Renal

Question 1

Hypernatremia

Answer 1

usually result of neruosurgery complicaiton or brain trauma

commo sx: muscle weakness, lethargy, restlessness, coma, death

Question 2

Euvolemia Hyponatremia

Answer 2

could be caused by

• glucocorticoid deficency (cortisol normally exerts negative fb on AVP secretion)
• hypothyroidism
• SIADH

(bc it is due to some limitaiton in H2O exretion, urine [Na+] is elevated)

Tx: water restriciton

Question 3

Hypervolemi Hyponatremia

Answer 3

loss of total body water and Na+

Intrarenal causes: duretics, osmotic diuresis, aldosterone deficiency

Signs/Sx:

• Clinical:
  
  • tachycardia
  • flattened neck veins
  • orthostatic hypotension
• Labs: (note- kidneys in ultra-conservation mode)
  
  • BUN would be elevated (due to decreased renal perfusion)
• Tx: isotonic saline

Question 4

Hypervolemic hyponatremia

Answer 4

Common cause: Heart Failure

• diminished cardiac output
• decreaed urine Na+
• decreased GFR
• high Na+ urine concentration (renal fxn impaired)

Question 5

Mineralocorticoid hyptertension

Answer 5

Characterized by:

• hypokalemia
• kaliuresis
• metabolic acidosis
• decreased plasma [renin]

Common cause: hyperaldosteronism (ie: one that hyperstimlates ENaC, Na+ reabsorption)

Question 6

Primary Hyperaldosteronism

Answer 6

due to adosterone-secreting tumor, adrenal hyperplasia, or adrenal carcinoma

Low PAC:PRA ration (low aldosterone to renin ratio)

Question 7

Secondary Hypoaldosteronism

Answer 7

high PAC:PRA ratio

Question 8

Pseudohypoaldosteronism

(Type I Hypoaldosteronism)

Answer 8

causes salt-wasting

fata, disrupt ENaC, Na+ reabsorption impaired

Causes mass excretion of Na+ (natriuresis) and H2O

Question 9

Diabetes Incipidus

Answer 9

Caused: (either)

• loss in AVP production
• disruption in V2R (AVP receptor) or AQP2 (aquaporin 2)

Symptoms

• polyuria
• polydipsia

Question 10

SIADH

(syndrome of inappropriate ADH secretion)

Answer 10

AVP = ADH

Can be:

• neurogenic: defect in level of hormone release
• nephrogenic: hormone responsivness defect in target tissue

Congenital: usually linked to mutation in V2-R so it is consituatively active in absence of AVP, thus having undetectable levels of serum AVP

Inappropriate regulation of AVP

Defining Characteristics:

• highly concentrated urine (osmolaity >100mOsm/kg)
• urine Na+ > 40meq/l despite normal intake
• euvolemic hyponatremia (serum Na+ <136meq/l)
• hypoosmoality (<275 mOsm/kg)

Tx: idenitfy underlying cause

• restrict fluid intake
• loop diuretic to increase free H2O excretion

Question 11

Hyperchloremia

Answer 11

can be realted to dehydration but not as likely

hyperchloremia can be induced as a compensatory mechanism during metabolic acidosis

(can be identified as a normal AG metabolic acidosis)