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Basics Flashcards

1
Q

Total Blood Osmolaity

A

2([Na+]blood) + (blood glucose / 18) + (BUN / 2.8)

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2
Q

Effective Osmolality

A

2([Na+]blood) + (blood glucose / 18)

  • created by effective solutes, which cannot passily diffuse across cell membranes
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3
Q

Effective Circulating Volume

A

the blood volume that is required for adequate perfusion of the vital organs

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4
Q

What do the kidneys regulate?

A
  • plasma volume
  • blood pressure (BP)
  • waste excretion
  • electrolyte balence
  • plasma pH
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5
Q

What 3 things mediate renal function?

A
  1. internal mechanisms
  2. extra- and intrarenal endocrine systems (e.g.: aldosterone, arginine vasopressin, angiotensin, and atrial natriuretic peptide)
  3. the autonomic nervous system (SNS)
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6
Q

Describe the ANS control in the kidney.

A

SNS activity controls

  • vasoconstriction of the renal microcirculation
  • Na+ reabsorption
  • stimulates the secretion of renin
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7
Q

What is filtration?

A

the movement of plasma constituents (e.g.: H2O, ions, glucose, urea, and very small proteins) from the glomerulus into Bowman’s capsule

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8
Q

What is reaborption?

A

the movement of constituents from teh tubule lumenal fluid (ie: forming urine) into the renal interstitium; and/or recycling of these substances back into circulation

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9
Q

What is secretion?

A

movement of constituents from renal circulation, interstitium and/or tubule epithelium into the forming urine

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10
Q

What is the significance of GFR?

A
  • it is the product of a single nephron
  • it will decrease prior to the onset of symptoms of renal disease
  • it decreases in direct correlation with the pathological severity of kidney disease
  • *can only be assessed in patients who are at some steady state
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11
Q

What pathophysiologic factors will affect GFR?

A
  • kidney disease
  • pregnancy
  • reduced kidney perfusion
  • marked changes in extracellular fluid volume
  • non-steroidal anti-inflammatory drug (NSAID) use
  • acute/habitual elevated protein ingestion
  • blood glucose
  • arterial BP
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12
Q

Explain glomerular regulation of intraglomerular pressure

A

Generally,

  • self-governing:
  • increased systemic BP induces a myogenic response within the afferent arterioles
    • resultant vasoconstriction of the afferents prevents potentially damaging inceases in glomerular pressure, and sustains GFR within optimal limits
  • Very low BP sensed within the kidney:
    • in response: hormonal mechanisms are mobilized to induce vasoconstriction within the efferent arterioles
    • maintains glomerular pressure within the fairly narrow range that is conducive to healthy GFR
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13
Q

What values of GFR are at risk?

A
  • GFR<60 is associated with a high risk for the development of cardiovascular disease and mortality from CV disease exceeds the risk of progression to renal failure
  • GFR<15 ml/min/1.73m3 indicates renal failure and would require replacemet via dialysis or kidney transplant
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14
Q

How do we measure GFR?

A

creatinine

assuming steady state:

Scr (serum/plasma creatinine) generally fall in standard range: (~0.4-1.5 mg/dl)

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15
Q

What factors affect creatinine levels?

A

HEALTHY PATIENT:

  • inceased GFR will induce a decreased in Scr
  • decreased GFR will cause increased Scr and increased BUN

General Levels:

  • Men excrete: 20-25 mg creatinine/kg/day
  • Women excrete: 15-20 mg creatinine/kg/day
  • *obesity has no effect on levels

Factors that Increase Scr:

  • Race: black
  • Kidney disease
  • Crushing injury (rhabdomyolysis)
  • Ketoacidosis (interferes with assay)
  • Ingestion of cooked meat (transient increase)
  • Large muscle mass
  • Various medications

Factors that Decrease Scr:

  • Race: hispanic, asian
  • Low muscle mass
  • Vegetarian diet
  • Malnutrition
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16
Q

What is BUN and what affects it?

A

Blood Urea Nitrogen

  • a product of protein metabolism
  • levels fluctuate with changes in diet, metabolism, and volume status
  • high protein diet and volume depletion will each raise BUN
    • This effect is see in volume depletion bc of increased renal tubule reabsorption of urea accompanies Na+ and H2O reabsorption
    • thus elevation in BUN is not reliable indicator of GFR
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17
Q

Explain fluid dynamics (forces) within the nephron

A
  • Within the afferent arteriole (and esp glomerular capillary), the hydraulic forces (Pcap +πBowman’s) that favor ultrafiltration win-out –> FILTRATION OCCURS
  • As plasma enters the efferent arteriole, the opposing forces (PBowman’s + πcap) increase concomitant with a decrease in thehydraulic forces; these forces oppose filtration)
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18
Q

What regulates input to the nephron?

A
  1. systemic BP which afects:
  2. blood flow (ie BP and renal perfusion) with in the afferent arteriole
  3. glomerular P which dictates GFR
  4. vasomotion within the afferent and efferent arterioles

*Afferent arteriole is key:

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19
Q

What is the role/significance of the afferent arteriole?

A

Significance:

  • GREATEST pressure drop occurs between the afferent arteriole and glomerulous
  • virtulally no pressure drop occurs between afferent and efferent end of the glomerulus
  • thus, vasoconstriction and vasodilation of the afferent arteriole has major impcat on renal perfusion and GFR

Role:

  • So goes the afferent arteriole, so does GFR
    • ​constriction of the efferent arteriole will cause back pressure within the glomerulus
    • healthy pt: any incrase in pressure wthin the glomerulus will incrase GFR
    • low pressure and high resistance (esp compared to systemic capillary network)
      • enables filtration of ~180 L of plasma/day
20
Q

What does “autoregulation” respond to?

A
  • autoregulation fuctions via the concertes actions of SNS, natriuretic peptides, paracrine factors, and RAAS
  • via autoregulation, GFR and RBF can be maintained within a narrorw rainge even in face of markedly changing MAP

​Autoregulation responds to

  1. ​pressure-induced distension of both the vascular smooth muscle and the vascular endothelium within the afferent arteriole
  2. the tubular-glomerular feedback system
21
Q

What regulates the tubular-glomerular-feedback (TGF) system?

A

concentration of Na+ (or NaCl) in the forming urine as it reaches the cortical thick ascending limb (TAL)

22
Q

What is PRA?

A

Plasma Renin Activity

volume depletion leads to lowered BP, this would cause the secretion of renin with a subsequent increase in PRA

23
Q

How does ACE support vasoconstriction?

A
  1. production of AII
  2. degradation of bradykinin (a vasodilator)
24
Q

Explain mobilization of the RAS during periods of hypovolemia

A

(measured by incrased PRA)

  • AII induces vasoconstriction of systemic arterioles, this raises BP
  • AII targets the renal arteriole –>2-prong approach to stopping and correcting volume depletion
    • 1) AII-dependent constriction of the efferent arteriole steadies glomerular P. With constriction of the efferent arterioles by AII, renal perfusion is reduced, leading to lowered P within the peritubualr capillaries
    • 2) conservation mechanism: reduced perfusio allows hemodynamics that favor reabsorption of Na+ and H2O from the glomerular filtrate into the renal interstitium and back into circulation
25
What is AT1?
* AII receptor * **predominant AT receptor isoform expressed in humans** * **expressed within smooth msucls of afferent and predominately efferent arterioles, renal tubules, and peripheral vasculature** * expressed witin renal tubules and cells within the adrenal zona glomerulosa * likely coupled to Na+ reabsorption * regionally expressed within renal tubule epithelium and JG cells * **AT1 is known to mediate AII-dependent vasoconstriction in the renal arterioles (predominant effect) and AII-stimulated Na+ reabsorption from the tubules**
26
What happens in a state of diminished ECV (ie low BP)?
* **AT binds and activates AT1 within the efferent arteriolar vascular smooth muscle** * This induces efferent vasoconstriction and maintains glomerular pressure in order to sustain optimal ultrafiltration across the glomerular capillaries
27
What is the role of AII?
* stimulates renal Na+ reabsorption by activating transporters (NHE3, NKCC2, NCC, and ENaC) * likely stimulates the Na+/K+ ATPase within the tubule epithelium * this collectively allows for the reabsorption of Na+ from forming urine back in to ciculation
28
Osmoles
total particles in solution
29
Osmolarity
total moles in solution
30
Osmolality
Solute/Kg H2O
31
Osmosis
Diffusion of H2O through a semipermeable membrane; from an area of high random motion to area of less random motion
32
Osmotic Pressure
created by effective osmoles; driving forve for osmosis
33
osmotic equilibrium
osmotic pressure = hydrostatic pressure
34
Explain the SNS response to Low BP
***\* To Conserve, we increase GFR \**** 1. Low BP (threshold) 1. SNS tone increased 2. AII production 3. **Selective constriction of efferent arterioles (major effect)** 4. Increases/maintains glomerular pressure 5. Increase GFR 1. maintain optimal reabsorptive gradients (conserve)
35
Volume Decrease and Osmole System
*Note: Osmole receptor system is not coupled to volume decrease due to dehydration or GI fluid loss.*
36
What are the intrarenal and extrarenal effects of AT1-R? Pathophysiologic?
* Intrarenal (in kidney): * vasocontriction * Na+ reabosorption * Extrarenal effects: * vasoconstriction * aldosterone secretion * Pathophysiologic: * LVH * Fibrosis (cardiac, renal) * Athrosclerosis
37
What does evidence suggest is the role of AT2-R?
* Bradykinin synthesis (vasodilation) * Reverse/block fibrosis * Anti-inflammatory * Proapoptotic (heart, favorable remodeling)
38
Wht are the physiologic and pathophysiologic effects of aldosterone?
* secreted from adrenals * myocardial production * mineralcorticoid receptor **_Physiologic:_** * Na+ conservtaion * K+ elimination * vasoconstriction **_Pathophysiologic:_** * direct vasoconstrictor * HTN * induces vascular inflammation * increases collagen synthesis in cardio fibroblasts * induces cardiomyocyte apoptosis
39
What occurs in the proximal tubule?
Na+ and glucose reabsorption _Lumen to Cyto Side_ * **SGLT:** Na+ and Glucose **reabsorbed** into epithelial cytoplasm from forming urine (lumen) * **NHE-3:** Sodium/proton epithelieal trans * trades **sodium reabsorption** into epithelial cell for **proton secretion** into lumen * *\*Important for acid-base balence* * **AT1-Receptors**: respond to reabsorb AII * coupled to/driving NHE-3 **_Cyto to Intersitium (vehicle to plasma)_** * **GLUT:** Glucose to plasma * Na+ has several options * **Na+/K+ ATPase** (**Na+ reabsorped and K+ secreted into cytoplasm)** * **​***activity of Na+/K+ ATPase may be upregulated by AII* * **Na+/HCO3- transporter** (**reabsorption of both)**
40
What happens in the Distal Nephron's Thick Ascending Limb?
Na+ and K+ handling _Lumen to Cytoplasm (apical):_ * **NKCC**: grabs Na+, K+, and 2 Cl-s to reabsorb them * driven by AII and * faciliated by K+ secretion - creates gradient dynamics * targeted by loop diuretics * **ROMK2**: K+ secretion that facilitates NKCC (K+ cycling) * **NHE**-3: think acid-base and Na+ reabsorption _Cyto to interstitum (basolateral):_ * **HCO3-/Cl- exchanger** (bicarb reabsorption and Cl secretion into lumen) * mechaism for Cl- reabsorption * also a **K+ leak** into interstitum * **Na+/K+ ATPase**
41
What happens in the distal convoluted tubule?
Na+, Cl-, and Ca2+ Reabsorption _Lumen to Cyto (apical)_ * **_NCC_**: reabsorps Na and 2 Chlorides * driven by AII * target for Thiazide diuretics * Ca2+ transporter - reasoprtion * primary place for Ca2+ regulation * **ENaC**: Na+ reabsorption * targeted/stimulated by AVP and AII _Cytoplasm to Interstitium (basolater:_ * Ca+/Na+ transporter (Na+ secreted into cytoplasm; Ca2+ reabsorbed) * Na+/K+ ATPase * Cl- transporter (reabsorption) * K+ reabsorbed
42
Diuretics
* **Acetazolamide**: * Carbonic anhydrase inhibitor, thus impairing the formatin of bicarbonate, and thus becomes useful as diuretic in certain acid-base disorders * **Furosemide** * blocks NKCC * by keeping more charged substances in the forming urine --\> acts as effective osmole * wherever there is a charge, that is where water wants to go * so if you keep more stuff in forming urine, water will be there --\> diuresis * *also screws up Ca2+ reabsorption bc changes charge gradient* * *when using furosemide, be careful with Ca2+ status of pts, esp if they are hypocalcemic* * *​*potent; uses reserved for pleural edema, etc * Ca2+ wasting * **Thiazides** * **​**blocks NCC transporter * changes electrochemical gradient, thiazides stimulate * K+ secretion - *be careful if ppl have K+ or Ca2+ issues* * Ca2+ reabsorption * **Amiloride** * K+ sparing (helps us hang onto K+) * blocks Na+ chanel in collecting tubules * **Eplerenone and Spironolactone** * block aldosterone * mineralocotoricoid receptor antagonists * **HCTZ** * weak; blocks Na+ and Cl- reabsorption * stimulates K+ secretion; stimulates Ca2+ reabsorption
43
Aldosterone (simplified)
* stimulated by: * elevated AII * Hyperkalemia * Causes: * Na+ reabsorption * K+ secretion
44
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45
Glomerulosa
* where aldosterone is synthesized * high [AT1-R] * this is how AII stimulates secretion of aldosterone from adrenal cortex (targeting AT1-R in zona glomerulosa)
46
Mineralicorticocoids
a family of steriods that include aldosterone
47

Renal/Endocrine/Repro (10 decks)

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