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Purpose of CVMP activation of the sympathetic drive
- Transfer volume to central circulation
- Cardiac inotropy, chronotropy
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Purpose of CVMP activation of sympathetic and endocrine outflow to the kidney
- Preserve GFR
- Produce concentrated, Na+-free urine
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Pathway by which sympathetic outflow to kidney causes increased GFR
Sympathetic stimulation of JGA → renin secretion → AI → AII → constriction of afferent/efferent arterioles → secretion of PGI → dilation of afferent arteriole → increase GFR
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Effect of antiotensin II on the PCT
Stimulate Na/H counter-transporter → increase Na+ reabsorption
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Aldosterone causes increased Na+ reabsorption in these nephron segments
Medullary and cortical collecting ducts
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In times of dehydration, the kidney can preserve up to [%] of the filtrate
99.3%
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What brainstem region might be involved in the salt appetite that accompanies thirst?
Nucleus of the solitary tract
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Increased extracellular fluid volume (ECFV) leads to inactivation of [?] and increased secretion of [?]
CVMP; ANP
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Atrial natriuretic peptide (ANP):
Stimulation for secretion
Effect on CCD and MCD
Relationship to ADH
Effect on afferent arteriole
- Atrial stretch
- Antagonize aldosterone
- Antagonize ADH → decreased water reabsorption
- Decrease resistance → increased GFR
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What effect does increased renal blood flow have on the medullary osmotic gradient?
Washes it out → decreased water reabsorption
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Severe intravascular volume depletion - Effects on:
Supine BP
Inferior vena cava filling
Pulmonary capillary wedge pressure (PCWP)
- Reduced (systolic < 80 mm Hg)
- Underfilling
- Reduced
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Sign of decreased systemic interstitial volume
Decreased skin turgor
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Signs of decreased transcellular volume
- Dry mouth, mucous membranes
- Diminished intraocular pressure
- Absent axillary sweat
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Intravascular volume overload – Effects on:
BP
Heart sounds
Jugular venous pressure
Hepatojugular reflux
- Hypertension
- S3 gallop (due to ventricular distension)
- Increased
- Present
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What is hepatojugular reflux?
Press on the liver → jugular veins distend
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Signs of increased systemic interstitial volume
- Dependent pitting edema
- Hepatic congestion
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Signs of increased pulmonary interstitial volume
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Define ascites
Fluid accumulation in the peritoneal cavity (e.g., secondary to increased extracellular fluid volume)
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Generalized, pitting edema:
Represents ECF overload of at least [#] L
Symmetric or asymmetric?
Noticeable or not?
- 3 L
- Symmetric
- Depends on the size of the person
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3 contributing factors to generalized, pitting edema
- Altered Starling balance
- Continued intake of salt and water
- Renal retention of salt and water
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Equation for Starling’s law of transcapillary volume flux (net flux, JV)
J V = σ K f (ΔP – Δπ)
- σ = solute reflection coefficient
- Kf = capillary permeability
- ΔP = hydrostatic pressure gradient
- Δπ = oncotic pressure gradient
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T/F: Renal retention of salt and water can be triggered either during intravascular volume depletion or during intravascular volume overload
True
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Why is generalized, pitting edema termed “dependent”?
It shifts around, based on your body position
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Generalized, pitting edema can accumulate in which spaces?
Peritoneal (ascites) or pleural (pleural effusion)
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Causes of localized, pitting edema
- Damage to a capillary bed
- Local obstruction of lymphatic or venous drainage
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Non-pitting swelling reflects increased [ICF or ECF]
ICF
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In non-pitting swelling, there is [more or less] excess water than excess salt
more
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How can hypothyroidism cause non-pitting swelling (myxedema)?
Interstitial mucopolysaccharides accumulate → trap water, albumin
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What disease process is associated with severe peri-orbital edema?
Nephrotic syndrome (you’re losing albumin through the nephron)
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3 disease processes that result in massive edema
- Congestive heart failure
- Nephrotic syndrome
- Cirrhosis
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What happens to the ECFV in a normal patient on a high-Na+ diet or mineralcorticoid (over several days)? Why?
- ECFV increases by a maximum of 2.5 L, then it remains stable
- Inactivate CVMP, increase ANP
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T/F: You can have increased salt intake without experiencing increased thirst
True
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What happens to the ECFV in a patient with CHF, nephrotic syndrome, or cirrhosis, on a high-Na+ diet or mineralcorticoid (over several days)? Why?
- Generalized edema
- Failure to inactivate CVMP and/or failure to respond to ANP
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Mechanisms of ineffective intravascular volume
- Baroreceptor malfunction
- Volume shunted into circulation without baroreceptors
- CVMP/kidney receives an overriding stimulus
- Kidney misinterprets signals
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Baroreceptor stimulation → [activation or inhibition] of CVMP
inhibition
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Mechanism by which the baroreceptor can misinterpret a pressure waveform
- CHF → desynchronized cardiac contraction → abnormal waveform
- Densensitivity of the baroreceptor to increased pressure, over time
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2 places volume can be shunted, where it is undetectable by baroreceptors
- Splanchnic vessels
- Arterial-venous fistulae
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2 circumstances in which splanchnic shunting could occur
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Effective perfusion = [?] x [?]
(cardiac output) x (systemic vascular resistance)
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In cirrhosis, hepatic venous outflow obstruction + A-V fistulae → activation of the [?] reflex for salt retention
hepato-renal
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Increased portal venous pressure (in cirrhosis) causes [?]-[?] venous shunting, resulting in [signs]
porto-systemic; hemorrhoids, varices
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In cirrhosis, what pathologic liver changes cause increased portal pressure?
- Distortion/fibrosis of the sinusoids
- Decreased clearance of vasoconstrictors/dilators
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T/F: Ascites is a sign of cirrhosis
True
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The cirrhotic liver is [underperfused or overperfused]
underperfused
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How does an underperfused, cirrhotic liver ultimately result in increased Na/water retention?
- Distressed liver sends signal to kidney → kidney retains salt and water (hepato-renal reflex)
- Example of an “overriding” stimulus leading to failure to inactivate CVMP
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T/F: Arterial-venous fistulae form in cirrhosis
True
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Describe the normal pathogenesis of nephrotic syndrome, leading to edema
Loss of albumin → fluid seeps out of capillaries → decreased IVF → CVMP activation → Na/water retention
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How can nephrotic syndrome result in edema when albumin is not very low?
IVF overfill → secretion of ANP; but patients have acquired ANP resistance and the kidneys cannot respond to ANP
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In patients with acquired ANP resistance + nephrotic syndrome, the edema subsides [before or after] the proteinuria, if the patient regains ANP sensitivity
before
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Define pre-renal azotemia
Rise in BUN despite good renal function
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BUN:
Stands for…
Is an indication of…
- Blood urea nitrogen
- Ability to clear nitrogenous waste
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T/F: An increase in BUN always correlates with decreased glomerular filtration
False – GFR can be normal; the nephron is simply reabsorbing more urea into the bloodstream
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What hormone controls urea reabsorption in the nephon?
ADH
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Effect of increased BUN on:
Urine volume
Urine Na+ content
Urine osmolarity
Acid/base balance
Urine K+ content
- Decreased
- Decreased
- Increased
- Metabolic alkalosis
- Decreased
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You should look for the symptoms of pre-renal azotemia in patients with…
Severe heart failure
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What hormones cause hypokalemia and metabolic alkalosis in pre-renal azotemia?
Aldosterone, AII
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What hormone causes hyponatremia and azotemia in pre-renal azotemia?
ADH
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CVMP activation results in the release of…
Aldosterone and catecholamines
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How does aldosterone induce metabolic alkalosis?
Increases ammoniagenesis (increase in H+ secretion and HCO3- production)
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How do aldosterone and ADH cause an increase in the medullary osmotic gradient?
- Aldosterone → increased Na+ reabsorption into interstitium
- ADH → increased urea reabsorption into interstitium
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What transporters are upregulated by aldosterone in the cortical collecting duct?
Apical ENaC and ROMK1, basolateral Na/K ATPase
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In the collecting duct, why does an increase in Na+ reabsorption contribute to hypokalemia and alkalosis?
Increases the transcellular electrical gradient favoring K+ and H+ secretion into the tubule lumen
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Cardio-renal syndrome results from acutely worsening [?]
CHF
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