Physio E3: Renal pt 2

3 process required for water balance to exist

3 process required for water balance to exist

-adequate glomerular filtration

-Na reabsorption w/o H20 reabsorption

-Variable water permeability in collecting duct (ADH controls)

glomerular filtration delivers ___ to loop of Henle

NaCl and H2O

ADH role

variation in water excretion

ADH is stimulated by

increases in plasma osmolarity or BV decreases

What organ does ADH effect?

kidneys: formation of concentrated urine and solute rentention

vasoconstrictors and their role

V1 receptors: vasoconstriction

V2 receptors: renal water retention

Where is ADH synthesized and secreted?

Hypothalamus; posterior pituitary

What detects low plasma volume?

Low pressure baroreceptors in atria and lungs

High pressure carotid baroreceptors

Nicotine effect on ADH

increases secretion of ADH

Ethanol effect on ADH

inhibits secretion

Effect of increase in plasma osmolarity on concentration levels

urine concentration > plasma concentration

Effect of decrease in plasma osmolarity on concentration levels

urine concentration < plasma concentration

T/F ADH effects whether the kidney produces concentrated or dilute urine

T

effect of water deprivation

decreased urine volume, increased urine concentration

effect of water excess

increased urine volume, decreased urine osmolarity

Two types of DI

Central: posterior pituitary does not secrete ADH

Nephrogenic: kidney’s do not respond to ADH

ECF is a function of total ___ in ECF

Na

Disorders of ECF volume (edema) reflect

difficulties with Na balance

perfusion decreases —>

stretch in afferent arteriolar wall —> renin release —> angio-aldosterone axis

response to low effective circulating volume

renin/angio/aldosterone axis activated —> SNS stimulated via baroreceptors —> increased ADH secretion —> increased fluid retention via Starling’s forces

response to high effective circulating volume

renin/angio/aldosterone/ADH/SNS have limited activity

Starling force’s continue

more fluid excreted

ANP secreted

ANP

promotes loss of Na and H2O

-response to stretch caused by high BV

-increase GFR

BNP is a marker of what

fluid overload

-lasts long than ANP

Mg homeostasis

essential cofactor; balanced by intestinal uptake and urinary excretion; reabsorbed in back end of distal tubule (w/Ca)

LOOP: cause loss of Mg and Ca

Urea

end product of nitrogen metabolism; excretion depends on urine flow rate

measured by BUN

elevated BUN can indicate

maker of dehydration

-increases with ADH

What are the major hormones that control Ca balance?

PTH and Vit D

Which form of Ca leads to kidney stones?

Ca Oxalate

3 forms of Ca

45% free ionized

45% bound to plasma protein

10% complexed with anions

liver failure = ___ albumin —>

NO; decreased Ca due to lack of binding

What stimulates Ca reabsorption in distal tubule?

PTH, Vit D, and thiazide diuretics

Phosphate concentration is influenced by

intestinal uptake, renal excretion, exchanges with bone

2 forms of Phosphate

80% alkaline phosphatase

20% acid phosphate

What is the most important regulator of phosphate?

PTH

Phosphate reabsorption

only in proximal tubule

-restricted to Na/phosphate co transporter

What effect does renal insufficiency have on phosphate excretion?

quickly results in inadequate excretion (plasma levels increase)

(HIGHLY dependent on GFR)

What percent of K is in the ICF?

98%

role of K

strong influence of resting membrane potential

What is the central hormone for controlling K balance?

Aldosterone (late distal tubule)

What stimulates Aldosterone secretion?

increased ECF K

-inc cell uptake of K in skeletal m. → lower ECF K

-renal K excretion is stimulated to remove excess K

Internal K homeostasis

shifts between ICF and ECF

external K homeostasis

balance between K ingestion and excretion

Insulin & Epinephrine are a part of internal/external K homeostasis. What do they do to K?

internal; movement from ECF to ICF

K levels in acidosis

Hyperkalemia; H buffered by ICF → K leaves cell —> increase plasma K

K levels in alkalosis

hypokalemia; H exits cell in exchange for K —> reduces plasma K → decreases ECF K

Renal K reabsorption

70% in proximal tubule

25% in ascending limb

Aldosterone stimulates __ secretion while promoting _ uptake

K; Na

Thiazide and Loop diuretics effects on K

inhibit Na reabsorption upstream → high Na deliver → furthers K secretion → dec ECF K

Normal pH, PCO2, HCO3- values

pH 7.35-7.45

PCO2 40mmHg

HCO3 24mmol/L

pH limit to sustain life

6.8-7.8

3 components of defense against pH disturbance

-buffers: limited but immediate

-changes in ventilation: secs-mins and provide second line of defense

-renal H excretion and HCO3 synthesis: final line of defense, hours-days to prevent sustained pH change

What is the most important buffer in ECF

bicarb system; reversibly bind H+

What drug causes bicarbonaturia?

carbonic anhydrase inhibitors

-ex: acetazolamide

Where does the acidification of urine occur?

Along the entire renal tubule

Na/H exchange in distal tubule is stimulated by

aldosterone

Factors of Acid Production

CO2, Sulfuric acid, Phosphoric Acid = H+

Tissue Acid Buffers

ICF: proteins, organic phosphates

Interstitium Acid Buffers

ECF: HCO3-, phosphate

Blood Acid Buffers:

RBC: Hgb

Acid removal resp. component

increase ventilation

Acid removal Met. component

reabsorb HCO3-

Diuretic use ___ Na delivery to CCD

increases (drives more secretion of H and K —> alkalosis & hypokalemia)

Review metabolic/respiratory acidosis/alkalosis and compensation mechanisms

see chart

Guarding reflex

prevents involuntary emptying of bladder

Stretch receptors in bladder signal pathway

send impulses from visceral afferent innervations to S2-4 —> Pons micturition center

SNS nerve of bladder

hypogastric; contract neck and urethra inhibits micturition

PNS nerve of bladder

pelvic; stimulates detrusor internal sphincter to contract

somatic nerve of bladder

pudenal; innervates the external sphincter to relax

___ must be inhibited for micturition

SNS —> urethral sphincter relaxes and opens

PNS neurons release ___ onto ___ receptors

ACh; muscarinic (M3) (detrusor)

role of PNS neurons

allow voiding

role of SNS neurons

inhibit voiding

SNS neurons release ___ onto ___ and ___ receptors

NA; B3 (bladder) and a1 (urethra)

Somatic nerve role

allow voiding

Somatic nerve inhibits release of ___ onto ___ receptors allowing the external sphincter to open

ACh; nicotinic -@external sphincter

T/F personal can control when they urinate

T

Internal urethral sphincter is made up of ____ and ___ control. ___ innervation relaxes for dilation

smooth muscle; involuntary; PNS

External urethral sphincter is made up of ___ and under ____ control. __ innervates

skeletal muscle; voluntary (opening); pudenal