Signs and symptoms indicative of diabetic ketoacidosis (DKA) include:
A. Unexplained increase in urine output of >200ml/hour x 2 hours, urine specific
gravity <1.005, hypernatremia.
B. Polyuria, polydipsia, Kussmaul's breathing, ketones in urine.
C. Polyuria, polydipsia, rapid shallow respirations, ketone free urine.
D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia.
Give this one a try later!
B. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic
Syndrome (HHNS) both present with polyuria and polydipsia. DKA
presentation includes Kussmaul's respiratory pattern (deep gasping air
hunger) secondary to metabolic acidosis and there are ketones present in
the urine. The respiratory pattern with HHNS is rapid and shallow and there
are no ketones present in the urine.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized
by an excess of antidiuretic hormone or an enhanced response. This results
in a volume overload state as the urine output drops considerably and fluid
retention occurs. As urine output decreases, the urine becomes more
concentrated and urine specific gravity will increase. Additionally, as the
patient becomes volume overloaded the sodium levels will decrease
secondary to the hypervolemia.
, Diabetes insipidus (DI) is characterized by a decrease or absence of
antidiuretic hormone. One early sign is an unexplained increase in urine
output of > 200 ml/hr over 2 hours. As excessive urine production
continues the urine becomes more dilute and the urine specific gravity
deceases. Hypernatremia occurs secondary to the dehydration.
You are monitoring the glucose levels hourly on your patient with diabetic
ketoacidosis and note that she was admitted with a glucose level of 532. Her hourly
levels have been as follows:
1 hour 486 mg/dL
2 hour 415 mg/dL
3 hour 302 mg/dL
In reviewing these values you know:
A. A reduction in blood sugar greater than 100 mg/dL is dangerous and can result in
the rapid development of cerebral edema and hypokalemia.
B. The blood glucose level remains too high putting the patient at risk for continued
hypovolemia and will need more aggressive treatment of the blood sugar.
C. The reduction in blood sugar is appropriate and the infusion of normal saline
should have glucose added to it to prevent the development of cerebral edema.
D. This gradual decline in blood glucose levels is appropriate and you should
continue current therapy.
Give this one a try later!
A. Blood sugar levels should not be reduced any faster than 100mg/dL. A
rapid reduction in blood sugar levels can result in the development of
cerebral edema as glucose quickly moves from outside the cell into the
cell. This transfer of the large glucose molecules will then draw volume into
the cell. If this is done too quickly cerebral edema can occur.
As similar effect occurs with potassium. As insulin moves glucose into the
cell potassium follows and moves from extracellular to intracellular. This will
drop the serum potassium level and hypokalemia can result if this occurs
too quickly.
Dextrose is added to normal saline solutions only after the blood sugar has
dropped to < 250 mg/dL.
,During the treatment of diabetic ketoacidosis the patient may experience a drop in
potassium as potassium moves back into the cell. Which of the following treatment
strategies is responsible for the movement of potassium from the extracellular fluid to
the cell:
A. Dextrose.
B. Bicarbonate infusion.
C. Insulin.
D. Potassium administration.
Give this one a try later!
C. Insulin will result in the movement of potassium from the extracellular
fluid back into the cell. As DKA and metabolic acidosis develops hydrogen
ions move from extracellular fluid into the cell. In an attempt to maintain
electrolyte balance potassium moves from the cell to the extracellular fluid.
The administration of insulin will move hydrogen ions back to the
extracellular fluid and allow potassium to reenter the cell.
Primary assessment findings consistent with the development of diabetes insipidus
(DI) include:
A. Polyuria, polydipsia, rapid shallow respirations, ketone free urine.
B. Polyuria, polydipsia, Kussmaul's Breathing, ketones in urine.
C. Unexplained increase in urine output of 200ml/hour x 2 hours, urine specific gravity
<1.005, hypernatremia.
D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia.
Give this one a try later!
, C. Diabetes insipidus (DI) is characterized by a decrease or absence of
antidiuretic hormone. One early sign is an unexplained increase in urine
output of > 200 ml/hr over 2 hours. As excessive urine production
continues the urine becomes more dilute and the urine specific gravity
deceases. Hypernatremia occurs secondary to the dehydration.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized
by an excess of antidiuretic hormone or an enhanced response. This results
in a volume overload state as the urine output drops considerably and fluid
retention occurs. As urine output decreases, the urine becomes more
concentrated and urine specific gravity will increase. Additionally, as the
patient becomes volume overloaded the sodium levels will decrease
secondary to the hypervolemia.
Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic
Syndrome (HHNS) both present with polyuria and polydipsia. DKA
presentation includes Kussmaul's respiratory pattern secondary to
metabolic acidosis and there are ketones present in the urine. The
respiratory pattern with HHNS is rapid and shallow and there are no
ketones present in the urine.
You patient with diabetic ketoacidosis was admitted 4 hours ago and is being treated
with IV fluids and IV insulin. His initial lab work demonstrated a blood glucose level of
585 mg/dl, pH of 7.30, potassium of 3.6 mEq/L. His repeat lab work is as follows:
glucose 302 mg/dl, pH of 7.35, potassium of 3.6 mEq/L. Based on these findings you
would anticipate the following changes:
A. Change from IV insulin to SQ insulin.
B. Administer bicarbonate to continue to correct the acidosis.
C. Change the IV fluid from 0.9% normal saline to D5.45%normal.
D. Administer potassium.
Give this one a try later!
D. As insulin administration continues, extracellular potassium will be driven
into the cell and the serum potassium level will continue to drop putting
the patient at risk for hypokalemia.
The pH is back to low normal. There is no support for the administration of
bicarbonate unless the patient is severely acidotic - pH < 7.0.
When the patient's blood sugar nears 250mg/dl it is important to add
dextrose to the IV fluids to prevent the development of cerebral edema.
A. Unexplained increase in urine output of >200ml/hour x 2 hours, urine specific
gravity <1.005, hypernatremia.
B. Polyuria, polydipsia, Kussmaul's breathing, ketones in urine.
C. Polyuria, polydipsia, rapid shallow respirations, ketone free urine.
D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia.
Give this one a try later!
B. Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic
Syndrome (HHNS) both present with polyuria and polydipsia. DKA
presentation includes Kussmaul's respiratory pattern (deep gasping air
hunger) secondary to metabolic acidosis and there are ketones present in
the urine. The respiratory pattern with HHNS is rapid and shallow and there
are no ketones present in the urine.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized
by an excess of antidiuretic hormone or an enhanced response. This results
in a volume overload state as the urine output drops considerably and fluid
retention occurs. As urine output decreases, the urine becomes more
concentrated and urine specific gravity will increase. Additionally, as the
patient becomes volume overloaded the sodium levels will decrease
secondary to the hypervolemia.
, Diabetes insipidus (DI) is characterized by a decrease or absence of
antidiuretic hormone. One early sign is an unexplained increase in urine
output of > 200 ml/hr over 2 hours. As excessive urine production
continues the urine becomes more dilute and the urine specific gravity
deceases. Hypernatremia occurs secondary to the dehydration.
You are monitoring the glucose levels hourly on your patient with diabetic
ketoacidosis and note that she was admitted with a glucose level of 532. Her hourly
levels have been as follows:
1 hour 486 mg/dL
2 hour 415 mg/dL
3 hour 302 mg/dL
In reviewing these values you know:
A. A reduction in blood sugar greater than 100 mg/dL is dangerous and can result in
the rapid development of cerebral edema and hypokalemia.
B. The blood glucose level remains too high putting the patient at risk for continued
hypovolemia and will need more aggressive treatment of the blood sugar.
C. The reduction in blood sugar is appropriate and the infusion of normal saline
should have glucose added to it to prevent the development of cerebral edema.
D. This gradual decline in blood glucose levels is appropriate and you should
continue current therapy.
Give this one a try later!
A. Blood sugar levels should not be reduced any faster than 100mg/dL. A
rapid reduction in blood sugar levels can result in the development of
cerebral edema as glucose quickly moves from outside the cell into the
cell. This transfer of the large glucose molecules will then draw volume into
the cell. If this is done too quickly cerebral edema can occur.
As similar effect occurs with potassium. As insulin moves glucose into the
cell potassium follows and moves from extracellular to intracellular. This will
drop the serum potassium level and hypokalemia can result if this occurs
too quickly.
Dextrose is added to normal saline solutions only after the blood sugar has
dropped to < 250 mg/dL.
,During the treatment of diabetic ketoacidosis the patient may experience a drop in
potassium as potassium moves back into the cell. Which of the following treatment
strategies is responsible for the movement of potassium from the extracellular fluid to
the cell:
A. Dextrose.
B. Bicarbonate infusion.
C. Insulin.
D. Potassium administration.
Give this one a try later!
C. Insulin will result in the movement of potassium from the extracellular
fluid back into the cell. As DKA and metabolic acidosis develops hydrogen
ions move from extracellular fluid into the cell. In an attempt to maintain
electrolyte balance potassium moves from the cell to the extracellular fluid.
The administration of insulin will move hydrogen ions back to the
extracellular fluid and allow potassium to reenter the cell.
Primary assessment findings consistent with the development of diabetes insipidus
(DI) include:
A. Polyuria, polydipsia, rapid shallow respirations, ketone free urine.
B. Polyuria, polydipsia, Kussmaul's Breathing, ketones in urine.
C. Unexplained increase in urine output of 200ml/hour x 2 hours, urine specific gravity
<1.005, hypernatremia.
D. Urine output less than 500 ml/24 hours, urine specific gravity >1.010, hyponatremia.
Give this one a try later!
, C. Diabetes insipidus (DI) is characterized by a decrease or absence of
antidiuretic hormone. One early sign is an unexplained increase in urine
output of > 200 ml/hr over 2 hours. As excessive urine production
continues the urine becomes more dilute and the urine specific gravity
deceases. Hypernatremia occurs secondary to the dehydration.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized
by an excess of antidiuretic hormone or an enhanced response. This results
in a volume overload state as the urine output drops considerably and fluid
retention occurs. As urine output decreases, the urine becomes more
concentrated and urine specific gravity will increase. Additionally, as the
patient becomes volume overloaded the sodium levels will decrease
secondary to the hypervolemia.
Diabetic Ketoacidosis (DKA) and Hypertonic Hyperosmolar Non-Ketotic
Syndrome (HHNS) both present with polyuria and polydipsia. DKA
presentation includes Kussmaul's respiratory pattern secondary to
metabolic acidosis and there are ketones present in the urine. The
respiratory pattern with HHNS is rapid and shallow and there are no
ketones present in the urine.
You patient with diabetic ketoacidosis was admitted 4 hours ago and is being treated
with IV fluids and IV insulin. His initial lab work demonstrated a blood glucose level of
585 mg/dl, pH of 7.30, potassium of 3.6 mEq/L. His repeat lab work is as follows:
glucose 302 mg/dl, pH of 7.35, potassium of 3.6 mEq/L. Based on these findings you
would anticipate the following changes:
A. Change from IV insulin to SQ insulin.
B. Administer bicarbonate to continue to correct the acidosis.
C. Change the IV fluid from 0.9% normal saline to D5.45%normal.
D. Administer potassium.
Give this one a try later!
D. As insulin administration continues, extracellular potassium will be driven
into the cell and the serum potassium level will continue to drop putting
the patient at risk for hypokalemia.
The pH is back to low normal. There is no support for the administration of
bicarbonate unless the patient is severely acidotic - pH < 7.0.
When the patient's blood sugar nears 250mg/dl it is important to add
dextrose to the IV fluids to prevent the development of cerebral edema.
