Class: Renal Sodium balance Flashcards
normal urine osmolality
285-295
intracellular volume is controlled by what
osmolality
extracellular volume is controlled by what
sodium
major intracellular ion
K+
major extracellular cation
Na+
hyponatremia water moves where?
to ICF
hyperglycemia/natremia water moves where
to ECF
What does the kideny regulate (volume-wise)
ECF volume and osmolality
ECF osmolality is regulated by what
renal ADH = water handling
ECF volume is regulated by what
renal Na+ handling = RAAS system
Which is tightly regulated and which varies all day- ECF volume or osmolality
osmolality is tightly regulated
min and max urine osmolality
min = 50 max = 1200
desert islnad no water = what type of state
hyperosmolar
in hyperosmolar state, what occurs
ADH released
sweating a lot and drinking water with no salt leads to what state
hyposmolar state
what 3 things will promote renin secretion:
Decreased NaCl to macula densa
Low BP in Afferent arteriole
Increased SNS activity
Decreased NaCl to macula densa –> what 2 things
dilation of AA
Prostaglandin release –> JG cells release renin
What do JG cells do in low BP independent of macula densa
release renin
SNS activity increased by what
low BP
SNS effects on kidney (3) and one systemic effect
i. Vasoconstriction (systemic)
ii. Renin release
iii. Decreased RBF, GFR (dt constriction of AA, EA)
iv. Increased reabsorption of NaCl (PCT, TAL, DT/CD)
Hypothalamus is activated by what 4 things
i. Hyperosmolarity
ii. decreased atrial receptor firing
iii. SNS
Angiotensin II
V1 receptor activation –> increased MAP via what MOA?
V1 is present on blood vessels–> increased SVR (vasoconstriction)
V2 receptor activation –> increased MAP via what MOA?
ADH receptor in tubule –> kidney water reabsorption–> increased BV
define hypern natremia
Sodium >145
4 causes of Diabetes insipidus
Neurosurgery
Head trauma
Neoplasms
Sarcoidosis
4 causes of hypernatermia
Inadequate water intake
Insensible water losses
Inability to concentrate urine (central or nephrogenic diabetes insipidus)
Salt toxicity
Diabetes insipidus 4 sx
Polyuria/polydipsia
Lethargy/weakness
Irritability
Seizures/coma
3 causes of Nephrogenic diabetes indipidus
Pregnancy
Lithium use
genetic mutations
Give ADH:
no response = what dx
no response = nephrogenic DI
Tx for Central DI:
Desmopressin (synthetic DDAVP)
Tx for Nephrogenic DI- 2 drugs and MOA
amiloride- competes with lithium
HCTZ - MOA unknown
Tx for Nephrogenic DI: (non-pharmacological) and MOA
reduce Na and protein in diet –> reduced urine volume
define hyponatremia
Sodium <135
presentation of hyponatremia (4)
Headache
Nausea/vomiting
Disorientation
Gait abnormality
3 reasons for Urine Osmolality <100 mOsm/kg in hyponatremia
primary polydypsia
beer potomania = decreased ADH secretion
tea/toast diet = urine has no osmotic pull
3 reasons for Urine osmolality >100 mOsm/kg in hyponatremia
impaired water excretion (RF, thiazides)
exccess ADH
ADH receptor dysfunction
urine sodium and urine osmolailty in both:
hypovolemic hyponatremia
hypervolemic hyponatremia
Both will have low urine sodium and high urine osmolality
SIADH urine sodium and urine osmolality
SIADH will have high urine sodium (<40) and high urine osmolality (>300),
What is a major cause for euvolemic hyponatremia
SIADH = medications
TX for Any patient with gait abnormality/disorientation/obtunded (mental status changes due to hyponatremia)-
give hypertonic saline
What can you give to treat acute hyponatremia that you can’t give in Chronic hyponatremia? Why?
can’t give hypertonic saline
bc: the brain cells have adjusted to the new normal by pumping out osmoles which keeps them from being filled with water too. (since in hyponatremia they have higher osmolarity than the ECF). If you give hypertonic saline in chronic, the cells will lose all their water and become demyelinated
