2500

2300: food and drink

200: cell metabolism

2500

kidneys: 1500 mL > primary regulator of water excretion at the hormonally controlled late DCT and collecting duct

skin: 600 mL > sweat, evaporation

lungs: 300 mL > evaporation

GI tract: 300 mL > vomiting, diarrhea

hypervolemia: increase water and solutes > infusion of isotonic solution

hypovolemia: decrease water and solutes > trauma, blood loss, hemorrhage, surgery, burns, vomiting, diarrhea

overhydration: increase too much water > drinking too much

dehydration: decrease too much water > sweating (sweat is primarily water, some solutes)

must lose more than 15 mg/kg of blood

-can be hemorrhagic or trauma caused

1. ADH

2. aldosterone

3. thirst center

4. SNS

binds to ADH receptor on principal cells of late DCT and collecting duct > GPCR > activates adenylate cyclase to make cAMP > activates PKA > cell signaling causes increased aquaporins > allow for water reabsorption

stimulus for release: osmoreceptors detecting high osmolality

-produced in the supraoptic nuclei of the hypothalamus, released through the posterior pituitary

regulates water intake

-stimulus:

1. dry mouth: stimulates thirst center in the hypothalamus

2. hypothalamic osmoreceptors: detects increased osmolality > stimulates thirst center

3. decreased blood pressure: detected by baroreceptors > baroreceptor reflex > production of angiotensin 2 > stimulates thirst center

stimulus

1. increased Na and decreased K concentration in plasma

2. low BP > renin angiotensin system > angiotensin 2

-aldosterone released from the adrenal cortex > places extra Na/K antiporters on the principal cells of the late DCT and collecting duct > Na reabsorption and K secretion

low BP in renal blood vessels > baroreceptors in heart, aortic arch, carotid arteries activated > send signal to medulla > increased sympathetic outflow causes:

1. increased renin from JG cells

2. vasoconstriction of systemic arterioles (except afferent arteriole because it is protected by NO)

-intense SNS stimulation causes extreme vasoconstriction > vasoconstrict afferent arteriole > decreased GFR > less fluid loss > increased BP/BV 

enter: food and beverage

leave: kidneys, skin, feces, severe vomiting that involves intestines, diarrhea

electrolyte = salt that dissociates in water

136-145 meq/L NORMAL

> 145 meq/L HYPERNATREMIA

< 136 meq/L HYPONATREMIA

3.5-5.1 meq/L NORMAL

> 5.1 meq/L HYPERKALEMIA

< 3.5 meq/L HYPOKALEMIA

edema = accumulation of fluid in the interstitium

1. decreased plasma colloid osmotic pressure (Po): liver disease

-albumins located in plasma pull blood from interstitium

2. increased hydrostatic pressure (PHb): hypertension

3. increased capillary permeability: local inflammation or injury

-fluid is able to flow out of capillaries easier

4. lymphatic obstruction/removal

-water usually leaves via the lymph

1. HYPERVOLEMIA: gain both water and solutes: infusion of isotonic fluid

2. HYPOVOLEMIA: loss of both water and solutes: blood loss, hemorrhage, trauma, burns, vomiting, diarrhea

3. OVERHYDRATION: gain water

-drinking too much water

4. DEHYDRATION: loss of water

-sweating (more water than solute loss)

roles of sodium

1. muscle contraction

2. nerve impulse

3. major extracellular positive ion

4. primary regulator of water movement in the body

-cotransports glucose and AA in the late DCT and collecting duct

associated with hypertonicity > water loss

1. sweating

2. excessive salt intake

results: cell shrinkage, increased thirst (high osmolarity), increased blood volume and pressure

clinical presentation

1. thirst

2. restlessness

3. irritability

4. spasticity

5. seizures

6. coma

7. death

8. intracranial bleeding

9. edema

1. hypervolemic hypernatremia: iatrogenic (caused my medication mistakes)

2. hypovolemia hypernatremia

3. isovolemic hypernatremia: diabetes insipidus (no ADH > water loss)

result: cell swelling, nervous impulse conduction, muscle contraction

clinical presentation

for hypovolemic hyponatremia: poor skin turgor, tachycardia, hypotension

1. cellular swelling:cerebral edema with increased intracranial pressure

2. lethargy

3. confusion

4. seizures

5. coma

depending on serum osmolality

1. hypertonic hyponatremia: hypertonic infusions

2. hypotonic hyponatremia: classified further

3. isotonic hyponatremia

depending on ECF volume

1. hypovolemic (low BP, high HR, poor skin turgor) hypotonic hyponatremia

2. hypervolemic hypotonic hyponatremia

3. isovolemic hypotonic hyponatremia: SIADH > too little ADH hormone

roles:

1. major intracellular positive ion

2. sets resting membrane potential

3. nerve impulse

4. muscle contraction

5. maintenance of normal cardiac rhythm

6. acid base balance (H/K antiporter on luminal membrane of intercalated cells of late dct and collecting tube)

loop diuretics: inhibit the Na/K/2Cl symporter on the luminal side of the thick ascending limb of the loop of henle

-causes more salt to stay in the urine > water moves from plasma to the urine > decreased BV > decreased BP

-K wasting > K goes out into the urine > can  cause hypokalemia > need to ingest extra K

caused by

1. excessive K intake: overuse of salt substitutes

2. decreased K excretion: renal failure

3. metabolic acidosis > H/K antiporter on the intercalated cells > high H > H secreted and K reabsorbed

results: 

1. muscle weakness: restlessness, neuromuscular irritability, paralysis

2. intestinal problems: cramping and diarrhea

3. cardiac problems: EKG problems

4. death by CARDIAC arrest

causes

1. decreased K intake: unbalanced diets

2. increased K secretion: potassium wasting diuretics (loop diuretics)

3. metabolic alkalosis: not enough H > need to reabsorb H and secrete K > using H/K antiporter on the luminal membrane of intercalated cells in the late DCT and collecting tubule

results:

1. muscle weakness: decreased tone in smooth muscles

2. intestinal problems

3. cardiac problems: bradycardia

4. death by RESPIRATORY arrest

roles

1. crucial to normal body function

1. thyroid gland releases calcitonin

2. calcitonin inhibits the actions of osteoclasts which breakdown bone

3. stimulates actions of osteoblasts which cause bone formation which uses Ca and PO4-

causes: cancer (lung, breast, multiple myeloma > metastatic > attacks bone which causes bone breakdown> increased Ca > leads to cardiac arrest), hyperthyroidism (too much PTH)

symptoms

1. heart dysrhythmias

2. fatigue

3. confusion

4. nausea

5. coma

6. cardiac arrest

7. calcification of the soft tissues

treatment: biphosphonates (bone loss inhibitors) and calcitonin

1. PTH is released from the parathyroid gland

2. PTH causes increased number and action of osteoclasts which break down bone into Ca

3. PTH causes increased Ca and Mg reabsorption at the kidneys

4. causes increased vitamin D at the kidney > vit D is activated to calcitriol > required for Ca and PO4 absorption in the GI tract 

causes: vit D deficiency (no calcitriol > cannot reabsorb Ca into GI tract > lose Ca in feces), parathyroid gland dysfunction (no PTH production)

symptoms

1. muscle spasms

2. tetanus around mouth and extremities: Ca is needed for NT release

3. ECG changes that lead to heart failure

4. respiratory arrest

NORMAL ECF: 7.35-7.45

ACIDEMIA: < 7.35

ALKALEMIA: > 7.45

acids = proton donors

bases = proton acceptors

pH = log [H+]

henderson hasselbalch equation: relates pH to the ratio of the concentrations of the conjugate base and acid

pH = pKa + log [A-]/[HA]

must be regulated because pH changes cause conformational changes in proteins which change their functions

H+ changes caused by

1. metabolism: CO2 as a byproduct which is then used by carbonic anhydrase

2. diet: ingest acids or bases

1. chemical

2. respiratory

3. renal

-fastest > buffers resist changes in pH and are most effective at their pKa

1. phosphate buffer system: intracellular and in urine

-H2PO4- + OH- > HPO42- + H+

-H+ secreted into the urine > cannot leave the body as H+ > converted to H2PO4 and excreted

2. protein buffers: bind or release H+

-NH2-X-COOH + H+ > NH3+-X-COOH

-NH2-X-COOH + OH- > NH2-X-COO-

3. carbonic acid/bicarbonate buffer system using carbonic anhydrase

CO2 + H2O > H2CO3 > H+ + HCO3-

-most important

chemoreceptors respond to changes in PaCO2, H+ and pH

1. hyperventilation > decreased PaCO2 > decreased H+ > increased pH

2. Hypoventilation > increased PaCO2 > increased H+ > decreased pH

slowest form of regulation (hours to days)

1. reabsorption of bicarb

2. formation of bicarb by kidney tubule cells

3. secretion of H+ in the PCT and DCT

-intercalated cells: H/K antiporter

-PCT: Na/H antiporter

-H+ is titrated with Na2HPO4 and NH3 to yield excretable acidic products > CANNOT URINATE H+ > will damage ureters

1. respiratory acidosis

2. respiratory alkalosis

3. metabolic acidosis

4. metabolic alkalosis

excess acid or loss of bicarb

causes of excess acid production:

1. diabetic ketoacidosis

2. starvation acidosis

3. lactic ketosis (lactic acid breakdown)

4. kidney disease (H+ not getting excreted)

5. hyperkalemia (H/K antiporter)

causes of loss of bicarb:

1. diarrhea

2. excessive vomiting that involves the intestines

compensation

1. increased ventilation: decrease PaCO2 > decrease H+ > increase pH

2. increased excretion of H+ > titrate with NH3 or PO4

respiratory alkalosis

caused by hypoventilation which increases PaCO2

compensation:

1. kidneys retain bicarb

2. secrete H+ (Na/H antiporter in the PCT, H/K antiporter at the intercalated cells of the late DCT/collecting duct)

excess bicarb or loss of acid

causes of loss of acid:

1. mild to moderate vomiting that only involves the stomach

2. hypokalemia (H/K antiporter)

causes of excess base:

1. ingesting too much bicarb

compensation

1. decrease ventilation > increase PaCO2 > increase H+ > decrease pH

2. increase bicarb secretion

1. blood pH > alkalosis vs acidosis

2. PaCO2 level > high PaCO2 = metabolic, low PaCO2 = respiratory

3. plasma HCO3 level >high bicarb = respiratory, low bicarb = metabolic

1. H+ secreting

2. bicarb secreting