NR 507 ENDOCRINE SYSTEM, NR507
MIDTERM, NR 507 FINAL EXAM
QUESTIONS AND ANSWERS
beta cells - Answer-responsible for secreting insulin and amylin
inhibits glucagon secretion
delta cells - Answer-responsible for secreting gastrin and somatostatin
F (PP) Cells - Answer-secrete pancreatic polypeptide that stimulates gastric secretions
and antagonizes cholecystokinin.
Criteria to diagnose Diabetes Type 1 and 2 - Answer-FPG ≥126 mg/dL (7.0 mmol/L).
Fasting is defined as no caloric intake for at least 8 h*
OR
2-h PG ≥200 mg/dL (11.1 mmol/L) during OGTT. The test should be performed as
described by the WHO, using a glucose load containing the equivalent of 75 g
anhydrous glucose dissolved in water*
OR
A1C ≥6.5% (48 mmol/mol). The test should be performed in a laboratory using a
method that is NGSP certified and standardized to the DCCT assay*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random
plasma glucose ≥200 mg/dL (11.1 mmol/L)
*In the absence of unequivocal hyperglycemia, diagnosis requires two abnormal test
results from the same sample or in two separate test samples
pre-screening for DM - Answer-HbA1c (as measured in a DCCT-referenced assay)
≥6.5%
OR
FPG ≥126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hr.
OR
2-hr plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random
plasma glucose ≥200 mg/dL (11.1 mmol/L)
Categories of Increased Risk for Diabetes (Prediabetes) - Answer-1. FPG 100 to 125
mg/dL
2. 2-hr PG in the range of 140 to 199 mg/dL during an OGTT
3. HbA1c 5.7% to 6.4%
,Symptoms of hypoglycemia can result from activation of the sympathetic nervous
system to cause neurogenic reactions that occur when the blood glucose drops rapidly:
- Answer-Tachycardia
Palpitations
Diaphoresis
Tremors
Pallor
Arousal anxiety
Other symptoms include:
Headache
Dizziness
Blurred vision
Irritability
Fatigue
Poor judgement
Confusion
Hunger
Seizures
Coma
Treatment of hypoglycemia - Answer-Immediate glucose replacement is required by
either oral or intravenous replacement. For patients who are at high risk for developing
hypoglycemia, glucagon is prescribed for home use. The practitioner should discuss
medications and diet management and proper monitoring of blood glucose levels in the
patient education plan.
DKA pathophysiology - Answer-Insulin deficiency and an increase in counter-regulatory
hormones (catecholamines, cortisol, glucagon and growth hormone) are the most
significant factors for developing DKA.
Under normal circumstances, the counter-regulatory hormones antagonize insulin by
increasing glucose production and decreasing use of glucose by the tissues. Extreme
insulin deficiency results in decreased uptake of glucose, increased fat mobilization and
release of fatty acids and gluconeogenesis, glycogenesis and ketogenesis.
Without insulin, the free fatty acids increase the production of ketone bodies in the liver
at a high rate that exceeds peripheral use. This causes ketone bodies to accumulate
and results in decreased pH and metabolic acidosis.
The buffer system is activated in response to metabolic acidosis. Remember that insulin
also has an antilipolytic effect. When insulin is deficient, there is increased circulating
ketones that contributes to DKA. Also, ketones are normally used by the tissues as an
energy source to produce bicarbonate.
In DKA, the number of ketones and bicarbonate cannot be balanced. Circulating
ketones increase because of impaired use by the peripheral tissues, thus increasing
,strong acids to freely circulate. Bicarbonate buffering does not occur which leads to
metabolic acidosis.
Clinical manifestations of DKA - Answer-Kussmaul respirations: the individual
hyperventilates to compensate for the metabolic acidosis
Postural dizziness
Central nervous system depression
Ketonuria
Anorexia, nausea, vomiting
Abdominal pain
Acetone breath
Dehydration
Thirst
Polyuria
Hyperglycemia causes an osmotic diuresis that leads to polyuria along with dehydration.
Large amounts of glucose are lost in the urine because the blood glucose is higher than
the renal threshold.
Electrolyte abnormalities also occur:
Hyponatremia
Hypophosphatemia
Hypomagnesemia
The most significant electrolyte disturbance is hypokalemia. The potassium drops
because of a shift out of the cell and into the blood caused by the metabolic acidosis.
The blood potassium level, though may appear normal
The diagnosis of DKA is based on the signs and symptoms described above. The
American Diabetes Association's criteria for the diagnosis of DKA include: - Answer-
Serum glucose level >250 mg/dL
Serum bicarbonate level <18
Serum pH <7.30
Presence of an anion gap
Presence of urine and serum ketones
Treatment of DKA - Answer-Treatment is aimed at decreasing the glucose level by
administering insulin. Before administering insulin aggressive fluid replacement and
correction of potassium must occur. Intravenous fluids are given to correct the
potassium level as well as sodium and phosphorous. Throughout treatment, volume
status and potassium levels are monitored closely. Once the individual is stable,
teaching is provided on the causes of DKA and how to avoid it.
Pathophysiology of Hyperosmolar Hyperglycemic Non-Ketoacidosis Syndrome
(HHNKS) - Answer-HHNKS involves insulin deficiency but it is not as pronounced as the
insulin deficiency seen in DKA. Also, the degree of elevated blood glucose and fluid
deficit is more pronounced in HHNKS than in DKA. The follow factors contribute to the
development of HHNKS:
Insulin deficiency
, Increased levels of counter-regulatory or stress hormones (glucagon, catecholamines,
cortisol and growth hormone)
Increased gluconeogenesis and glycogenolysis
Inadequate use of glucose by peripheral tissues (primarily muscle)-characterized by
lack of ketosis
Proinflammatory mediators (TNF-α, IL-6, IL-1β) are also involved that also contribute to
insulin resistance and hyperglycemia.
Less insulin is needed to inhibit fat breakdown needed for effective glucose transport.
Therefore, insulin levels are enough to prevent excessive lipolysis but not to use
glucose effectively.
Clinical manifestations of HHNKS - Answer-Patients with HHNKS will have an extremely
high glucose level. As a result, there will be glycosuria and polyuria. Because of the
amount of glycosuria, the patient is at risk for developing severe volume depletion,
increased serum osmolarity, intracellular dehydration and loss of potassium and other
electrolytes. Neurological symptoms (stupor and coma) may appear as well and worsen
with the degree of hyperosmolarity.
Diagnosis of HHNKS - Answer-The diagnostic features of HHNKS include:
Elevated serum glucose (>600 mg/dL)
Near normal serum bicarbonate level and pH
Serum osmolarity > 320 mOsm/L
Absent or low ketone levels in the urine and serum
Treatment of HHNKS - Answer-The patient will receive an insulin infusion and fluid
replacement. The hypokalemia may be extreme and require several days of infused
potassium to return it to a normal level. Sodium and phosphorous replacement may be
needed as well.
Symptoms of hypoglycemia select all that apply - Answer-Symptoms associated with
hypoglycemia include pallor, sweating, tachycardia, hunger, restlessness, anxiety,
tremors.
An individual who presents with Diabetic Ketoacidosis (DKA) will have a blood glucose
level of >250 mg/dL. - Answer-This statement is true.
Metabolic syndrome is characterized by - Answer-Metabolic syndrome is characterized
by hyperlipidemia, obesity, hypertension.
HHNKS is characterized by increased gluconeogenesis and glycogenolysis - Answer-
true
Vitamin D works with parathyroid hormone (PTH) to promote calcium and phosphate
absorption in the GI tract and bone - Answer-True
MIDTERM, NR 507 FINAL EXAM
QUESTIONS AND ANSWERS
beta cells - Answer-responsible for secreting insulin and amylin
inhibits glucagon secretion
delta cells - Answer-responsible for secreting gastrin and somatostatin
F (PP) Cells - Answer-secrete pancreatic polypeptide that stimulates gastric secretions
and antagonizes cholecystokinin.
Criteria to diagnose Diabetes Type 1 and 2 - Answer-FPG ≥126 mg/dL (7.0 mmol/L).
Fasting is defined as no caloric intake for at least 8 h*
OR
2-h PG ≥200 mg/dL (11.1 mmol/L) during OGTT. The test should be performed as
described by the WHO, using a glucose load containing the equivalent of 75 g
anhydrous glucose dissolved in water*
OR
A1C ≥6.5% (48 mmol/mol). The test should be performed in a laboratory using a
method that is NGSP certified and standardized to the DCCT assay*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random
plasma glucose ≥200 mg/dL (11.1 mmol/L)
*In the absence of unequivocal hyperglycemia, diagnosis requires two abnormal test
results from the same sample or in two separate test samples
pre-screening for DM - Answer-HbA1c (as measured in a DCCT-referenced assay)
≥6.5%
OR
FPG ≥126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hr.
OR
2-hr plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random
plasma glucose ≥200 mg/dL (11.1 mmol/L)
Categories of Increased Risk for Diabetes (Prediabetes) - Answer-1. FPG 100 to 125
mg/dL
2. 2-hr PG in the range of 140 to 199 mg/dL during an OGTT
3. HbA1c 5.7% to 6.4%
,Symptoms of hypoglycemia can result from activation of the sympathetic nervous
system to cause neurogenic reactions that occur when the blood glucose drops rapidly:
- Answer-Tachycardia
Palpitations
Diaphoresis
Tremors
Pallor
Arousal anxiety
Other symptoms include:
Headache
Dizziness
Blurred vision
Irritability
Fatigue
Poor judgement
Confusion
Hunger
Seizures
Coma
Treatment of hypoglycemia - Answer-Immediate glucose replacement is required by
either oral or intravenous replacement. For patients who are at high risk for developing
hypoglycemia, glucagon is prescribed for home use. The practitioner should discuss
medications and diet management and proper monitoring of blood glucose levels in the
patient education plan.
DKA pathophysiology - Answer-Insulin deficiency and an increase in counter-regulatory
hormones (catecholamines, cortisol, glucagon and growth hormone) are the most
significant factors for developing DKA.
Under normal circumstances, the counter-regulatory hormones antagonize insulin by
increasing glucose production and decreasing use of glucose by the tissues. Extreme
insulin deficiency results in decreased uptake of glucose, increased fat mobilization and
release of fatty acids and gluconeogenesis, glycogenesis and ketogenesis.
Without insulin, the free fatty acids increase the production of ketone bodies in the liver
at a high rate that exceeds peripheral use. This causes ketone bodies to accumulate
and results in decreased pH and metabolic acidosis.
The buffer system is activated in response to metabolic acidosis. Remember that insulin
also has an antilipolytic effect. When insulin is deficient, there is increased circulating
ketones that contributes to DKA. Also, ketones are normally used by the tissues as an
energy source to produce bicarbonate.
In DKA, the number of ketones and bicarbonate cannot be balanced. Circulating
ketones increase because of impaired use by the peripheral tissues, thus increasing
,strong acids to freely circulate. Bicarbonate buffering does not occur which leads to
metabolic acidosis.
Clinical manifestations of DKA - Answer-Kussmaul respirations: the individual
hyperventilates to compensate for the metabolic acidosis
Postural dizziness
Central nervous system depression
Ketonuria
Anorexia, nausea, vomiting
Abdominal pain
Acetone breath
Dehydration
Thirst
Polyuria
Hyperglycemia causes an osmotic diuresis that leads to polyuria along with dehydration.
Large amounts of glucose are lost in the urine because the blood glucose is higher than
the renal threshold.
Electrolyte abnormalities also occur:
Hyponatremia
Hypophosphatemia
Hypomagnesemia
The most significant electrolyte disturbance is hypokalemia. The potassium drops
because of a shift out of the cell and into the blood caused by the metabolic acidosis.
The blood potassium level, though may appear normal
The diagnosis of DKA is based on the signs and symptoms described above. The
American Diabetes Association's criteria for the diagnosis of DKA include: - Answer-
Serum glucose level >250 mg/dL
Serum bicarbonate level <18
Serum pH <7.30
Presence of an anion gap
Presence of urine and serum ketones
Treatment of DKA - Answer-Treatment is aimed at decreasing the glucose level by
administering insulin. Before administering insulin aggressive fluid replacement and
correction of potassium must occur. Intravenous fluids are given to correct the
potassium level as well as sodium and phosphorous. Throughout treatment, volume
status and potassium levels are monitored closely. Once the individual is stable,
teaching is provided on the causes of DKA and how to avoid it.
Pathophysiology of Hyperosmolar Hyperglycemic Non-Ketoacidosis Syndrome
(HHNKS) - Answer-HHNKS involves insulin deficiency but it is not as pronounced as the
insulin deficiency seen in DKA. Also, the degree of elevated blood glucose and fluid
deficit is more pronounced in HHNKS than in DKA. The follow factors contribute to the
development of HHNKS:
Insulin deficiency
, Increased levels of counter-regulatory or stress hormones (glucagon, catecholamines,
cortisol and growth hormone)
Increased gluconeogenesis and glycogenolysis
Inadequate use of glucose by peripheral tissues (primarily muscle)-characterized by
lack of ketosis
Proinflammatory mediators (TNF-α, IL-6, IL-1β) are also involved that also contribute to
insulin resistance and hyperglycemia.
Less insulin is needed to inhibit fat breakdown needed for effective glucose transport.
Therefore, insulin levels are enough to prevent excessive lipolysis but not to use
glucose effectively.
Clinical manifestations of HHNKS - Answer-Patients with HHNKS will have an extremely
high glucose level. As a result, there will be glycosuria and polyuria. Because of the
amount of glycosuria, the patient is at risk for developing severe volume depletion,
increased serum osmolarity, intracellular dehydration and loss of potassium and other
electrolytes. Neurological symptoms (stupor and coma) may appear as well and worsen
with the degree of hyperosmolarity.
Diagnosis of HHNKS - Answer-The diagnostic features of HHNKS include:
Elevated serum glucose (>600 mg/dL)
Near normal serum bicarbonate level and pH
Serum osmolarity > 320 mOsm/L
Absent or low ketone levels in the urine and serum
Treatment of HHNKS - Answer-The patient will receive an insulin infusion and fluid
replacement. The hypokalemia may be extreme and require several days of infused
potassium to return it to a normal level. Sodium and phosphorous replacement may be
needed as well.
Symptoms of hypoglycemia select all that apply - Answer-Symptoms associated with
hypoglycemia include pallor, sweating, tachycardia, hunger, restlessness, anxiety,
tremors.
An individual who presents with Diabetic Ketoacidosis (DKA) will have a blood glucose
level of >250 mg/dL. - Answer-This statement is true.
Metabolic syndrome is characterized by - Answer-Metabolic syndrome is characterized
by hyperlipidemia, obesity, hypertension.
HHNKS is characterized by increased gluconeogenesis and glycogenolysis - Answer-
true
Vitamin D works with parathyroid hormone (PTH) to promote calcium and phosphate
absorption in the GI tract and bone - Answer-True
