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851 diuretics 1
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Flashcards in this deck (214)

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  • Name the major structures shown in a sagittal view of the kidney.

    • Renal vein
    • Renal cortex
    • Renal papilla
    • Renal pyramids
    • Renal columns
    • Fibrous capsule
    • Renal pelvis
    • Ureter

    sagittal kidney view

  • What are the primary learning goals regarding diuretic classes in this review?

    • Differentiate among major diuretic classes by site, mechanism, and relative potency

  • What clinical decisions should be identified for each diuretic class?

    • Clinical indications and contraindications for perioperative and chronic management

  • What adverse effects must be evaluated for each diuretic class?

    • Common and clinically significant side effects, including implications for anesthesia practice

  • What should an anesthesia plan incorporate for patients taking diuretics?

    • Fluid and electrolyte management, drug interactions, and physiologic response

  • How many times per day does the kidney filter the extracellular fluid volume (ECV) across the renal glomeruli?

    ~ 12 times/day

  • What are the primary regulatory functions of nephrons?

    • Regulate bodily fluid and electrolytes
    • Via secretion and reabsorption

  • What are the main anatomical segments of a nephron?

    • Glomerular capsule
    • Proximal convoluted tubule
    • Loop of the nephron (loop of Henle)
    • Distal convoluted tubule
    • Collecting duct

  • Which blood vessels are directly associated with the nephron's blood supply?

    • Afferent arteriole
    • Peritubular capillary network
    • Interlobular artery
    • Interlobular vein

  • Describe the path urine takes from the nephron to the ureter.

    • Urine flows from collecting duct
    • into minor calyx → major calyx → renal pelvis → ureter

  • Name the major renal vessels and structural parts shown in the kidney diagram.

    • Renal artery
    • Segmental artery
    • Interlobar artery and vein
    • Arcuate artery and vein
    • Cortical radiate artery
    • Renal vein
    • Renal pyramid
    • Renal column

  • What structure surrounds the glomerulus in the nephron?

    • Glomerular capsule

  • What is the primary pharmacologic effect of diuretics?

    Increase the rate of sodium excretion and urine volume

  • By what general mechanism do most diuretics act within the nephron?

    Most work by increasing Na+ reabsorption at varying sites within the nephron

  • What are common clinical indications for diuretic use?

    • Fluid retention/overload
    • Hypertension
    • CHF

  • Which diuretic classes act at these nephron sites: proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct?

    • Carbonic anhydrase inhibitors: proximal convoluted tubule
    • Loop diuretics: loop of Henle
    • Thiazide diuretics: distal convoluted tubule
    • Potassium-sparing diuretics: collecting duct

  • Which diuretic classes and related agents are depicted in the nephron diagram?

    • Carbonic anhydrase inhibitors
    • Loop diuretics
    • Thiazide diuretics
    • Potassium-sparing diuretics
    • Osmotic diuretics
    • Arginine vasopressin

  • Which hormone is shown in the diagram as relevant to renal water handling?

    • Arginine vasopressin

    Answer illustration: Nephron diagram showing diuretic sites and arginine vasopressin

  • Which nephron segment is highlighted as the site of carbonic anhydrase action?

    • Proximal convoluted tubule

    Nephron PCT and carbonic anhydrase

  • Which nephron segment is highlighted for the action of osmotic diuretics?

    • Loop of Henle

    Loop of Henle and osmotic diuretics

  • What general nephron features does the diagram indicate relevant to diuretic pharmacology?

    • Ion transport mechanisms and sites of action for various diuretic classes

  • Where in the nephron is carbonic anhydrase activity primarily described in the text?

    • Proximal convoluted tubule
    • Collecting ducts

  • What is the role of the Na+/H+ exchanger in the renal tubule as described?

    Reabsorbs Na+ and secretes H+ into the renal tubule, contributing to urine acidification.

  • Write the sequence of reactions involving bicarbonate and carbonic acid described in the text.

    \(H^+ + HCO_3^- \rightleftharpoons H_2CO_3 \rightleftharpoons H_2O + CO_2\)

  • According to the text, which molecule crosses the tubular cell membrane during bicarbonate handling?

    Carbon dioxide (CO2) crosses the tubular cell membrane.

  • What happens to carbonic acid within tubular cells and how are the products handled?

    Carbonic acid is converted to H2O + CO2; intracellularly H+ is used by the Na+/H+ exchanger and HCO_3^- is released into the circulation.

  • What is the amount of acetazolamide per vial for injection labelled in the material?

    • 500 mg

  • To which drug class does acetazolamide belong?

    • Sulfonamide class

  • What is the mechanism of enzyme inhibition of acetazolamide?

    • Non-competitive inhibition of carbonic anhydrase

  • Which nephron segment is primarily affected by acetazolamide's diuretic action?

    • Proximal renal tubule

  • What reabsorptions are decreased by acetazolamide in the kidney?

    • Sodium (Na)\n- Bicarbonate (HCO3)\n- Water (H2O)

  • Show the vial image of acetazolamide for intravenous use.

    • Vial of Acetazolamide Sodium for Injection, USP.\n- Label: Acetazolamide for injection, for intravenous use.

  • Where in the nephron does acetazolamide primarily act?

    • Proximal convoluted tubule

  • What is the mechanism of action of acetazolamide and its immediate effects on ion transport in the proximal tubule?

    • Inhibits carbonic anhydrase (CA) → decreases HCO3- reabsorption, reduces H+ secretion, and reduces Na+ reabsorption

    Diagram illustrating acetazolamide effects

  • What are the primary clinical applications of acetazolamide (diamox)?

    • Increased IOP/Glaucoma
    • Idiopathic intracranial hypertension (formerly pseudotumor cerebri)
    • Altitude sickness
    • Edematous states
    • HTN states
    • Metabolic alkalosis

    background image

  • Which enzyme is present in the ciliary process of the eye involved in aqueous humor production?

    • Carbonic anhydrase

  • What is the effect of inhibiting carbonic anhydrase in the ciliary process on aqueous humor and intraocular pressure (IOP)?

    • Decreased aqueous humor production → Decreased IOP

  • What major structural damage can result from buildup of aqueous humor fluid in glaucoma?

    • Damage to the optic nerve

    Diagrams comparing a normal eye with an eye affected by glaucoma.

  • What is 'Pseudotumor cerebri' (Idiopathic Intracranial Hypertension)?

    • A condition with elevated CSF pressure and normal brain imaging

  • What does the mnemonic 'HEAD PRESS' summarize for Idiopathic Intracranial Hypertension?

    • Headache (daily, throbbing)
    • Elevated ICP (with normal brain imaging)
    • Absence of focal neurological signs (except CN VI palsy)
    • Diplopia (CN VI palsy)
    • Papilledema (bilateral)
    • Risk: obese women of childbearing age
    • Empty sella may be seen on MRI
    • Swooshing sound (pulsatile tinnitus)
    • Sight loss (transient or permanent)

  • What key diagnostic combination defines Idiopathic Intracranial Hypertension?

    • Normal brain imaging with elevated CSF pressure

  • What are the main treatments for Idiopathic Intracranial Hypertension?

    • Acetazolamide
    • Weight loss
    • Shunt if severe

    Pseudotumor cerebri slide

  • What is 'acute high-altitude illness' (AHAI) or 'acute mountain sickness' (AMS)?

    • Illness occurring at high altitudes due to insufficient acclimation leading to hypoxia-related symptoms

  • What is the primary initial physiological response to hypoxia at high altitude?

    • Hyperventilation

  • Describe the ventilatory chemical sequence that can follow hypoxia at high altitude.

    • Hypoxia → hyperventilation → respiratory alkalosis → ventilatory depression

  • How can metabolic acidosis affect ventilation in high-altitude illness?

    • Metabolic acidosis can reverse hypoventilation

  • What drug is described as the cornerstone of therapy for acute high-altitude illness?

    • Acetazolamide

  • What is Acute Mountain Sickness (AMS) primarily associated with?

    Exposure to high altitude leading to physiological symptoms from hypobaric hypoxia

  • What cognitive or neuroimaging changes occur above 7000 m?

    • MRI changes, including white matter hyperintensities
    • Cortical atrophy

  • At what altitude do about 32% of climbers experience hallucinations?

    Above 7500 m

  • Name some detectable psychomotor or cognitive impairments at high altitude (examples from the diagram).

    • Psychomotor impairment detectable with FTT/pegboard
    • Slowed complex reaction time
    • Impaired learning and spatial memory
    • Impaired memory retrieval

  • What altitude equivalent are commercial aircraft typically pressurised to?

    An altitude equivalent of 1500–2500 m

  • What is the pharmacokinetic property of carbonic anhydrase (CA) inhibitors regarding excretion?

    • CA inhibitors are given orally and are excreted unchanged

  • How should dosing of CA inhibitors be adjusted for elderly patients and those with chronic renal impairment (CRI)?

    • Reduce dose in elderly and in patients with CRI

  • Should CA inhibitors be used in patients with severe chronic renal impairment (CRI)?

    • Avoid CA inhibitors in patients with severe CRI

  • What is the primary pharmacodynamic effect of CA inhibitors on bicarbonate and urine pH?

    • Increase excretion of HCO3- leading to alkaline urine and metabolic acidosis

  • What type of metabolic acidosis do CA inhibitors cause and what ion change accompanies it?

    • Cause hyperchloremic metabolic acidosis with increased Cl- reabsorption in the loop of Henle

  • What are the effects of CA inhibitors on natriuresis and potassium balance?

    • Produce modest natriuresis (up to 5% Na+ excretion) and increase distal Na+ delivery causing K+ loss

  • Is long-term administration of CA inhibitors considered a problem according to the notes?

    • Long-term administration is noted as 'no problem with long-term admin'

  • What are common side effects of carbonic anhydrase inhibitors?

    • Fatigue
    • Decreased appetite
    • Paresthesias
    • Depression

    sad emoticon

  • Which diuretic class is shown?

    Loop diuretics

  • Where do loop diuretics act in the nephron?

    • Medullary portion of the thick ascending limb of the Loop of Henle

  • Which transport protein is inhibited by loop diuretics?

    • Na-K-2Cl transport protein

  • Which ions' reabsorption is inhibited by loop diuretics?

    • Na+, K+, and Cl-

  • What proportion of filtered sodium is reabsorbed in the thick ascending limb?

    • 20–30% of filtered Na+

  • Is the thick ascending limb of the Loop of Henle permeable to water?

    • No — it is impermeable to H2O

  • What are two main physiological effects of diuresis from loop diuretics?

    • Reduced intravascular volume
    • Peripheral vasodilation

    Three vials of Furosemide Injection, USP

  • What is the relative potency of loop diuretics among diuretic classes?

    • Loop diuretics are the most potent class of diuretics

  • How does response to loop diuretics change with dose?

    • They have a dose-dependent response

  • What is the first-line indication for loop diuretics related to fluid overload?

    • First-line therapy for heart failure-related fluid overload

  • Are loop diuretics first-line for treating hypertension in patients with normal kidney function?

    • No; they are not first-line for hypertension with normal kidney function

  • Which transporter in the thick ascending limb is inhibited by loop diuretics?

    • Na+/K+/2Cl cotransporter (NKCC2)

    Diagram showing the mechanism of loop diuretics in the nephron

  • What fraction of filtered sodium is normally reabsorbed in the loop of Henle?

    • 25% of filtered Na

  • How do loop diuretics affect divalent cation reabsorption (Ca2+, Mg2+)?

    • Increase Ca2+ and Mg2+ loss

  • What acid-base and potassium disturbance is associated with loop diuretics?

    • Hypokalemic metabolic alkalosis

  • Why do loop diuretics cause increased K+ loss in the collecting duct?

    • Enhanced distal Na delivery results in K+ loss in the collecting duct

  • What class of diuretic is furosemide?

    • Loop diuretic

  • How does furosemide affect cerebrospinal fluid (CSF) and intracranial pressure (ICP)?

    • Reduces CSF production and ICP

  • Can alterations in the blood-brain barrier (BBB) change furosemide's effect on ICP?

    • No; BBB alterations do not affect furosemide's effects on ICP

  • In what ways can furosemide be administered for ICP reduction?

    • Single dose or in combination with mannitol

  • What are furosemide's oral absorption and protein binding characteristics?

    • Oral absorption ~50%
    • Protein binding 90% (albumin)

  • What is the elimination half-life and typical dose range of furosemide?

    • Elimination half-life 1–2 hours (short duration)
    • Dose 20–200 mg

  • What is the onset time of intravenous furosemide?

    • Onset: 5–10 minutes

  • What is the peak effect time of furosemide?

    • Peak: 30 minutes

  • What is the duration of action (DOA) of furosemide?

    • DOA: 2–6 hours

  • What is the elimination half-life of furosemide?

    • Elimination half-life: 1–2 hours

  • How is furosemide excreted?

    • Excretion:
    • 50–60% via glomerular filtration and tubular secretion
    • 40–50% conjugated to glucuronide

  • What is the usual IV dose of furosemide in normal renal function and the typical range for renal insufficiency?

    • Normal renal function: 20 mg
    • Renal insufficiency: increased dose required, typically 160–200 mg

  • Is there benefit to giving more than 200 mg of furosemide IV?

    • > 200 mg: no additional benefit

  • What ototoxic adverse effect can occur if furosemide is administered too quickly?

    • Adverse effect: tinnitus if given too fast

  • Relative potency: how potent is bumetanide compared with furosemide?

    • ~40× potency compared with furosemide

  • Key pharmacokinetics and usual dose for bumetanide (Bumex)?

    • Bioavailability: 80–90% (PO)
    • Routes: PO, IV, IM
    • Metabolism: Mostly liver
    • Dose: 0.5–2 mg

  • Core properties and starting dose for torsemide (Demadex)?

    • Potency: ~3× furosemide
    • Metabolism: Mostly liver
    • Duration: Longer DOA; ½-life 3–4 hours (once-daily dosing)
    • Dose (start): 10–20 mg

    Torsemide box and blister pack

  • What is a key chemical characteristic of ethacrynic acid (Edecrin)?

    • Non-sulfonamide

    Boxes of Ethacrynic Acid Tablets, USP 25 mg

  • How does the potency of ethacrynic acid compare to furosemide?

    • 70% potency of furosemide

  • What is the usual dose range for ethacrynic acid?

    • 25-100 mg

  • What are the notable adverse effects of ethacrynic acid?

    • Notable risk for ototoxicity
    • Nausea

  • What are the main fluid/electrolyte and metabolic side effects of loop diuretics?

    • Hypokalemia
    • Hypovolemia
    • Hyponatremia
    • Hypomagnesemia
    • Hyperglycemia

  • What is the 'braking phenomenon' with loop diuretics and what causes acute versus chronic tolerance?

    • Braking phenomenon: acute or chronic tolerance to diuretic effects
    • Acute cause: activation of the RAS
    • Chronic cause: hypertrophy of the renal tubule

  • What ototoxicity risks are associated with loop diuretics?

    • Ototoxicity occurs with all loop diuretics
    • Can be transient or permanent
    • Ethacrynic acid is noted in association with ototoxicity

  • Do loop diuretics have cross reactivity concerns with sulfa allergy?

    • Yes — cross reactivity in patients with sulfa allergy

  • How do loop diuretics interact with nondepolarizing neuromuscular blocking agents (NMBAs)?

    • Loop diuretics potentiate nondepolarizing NMBAs

  • What is the primary mechanism of action of thiazide diuretics?

    • Inhibit the Na-Cl cotransporter in the renal tubule

  • At which nephron segment do thiazide diuretics act?

    • Early distal convoluted tubule

  • Which major electrolyte changes do thiazide diuretics cause in urine and blood?

    • Increase urinary excretion: Na+, Cl-, K+
    • Increase renal reabsorption: Ca++

  • What are the early and sustained physiological effects of thiazide diuretics?

    • Early: decrease ECF volume and cardiac output
    • Sustained: vasodilatation developing over weeks

  • What is the primary antihypertensive indication for thiazide diuretics?

    • Essential hypertension

  • How are thiazide diuretics commonly used in relation to other antihypertensives?

    • Often given with other antihypertensives

  • Name two cardiovascular or fluid-overload conditions treated with thiazide diuretics.

    • Edema
    • Congestive heart failure (CHF)

  • Which renal concentrating disorder is treated with thiazide diuretics?

    • Diabetes insipidus (DI)

  • What is the effect of thiazide diuretics on urinary calcium and which two conditions does this support treating?

    • Reduce urinary Ca++ excretion
    • Used for hypocalcemia
    • Used for osteoporosis

  • Which thiazide diuretic is the 2nd most commonly prescribed antihypertensive?

    • Hydrochlorothiazide (HCTZ)

  • Name other common thiazide or thiazide‑like diuretics and their typical oral dose ranges.

    • Hydrochlorothiazide (HCTZ): 12.5–50 mg
    • Chlorthalidone: 12.5–50 mg
    • Indapamide: 1.25–5 mg
    • Metolazone: 1.25–5 mg

  • How are thiazide diuretics absorbed when given orally?

    • Readily absorbed

  • What is the plasma protein binding characteristic of thiazide diuretics?

    • Highly protein bound

  • How are most thiazide diuretics eliminated and which one is metabolized by the liver?

    • Most eliminated unchanged
    • Indapamide is metabolized by the liver

  • What are the typical half-lives of thiazide diuretics and of chlorthalidone?

    • Thiazides: 8–12 hours
    • Chlorthalidone: 50–60 hours

  • What acid-base disturbance is commonly caused by thiazide diuretics?

    • Hypokalemic, hypochloremic metabolic alkalosis

  • Which two electrolytes are decreased by thiazide diuretics?

    • Potassium (hypokalemia)
    • Magnesium (hypomagnesemia)

  • Which electrolytes or metabolic parameters can be increased by thiazide diuretics?

    • Calcium (hypercalcemia)
    • Uric acid (hyperuricemia)

  • How can thiazides affect blood glucose in diabetics and why might this be worse with beta blockers?

    • Can cause hyperglycemia in diabetics, possibly from decreased insulin release; effect may be greater in patients taking beta blockers

  • Name two cardiovascular-related adverse effects or interactions of thiazide diuretics.

    • Dysrhythmias
    • Can potentiate nondepolarizing neuromuscular blockers (NMBAs)

  • Which common drug class can decrease the effectiveness of thiazide diuretics?

    • NSAIDs

  • What toxicity risk is increased by concomitant thiazide use?

    • Potential for lithium toxicity

  • What allergy cross-reactivity concern exists with thiazide diuretics?

    • Cross reactivity in patients with sulfa allergy

  • Name two non-electrolyte adverse effects of thiazide diuretics mentioned.

    • Hyperlipidemia
    • Sexual dysfunction

  • What nephron segment is the main site of action for thiazide diuretics?

    The distal convoluted tubule (DCT)

  • Which transporter is primarily inhibited by thiazide diuretics in the DCT?

    • Na+/Cl− cotransporter (NCC)

  • Approximately what percentage of filtered Na+ is normally reabsorbed in the distal convoluted tubule?

    About 10% of filtered Na+ is reabsorbed in the DCT

  • List the main systemic effects of thiazide diuretics noted in the diagram.

    • Loss of Na & Water
    • Hypokalemic metabolic alkalosis
    • Increased Ca²+ reabsorption

  • Why do thiazides cause increased K+ loss in the collecting duct?

    Enhanced distal Na+ delivery increases Na+ reabsorption in the collecting duct, causing K+ loss

  • How do thiazides increase Ca²+ reabsorption in the DCT?

    • Lower intracellular Na+ facilitates Ca²+ reabsorption via apical TRPV5 and basolateral Na+/Ca²+ exchange

  • Refer to the diagram illustrating thiazide mechanism in the DCT (image). What is shown affecting Na+/Cl− transport?

    Diagram illustrating the mechanism of thiazide diuretics in the distal convoluted tubule - Thiazide inhibition of the Na+/Cl− cotransporter (NCC)

  • For a patient taking HCTZ who is having surgery, what immediate action is advised regarding the medication?

    • Hold the dose

  • What patient status should be assessed preoperatively for someone on HCTZ?

    • Intravascular fluid volume status

  • What volume state is noted for the patient taking HCTZ in this note?

    • Volume contracted

  • Where do potassium-sparing diuretics act in the nephron?

    • Late distal tubule (Late DT)
    • Collecting ducts

  • What are the two classes of potassium-sparing diuretics?

    • Pteridine analogues
    • Aldosterone receptor blockers

  • What is the primary electrolyte effect of potassium-sparing diuretics?

    They decrease Na+ absorption without increased K+ secretion, sparing potassium.

  • How are potassium-sparing diuretics used clinically for hypertension?

    They are not used as single treatment for hypertension; used in combination with loop or thiazide diuretics.

  • Give an example of an aldosterone receptor blocker.

    • Spironolactone (Aldactone)

    Box of Spironolactone Aldactone 25 mg Film-Coated Tablets

  • What is the primary therapeutic class name for drugs that conserve potassium?

    • K+ sparing diuretics

  • What is the main mechanism of action of K+ sparing diuretics listed?

    • Block renal epithelial Na+ channels

  • Name two examples of K+ sparing diuretics with their listed doses.

    • Amiloride 5–10 mg
    • Triamterene 50–150 mg

  • Are the listed K+ sparing diuretics dependent on aldosterone to work?

    • Independent of Aldosterone

  • Which listed K+ sparing diuretic is more potent?

    • Amiloride > Triamterene

  • What is the mechanism/class of inhibitors of renal epithelial Na+ channels?

    • K+-sparing diuretics
    • Mechanism: Inhibition of renal epithelial Na+ channels

  • Which of the two drugs has higher relative potency: amiloride or triamterene?

    • Amiloride: relative potency 1
    • Triamterene: relative potency 0.1

  • Compare oral bioavailability, half-life, and route of elimination for amiloride versus triamterene.

    • Amiloride: oral bioavailability 15%–25%, t<sub>1/2</sub> ~21 h, route renal excretion (R)
    • Triamterene: oral bioavailability ~50%, t<sub>1/2</sub> ~4 h, route metabolism to active metabolite, urinary excretion (M)

    Table: Inhibitors of Renal Epithelial Na+ Channels

  • What class of potassium-sparing diuretics blocks aldosterone receptors?

    Aldosterone receptor blockers (potassium-sparing diuretics).

  • Name two aldosterone receptor blocker drugs and their dose ranges.

    • Spironolactone: 12.5–100 mg
    • Eplerenone: 25–50 mg

  • What is the primary mechanism of action of aldosterone receptor blocker diuretics?

    They prevent synthesis and activation of the aldosterone-dependent Na-K-ATPase pump.

  • What are two classes of K-sparing diuretics listed?

    • Pteridine analogues
    • Aldosterone antagonists

  • What is the primary electrolyte adverse effect of K-sparing diuretics?

    • Hyperkalemia

  • Name three other side effects mentioned for K-sparing diuretics.

    • Metabolic acidosis
    • GI disturbances
    • Nephrolithiasis

  • Which medications increase risk of adverse effects when given with K-sparing diuretics?

    • ACE inhibitors
    • NSAIDs

  • Which additional adverse effects are listed when K-sparing diuretics are given with ACE inhibitors or NSAIDs?

    • Metabolic acidosis
    • GI disturbances
    • Libido changes (impotence)
    • Gynecomastia

  • What is an osmotic diuretic?

    An inert substance that is filtered freely at the glomerulus and promotes diuresis.

  • How are osmotic diuretics handled at the glomerulus?

    They are filtered freely at the glomerulus.

  • What are the primary sites of action for osmotic diuretics in the nephron?

    • Loop of Henle
    • Proximal tubules

  • Do osmotic diuretics cause greater excretion of water or electrolytes?

    Water excreted > electrolytes

  • What does it mean that an osmotic diuretic is described as inert?

    It does not undergo metabolism.

  • Give a common example of an osmotic diuretic.

    • Mannitol

    Bottle of MANNITOL INJECTION USP 25%

  • What are the primary clinical uses of osmotic diuretics?

    • Increased intracranial pressure in TBI
    • Reducing cerebral edema & brain mass in neurosurgery
    • Glaucoma

  • How do osmotic diuretics affect renal tubular fluid?

    • Increase renal tubular fluid osmolality

  • How does plasma osmolality contribute to the action of osmotic diuretics?

    • Increased plasma osmolality draws fluid from the extracellular space (ECF) into the intravascular compartment

  • Name two additional pharmacologic effects of osmotic diuretics.

    • Osmotic diuresis
    • Scavenging of O2 free radicals

  • What is the only osmotic diuretic currently in clinical use?

    • Mannitol

  • Name other compounds that are osmotic agents mentioned alongside mannitol.

    • Urea
    • Isosorbide
    • Glycerin

  • What is the chemical classification of mannitol?

    • Six-carbon sugar alcohol

  • How is mannitol metabolized in the body?

    • It undergoes no metabolism

  • Why must mannitol be given intravenously to achieve a diuretic effect?

    • It is not absorbed in the GIT; IV administration is required for diuresis

  • By what route is mannitol cleared from the body?

    • Clearance occurs only by glomerular filtration

  • What are the key pharmacokinetic timing parameters of mannitol (onset, peak, duration)?

    • Onset: 10–15 min
    • Peak: 40–45 min
    • Duration of action: 6 hours

  • What is a main pharmacodynamic electrolyte risk of mannitol related to its diuretic effect?

    • Potential hypernatremia from water diuresis

  • What pulmonary risk does IV mannitol pose in patients with reduced ejection fraction (EF)?

    • Pulmonary edema (due to initial IV volume expansion)

  • What volume-related effect can prolonged mannitol use cause?

    • Hypovolemia

  • Which acid–base and electrolyte disturbance can mannitol cause?

    • Hypokalemic, hypochloremic alkalosis

  • What plasma change can occur with mannitol related to solute concentration?

    • Plasma hyperosmolarity

  • What is the mechanism given for mannitol-induced plasma hyperosmolarity?

    • Excessive Na+ and water excretion

  • What risk does mannitol carry if the blood–brain barrier (BBB) is disrupted?

    • Rebound intracranial hypertension

  • How can mannitol affect cerebral edema in the context of a disrupted BBB?

    • It can worsen cerebral edema

  • What are the main acute fractional excretion changes caused by inhibitors of carbonic anhydrase in the proximal tubule?

    • Na+: ++
    • K+: +
    • HCO3-: +

  • What are the main acute fractional excretion changes caused by osmotic diuretics (loop of Henle)?

    • Na+: +
    • K+: ++
    • Mg2+: +
    • Cl-: +
    • HCO3-: +
    • H2PO4-: +

  • What are the main acute fractional excretion changes caused by inhibitors of the Na+-K+-2Cl- symport (thick ascending limb)?

    • Na+: ++
    • Ca2+: ++
    • Mg2+: +
    • Cl-: ++
    • HCO3-: +
    • H2PO4-: +

  • What are the main acute fractional excretion changes caused by inhibitors of the Na+-Cl- symport (distal convoluted tubule)?

    • Na+: +
    • K+: +
    • Ca2+: +
    • Mg2+: +
    • Cl-: +
    • HCO3-: +
    • H2PO4-: +

  • What are the main acute fractional excretion changes caused by inhibitors of renal epithelial Na+ channels (late distal tubule, collecting duct)?

    • Na+: +
    • K+: -
    • Other anions/cations: NC

  • How do antagonists of mineralocorticoid receptors (late distal tubule, collecting duct) affect Na+ and K+ fractional excretion acutely?

    • Na+: +
    • K+: -

  • What does the table note say about the context for the listed diuretic effects?

    • Effects (except uric acid) are for acute diuretic use in the absence of significant volume depletion, which would trigger complex adjustments.

  • Which nephron segment is the main site of action for loop diuretics?

    Medullary thick ascending loop of Henle

  • Where do thiazide diuretics mainly act in the nephron?

    Cortical ascending loop of Henle

  • What is the main nephron site of action for carbonic anhydrase inhibitors?

    Proximal convoluted tubule

  • Which diuretic class primarily acts on the collecting duct via the epithelial Na+ channel?

    Potassium-sparing diuretics

  • What is a key clinical use of loop diuretics listed in the table?

    First-line diuretics in renal impairment

  • What is a primary clinical use of thiazide diuretics listed in the table?

    First-line therapy of hypertension

  • Name the notable electrolyte-related side effect common to loop and thiazide diuretics.

    Hypokalemia

  • What notable side effect is associated with carbonic anhydrase inhibitors?

    Metabolic acidosis

  • Which diuretics are noted to cause hyperkalemia in the table?

    Aldosterone blockers and potassium-sparing diuretics

  • Provide a visual summary of diuretic classes, sites, uses, and side effects.

    • See table image summarizing classes, sites, clinical uses, and notable side effects:

    Table showing diuretics and their sites of action, clinical uses, and notable side effects.

  • Which nephron segment is the primary site of action for loop diuretics?

    Thick ascending limb (Loop of Henle)

  • Which nephron segment is associated with K+‑sparing diuretics?

    Collecting duct (principal cells)

  • Which solute is shown as being handled in the proximal convoluted tubule (PCT) on the diagram?

    NaHCO3 (sodium bicarbonate)

  • Which ions are labeled as transported in the distal convoluted tubule (DCT) on the diagram?

    Na+ and Cl-

  • What effect does ADH have on the collecting duct as shown in the diagram?

    Increases water (H2O) reabsorption

    Diagram of a nephron showing filtration and transport in different segments.

  • Name the main nephron parts illustrated in the diagram.

    • Afferent Arteriole
    • Bowman's Capsule
    • Proximal Convoluted Tubule (PCT)
    • Loop of Henle
    • Distal Convoluted Tubule (DCT)
    • Collecting Duct

    nephron diagram

  • Which enzyme is targeted by acetazolamide as shown in the diagram?

    • Carbonic Anhydrase II

  • Which transporter is targeted by thiazide diuretics according to the diagram?

    • Na-Cl cotransporter

  • Which drugs are listed in the diagram as associated with the epithelial Na+ cotransporter?

    • Spironolactone
    • Eplerenone
    • Amiloride
    • Triamterene

  • Which diuretic class is explicitly named 'Osmotic Diuretics' in the diagram?

    • Osmotic Diuretics

  • What is the recommended perioperative action for chronic diuretics on the day of surgery (DOS)?

    • Hold diuretics on the day of surgery (DOS).

    stethoscope image

  • What preoperative assessments should be considered for patients on diuretics?

    • Review recent lab work, acid-base status, and volume status.

  • Which diuretics may be given during neurosurgical cases?

    • Mannitol
    • Lasix (furosemide)

  • Which diuretic is often used in ophthalmology (eye) cases?

    • Acetazolamide

  • Which diuretic may be used if negative pressure pulmonary edema (NPPE) needs treatment?

    • Lasix (furosemide)
Appunti di studio

Overview

  • Diuretics increase urinary sodium excretion and urine volume by inhibiting specific transporters along the nephron.
  • Major clinical uses: fluid overload, hypertension, heart failure, edema, and specific indications (e.g., glaucoma, altitude sickness, raised intracranial pressure).

Kidney & Nephron (quick reference)

Kidney sagittal view Alt: Sagittal kidney view with major structures.

  • The nephron segments and major transporters determine where each diuretic acts.

Nephron sites of diuretic action Alt: Nephron diagram showing diuretic class action sites.

Classification & Key actions (concise table)

Class Main site Primary effect Clinical highlight
Carbonic anhydrase inhibitors Proximal tubule ↑HCO3- excretion, mild natriuresis Altitude sickness, glaucoma, IIH
Loop diuretics Thick ascending limb (TAL) Potent Na+ loss; inhibit NKCC2 Most potent; acute pulmonary edema
Thiazides Early distal convoluted tubule (DCT) ↓NaCl reabsorption; ↑Ca2+ reabsorption First-line HTN therapy
K+-sparing (ENaC blockers / aldosterone antagonists) Late DCT / collecting duct Reduce Na+ reabsorption without K+ loss Use with loops/thiazides to spare K+
Osmotic diuretics PCT & loop Water diuresis > electrolyte loss Mannitol for increased ICP/brain edema

Carbonic Anhydrase Inhibitors (e.g., Acetazolamide)

  • Mechanism: Noncompetitive inhibition of carbonic anhydrase in proximal tubule and collecting ducts → ↓HCO3- reabsorption, alkaline urine, metabolic hyperchloremic acidosis.
  • Effect size: Modest natriuresis (≈ up to 5% filtered Na+).
  • Indications: Acute mountain sickness, glaucoma (↓aqueous humor), idiopathic intracranial hypertension (pseudotumor cerebri), some metabolic alkalosis states.
  • PK/PD notes: Oral drug largely excreted unchanged; reduce dose with renal impairment; avoid in severe CRI.
  • Adverse effects: Fatigue, paresthesias, metabolic acidosis, hypokalemia (due to distal K+ loss).
  • Anesthesia considerations: Often held day of surgery; consider acid-base and volume status; acetazolamide sometimes seen preop for eye cases or IIH.

Loop Diuretics (e.g., Furosemide, Bumetanide, Torsemide, Ethacrynic acid)

  • Mechanism: Inhibit Na+-K+-2Cl- cotransporter (NKCC2) in TAL → loss of Na+, K+, Cl- and increased Ca2+/Mg2+ excretion.
  • Physiology: TAL normally reabsorbs about \(20\%-30\%\) of filtered Na+; inhibition causes powerful natriuresis and diuresis.
  • Potency & examples: Most potent diuretics. Bumetanide ≈ 40× furosemide potency; torsemide longer duration; ethacrynic acid is non-sulfonamide (use if sulfa allergy) but has higher ototoxicity risk.
  • PK highlights (furosemide): Onset IV 5–10 min; peak ≈30 min; DOA 2–6 h; half-life ~1–2 h; bioavailability ≈50% PO; highly protein bound.
  • Indications: Acute pulmonary edema, heart failure with fluid overload, refractory edema, sometimes to lower ICP (adjunct).
  • Adverse effects: Hypokalemia, hyponatremia, hypomagnesemia, metabolic alkalosis, ototoxicity (esp. with aminoglycosides or ethacrynic acid), hypotension, volume depletion.
  • Drug interactions: NSAIDs blunt effect; aminoglycosides increase ototoxicity; digoxin toxicity risk with hypokalemia; potentiation of nondepolarizing neuromuscular blockers.
  • Anesthesia considerations: Hold chronic diuretics DOS; check electrolytes & intravascular volume; be ready to manage hypovolemia and dysrhythmias; note interactions with NMBAs.

Thiazide Diuretics (e.g., HCTZ, Chlorthalidone, Indapamide, Metolazone)

  • Mechanism: Inhibit Na+-Cl- cotransporter (NCC) in early DCT → ↑Na+ and Cl- excretion, reduce urinary Ca2+ excretion (↑Ca2+ reabsorption).
  • Physiology: DCT normally handles ≈ \(10\%\) of filtered Na+; thiazides cause mild-moderate natriuresis but have chronic vasodilatory effects for BP reduction.
  • Indications: First-line for essential hypertension, mild edema, nephrogenic diabetes insipidus (low doses reduce polyuria), reduce urinary Ca2+ (benefit in kidney stones/osteoporosis).
  • PK notes: Orally absorbed; chlorthalidone has a long half-life (≈50–60 h).
  • Adverse effects: Hypokalemic, hypochloremic metabolic alkalosis; hyperglycemia; hyperuricemia; hypercalcemia; hypomagnesemia; dyslipidemia; can potentiate NMBAs.
  • Anesthesia considerations: Hold day of surgery; evaluate volume status and electrolytes; watch glucose and uric acid in susceptible patients.

Potassium-sparing Diuretics

  • Two subtypes:
  • ENaC blockers (amiloride, triamterene): Directly block epithelial Na+ channels in collecting duct; reduce Na+ reabsorption and K+ excretion.
  • Aldosterone antagonists (spironolactone, eplerenone): Block mineralocorticoid receptor → reduce synthesis/activation of Na+-K+ pump; useful in hyperaldosteronism and heart failure.
  • Indications: Adjunct to loop/thiazide to prevent hypokalemia; spironolactone for heart failure and hyperaldosteronism.
  • Adverse effects: Hyperkalemia (especially with ACE inhibitors, ARBs, NSAIDs), metabolic acidosis, GI upset; spironolactone may cause gynecomastia/sexual side effects; eplerenone is more selective (less endocrine effects).
  • Anesthesia considerations: Check K+ preop; avoid perioperative hyperkalemia risk with ACE inhibitors/ARB overlap.

Osmotic Diuretics (Mannitol)

  • Mechanism: Freely filtered inert osmole that increases tubular fluid osmolality → water diuresis > electrolyte loss.
  • Uses: Reduce intracranial pressure and cerebral edema (acute TBI, neurosurgery), acute renal protection in some settings, and to decrease intraocular pressure.
  • PK: IV only; onset 10–15 min, peak 40–45 min, duration ≈ 6 h; eliminated by glomerular filtration.
  • Adverse effects & cautions: Initial intravascular volume expansion (can precipitate pulmonary edema in heart failure), subsequent hypovolemia with continued diuresis, hypernatremia, plasma hyperosmolarity, risk of rebound intracranial hypertension if blood–brain barrier is disrupted.
  • Anesthesia considerations: Use cautiously in low EF patients; monitor hemodynamics and serum osmolality; mannitol often given intraop in neurosurgical cases.

Electrolyte & Acid-Base Patterns (practical)

  • Loops & thiazides: typically cause hypokalemia and metabolic alkalosis.
  • Carbonic anhydrase inhibitors: cause metabolic acidosis with alkaline urine.
  • Potassium-sparing/aldosterone antagonists: risk hyperkalemia and metabolic acidosis.
  • Osmotics: risk hypernatremia (water loss) and transient volume changes.

Perioperative Practical Points

  • General: Hold most diuretics on day of surgery (DOS) unless directed otherwise; assess recent labs, volume status, and electrolytes.
  • When diuretics may be given periop: Mannitol or furosemide may be administered intraop for neurosurgical indications or acute pulmonary edema (NPPE).
  • Electrolyte monitoring: Check K+, Na+, Mg2+, glucose, and acid–base status preop; correct significant abnormalities.
  • Drug interactions to note: NSAIDs reduce diuretic efficacy; hypokalemia increases risk of digoxin toxicity and arrhythmias; diuretics can potentiate nondepolarizing neuromuscular blockers.

Quick clinical tips

  • If patient takes HCTZ and is having surgery: hold the dose DOS and evaluate intravascular volume—they may be volume-contracted.
  • For severe loop-diuretic resistance consider combination therapy (loop + thiazide/metolazone) under supervision.
  • Be cautious combining ACE inhibitors/ARBs with K+-sparing agents.

High-yield summary (one-line reminders)

  • Loops: most potent → careful with electrolytes and ototoxicity.
  • Thiazides: HTN first-line, watch glucose/uric acid and K+.
  • CA inhibitors: altitude, glaucoma, IIH, cause metabolic acidosis.
  • K+-sparing: prevent hypokalemia but risk hyperkalemia.
  • Mannitol: reduce ICP, but watch for volume shifts and rebound edema.

References / further reading

  • Stoelting's Pharmacology & Physiology in Anesthetic Practice, Ch. 22: Diuretics.
  • Goodman & Gilman: Drugs affecting renal excretory function (selected sections).