Renal - Hormonal Regulation of Body Fluid - Lecture 6 Flashcards
What is the responsible for the major elimination of water?
What are 4 other ways that water loss can be facilitated?
Kidneys! - regulate water balance and are the major route for elimination of water from the body
- Insensible water loss - evaporation from cells of the skin & respiration
- Sweat
- GI tract via fecal water (100mL/day)
- Diarrhea - increased dramatic water loss (20L/day)
State the order of magnitude of water loss for the following:
Urine, Insensible, feces, sweat
Urine > Insensible (skin/respiration) > Feces > Sweat
1500 mL > 700 ml > 200 mL > 100 mL
What is the TBW (total body water) amount?
What is ICF?
ECF?
42 L
ICF = 28L
ECF = 14L ( Plasma: 3.5L and Interstitial: 10.5 L)
Which selective permeabilities are similar?
P, ICF, ISF, ECF
P and ECF, ISF and ICF
What is the osmolarity in each fluid compartment?
300 mosm/L
What is the major electrolyte composition of the following:
- Plasma
- Interstitial Fluid
- Intracellular fluid
- Plasma - Na & Cl-
- Interstitial Fluid - Na + and Cl-
- Intracellular Fluid (skeletal muscle) - K+
Describe:
- Positive Water Balance
- Negative Water Balance
- Intake Exceeds Loss
2. Intake is Less than Loss
What is the major determinant of plasma osmolality? (or body fluid osmolality)
Na+
What kind of urine does high water intake produce?
Low intake/Loss of Water?
- Hypoosmotic Urine
2. Hyperosmotic Urine
Where is ADH stored? How is it released?
- ADH is stored in the posterior Pituitary
2. It is released via exocytosis when the nerve endings are stimulated
What kind of feedback system does ADH utilize?
What kind of Physiologic regulation does it perform?
Where are the sensors located?
What is the effector?
What is the target of ADH?
What is the response of ADH
- Negative feedback
- Osmolality regulation of plasma, volume & pressure of the vascular system
- Effector - EXOCYTOSIS of ADH from terminal axons of supraoptic neurons & paraventricular neurons into the blood of the posterior pituitary
- The target is Extracellular ADH receptors in distal tubules & collecting duct
- Response: change in cytoarchitecture and cellular matrix remodeling, increased passive water reabsorption into RENAL MEDULLA
Which of the 5 factors that inhibit/stimulate ADH release?
- Nicotine
- Angiotensin II
- ANP
- Ethanol
- Nicotine - stimulates ADH release (water reabsorption increases)
- Angotensin II - stimulates ADH release (water reabsorption increases)
- ANP - inhibits ADH release (reduce ECFV)
- Ethanol - inhibit ADH release (producing large amounts of urine due to decreased water reabsorption)
Where are afferent fibers from the Baroreceptors carried?
CN 9 and 10
- leads to posterior pituitary of hypothalamus
What is ADH most sensitive to? (3)
What is the ADH release threshold? (in mosm/kgH20)
What is the thirst threshold?
- High sensitivity to increases and decreases in plasma osmolality
& DECREASES in BP or VOLUME! - ADH threshold is near 280 most/kgH20
- Thirst threshold - 298 mOsm/kgH20
What are some ADH disorders?
- Central (pituitary) diabetes insipidus - Polyuria, polydipsia
- Nephrogenic Diabetes Insipidus - Polyuria, Polydipsia
What is polyuria? Polydipsia?
Polyuria - copious amounts of dilute urine
Polydipsia - excessive thirst
What is SIADH? How is water reabsorption affected?
SIADH - Syndrome of Inappropriate ADH secretion
very high water retention
Where does ADH increase water permeability? (specifically)
Upper & Lower collecting duct
Describe the ADH activation pathway (cellular pathway).
ADH –> ADH receptor stimulation –> Increase Gs –> cAMP –> PKA –> insertion of aquaporin 2 water channels –> increase water permeability
There are active transports for water and UREA in the collecting duct. True or False.
FALSE
- both have no active transport in the nephron
What does ADH do to the urea permeability?
Increases Urea permeability of the LOWER COLLECTING duct
- increases urea reabsorption in the DEEP RENAL MEDULLA
What 2 things can lead to a decrease in ADH release?
- Increase in Blood Volume
2. Decrease in serum osmolality
What are the 6 challenges to homeostasis?
- Hyperosmotic Volume EXPANSION
- Hypoosmotic Volume EXPANSION
- Isoosmotic Volume EXPANSION
- Hyperosmotic Volume CONTRACTION
- Hypoosmotic Volume CONTRACTION
- Isomotic Volume CONTRACTION
How do you compute Osmolarity?
Amount in g (or if 0.9% then .9 g) / MW * 1000 mol/mol * Dissociation constant (NaCl is 2, D5W and LMW Dextran is 1) * 1000 mL/L
ex: the osmolarity for 0.9% NaCl
0. 9g/58.4 * 1000 mmol/mol * 2 mOsm/mmol * 1000 mL/L
What Happens to the following in ISOSMOTIC VOLUME EXPANSION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF Volume increases
- Osmolarity DOES NOT CHANGE
- plasma protein and hematocrit DECREASE - addition of fluid dilutes protein
- BP RISES
Ex; Infusion of Isotonic NaCl, Blood transfusion
What Happens to the following in ISOSMOTIC VOLUME CONTRACTION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF volume decreases
- Osmolarity DOES NOT CHANGE
- plasma concentration/hematocrit INCREASE - removal of volume concentrates
- BP DECREASES
EX: Sever the radial artery in a car accident, diarrhea
What Happens to the following in Hyperoosmotic VOLUME EXPANSION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF volume increases
- Osmolarity increases of ECF
- ICF osmolarity INCREASES
- ICF Volume DECREASES
- plasma protein/hematocrit concentration DECREASES
What Happens to the following in Hyperosmotic VOLUME CONTRACTION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF Volume decreases
- ECF osmolarity INCREASES
- ICF osmolarity INCREASES
- ICF volume decreases
- plasma protein INCREASES, hematocrit CONSTTANT (since h20 moves out of RBC ; offsetting the decrease in ECF volume)
EX: Sweating in the desert, Produce Hypoosmotic Sweat (H20 loss)
What Happens to the following in Hypo-osmotic VOLUME EXPANSION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF Volume increases
- ECF osmolarity decreases
- ICF Osmolarity Decreases
- ICF Volume INCREASES
- plasma protein concentration decreases, HEMATOCRIT unchanged (increase in volume is offset by the swelling of RBC’s)
Ex: SIADH, (gain of H20) or Infuse Physiological saline into a dehydrated person
What Happens to the following in Hypo-osmotic VOLUME CONTRACTION:
- ECF Volume
- Osmolarity of ECF
- Osmolarity of ICF
- Volume of ICF
Give an example
- ECF volume decreases
- ECF osmolarity DECREASES
- ICF osmolarity DECREASES
- ICF volume INCREASES
- plasma protein concentration INCREASES, hematocrit INCREASES (volume loss & water moves OUT of the cell)
Ex: Adrenocortical Insufficiency (no aldosterone)
or Production of Concentrated Urine
What equation defines the anion gap?
={Na - (Cl + HCO3-)]
What is the anion gap?
Calculated measure representing unmeasured ions in plasma or serum
- this includes phosphate, citrate, sulfate, and protein
- In metabolic acidosis , the serum HCO3 - decreases as it is depleted in buffering fixed acid
- thus another anion must increase to offset this change (Cl increases)
What type of metabolic disorders are the following:
1. RTA Type 2 Kidney
- Vomiting
- Diabetes Mellitis
What changes in these conditions?
- Metabolic Acidosis - increase in Cl, decrease in HCO3-( so increase in CO2)
- Metabolic Alkalosis - decrease Cl-, increase in HCO3- (decrease CO2)
- KetoAcidosis due to increased Lactate Ion
- decrease in Cl-
- increase in Anion Gap!!! (35)
What is the only example that causes a change to the anion gap?
Diabetes Mellitus
When does the serum anion gap increase?
When is the serum anion gap normal?
When the concentration of an unmeasured anion (phosphate, lactate etc) is increased to replace HCO3-!
(so HCO3 - must decrease)
- serum anion gap is normal if the concentration of Cl- is increased to replace HCO3 - (hyperchloremic metabolic acidosis)
How does vomiting result in metabolic alkalosis?
Loss of H+ ions
- causes an increase in HCO3- in arterial blood
Define the following for Azetazolamide Inhibitors:
- Class of Diuretic
- Site of Action
- Mechanism
- Major Effects
- Carbonic Anhydrase Inhibitor
- Proximal Tubule
- Inhibition of Carbonic Anhydrase
- Increase HCO3- Excretion
- causes Metabolic Acidosis
- Shifts p50 to the RIGHT
Define the following for Furosemide(Lasix); Ethacrynic Acid, Bumetanide:
- Class of Diuretic
- Site of Action
- Mechanism
- Major Effects
- Loop Diuretics
- Thick Ascending Limb of the Loop of Henle
- Inhibits Na-K - 2Cl cotransport in TAL
- increased NaCl excretion,
Increased K+ excretion
increased Ca excretion
Decreased ability to CONCENTRATE urine (decreased cortiocopappilary gradient)
Decreased ability to DILATE urine (inhibition of diluting segment)
Define the following for Hydrochlorothiazide(HydroDiuril), Chlorothiazide
- Class of Diuretic
- Site of Action
- Mechanism
- Major Effects
- Thiazide Diuretic
- Early Distal Tubule (cortical diluting segment)
- increased NaCl excretion,
Increased K+ excretion
DECREASED Ca excretion
Decreased ability to DILATE urine (inhibition of diluting segment)
No affect on ability to concentrate urine**
Define the following for Spironolactone, Triamterene, Amiloride (STA)
- Class of Diuretic
- Site of Action
- Mechanism
- Major Effects
- K+ SPARING Diuretics (the previously mentioned ones are all K+ wasting)
- Late Distal Tubule & COllecting Duct
- Inhibition of Na Reabsorption
Inhibition of K secretion
Inhibition of H secretion
- Increased Na excretion
DECREASED K excretion
Decreased H+ excretion
If there is a pH change and the serum anion gap is GREATER than 15 mEq/mL what is NOT a likely cause?What COULD be the cause?
Renal or GI –> serum anion gap is normal in these issues
Could be ketoacidosis (diabetes Mellitus), Lactic Acidosis, Renal Failure,
Vomiting induces what kind of metabolic issue? This is due to a decrease in what ion? What is left behind?
Metabolic Alkalosis
- a decrease in H+ , HCO3 - is left behind
(steady state relationship between acid/base formation)
