CCRN REVIEW EXAM 2025
QUESTIONS AND ANSWERS
SIADH - ANSWER-too much ADH
low Na, hypo-osmolar, low UOP
ADH - ANSWER-made in hypothalamus
stored in pituitary
released to kidney and makes kidney hold onto h20
serum osmolarity - ANSWER-Na X2
275-295
low=fluid overloaded
high=concentrated
SIADH CAUSES - ANSWER-oat cell carcinoma (bronchogenic CA)-makes its
own ADH
Viral PNA
Head Problem
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 1
,inc. serum osmo, anesthesia, analgesics, stress
COMPLICATIONS OF SIADH - ANSWER-Sz's
TREATMENT of SIADH - ANSWER-get rid of causes
fluid restrictions
hypertonic solutions (3%, D5NS, D51/2NS) give 25-50cc/hr d/t CHF
DI - ANSWER-No ADH (no h20 at kidney)
inc Na+ levels, inc osmolarity, inc. UOP (spec grav 1.001-1.005)
DI Causes - ANSWER-head problems
dilantin
DI Treatment - ANSWER-Give ADH (PItressin or vasopressin)
Give fluids to increase Intravascular volume
monitor UOP
*monitor fo ischemia
Hypoglycemia - ANSWER-CVS s/s
tachycardia, palpitations, diaphoresis, irritable, restlessness
CNS s/s
confusion, lethargy, slurred speech, sz, coma
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 2
,hypoglycemia pathophys - ANSWER-low glucose->adrenal medulla knows and
releases adrenaline->liver releases glycogen which is converted into glucose to
increase BGL
if block in adrenaline or liver cant convert glycogen into glucose (AKA BETA
BLOCKERS) then CVS s/s wont occur
DKA s/s - ANSWER-only in insulin dependent diabetics
BGL 400-900
dehydrated (4-6L lost)
No circulating insulin
+acidosis b/c body breaks down fat into ketones
Kussmaul (inc rate depth to blow off c02)
DKA and HHNK treatment - ANSWER-insulin gtt
IVF (more for HHNK)
NS 1st- to hydrate vascular compartment
1/2NS to hydrate cell
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 3
, D51/2NS to prevent hypoglycemia
**for every decrease in pH by 0.1, K+increases by 0.6
HHNK vulnerable population - ANSWER-OLD AGE (pancrease gets tired)
diet controlled diabetics
people on TPN (gets 80% glucose IV->pancreatic fatigue
pancreatitis
HHNK s/s - ANSWER-BGL 1000-2000
Severe dehydration (6-8L lost)
+insulin (prevents breakdown of fat)
No acidosis (baby breaths)
somogyi phenomenon - ANSWER-Rapid decrease in serum glucose, usually at
night, that generates the release of glucose-elevating hormones that manifests as an
elevated glucose level in the morning.
dehydration is not a component of this
NPH peak - ANSWER-6-10 hrs
Pancreatitits - ANSWER-obstruction of pancreatic ducts
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 4
QUESTIONS AND ANSWERS
SIADH - ANSWER-too much ADH
low Na, hypo-osmolar, low UOP
ADH - ANSWER-made in hypothalamus
stored in pituitary
released to kidney and makes kidney hold onto h20
serum osmolarity - ANSWER-Na X2
275-295
low=fluid overloaded
high=concentrated
SIADH CAUSES - ANSWER-oat cell carcinoma (bronchogenic CA)-makes its
own ADH
Viral PNA
Head Problem
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 1
,inc. serum osmo, anesthesia, analgesics, stress
COMPLICATIONS OF SIADH - ANSWER-Sz's
TREATMENT of SIADH - ANSWER-get rid of causes
fluid restrictions
hypertonic solutions (3%, D5NS, D51/2NS) give 25-50cc/hr d/t CHF
DI - ANSWER-No ADH (no h20 at kidney)
inc Na+ levels, inc osmolarity, inc. UOP (spec grav 1.001-1.005)
DI Causes - ANSWER-head problems
dilantin
DI Treatment - ANSWER-Give ADH (PItressin or vasopressin)
Give fluids to increase Intravascular volume
monitor UOP
*monitor fo ischemia
Hypoglycemia - ANSWER-CVS s/s
tachycardia, palpitations, diaphoresis, irritable, restlessness
CNS s/s
confusion, lethargy, slurred speech, sz, coma
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 2
,hypoglycemia pathophys - ANSWER-low glucose->adrenal medulla knows and
releases adrenaline->liver releases glycogen which is converted into glucose to
increase BGL
if block in adrenaline or liver cant convert glycogen into glucose (AKA BETA
BLOCKERS) then CVS s/s wont occur
DKA s/s - ANSWER-only in insulin dependent diabetics
BGL 400-900
dehydrated (4-6L lost)
No circulating insulin
+acidosis b/c body breaks down fat into ketones
Kussmaul (inc rate depth to blow off c02)
DKA and HHNK treatment - ANSWER-insulin gtt
IVF (more for HHNK)
NS 1st- to hydrate vascular compartment
1/2NS to hydrate cell
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 3
, D51/2NS to prevent hypoglycemia
**for every decrease in pH by 0.1, K+increases by 0.6
HHNK vulnerable population - ANSWER-OLD AGE (pancrease gets tired)
diet controlled diabetics
people on TPN (gets 80% glucose IV->pancreatic fatigue
pancreatitis
HHNK s/s - ANSWER-BGL 1000-2000
Severe dehydration (6-8L lost)
+insulin (prevents breakdown of fat)
No acidosis (baby breaths)
somogyi phenomenon - ANSWER-Rapid decrease in serum glucose, usually at
night, that generates the release of glucose-elevating hormones that manifests as an
elevated glucose level in the morning.
dehydration is not a component of this
NPH peak - ANSWER-6-10 hrs
Pancreatitits - ANSWER-obstruction of pancreatic ducts
....COPYRIGHT ©️ 2025 ALL RIGHTS RESERVED...TRUSTED & VERIFIED 4
