Obligatory Water losses
losing water thru organs that are not water handlers... nothing yu can do about it ..
insensible water loss
imperceptible, this H20 loss occurs via evaporation & moisture exhaled in breaths.
imperceptible
unnoticeable; impossible to perceive; undetectable
Insensible water loss:
- from lungs (that vaporizes out in expired air)
- or skin (diffuses directly through)
- Perspiration
- Feces
Minimum daily sensible water loss of
500 ml in urine to excrete wastes
Body water and Na+ content are regulated in tandem by mechanisms that maintain
- cardiovascular function
- and blood pressure
Water reabsorption in collecting ducts is proportional to ADH release
decreased ADH = dilute urine and decreased volume of body fluids
increased ADH = concentrated urine
Hypothalamic osmoreceptors trigger or inhibit
ADH release
Other factors may trigger ADH release via large changes in blood volume or pressure,
e.g.,
- fever,
- sweating,
- vomiting,
- or diarrhea;
- blood loss; and traumatic burns
increased osmolalilty or increased Na+ in plasma stimulates
osmoreceptors in hypothalamus
osmoreceptors in hypothalamus stimules
posterior pituituary
posterior pituituary releases
ADH
ADH target
collecting ducts of kidneys
effects of collecting ducts of kidneys
increased water reabsorption
increased water reabsorption results in
decreased osmolality
increased plasma volume
- scant urine
decreased plasma volume and BP inhibits
baroreceptors in atrium and large vessles
inhibition of baroreceptors in atrium and large vessles stimulates
posterior pituitary to release ADH
ADH targets
collecting ducts of kidneys
effects
- inc. water reabsorption
results in
- dec osmolaltiu
increased plasma vol
- scant urine
dehydation signs and Sx
thirst
dry flushed skin
oliguria
May lead to
- weight loss,
- fever,
- mental confusion,
- hypovolemic shock,
- and loss of electrolytes
ECF is diluted = hyponatremia and leads to a
net osmosis into tissue cells = swelling of cells = severe metabolic disturbances (nausea,
vomiting,
muscular cramping,
cerebral edema) possible death
Edema due to anything that increases flow of fluid out of the blood or hinders its return
1. increased blood pressure
2. Capillary permeability (usually due to inflammatory chemicals)
3. Incompetent venous valves, localized blood vessel blockage
4. Congestive heart failure, hypertension, and increased blood volume
Hindered fluid return occurs with an imbalance in colloid osmotic pressures, e.g., hypoproteinemia (decreased plasma proteins)
- Fluids fail to return at the venous ends of capillary beds
Results from
- protein malnutrition,
- liver disease, or
- Glomerulonephritis
Blocked (or surgically removed) lymph vessels
Cause
leaked proteins to accumulate in IF
- increased colloid osmotic pressure of IF draws fluid from the blood
Results in
- low blood pressure and
- severely impaired circulation
Importance of salts CSEM
1. Controlling fluid movements
2. Excitability
3. Secretory activity
4. Membrane permeability
Central Role of Sodium
Most abundant cation in the ECF
Sodium salts in the ECF contribute
280 mOsm of the total 300 mOsm ECF solute concentration
Na+ leaks into cells and
is pumped out against its electrochemical gradient
Na+ content may change but ECF
Na+ concentration remains stable due to osmosis
Changes in plasma Na+ levels affect
Plasma volume, blood pressure
ICF and IF volumes
Renal acid-base control mechanisms are coupled to Na+ ion transport
No receptors are known that monitor Na+ levels in body fluids
Na+ - water balance is linked to
Blood pressure and blood volume control mechanisms
Na+ reabsorption
65% is reabsorbed in the proximal tubules 25% is reclaimed in the loops of Henle
Aldosterone
active reabsorption of remaining Na+
Water follows Na+ if ADH is present
Renin-angiotensin mechanism is the main trigger for
aldosterone release
Granular cells of JGA secrete
renin in response to:
- Sympathetic nervous system stimulation
- Filtrate osmolality
- decreased stretch (due to decreased blood pressure)
Renin catalyzes the production of angiotensin II which prompts
aldosterone release from the adrenal cortex
Aldosterone release is also triggered by
elevated K+ levels in the ECF
Aldosterone brings about its effects
slowly (hours to days)
increased K+ or Na+ in blood plasma
RAAS activates and stimulates
adrenal cortex which releases
aldosterone
aldosterne targets
kidney tubules
kindey tubules
na+ reabsopriton
k+ secretion
k+ secretion restores
homeostatic plasma levels of Na+ and K+
RAAS
Adrenal cortex
Aldosterone
Kidney Tubules
Na+ reabsorption
Increased K+ secretion
= homeostatic plasma levels of Na and K
ANP released by atrial cells in response to
stretch - increased blood pressure
ANP Effects
Decreases blood pressure and blood volume:
- decreases ADH, renin and aldosterone production
- increases Excretion of Na+ and water
- Promotes vasodilation directly and also by decreasing production of angiotensin II
ANP
targets hypothal and posterior pituitary gland
- decreases ADH release
Estrogens:
Increases NaCl reabsorption (like aldosterone)
H2O retention during menstrual cycles and pregnancy
Glucocorticoids
increases Na+ reabsorption and promote edema
Progesterone:
decreases Na+ reabsorption
(blocks aldosterone)
Promotes Na+ and H2O loss
Cardiovascular System Baroreceptors alert the brain of
increases in blood volume and pressure
- Sympathetic nervous system impulses to the kidneys decline
- Afferent arterioles dilate
- GFR increases
- Na+ and water output increase
ANP effect
Importance of potassium K+:
Affects RMP in neurons and muscle cells (especially cardiac muscle)
Increased ECF [K+] leads to
(hyperkalemia)
decreased RMP = depolarization = reduced excitability
Decreased ECF [K+]
hypokalemia
hyperpolarization and non-responsiveness
H+ shift in and out of cells
Leads to corresponding shifts in K+ in the opposite direction to maintain cation balance
Interferes with activity of excitable cells
K+ balance is controlled in the cortical collecting ducts by
changing the amount of potassium secreted into filtrate
High K+ content of ECF favors
principal cell secretion of K+
When K+ levels are low,
type A intercalated cells reabsorb some K+ left in the filtrate
Influence of aldosterone
Stimulates K+ secretion
(and Na+ reabsorption) by principal cells
Increased K+ in the adrenal cortex causes
Release of aldosterone
Potassium secretion
Ca2+ in ECF is important for
NBCS
Neuromuscular excitability
Blood clotting
Cell membrane permeability
Secretory activities
Hypocalcemia =
increased cell excitability and muscle tetany
Hypercalcemia =
Inhibits neurons and muscle cells, may cause heart arrhythmias
Calcium balance is controlled by
-parathyroid hormone (PTH) and calcitonin
Bones are the largest reservoir for
Ca2+ and phosphates
PTH promotes increase in calcium levels by targeting
- bones,
- kidneys, and
- small intestine (indirectly through vitamin D)
Calcium reabsorption and phosphate excretion
go hand in hand
Normally 75% of filtered phosphates are
actively reabsorbed in the PCT
PTH inhibits this by decreasing the Tm
Cl- is the major anion in the ECF
1. Helps maintain the osmotic pressure of the blood
2. 99% of Cl- is reabsorbed under normal pH conditions
When acidosis occurs,
fewer chloride ions are reabsorbed
Other anions have
transport maximums and excesses are excreted in urine
18) Angiotensin II
A) causes widespread vasoconstriction throughout the body.
B) stimulates thirst.
C) causes the synthesis and release of aldosterone from the
adrenal cortex.
D) A and B
E) A, B and C
E) A, B and C
Atrial natriuretic peptide
A) acts as both a hormone and a neurotransmitter.
B) is secreted by neurons originating in the hypothalamus.
C) is produced by specialized myocardial cells.
D) A and B
E) A, B and C
E) A, B and C
Which of the following is not true about angiotensin II?
A) is a potent vasoconstrictor
B) elevates blood pressure
C) activates parasympathetic output
D) stimulates thirst
E) increases cardiac output
C) activates parasympathetic output
Dangers of low plasma potassium include (hypokalemia)
A) skeletal muscle weakness.
B) arrhythmias.
C) weakness and failure of the muscles of respiration.
D) A and B
E) A, B and C
E) A, B and C
When large amounts of pure water are consumed,
A) a fluid shift occurs and the volume of the ICF decreases.
B) the ECF becomes hypertonic to the ICF.
C) osmolarities of both ECF and ICF will be slightly lower.
D) the volume of the ECF will decrease.
E) th
C) osmolarities of both ECF and ICF will be slightly lower.
If plasma levels of potassium K+ get too high, (hyperkalemia)
A) cells are unable to repolarize fully.
B) excitable cells depolarize readily.
C) action potentials become smaller or nonexistent.
D) muscle weakness occurs.
E) All of these events occur.
E) All of these events occur.
The kidneys can alter extracellular fluid volume and osmolarity by
A) changing the amount of water excreted.
B) changing the amount of sodium excreted.
C) both of these
D) neither of these
C) both of these
As a result of respiratory alkalosis,
A) the kidneys conserve bicarbonate.
B) the tidal volume increases.
C) the body retains less carbon dioxide.
D) the respiratory rate increases.
E) the kidneys secrete less hydrogen ions.
C) the body retains less carbon dioxide.
Juxtaglomerular cells in the nephron secrete
A) angiotensinogen.
B) renin.
C) angiotensin I.
D) angiotensin converting enzyme.
E) aldosterone.
B) renin.
The enzyme renin is responsible for the activation of
A) erythropoietin.
B) atrial natriuretic peptide.
C) adrenaline.
D) angiotensin.
E) cortisol.
D) angiotensin.
When plasma water is lost but electrolytes are retained,
A) the osmolarity of the ECF falls.
B) both the ECF and the ICF become more dilute.
C) there is an increase in the volume of the ICF.
D) osmosis moves water from the ICF to the ECF.
E) all of the ab
D) osmosis moves water from the ICF to the ECF.
A mountain climber at high altitude may develop
A) respiratory alkalosis. (lower oxygen exists in high altitudes)
B) respiratory acidosis.
C) metabolic acidosis.
D) metabolic alkalosis.
E) none of the above
A) respiratory alkalosis. (lower oxygen exists in high altitudes)
ACE inhibitors
A) lower blood pressure.
B) block the conversion of angiotensin I to II.
C) reduce Na+ reabsorption and decrease extracellular fluid volume.
D) A and B
E) A, B and C
E) A, B and C
When the concentration of sodium ion in the ECF increases,
A) osmoreceptors are stimulated.
B) there is a decreased thirst.
C) ADH secretion decreases.
D) there is an increase in the volume of urine produced.
E) aldosterone secretion increases.
A) osmoreceptors are stimulated.
The hormone ADH
A) causes the kidneys to produce a large volume of urine.
B) is secreted by the anterior pituitary gland in response to changes in blood osmolarity.
C) stimulates the kidneys to retain sodium ion.
D) stimulates water conservation at the ki
D) stimulates water conservation at the kidneys.
The hormone that controls water excretion by the kidneys is
A) aldosterone.
B) angiotensin.
C) ANP.
D) ADH.
E) epinephrine.
D) ADH.
The hormone that controls water excretion by the kidneys is
A) aldosterone.
B) angiotensin.
C) ANP.
D) ADH.
E) epinephrine.
D) ADH.