NR 507 Endocrine System With 100% correct answers + rationales 2026

The only way for a hormone to work is through the blood stream.

False.

The endocrine cell can also secrete hormones that target cells directly close it. When this occurs, this type of secretion is known as paracrine signaling.

Lipid-derived hormones cross the cell membrane and bind to receptors in the cell's cytoplasm

True.

This statement is true. Lipid-derived hormones cross the cell membrane and bind to receptors in the cell's cytoplasm.

The anterior lobe of the pituitary produces its own hormones

True.

This statement is true. The anterior lobe of the pituitary produces its own hormones

To be considered a lipid hormone, it must be bound to a protein and it must bind to receptors inside the cell membrane

False.

It must be bound to a protein and it bind to receptors on the cell membrane rather than inside the cell membrane.

The pineal gland is responsible for regulating the sleep-wake cycle

True.

The posterior lobe of the pituitary produces its own hormones

False.

The posterior pituitary receives its hormones (oxytocin and ADH) from the hypothalamus. The anterior pituitary produces its own hormones.

Aldosterone promotes sodium reabsorption and potassium excretion in the kidneys.

This statement is true.

Hyperthyroidism

Elevated Thyroid Hormone

Suppressed TSH

Enlarged liver

Hand tremors

Hypothyroidism

Decreased thyroid hormone and

Elevated TSH

Fatigue

Diminished deep tendon reflexes

Type 1 DM

Onset 1<10-20 years

Associated with diabetic ketoacidosis

Symptoms: polyuria, polyphagia, polydipsia

Autoimmune:Genetic and environmental factors, resulting in gradual process of autoimmune destruction in genetically susceptible individuals

Nonautoimmune:Unknown

Strong association with HLA-DQA and HLA-DQB genes

acute complications: Diabetic ketoacidosis

Type 2 DM

Usually > 40 years of age

Associated with hyperosmolar nonketotic coma

Symptoms: weakness, weight loss, infections

Results from genetic susceptibility (polygenic) combined with environmental determinants and other risk factors

Inherited defects in beta-cell mass and function combined with peripheral tissue insulin resistance

Associated with long-duration obesity

strong genetic association

Acute complications: Hyperosmolar nonketotic coma

alpha cells

responsible for secreting glucagon

beta cells

responsible for secreting insulin and amylin

inhibits glucagon secretion

delta cells

responsible for secreting gastrin and somatostatin

F (PP) Cells

secrete pancreatic polypeptide that stimulates gastric secretions and antagonizes cholecystokinin.

Criteria to diagnose Diabetes Type 1 and 2

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

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)

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:

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

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

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

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:

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

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)

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

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

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

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

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.

This statement is true.

Metabolic syndrome is characterized by

Metabolic syndrome is characterized by hyperlipidemia, obesity, hypertension.

HHNKS is characterized by increased gluconeogenesis and glycogenolysis

true

Vitamin D works with parathyroid hormone (PTH) to promote calcium and phosphate absorption in the GI tract and bone

True

hyperparathyroidism

Primary hyperparathyroidism- Hyperfunction of parathyroid cells due to adenoma

Secondary: Stimulation of parathyroid in response to hypocalcemia

Tertiary: Long term stimulation of parathyroid leads to hyperplasia

Treatment of secondary hyperparathyroidism involves calcium replacement, dietary phosphate restriction, phosphate binders and vitamin D replacement.

true

Decreased circulating PTH results in decreased serum calcium levels and decreased serum phosphate levels.

FALSE- Serum phosphate levels increase.

Chvostek sign is elicited by tapping the cheek that will result in twitching of the upper lip

True. associated with hypocalcemia

Primary hyperparathyroidism

pathology: Hyperfunction of parathyroid cells due to hyperplasia, adenoma or carcinoma.

May be associated with multiple endocrine neoplasia.

high serum calcium

low/normal serum phosphate

Management: Usually surgery if symptomatic. Cincacalcet can be considered in those not fit for surgery.

Secondary hyperparathyroidism

Physiological stimulation of parathyroid in response to hypocalcaemia.

Usually due to chronic renal failure or other causes of Vitamin D deficiency.

low/normal serum calcium

high serum phosphate

treatment of underlying cause

Tertiary hyperparathyroidism

Following long term physiological stimulation leading to hyperplasia

Seen in chronic renal failure

high serum Calcium

high serum phosphate

Usually cinacalcet or surgery in those that don't respond.

MEN 1 (multiple endocrine neoplasia)

involves tumors of the pancreas, parathyroid glands or pituitary gland. Tumors most often appear in the parathyroid glands which can lead to the first sign of disease, hypercalcemia.

MEN 2

divided into three subtypes

Type IIA: (90% of cases), parathyroid hyperplasia, medullary thyroid carcinoma, pheochromocytoma (pheochromocytoma which is an adrenal gland tumor that can cause extreme hypertension.)

Type IIB: mucosal nueromas, marfanoid body habitus, medullary thyroid carcinoma, pheochromocytoma

Familial medullary thyroid carcinoma (FMTC)

Hypercalcemic manifestations

neuromuscular: includes paresthesias, muscle cramps and weakness and diminished deep tendon reflexes.

CNS: may include malaise, fatigue, headache, mental exhaustion, insomnia, irritability and depression

Cardio: may include hypertension, palpitations, prolonged P-R interval, shortened Q-T interval, bradyarrhythmias, heart block and asystole.

Kidney: polyuria and polydipsia due to hypercalcemia-induced diabetes insipidus

GI: anorexia, nausea, heartburn, vomiting, weight loss, abdominal pain, and constipation.

hypercalcemia is the hallmark finding of primary hyperparathyroidism.

Serum adjust total calcium level will be greater than 10.5 mg/dL.

Assessment of urinary calcium excretion is recommended to confirm the diagnosis of hyperparathyroidism.

Urine calcium excretion may be high or normal in primary hyperthyroidism (100-300 mg/day).

Serum phosphate will be less than 2.5 mg/dL due to the excessive loss of phosphate in the urine. A serum calcium-phosphate ratio above 2.5 mg/dL helps to confirm the diagnosis of primary hyperparathyroidism

Vitamin D deficiency is common in hyperparathyroidism. Patient should be screened. Serum 25-OH vitamin D levels below 20 mcg/L can enhance hyperparathyroidism and bone-related symptoms.

Hypoparathyroidism

is an abnormally low PTH level cause by damage or removal of the parathyroid glands during thyroid surgery. Is also associated with genetic syndromes (DiGeorge syndrome), autoimmunity and familial disposition. A low magnesium can also cause a decrease in PTH secretion.

diagnosis of hypoparathyroidism

The patient will present with a low serum calcium level and a high phosphorous level. PTH levels will be low. A serum magnesium and urinary calcium excretion will help in diagnosing hypoparathyroidism.

treatment of hypoparathyroidism

The goal of treatment is to alleviate hypocalcemia. In an acute state, the patient will receive intravenous calcium to quickly correct the serum calcium. Maintenance of calcium level is managed through oral calcium and an active form of vitamin D. PTH replacement therapy with recombinant human parathyroid hormone (thPTH [1-84]) will help to reduce the need for supplemental calcium and vitamin D. Serum calcium and phosphate levels will be monitored for return to normal following treatment.

Trousseau sign will result in painful, carpal spasm.

true

serum magnesium and urinary calcium excretion will help in diagnosing hypoparathyroidism

true

Signs of hypocalcemia

Dry skin

Loss of body and scalp hair

Hypoplasia of developing teeth

Horizontal ridges on the nails

hypocalcemia lab values would reflect:

Correct lab values for hypocalcemia are high phosphorous level, and low PTH level.

Chromaffin cells are the site of production for epinephrine and norepinephrine.

This statement is true.

The adrenal cortex is stimulated by the adrenocorticotropic hormone (ACTH) from the anterior pituitary.

This statement is true. The adrenal cortex is stimulated by the adrenocorticotropic hormone (ACTH) from the anterior pituitary.

Cortisol secretion is regulated by the hypothalamus and the anterior pituitary

true

Zona glomerulosa

Aldosterone is produced

Zona fasciculata

Cortisol is secreted

Zona reticularis

Aldosterone is secreted

Glucocorticoids also have effects on other areas:

Inhibits bone formation

Inhibits antidiuretic hormone (ADA) secretion

Stimulate gastric acid secretion

Potentiates the effects of catecholamines

Potentiates the effects of thyroid and growth hormone effects on adipose tissue

Altered mood due to one of the metabolites of cortisol that depresses nerve cell function in the brain. Mood can fluctuate with steroid level fluctuations that occur in disease or stress states.

Increased number of circulating erythrocytes (polycythemia)

Increased appetite

Promotion of fat deposition in the face and cervical area

Increased uric acid excretion

Decreased calcium level (inhibits GI absorption of calcium)

Suppressed synthesis and secretion of ACTH

Inhibits somatic growth (interferes with action of growth hormone)

Adrenal cortex effects

Maintenance of gland size

Depletion of ascorbic acid

Activation of adenylyl cyclase

Conversion of cholesterol to pregnenolone

Maintenance of enzymes active in converting pregnenolone to other steroids

Accumulation of cholesterol for steroid hormone synthesis

Secretion of cortisol and adrenal androgens

extra-adrenal effects

Stimulation of melanocytes

Activation of tissue lipase

Co-morbidities of Cushing's syndrome

include diabetes, osteoporosis, psychiatric disorders, muscle weakness, hypokalemia, infections.

Diagnostic tests appropriate for Cushing's syndrome include

No cortisol diurnal variation.

No suppression of cortisol after dexamethasone administration.

Increased production of cortisol.

Suppression of plasma ACTH by hypercortisolism due to an adrenal nodule.

Primary hypocortisolism

Lack of production and secretion of the adrenocortical hormones

Secondary hypocortisolism

Caused by inadequate stimulation of the adrenal glands by ACTH.

tertiary hypocortisolism

caused when exogenous glucocorticoids are abruptly withdrawn

The effect of catecholamines is vasodilation

False (vasoconstriction)

Which of the following is considered a treatment option for Cushing's disease

Transsphenoidal

hypophysectomy

LaparoscopyResection