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Purpose of CVMP activation of the sympathetic drive
- Transfer volume to central circulation
- Cardiac inotropy, chronotropy
Purpose of CVMP activation of sympathetic and endocrine outflow to the kidney
- Preserve GFR
- Produce concentrated, Na+-free urine
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
Effect of antiotensin II on the PCT
Stimulate Na/H counter-transporter → increase Na+ reabsorption
Aldosterone causes increased Na+ reabsorption in these nephron segments
Medullary and cortical collecting ducts
In times of dehydration, the kidney can preserve up to [%] of the filtrate
What brainstem region might be involved in the salt appetite that accompanies thirst?
Nucleus of the solitary tract
Increased extracellular fluid volume (ECFV) leads to inactivation of [?] and increased secretion of [?]
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
What effect does increased renal blood flow have on the medullary osmotic gradient?
Washes it out → decreased water reabsorption
Severe intravascular volume depletion - Effects on:
Inferior vena cava filling
Pulmonary capillary wedge pressure (PCWP)
- Reduced (systolic < 80 mm Hg)
Sign of decreased systemic interstitial volume
Decreased skin turgor
Signs of decreased transcellular volume
- Dry mouth, mucous membranes
- Diminished intraocular pressure
- Absent axillary sweat
Intravascular volume overload – Effects on:
Jugular venous pressure
- S3 gallop (due to ventricular distension)
What is hepatojugular reflux?
Press on the liver → jugular veins distend
Signs of increased systemic interstitial volume
- Dependent pitting edema
- Hepatic congestion
Signs of increased pulmonary interstitial volume
Fluid accumulation in the peritoneal cavity (e.g., secondary to increased extracellular fluid volume)
Generalized, pitting edema:
Represents ECF overload of at least [#] L
Symmetric or asymmetric?
Noticeable or not?
- 3 L
- Depends on the size of the person
3 contributing factors to generalized, pitting edema
- Altered Starling balance
- Continued intake of salt and water
- Renal retention of salt and water
Equation for Starling’s law of transcapillary volume flux (net flux, JV)
= σ Kf
(ΔP – Δπ)
- σ = solute reflection coefficient
- Kf = capillary permeability
- ΔP = hydrostatic pressure gradient
- Δπ = oncotic pressure gradient
T/F: Renal retention of salt and water can be triggered either during intravascular volume depletion or during intravascular volume overload
Why is generalized, pitting edema termed “dependent”?
It shifts around, based on your body position
Generalized, pitting edema can accumulate in which spaces?
Peritoneal (ascites) or pleural (pleural effusion)
Causes of localized, pitting edema
- Damage to a capillary bed
- Local obstruction of lymphatic or venous drainage
Non-pitting swelling reflects increased [ICF or ECF]
In non-pitting swelling, there is [more or less] excess water than excess salt
How can hypothyroidism cause non-pitting swelling (myxedema)?
Interstitial mucopolysaccharides accumulate → trap water, albumin
What disease process is associated with severe peri-orbital edema?
Nephrotic syndrome (you’re losing albumin through the nephron)
3 disease processes that result in massive edema
- Congestive heart failure
- Nephrotic syndrome
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
T/F: You can have increased salt intake without experiencing increased thirst
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
Mechanisms of ineffective intravascular volume
- Baroreceptor malfunction
- Volume shunted into circulation without baroreceptors
- CVMP/kidney receives an overriding stimulus
- Kidney misinterprets signals
Baroreceptor stimulation → [activation or inhibition] of CVMP
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
2 places volume can be shunted, where it is undetectable by baroreceptors
- Splanchnic vessels
- Arterial-venous fistulae
2 circumstances in which splanchnic shunting could occur
Effective perfusion = [?] x [?]
(cardiac output) x (systemic vascular resistance)
In cirrhosis, hepatic venous outflow obstruction + A-V fistulae → activation of the [?] reflex for salt retention
Increased portal venous pressure (in cirrhosis) causes [?]-[?] venous shunting, resulting in [signs]
porto-systemic; hemorrhoids, varices
In cirrhosis, what pathologic liver changes cause increased portal pressure?
- Distortion/fibrosis of the sinusoids
- Decreased clearance of vasoconstrictors/dilators
T/F: Ascites is a sign of cirrhosis
The cirrhotic liver is [underperfused or overperfused]
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
T/F: Arterial-venous fistulae form in cirrhosis
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
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
In patients with acquired ANP resistance + nephrotic syndrome, the edema subsides [before or after] the proteinuria, if the patient regains ANP sensitivity
Define pre-renal azotemia
Rise in BUN despite good renal function
Is an indication of…
- Blood urea nitrogen
- Ability to clear nitrogenous waste
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
What hormone controls urea reabsorption in the nephon?
Effect of increased BUN on:
Urine Na+ content
Urine K+ content
- Metabolic alkalosis
You should look for the symptoms of pre-renal azotemia in patients with…
Severe heart failure
What hormones cause hypokalemia and metabolic alkalosis in pre-renal azotemia?
What hormone causes hyponatremia and azotemia in pre-renal azotemia?
CVMP activation results in the release of…
Aldosterone and catecholamines
How does aldosterone induce metabolic alkalosis?
Increases ammoniagenesis (increase in H+ secretion and HCO3- production)
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
What transporters are upregulated by aldosterone in the cortical collecting duct?
Apical ENaC and ROMK1, basolateral Na/K ATPase
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
Cardio-renal syndrome results from acutely worsening [?]