonic Anhydrase inhibitor MOA

A
  • acetazolamide
  • inhibits the membrane-bound and cytoplasmic forms of carbonic anhydrase
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41
Q

Carbonic anhydrase inhibitor actions

A
  • decreased H+ formation inside PCT cell and decreased Na+/H+ antiport
  • increased Na+ and HCO3- in lumen
  • increased diuresis
  • urine pH is increased and body pH is decreased
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42
Q

Carbonic anhydrase inhibitor clinical indications

A
  • rarely used as antihypertensives due to low efficacy as single agents and development of metabolic acidosis
  • used for glaucoma, acute mountain sickness, and metabolic alkalosis
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43
Q

Carbonic anhydrase inhibitor adverse effects

A

-acidosis, hypokalemia, renal stones, paresthesias (with high doses), sulfonamide hypersensitivity

44
Q

Loop Diuretics MOA

A
  • furosemide and ethacrynic acid are prototypes
  • inhibit the luminal Na+/K+/2Cl- cotransporter (NKCC2) in the TAL of the loop of Henle
45
Q

Loop Diuretic Action

A
  • decreased intracellular Na+/K+/Cl- in TAL
  • decreased back diffusion of K+ and positive potential -decreased reabsorption of Ca2+ and Mg2+
  • increased diuresis
  • ion transport is virtually nonexistent -among the most efficacious diuretics available
46
Q

Loop Diuretic diuretic activity

A
  • tied to secretion rates (act at luminal side of tubule)
  • half-life correlated to kidney function -0.5-2 hours (healthy) vs. 9 hrs (ESRD) for furosemide
47
Q

Loop Diuretics are used for

A

edema, heart failure, hypertension, acute renal failure, anion overdose, hypercalcemic states

48
Q

Loop Diuretic Adverse Effects

A

-hypokalemia, alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia, ototoxicity, sulfonamide hypersensitivity (not all)

49
Q

Thiazide Diuretic MOA

A
  • prototype hydrochlorothiazide (HCTZ)
  • cause inhibition of the Na+/Cl- cotransporter (NCC) and block NaCl reabsorption in the DCT
50
Q

Thiazide Diuretic Action

A

Thiazide Diuretic Action -increased luminal Na+ and Cl- in DCT -increased diuresis

  • enhance the reabsorption of Ca2+ in both DCT and PCT
  • largest class of diuretic agents
51
Q

Thiazide Diuretic Uses:

A

-hypertension, mild heart failure, nephrolithiasis (calcium stones), nephrogenic diabetes insipidus

52
Q

Thiazide Diuretic Adverse Effects

A
  • hypokalemia, alkalosis, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, sulfonamide hypersensitivity
  • more hyponatremic effects that loop diuretics
  • use with caution in patients with diabetes mellitus
53
Q

Collecting Tubule

A
  • most important site of K+ secretion at the kidney
  • site at which all diuretic-induced changes in K+ balance occur

–more Na+ delivered to collecting tubule leads to more K+ secretion

54
Q

K+ sparing diuretics: mineralocorticoid receptor antagonists uses

A
  • spironolactone and eplerenone
  • hyperaldosteronism, adjunct ot K+-wasting diuretics, antiandrogenic uses (female hirsutism), heart failure (reduces mortality)
  • do not require access to tubular lumen to induce diuresis
55
Q

Adverse effects of Mineralocorticoid receptor antagonists

A

-hyperkalemia, acidosis, and antiandrogenic effects

56
Q

K+ sparing diuretics: Na+ channel (ENaC) inhibitors uses

A
  • amiloride and triamterene
  • adjunct to K+-wasting diuretics and lithium-induced nephrogenic diabetes insipidus (amiloride)
57
Q

ENaC inhibitor adverse effects

A

hyperkalemia and acidosis

58
Q

Mineralocorticoid (aldosterone) receptor

A
  • nuclear hormone receptor responsible for regulating the expression of multiple gene products
  • natural agonists include mineralocorticoids
  • a class of hormones that influence salt and water balance
59
Q

Loop agents and thiazide diuretics

A
  • can be combined if patients fail or become refractory to the usual dose of loop diuretics
  • often produce diuresis when either agent acting alone is minimally effective
  • salt and water reabsorption in either the TAL (loop diuretics) or DCT (thiazides) can increase when the other is blocked; inhibition can produce more than an additive diuretic response
  • Thiazides often produce mild natriuresis in the PCT that is usually masked by increased absorption in the TAL; this combo can therefore block Na_ reabsorption from all 3 segments (PCT, ascending loop, and DCT)
60
Q

Combination of loop agents and thiazide diuretics can cause

A

profuse diuresis and therefore, routine outpatient use is not recommended

61
Q

Potassium-sparing diuretics and loop agents or thiazides

A
  • hypokalemia is a common side effect of loop agents and thiazides, which can be initially managed with dietary NaCL restriction or KCl supplementation
  • when unmanageable in this way, K+-sparing diuretics can lower K+ secretion
  • avoid this combo in patients with renal insufficiency and in those receiving angiotensin antagonists
62
Q

Common use for diuretics is

A
  • for the reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney
  • physiologically, this reduction is sensed as a lack of effective arterial blood volume and leads to salt and water retention, followed by edema formation
63
Q

Edematous states that are treated with diuretics

A
  • Heart failure
  • Kidney disease
  • Hepatic Cirrhosis
64
Q

Heart failure

A
  • reduces CO, which results in a decreased in BP and blood flow to kidney
  • decreases in BP and blood flow is sensed as hypovolemia and leads to renal retention of salt and water
  • pulmonary or interstitial edema occur when the plasma volume increases and the kidney continues to retain salt and water, which then leaks form the vasculature
65
Q

Kidney disease

A
  • most cause retention of salt and water
  • when loss of renal function is severe, there is insufficient glomerular filtration to sustain a natriuretic response and diuretic agents are of little benefit
  • patients with mild cases of renal disease can be effectively treated with diuretics when they retain sodium
  • loop and thiazide diuretics beneficial in individuals that develop hyperkalemia associated with ESRD
66
Q

Diuretics are beneficial in glomerular diseases, such as

A

systemic lupus erythematosus or diabetes mellitus, that exhibit renal retention of salt and water

67
Q

Hepatic cirrhosis

A
  • diuretics are useful when edema and ascites become severe due to liver disease
  • aggressive use of diuretics can be disastrous in patients with liver disease
68
Q

Non edematous states that are treated with diuretics

A
  • Hypertension
  • Nephrolithiasis
  • Hypercalcemia
  • Diabetes insipidus
69
Q

Hypertension

A
  • thiazides are often used because of their diuretic and mild vasodilator activities
  • loop diuretics are often reserved for patients with renal insufficiency or HF
  • diuretics are often used in combo with vasodilators because vasodilators cause significant salt and water retention
70
Q

Nephrolithiasis

A
  • 2/3 of kidney stones contain calcium phosphate or calcium oxalate
  • thiazide diuretics enhance Ca2+ reabsorption in the DCT and reduce urinary Ca2+ concentration, making them appropriate agents in the treatment of kidney stones
71
Q

Hypercalcemia

A
  • loop diuretics reduce and promote Ca2+ diuresis, but can also cause marked volume contraction when used alone
  • saline can be administered simultaneously with loop diuretics to maintain effective Ca2+ diuresis
72
Q

Diabetes insipidus

A
  • can be due to either deficient production of ADH (neurogenic or central DI) or inadequate responsiveness to ADH (nephrogenic DI)
  • supplementary ADH or one of its analogs is only effective in central DI
  • thiazide diuretics can reduce polyuria and polydipsia in both types of DI
73
Q

Renin

A
  • an aspartyl protease that specifically catalyzes the hydrolytic release of angiotensin I from angiotensinogen
  • enters circulation from kidneys where it is synthesized and stored in the juxtaglomerular apparatus of the nephron
  • sympathetic nervous system stimulation causes activation of B1-adrenergic receptors on juxtaglomerular cells, which stimulates the release of renin from these cells
74
Q

Angiotensinogen

A
  • circulating protein substrate (synthesized in the liver) from which renin cleaves angiotensin I
  • amino terminal 10 AAs are cleaved by renin, resulting in the formation of angiotensin I
75
Q

Angiotensinogen production is increased by

A

corticosteroids, estrogens (elevated during pregnancy and in women taking estrogen-containing oral contraceptives), thyroid hormones, an angiotensin II

76
Q

Angiotensin I

A
  • first 10 amino terminal AAs of angiotensinogen
  • little to no biologic activity
  • cleaved to angiotensin II by angiotensin converting enzyme (ACE)
  • when given IV, angiotensin I is converted to angiotensin II so rapidly that the pharmacological responses to these peptides are indistinguishable
77
Q

Angiotensin II

A
  • exerts actions at vascular smooth muscle (contraction), adrenal cortex (stimulation of aldosterone synthesis), kidney (renin secretion inhibition), heart (cardiac hypertrophy and remodeling), and brain (resets the baroreceptor reflex control of HR to a higher pressure) and regulates fluid and electrolyte balance and arterial blood pressure
  • 40x more potent than epinephrine
  • Activates GPCR angiotensin II receptors
78
Q

Rate of Angiotensin II synthesis is determined by

A

the amount of renin released by the kidneys
-removed rapidly from circulation by peptidases referred to as angiotensinase

79
Q

Converting enzyme (ACE or kininase II)

A
  • catalyzes removal of carboxyl terminal AAs form substrate peptides
  • most important substrates are angiotensin I and bradykinin (vasodilator which is inactivated by converting enzyme)
  • located on luminal surface of vascular endothelial cells in most tissues
80
Q

Angiotensin II receptors

A
  • ang II binds to 2 subtypes of GPCRs (AT1 and AT2)
  • AT1 is the major one in adults
81
Q

AT1 receptors

A
  • Gq GPCR
  • activation of PLC, production of IP3 and DAG, and smooth muscle contraction
82
Q

Consequences of AT2 receptor activation

A

-bradykinin and nitric oxide (NO) production, which results in vasodilation

83
Q

Aldosterone

A
  • promotes reabsorption of Na+ fro the distal part of the DCT and from the cortical collecting renal tubules
  • increases activity of both the epithelial sodium channel ENaC and the basolateral Na+/K+-ATPase, leading to an increase in Na+ reabsorption and K+ secretion (which causes retention of water, an increase in blood volume, an increase in BP, and hypokalemia)
84
Q

ACE Inhibitors include

A
  • benazepril
  • captopril
  • enalapril
  • enalaprilat
  • fosinopril
  • lisinopril
  • moexipril
  • perindopril
  • quinapril
  • ramipril
  • trandolapril
85
Q

Angiotensin Receptor Blockers (ARPs) include

A
  • azilsartan
  • candesartan
  • eprosartan
  • irbesartan
  • losartan
  • olmesartan
  • telmisartan
  • valsartan
86
Q

Drugs that block renin secretion include

A
  • clonidine
  • propranolol
87
Q

Renin inhibitors include

A

aliskiren

88
Q

Angiotensin II effects

A
  • Na+ and H2O retention
  • release of corticotropin and adiuretin, thirst
  • increased aldosterone production
  • vasoconstriction; increased blood pressure
89
Q

Major Effects of Angiotensin II

A
  • altered peripheral resistance
  • altered renal function
  • alterated cardiovascular structure
90
Q

Ang II Altered Peripheral resistance

A
  • direct vasoconstriction
  • enhancement of peripheral noradrenergic neurotransmission: increased NE release; decreased NE repute; increased vascular responsiveness
  • increased sympathetic discharge
  • release of catecholamines form adrenal medulla
  • result is rapid pressor response
91
Q

Ang II altered renal function

A
  • direct effect to increase Na+ reabsorption in proximal tubule
  • release of aldosterone from adrenal cortex (increased Na+ reabsorption and K+ excretion in distal nephron)
  • direct renal vasoconstriction
  • enhanced noradrenergic neurotransmission in kidney
  • increased renal sympathetic tone
  • result is slow pressor response
92
Q

ACE Inhibitor MOA

A
  • prototypes are captopril and enalapril
  • inhibit the conversion of angiotensin I to the more active angiotensin II; also prevent degradation of bradykinin and the vasodilator peptides (bogo!)
93
Q

ACE Inhibitors used for

A

-hypertension, heart failure, left ventricular dysfunction, prophylaxis of future cardiovascular events (e.g., MI, CAD, stroke) and nephropathy (+/- diabetes)

94
Q

Benefits of ACE inhibitors in hypertension

A
  • lowers TPR and mean, diastolic, and systolic BP
  • cardiac function in patients with uncomplicated hypertension is little changed–stroke volume and cardiac output may increase slightly with sustained treatment
  • baroreceptor function and cardiovascular reflexes are not compromised–responses to postural changes and exercise are little impaired
  • evidence that ACEIs are superior in treating HTN in patients with diabetes–improve endothelial function and reduce CV events more so than CCBs or diuretic and B-blocker combo
95
Q

Adverse Effects of ACE inhibitors

A
  • hypotension
  • cough
  • angiodema
  • hyperkalemia–avoid K+-sparing diuretics
  • acute renal failure–particularly in patients with renal artery stenosis
  • fetopathic potential (teratogen)–contraindicated in pregnancy
96
Q

ACE Inhibitor drug interactions

A

-antacids, capsaicin, NSAIDs, K+-sparing diuretics, digoxin, lithium, allopurinol

97
Q

Renal Considerations with ACEIs

A
  • prevent/delay the progression of renal disease in type I diabetics and in patients with non diabetic nephropathies (results mixed in type 2 diabetics)
  • ACEIs vasodilate efferent arterioles>afferent arterioles -reduces back pressure on the glomerulus and reduces protein excretion
  • ACEIs usually improve renal blood flow and Na+ excretion in CHF
  • in rare cases, can cause a rapid decrease in GFR, leading to acute renal failure
98
Q

Risk Factors for ACEI-Induced acute renal failure

A
  • MAP insufficient for adequate renal perfusion–poor CO; low systemic vascular resistance -volume depletion (diuretic use)
  • renal vascular disease: bilateral renal artery stenosis; stenosis of dominant or single kidney; AA narrowing (HTN, cyclosporin A); diffuse atherosclerosis in smaller renal vessels
  • vasoconstrictor agents (NSAIDs, cyclosporine)
  • all cause renal hypo perfusion
99
Q

Angiotensin II receptors

A

Angiotensin II receptors

  • GPCRs
  • AT1 and AT2
100
Q

AT1 receptors

A

major subtype of ang II receptors in adults

-Gq–>PLC–>IP3 + DAG–>SM contraction

101
Q

AT2 receptors

A
  • activation causes production of NO and bradykinin
  • smooth muscle dilation
102
Q

Angiotensin II Receptor Blockers (ARBs) MOA

A
  • prototypes are losartan and valsartan
  • selectively block AT1 receptors, which leads to decreased contraction of vascular SM, decreased aldosterone secretion, decreased pressor responses, decreased cardiac cellular hypertrophy and hyperplasia
  • no effect on bradykinin metabolism
103
Q

ARBs uses

A

-hypertension, diabetic nephropathy, HF, HF or left ventricular dysfunction after AMI, and prophylaxis of cardiovascular events

104
Q

ARB adverse effects

A

-similar to ACEIs but less cough and edema; contraindicated during pregnancy

105
Q

ACE inhibitors vs. ARBs

A
  • ARBs reduce activation of AT1 receptors more effectively than do ACE inhibitors
  • ARBs permit activation of AT2 receptors
  • ACEIs increase the levels of a number of ACE substrates, including bradykinin
  • unknown whether or not these pharmacologic differences result in significant differences in therapeutic outcomes
106
Q

Aliskiren

A
  • direct renin inhibitor
  • inhibits renin and blocks the conversion of angiotensinogen to angiotensin I
  • does not increase bradykinin
  • rise in plasma renin levels but decreased plasma renin activity
  • contraindicated in pregnancy
  • adverse effects similar to ACEIs and ARBs

Renal 2 Final (5 decks)

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