PORTH'S PATHOPHYSIOLOGY
COMPREHENSIVE REVIEW 2026 VERIFIED
QUESTIONS AND SOLUTIONS
◉Vasopressin (ADH). Answer: *regulates blood volume and salt
concentration
* synthesized by cells in hypothalamus
*stored in pituitary gland
exerts effects on V1 and V2 receptors
*pores (aquaporins) stimulated to move into membrane and make
tubular epithelial cells permeable to water
*levels controlled by ECF volume and osmolality
◉Disorders of ADH. Answer: DI and SIADH
◉SIADH. Answer: syndrome of inappropriate antidiuretic hormone
◉Causes of SIADH. Answer: -lung, brain tumors
-cancers of lymphoid tissue
-Prostate CA
,-pancreatic CA
-advanced TB
-severe PNA
◉manifestations of SIADH. Answer: * dilutional hyponatremia
(sodium <135mEq/L)
*crackles
*high urine osmol
*low serum osmol
*low HCT, BUN
*no edema or volume depletion
*normal renal, thyroid and adrenal function
◉diabetes insipidus (DI). Answer: antidiuretic hormone (ADH) is
not secreted, or there is a resistance of the kidney to ADH
◉causes of DI. Answer: Central (failure to produce ADH in brain),
Nephrogenic (insensitivity of the kidney)
◉clinical manifestations of DI. Answer: *classic*
-polydipsia & polyuria- can be so dilute it looks clear, very thirsty
-polydipsia bc serum sodium increased, dilute urine
, *CV- fluid volume depletion*
-hypotension, dec pulse pressure, tachycardia, weak pulsess,
hemoconcentration
*renal*
-inc output (2-20 L/d), dec urine specific gravity
*integumentary*
-dry skin, poor turgor, dry mucous membranes
*neurological- related to hypernatremia*
-inc sensation of thirst, dec cognition, irritability, lethargy to coma,
ataxia
-high sodium not as life threatening as in SIADH
◉Hypertonic hyponatremia. Answer: osmotic shift of water from ICF
to ECF compartment (hyperglycemia).
◉hypotonic (dilutional) hyponatremia. Answer: most common
caused by water retention;
water intoxication
-will see fingerprint edema
◉hypovolemic hypotonic hyponatremia. Answer: -Water and
sodium are both lost, but unequally, with the sodium loss being
greater.
COMPREHENSIVE REVIEW 2026 VERIFIED
QUESTIONS AND SOLUTIONS
◉Vasopressin (ADH). Answer: *regulates blood volume and salt
concentration
* synthesized by cells in hypothalamus
*stored in pituitary gland
exerts effects on V1 and V2 receptors
*pores (aquaporins) stimulated to move into membrane and make
tubular epithelial cells permeable to water
*levels controlled by ECF volume and osmolality
◉Disorders of ADH. Answer: DI and SIADH
◉SIADH. Answer: syndrome of inappropriate antidiuretic hormone
◉Causes of SIADH. Answer: -lung, brain tumors
-cancers of lymphoid tissue
-Prostate CA
,-pancreatic CA
-advanced TB
-severe PNA
◉manifestations of SIADH. Answer: * dilutional hyponatremia
(sodium <135mEq/L)
*crackles
*high urine osmol
*low serum osmol
*low HCT, BUN
*no edema or volume depletion
*normal renal, thyroid and adrenal function
◉diabetes insipidus (DI). Answer: antidiuretic hormone (ADH) is
not secreted, or there is a resistance of the kidney to ADH
◉causes of DI. Answer: Central (failure to produce ADH in brain),
Nephrogenic (insensitivity of the kidney)
◉clinical manifestations of DI. Answer: *classic*
-polydipsia & polyuria- can be so dilute it looks clear, very thirsty
-polydipsia bc serum sodium increased, dilute urine
, *CV- fluid volume depletion*
-hypotension, dec pulse pressure, tachycardia, weak pulsess,
hemoconcentration
*renal*
-inc output (2-20 L/d), dec urine specific gravity
*integumentary*
-dry skin, poor turgor, dry mucous membranes
*neurological- related to hypernatremia*
-inc sensation of thirst, dec cognition, irritability, lethargy to coma,
ataxia
-high sodium not as life threatening as in SIADH
◉Hypertonic hyponatremia. Answer: osmotic shift of water from ICF
to ECF compartment (hyperglycemia).
◉hypotonic (dilutional) hyponatremia. Answer: most common
caused by water retention;
water intoxication
-will see fingerprint edema
◉hypovolemic hypotonic hyponatremia. Answer: -Water and
sodium are both lost, but unequally, with the sodium loss being
greater.
