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NR 507 Advanced Pathophysiology Midterm & Final Exam 2026–2027 | Endocrine System Questions & Verified Answers

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Prepare for the NR 507 Advanced Pathophysiology Midterm and Final Exam 2026–2027 at Chamberlain University with this focused endocrine-system review featuring exam-style questions and verified answers. The material reinforces essential endocrine pathophysiology concepts including hormone regulation, hypothalamic-pituitary function, thyroid and parathyroid disorders, diabetes mellitus, adrenal disorders, pituitary dysfunction, glucose regulation, endocrine feedback mechanisms, hormonal imbalances, clinical manifestations, disease mechanisms, and related physiological alterations. Designed for NR507 graduate nursing students, this resource provides targeted practice for mastering endocrine-system concepts encountered throughout Advanced Pathophysiology exam preparation.

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NR 507 Advanced Pathophysiology Midterm & Final Exam
Endocrine System Questions & 100% Verified Answers |
Complete Exam Review
2026–2027

,The only way for a hormone to work is through the blood False.
stream.
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 True.
to receptors in the cell's cytoplasm
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 True.
hormones
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 False.
protein and it must bind to receptors inside the cell
membrane 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- True.
wake cycle



The posterior lobe of the pituitary produces its own False.
hormones
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 This statement is true.
excretion in the kidneys.



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 Tachycardia
the sympathetic nervous system to cause neurogenic Palpitations
reactions that occur when the blood glucose drops rapidly: 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.

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