Chapter 19 Flashcards
To maintain homeostasis, what comes in the body
must eventually be
used or excreted
Input + production =
utilization + output
Factors Affecting the Plasma Composition
- Kidneys regulate solute and water content, which also
determines volume - Regulate acid-base balance
Composition is also affected by exchange between what compartments of body
Cells
* Connective tissue
* Gastrointestinal tract
* Sweating
* Respiration
figure 19.1
Balance
- Solutes and water enter and exit plasma
at the same rate - Quantity stays the same
Positive balance
- Solute or water enters plasma faster than it exits
- Quantity increases
Negative balance
- Solute or water exits plasma faster than it enters
- Quantity decreases
Cells in late distal tubules and collecting ducts that
regulate balance
- Principal cells (Water
and Electrolytes) - Intercalated cells (Acid-base balance)
Water intake + metabolically produced =
water output +
water used
water Intake
- Gastrointestinal tract
- Metabolism
Water output
- Insensible loss
- Sweating
- Gastrointestinal tract
- Kidneys
Normovolemia
normal blood volume
Hypervolemia
high blood volume due
to positive water balance
Hypovolemia
low blood volume due
to negative water balance
Osmosis
- Water diffuses down the concentration gradient
- Water reabsorption follows solute reabsorption
Water moves from area of ___ solute concentration to
area of ___ solute concentration
low ; high
kidney’s role in osmolarity
Kidneys compensate for changes in osmolarity of
extracellular fluid by regulating water reabsorption
Water reabsorption is a ____ process
passive
Proximal tubules
70% of filtered water is reabsorbed
* Not regulated
Distal tubules and collecting ducts
Most remaining water is reabsorbed
* Regulated by ADH (vasopressin)
Water reabsorption follows
solute reabsorption
What is the primary solute
sodium
Na+ is ____ transported across the _____
membrane
actively ; basolateral
figure 19.5
Osmolarity of interstitial fluid of renal medulla
varies with?
- depth
- Lower osmolarity near cortex
- Greater osmolarity near renal pelvis
Osmotic gradient is established by the
countercurrent
multiplier
Ascending limb (loop of henle)
Impermeable to water
* Active transport of Na+, Cl–, and K+
Descending limb (loop of henle)
Permeable to water
* No transport of Na+, Cl–, or K+
Fluid in descending limb
- osmolarity increases as it descends
- Osmolarity = interstitial fluid
- Osmolarity > descending limb
Fluid in ascending limb
osmolarity decreases as it ascends
* Osmolarity < interstitial fluid
* Osmolarity < descending limb
Role of urea in the medullary osmotic gradient
- Generated by liver
- Nitrogen elimination
- Extremely water soluble
- Requires urea transporters: UTA, UTB, and UTC
Role of the vasa recta
capillaries prevents the
diffusion of water and solutes from dissipating the medullary osmotic gradient
Descending limb of vasa recta
As it descends, water leaves capillaries by osmosis and solutes enter by diffusion
Ascending limb of vasa recta
Water moves into plasma and solutes move into interstitial fluid
* Osmolarity is higher due to the lack of urea transporters
Water permeability dependent on what water channels
Aquaporin-3
Aquaporin-2
Aquaporin-2
present in apical membrane only when ADH present in blood
Aquaporin-3
present in basolateral membrane always
When membrane of late distal tubule and collecting duct is impermeable to water what happens
Water cannot leave the tubules
* No water reabsorption
* More water is excreted in urine
ADH stimulates the insertion of water channels
_____ into ___ membrane
aquaporin-2 ; apical
Maximum amount of water reabsorbed depends on ___ of ____
length ; loop of Henle
Obligatory water loss
Minimum volume of water that must be excreted in the
urine per day
Effects of ADH on water reabsorption
- ADH regulates permeability of late distal tubules and
collecting ducts - Urine osmolarity range: 100–1400 mOsm
- Aquaporin-2 varied by ADH
- Antidiuretic
Regulation of ADH secretion
Released from terminals in the posterior pituitary from
cell bodies originating in the hypothalamus
* Osmoreceptors in the organum vasculosum of laminae
terminalis (OVLT) sense osmolarity
* OVLT is not surrounded by the blood-brain barrier
* ADH is also affected by baroreceptors detecting blood
volume and pressure
* increase baroreceptor activity = increase ADH secretion
Figure 19.13
Hypernatremia
high plasma sodium
Hyponatremia
low plasma sodium
Sodium
primary solute in ECF
Why is sodium needed?
- Critical for normal osmotic pressure
- Critical to function of excitable cells
Where is Na reabsorbed?
Reabsorbed (70%) in proximal tubules, distal tubules, and
collecting ducts
Where is Na reabsorption regulated?
- Reabsorption regulated by aldosterone and ANP
- Reabsorption regulated at principal cells of distal tubules and
collecting ducts
Is reabsorption of Na passive or active?
active
What drives Na reabsorption?
Na+/K+ pump on basolateral membrane
Know figure 19.14
What are the effects of aldosterone?
Increases sodium reabsorption
* Steroid hormone secreted from adrenal cortex
Function of aldosterone
- Acts on principal cells of distal tubules and
collecting ducts - Increases number of Na+/K+ pumps on basolateral
membrane - Increases number of open Na+ and K+ channels on
apical membrane
Granular cells of juxtaglomerular apparatus secrete what?
Renin-angiotensin-aldosterone system (RAAS)
Angiotensinogen is converted by___ into _____
renin ; angiotensin I
Liver secretes?
angiotensinogen
Angiotensin II stimulates?
aldosterone production
Angiotensin I is converted by ___ into angiotensin II
ACE; angiotensin II
Capillary walls contain ______, especially in lungs
angiotensin-converting enzyme (ACE)
Know figure 19.16
Know figure 19.17
Atrial Natriuretic Peptide
Secreted by atrial cells in response to distension
of atrial wall
Atrial Natriuretic Peptide increases?
GFR
* Dilation of afferent arteriole
* Constriction of efferent arteriole
Atrial Natriuretic Peptide decreases?
Na+ reabsorption by closing Na+
channels in apical membrane
Overall effect of Atrial Natriuretic Peptide
increased Na+ excretion
Hyperkalemia
high plasma potassium
Hypokalemia
low plasma potassium
Potassium is crucial to function of _____
excitable cells
Renal Handling of Potassium Ions in the glomerulus
freely filtered
Renal Handling of Potassium Ions in the proximal tubules
reabsorbed
Renal Handling of Potassium Ions in the Distal tubules and collecting ducts
reabsorbed and
secreted
Aldosterone regulates
principal cells
K+ in plasma directly stimulates
aldosterone release
As K+ increases, more ____ is released
aldosterone
Hypercalcemia
high plasma calcium
Hypocalcemia
low plasma calcium
Calcium balance is critical for?
- Triggers exocytosis
- Triggers secretion
- Triggers muscle contraction
- Increases contractility of cardiac and smooth muscle
Know figure 19.21
Blood calcium
- Bound to carrier proteins
- Free in plasma
- Free calcium: freely filtered at glomerulus
Parathyroid hormone (PTH)
released from parathyroid
glands
Stimulus for the release of PTH
decreased Ca2+ in plasma
Functions of PTH
- Increases Ca2+ reabsorption by kidneys
- Stimulates activation of 1,25-dihydroxycholecalciferol in kidneys
- Stimulates resorption of bone
- Stimulates small increase in calcium absorption
Overall effect of PTH
increased blood calcium
1,25-dihydroxycholecalciferol
steroid hormone
derived from vitamin D3
Calcitonin is secreted from?
C cells of thyroid gland
What triggers the release of calcitonin?
high plasma [Ca2+]
Actions of calcitonin at target cells
- Increases bone formation
- Decreases calcium reabsorption by kidneys
Normal pH of arterial blood
7.35–7.45
pH < 7.35 =
acidosis
pH > 7.45 =
alkalosis
Complications with acid-base disturbance
- Conformation change in protein structure
- Changes in excitability of neurons
- Changes in potassium balance
- Cardiac arrhythmias
Vasodilation
Normal PCO2 arterial blood =
40 mm Hg
Sources of CO2
metabolism
Output of Co2
through respiratory system
Increased plasma [CO2] →
respiratory acidosis
Decreased plasma [CO2] →
respiratory alkalosis
What causes acidosis?
- High-protein diet
- High-fat diet
- Heavy exercise
- Severe diarrhea (loss of bicarbonate)
- Renal dysfunction
Metabolic alkalosis causes
- Excessive vomiting (loss of hydrogen ions)
- Consumption of alkaline products (baking soda)
- Renal dysfunction
Three lines of defense against Acid-Base Disturbances
- Buffering of hydrogen ions
- Respiratory compensation
- Renal compensation
Most important ECF buffer=
bicarbonate
ICF buffers
proteins and phosphates
Increased ventilation →
decreased CO2
Decreased ventilation →
increased CO2
Renal compensation
- Regulates excretion of hydrogen ions and bicarbonate in urine
- Regulates synthesis of new bicarbonate in renal tubules
Effects of increased acidity
- Increased secretion of hydrogen ions
- Increased reabsorption of bicarbonate
- Increased synthesis of new bicarbonate
Renal handling of hydrogen and bicarbonate ions in the Proximal tubule
Bicarbonate reabsorption coupled to hydrogen ion secretion
Renal handling of hydrogen and bicarbonate ions in the Distal tubule and collecting duct
Secretion of hydrogen ions coupled to synthesis of new bicarbonate ions
Compensation for Acid-Base Disturbances: PH
7.4, [HCO3–]/[CO2] = 20:1
Compensation for Acid-Base Disturbances: ACIDOSIS
[HCO3–]/[CO2] < 20:1
Compensation for Acid-Base Disturbances: ALKALOSIS
[HCO3–]/[CO2] > 20:1
Kidneys regulate?
HCO3–
Lungs regulate
CO2
Cause of Respiratory acidosis
hypoventilation
Increased CO2 →
increased H+
Compensation of Respiratory acidosis
- renal
- Increased H+ secretion
- Increased HCO3– reabsorption
Cause of Respiratory alkalosis
hyperventilation
Decreased CO2 →
decreased H+
Compensation of Respiratory alkalosis
- renal
- Decreased H+ secretion
- Decreased HCO3– reabsorption
Metabolic acidosis
Cause
increased H+ independent of CO2
Metabolic acidosis compensation
- respiratory and renal
- Increased H+ secretion
- Increased HCO3– reabsorption
- Increased synthesis of new bicarbonate
Metabolic alkalosis
Cause
decreased H+ independent of CO2
Respiratory compensation
Decreased ventilation → increased CO2
Renal compensation
- Decreased H+ secretion
- Decreased HCO3– reabsorption
- Decreased synthesis of new bicarbonate
figure 19.29