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MARYVILLE UNIVERSITY NURSING PROGRAM NURS 611 – ADVANCEDPATHOPHYSIOLOG Y Study Guide Questions for Exam 3 LATEST 2023/2024

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MARYVILLE UNIVERSITY NURSING PROGRAM NURS 611 – ADVANCEDPATHOPHYSIOLOG Y Study Guide Questions for Exam 3 LATEST 2023/2024 Study Guide Questions for Exam 3 1. Explain the pathophysiology associate with Type 1 and Type 2 DM. Type 1 diabetes occurs as a result of the body's immune system attacking the insulin producing beta cells of the pancreas, although it is not clear why this happens. A lack of insulin in the blood means inadequate amounts of glucose are taken up by cells of the body to provide energy for cellular functions. Consequently, glucose remains in the blood leading to a high blood sugar level. Exactly what causes the immune system to do this is not yet clearly understood. Type 2 diabetes mellitus consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. 2. Explain what occurs in panhypopituitarism. Panhypopituitarism is the term correctly associated with the lack of all anterior pituitary hormones. 3. List the clinical manifestations of hypothyroidism. Constipation, decreased heat rate, and lethargy. The lower levels of thyroid hormone result in decreased energy metabolism resulting in constipation, bradycardia, and lethargy. 4. Differentiate diabetes insipidus, diabetes mellitus and SIADH. Diabetes insipidus is a result of insufficient ADH. 5. What causes the microvascular complications of DM. Microvascular complications are a result of capillary basement membranes thickening and endothelial cell hyperplasia. 6. What is the cause of diabetes insipidus. Diabetes insipidus is a result of insufficient ADH. 7. Describe the pathophysiological changes associated with Addison’s Disease. Addison disease (or Addison's disease) is adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex. It affects glucocorticoid and mineralocorticoid function. T

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MARYVILLE UNIVERSITY
NURSING PROGRAM NURS 611 –
ADVANCEDPATHOPHYSIOLOG
Y Study Guide Questions for Exam 3
LATEST 2023/2024

,Study Guide Questions for Exam 3
1. Explain the pathophysiology associate with Type 1 and Type 2 DM.
Type 1 diabetes occurs as a result of the body's immune system attacking the insulin producing beta

cells of the pancreas, although it is not clear why this happens. A lack of insulin in the blood means

inadequate amounts of glucose are taken up by cells of the body to provide energy for cellular

functions. Consequently, glucose remains in the blood leading to a high blood sugar level. Exactly

what causes the immune system to do this is not yet clearly understood. Type 2 diabetes mellitus

consists of an array of dysfunctions characterized by hyperglycemia and resulting from the

combination of resistance to insulin action, inadequate insulin secretion, and excessive or

inappropriate glucagon secretion.


2. Explain what occurs in panhypopituitarism.
Panhypopituitarism is the term correctly associated with the lack of all anterior pituitary hormones.


3. List the clinical manifestations of hypothyroidism.
Constipation, decreased heat rate, and lethargy. The lower levels of thyroid hormone result in

decreased energy metabolism resulting in constipation, bradycardia, and lethargy.


4. Differentiate diabetes insipidus, diabetes mellitus and SIADH.
Diabetes insipidus is a result of insufficient ADH.


5. What causes the microvascular complications of DM.
Microvascular complications are a result of capillary basement membranes thickening and endothelial

cell hyperplasia.


6. What is the cause of diabetes insipidus.
Diabetes insipidus is a result of insufficient ADH.


7. Describe the pathophysiological changes associated with Addison’s Disease.
Addison disease (or Addison's disease) is adrenocortical insufficiency due to the destruction or

dysfunction of the entire adrenal cortex. It affects glucocorticoid and mineralocorticoid function. The

, onset of disease usually occurs when 90% or more of both adrenal cortices are dysfunctional or

destroyed.


8. Describe the pathophysiological changes associated with hypoparathyroidism.
Hypoparathyroidism is a condition of parathyroid hormone (PTH) deficiency. Primary

hypoparathyroidism is a state of inadequate PTH activity. In the absence of adequate PTH activity, the

ionized calcium concentration in the extracellular fluid falls below the reference range. Primary

hypoparathyroidism, the subject of this article, is a syndrome resulting from iatrogenic causes or one

of many rare diseases. Secondary hypoparathyroidism is a physiologic state in which PTH levels are

low in response to a primary process that causes hypercalcemia.


9. What are the causes and pathophysiological changes associate with ketoacidosis?
Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency,

associated with high blood levels of sugar level and organic acids called ketones. Diabetic

ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with

proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus

(T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes

typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it

may occur at any age. Males and females are equally affected.


10. What is acromegaly?
Acromegaly is a hormonal disorder that develops when your pituitary gland produces too much

growth hormone during adulthood. When this happens, your bones increase in size, including those of

your hands, feet and face. Acromegaly usually affects middle-aged adults.


11. Differentiate hypothyroidism and Graves’ disease.
Hypothyroidism is a lack of thyroid hormone. Graves' disease is over production of thyroid hormone.


12. Describe the pathophysiology related to chronic DM.
Chronic symptoms of diabetes are due to vascular damage from persistent hyperglycemia. Vascular
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