Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH.

Question 1
Needs Grading

A 67-year-old Caucasian woman was brought to the clinic by her son who stated that his mother had become slightly confused over the past several days. She had been stumbling at home and had fallen once but was able to ambulate with some difficulty. She had no other obvious problems and had been eating and drinking. The son became concerned when she forgot her son’s name, so he thought he better bring her to the clinic.
PMH-Type II diabetes mellitus (DM) with peripheral neuropathy x 20 years. COPD. Depression after death of spouse several months ago

Social/family hx – non contributary except for 30 pack/year history tobacco use.

Meds: Metformin 500 mg po BID, ASA 81 mg po qam, escitalopram (Lexapro) 5 mg po q am started 2 months ago

Labs-CBC WNL; Chem 7- Glucose-92 mg/dl, BUN 18 mg/dl, Creatinine 1.1 mg/dl, Na+120 mmol/L,

K+4.2 mmol/L, CO237 m mol/L, Cl–97 mmol/L.

The APRN refers the patient to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH).

Question:

Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH.

Correct Answer:
SIADH is a group of symptoms that occurs when antidiuretic hormone (ADH, arginine vasopressin) is secreted in the absence of osmotic or physiologic stimuli. These stimuli include: Increased serum osmolality, decreased plasma volume, and hypotension. A decrease in plasma osmolality normally inhibits ADH production and secretion. SIADH is characterized by fluid retention, dilutional hyponatremia, hypochloremia, concentrated urine, and lack of intravascular volume depletion. SIADH is characterized by normal to increased blood volume in normoproteinemia, nonedematous, and hyponatremic patients with normal renal and endocrine function. ADH regulates the body’s water balance. It is synthesized in the hypothalamus and stored in the posterior pituitary gland. When released into the circulation, it acts on the kidney’s distal tubules and collecting ducts, increasing their permeability to water. This decreases urine volume because more water is being reabsorbed and returned to the circulation. It also serves to produce more concentrated urine.

Question 2
Needs Grading

A 43-year-old female presents to the clinic with a chief complaint of fever, chills, nausea and vomiting and weakness. She has been unable to keep any food, liquids or medications down. The symptoms began 3 days ago and have not responded to ibuprofen, acetaminophen, or Nyquil when she tried to take them. The temperature has reached as high as 102˚F.

Allergies: none known to drugs or food or environmental

Medications-20 mg prednisone po qd, omeprazole 10 po qam

PMH-significant for 20-year history of steroid dependent rheumatoid arthritis (RA). GERD. No other significant illnesses or surgeries.

Social-denies alcohol, illicit drugs, vaping, tobacco use

Physical exam

Thin, ill appearing woman who is sitting in exam room chair as she said she was too weak to climb on the exam table. VS Temp 101.2˚F, BP 98/64, pulse 110, Resp 16, PaO2 96% on room air.

ROS negative other than GI symptoms.

Based on the patient’s clinical presentation, the APRN diagnoses the patient as having secondary hypocortisolism due to the lack of prednisone the patient was taking for her RA secondary to vomiting.

Question:

Explain why the patient exhibited these symptoms?

Correct Answer:
An adrenal insufficiency requires some type of trigger or stressor such as surgery, trauma, infection or acute withdrawal of glucocorticoids. The patient had several factors contributing to her present situation. She had RA x 20 years that necessitated oral prednisone. Increased levels of both glucocorticoids (primarily cortisol) and mineralocorticoids (primarily aldosterone) are needed for the body to adapt to the stress Corticotropin-releasing hormone (CRH) from the hypothalamus eventually prompts release of ACTH from the anterior pituitary gland. ACTH then stimulates release and 3 synthesis of cortisol from the adrenal cortex. Cortisol mobilizes amino acids from skeletal muscle and generally enhances the liver’s capacity for gluconeogenesis as well as enhances normal immune activity and maintenance of cardiovascular integrity. It also influences fat, carbohydrate and protein. Catecholamines cause vasoconstriction, which in the kidney, probably initiates release of renin, stimulating the rennin-angiotensionaldosterone-system (RAAS). Antidiuretic hormone (ADH, also called vasopressin), is released from the hypothalamus and posterior pituitary during periods of stress. Both aldosterone and ADH attempt to conserve water and electrolytes to sustain a sufficient vascular volume.

Question 3
Needs Grading

A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had about of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved.
The APRN examining the patient orders a Chem 7 which revealed a serum Ca++ of 13.1 mg/dl. The APN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist who does a complete work up and concurs with the APRN’s diagnosis.

Question:

What is the role of parathyroid hormone in the development of primary hyperparathyroidism?

Correct Answer:
Primary hyperparathyroidism is the unregulated overproduction of parathyroid hormone (PTH) resulting in abnormal calcium balance. PTH secretion is increased and is not under the usual feedback control mechanisms. The Ca++ level in the blood increase because of increased resorption and GI absorption of calcium but fails to inhibit PTH secretion at normal levels of calcium because the feedback threshold for calcium is set at a higher level in the abnormal parathyroid tissues. Hypercalcemia and hypophosphatemia are the clinical hallmarks of hyperparathyroidism.

Question 4
Needs Grading

A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had a fracture of her right metatarsal without trauma and currently is wearing a walking boot. She also had a bout of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved.

The APRN examining the patient orders a Chem 12 which revealed a serum Ca++ of 13.1 mg/dl. The APRN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist who does a complete work up and concurs with the APRN’s diagnosis.

Question 1 of 2:

Explain the processes involved in the formation of renal stones in patients with hyperparathyroidism.

Correct Answer:
Increased renal filtration load of calcium leads to hypercalciuria. Hypercalcemia also affects proximal renal tubular functions, causing metabolic acidosis and production of abnormally alkaline urine. PTH hypersecretion enhances real phosphate excretion and results in hypophosphatemia and hyperphosphatemia. The combination of hypercalciuria, alkaline urine, and hyperphosphaturia leads to the formation of renal stones

Question 5
Needs Grading

A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had a fracture of her right metatarsal without trauma and currently is wearing a walking boot. She also had a bout of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved.
The APRN examining the patient orders a Chem 12 which revealed a serum Ca++ of 13.1 mg/dl. The APRN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist who does a complete work up and concurs with the APRN’s diagnosis.

Question 2 of 2:

Explain how a patient with hyperparathyroidism is at risk for bone fractures.

Correct Answer:
Excessive osteoclastic and osteocytic activity results in increased bone reabsorption that weakens the bone. Kyphosis of the dorsal spine and compression fractures of the vertebral bodies are also seen in patients with hyperparathyroidism.

Question 6
Needs Grading

A 64-year-old Caucasian female who is 4 weeks status post total parathyroidectomy with forearm gland insertion presents to the general surgeon for her post-operative checkup. She states that her mouth feels numb and she feels “tingly all over. The surgeon suspects the patient has hypoparathyroidism secondary to the parathyroidectomy with delayed vascularization of the implanted gland. She orders a Chem 20 to determine what electrolyte abnormalities may be present. The labs reveal a serum Ca++ of 7.1 mg/dl (normal 8.5 mg/dl-10.5 mg/dl) and phosphorous level of 5.6 mg/dl (normal 2.4-4.1 mg/dl).

Question:

What serious consequences of hypoparathyroidism occur and why?

Correct Answer:
Hypoparathyroidism occurs when there is destruction of the parathyroid glands (autoimmune, surgical), abnormal parathyroid gland development, altered regulation of PTH production, or impaired PTH action. The acute manifestations of hypoparathyroidism (postsurgical hypoparathyroidism) are due to acute hypocalcemia. The hallmark of acute hypocalcemia is tetany, which is a disorder of neuromuscular irritability. The symptoms of tetany may be mild (perioral numbness, paresthesia of the hands and feet, muscle cramps) or severe (carpopedal spasm, laryngospasm, and focal or generalized seizures, which must be distinguished from the generalized tonic muscle contractions that occur in severe tetany). The classic physical findings in patients with neuromuscular irritability due to latent tetany are Trousseau’s and Chvostek’s signs.

Question 7
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 1 of 6:

The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polydipsia.”

Correct Answer:
Because elevated blood glucose levels, water is osmotically attracted from body cells which results in intracellular dehydration and hypothalamic stimulation of thirst.

Question 8
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 2 of 6:

The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polyuria.”

Correct Answer:
Hyperglycemia acts as an osmotic diuretic. The amount of glucose filtered by the glomeruli of the kidneys exceeds the amount that can be reabsorbed by the renal tubules. Glycosuria results accompanied by large amounts of water lost in the urine.

Question 9
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.
PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 3 of 6:

The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polyphagia.”

Correct Answer:
Depletion of cellular stores of carbohydrates, fats, and proteins results in cellular starvation and a corresponding increase in hunger.

Question 10
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 4 of 6:

The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “weight loss.”

Correct Answer:
Weight loss occurs because of fluid loss in osmotic diuresis and the loss of body tissue as fat and proteins are used for energy as a result of the effects of insulin deficiency.

Question 11
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.
PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 5 of 6:

The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “fatigue.”

Correct Answer:
Metabolic change result in poor use of food products, contributing to lethargy and fatigue. Sleep loss from severe nocturia also contributes to fatigue.

Question 12
Needs Grading

A 17-year-old boy is brought to the pediatrician’s office by his parents who are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with his school/work activities. He had been seemingly healthy until about 3 months ago when his parents started noticing these symptoms but put these symptoms down to his busy schedule including a part time job. He admits to sleeping more and tires very easily. He denies any other symptoms.
PMH-noncontributory. No surgeries or major medical problems. Usual colds and ear infections as a child

Allergies-none know

Family history- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process

Social-denies alcohol, tobacco or illicit drug use. Not sexually active. Junior at local high school and works in a fast food store after school and on weekends.

Labs in office: random glucose 220 mg/dl.

Based on his symptoms and the glucose level, the pediatrician makes a tentative diagnosis of Diabetes Mellitus type 1 and refers the boy and his parents to an endocrinologist for further work up and management plan.

Question 6 of 6:

How do genetics and environmental factors contribute to the development of Type 1 diabetes?

Correct Answer:
Islet cell autoantibodies (ICAs) were detected in serum from patients with autoimmune polyendocrine deficiency. They have subsequently been identified in 85 percent of patients with newly diagnosed type 1 diabetes and in prediabetic people.

Autoantigens form on insulin producing beta cells and circulate in the blood and lymphatics. This leads to processing and presentation of autoantigen by antigen presenting cells

There is activation of T helper 1 lymphocytes and T helper 2 lymphocytes There is activation of macrophages that release IL-1 and TNFα and activation of autoantigen specific T cytotoxic CD8 cells.

There is activation of B lymphocytes to produce islet cell autoantibodies and antiGAD65 antibodies. This cascade results in destruction of beta cells with decreased insulin production.

Question 13
Needs Grading

A 17-year-old boy recently diagnosed with Type I diabetes is brought to the pediatrician’s office by his parents with a chief complaint of “having the flu”. His symptoms began 2 days ago, and he has vomited several times and has not eaten very much. He can’t remember if he took his prescribed insulin for several days because he felt so sick. Random glucose in the office reveals glucose 560 mg/dl and the pediatrician made arrangements for the patient to be admitted to the hospitalist service with an endocrinology consult.

BP 124/80mmHg; HR 122bpm; Respirations 32 breaths/min; Temp 97.2˚F; PaO297% on RA

Admission labs: Hgb 14.6 g/dl; Hct 58%

CMP- Na+ 122mmol/L; K+ 5.3mmol/L; Glucose 560mg/dl; BUN 52mg/dl; Creatinine 4.9mg/dl;

Cl- 95mmol/L; Ca++ 8.8mmol/L; AST (SGOT) 248U/L; ALT 198U/L; CK 34/35 IU/L; Cholesterol 198mg/dl;

Phosphorus 6.8mg/dl; Acetone Moderate; LDH38U/L; Alkaline Phosphatase 132U/L.

Arterial blood gas values were as follows: pH 7.09; Paco220mm Hg; Po2100mm Hg; Sao2 98% (room air)

HCO3-7.5mmol/L; anion gap 19.4

A diagnosis of diabetic ketoacidosis was made, and the patient was transferred to the Intensive Care Unit (ICU) for close monitoring.

Question:

The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA.

Correct Answer:
The most important concept is that DKA is caused by insulin deficiency and an increase in counterregulatory hormones that include glucagon, catecholamines, cortisol, and growth hormone. These counter regulatory hormones normally antagonize insulin buy increasing glucose production and decreasing tissue use of glucose. Insulin deficiency results in decreased glucose uptake, increased fat mobilization with release of fatty acids and accelerated gluconeogenesis, glycogenesis, and ketogenesis. In the absence of insulin, the release of free fatty acids from adipocytes increases production of ketone bodies by the mitochondria of the liver that exceeds peripheral use. Accumulation of ketone bodies causes a drop in pH and triggers the buffering system associated with metabolic acidosis. Hyperketonemia may result from impaired use of ketones by peripheral tissue, which permits strong organic acids to circulate freely. Bicarbonate buffering then does not occur and the individual develops a metabolic acidosis.

Question 14
Needs Grading

A 67-year-old African American male presents to the clinic with a chief complaint that he has to “go to the bathroom all the time and I feel really weak.” He states that this has been going on for about 3 days but couldn’t come to the clinic sooner as he went to the Wound Care clinic for a dressing change to his right great toe that has been chronically infected, and he now has osteomyelitis. Patient with known Type II diabetes with poor control. His last HgA1C was 10.2 %. He says he can’t afford the insulin he was prescribed and only takes half of the oral agent he was prescribed. Random glucose in the office revealed glucose of 890 mg/dl. He was immediately referred to the ED by the APRN for evaluation of suspected hyperosmolar hyperglycemic non ketotic syndrome (HHNKS). Also called hyperglycemic hyperosmolar state (HHS).

Question:

Explain the underlying processes that lead to HHNKS or HHS.

Correct Answer:
HHNKS differs from DKA in the degree of insulin deficiency (more profound I DKA) and the elevation of glucose levels and degree of fluid deficiency which are more marked in HHKS.

The basic underlying mechanism of HHS is a relative reduction in effective circulating insulin with a concomitant rise in counterregulatory hormones. Unlike patients with DKA, most patients with HHS do not develop significant ketoacidosis. Insulin remains available in amounts sufficient to inhibit lipolysis and ketogenesis but insufficient to prevent hyperglycemia. Hyperosmolarity itself may also decrease lipolysis, limiting the amount of free fatty acids available for ketogenesis.

Patients with HHS have a very high serum glucose concentration, a near normal serum bicarbonate level and pH, a serum osmolarity that is usually greater than 320 mOsm/L (normal 275–295 mOsm/L), and either absent or low levels of ketones in both the urine and serum. Electrolyte imbalances are common, with severe potassium deficits that need to be corrected, usually over several days. Phosphorous and sodium replacement may also be needed.

Question 15
Needs Grading

A 32-year-old woman presented to the clinic complaining of weight gain, swelling in her legs and ankles and a puffy face. She also recently developed hypertension and diabetes type 2. She noted poor short-term memory, irritability, excess hair growth (women), red-ruddy face, extra fat around her neck, fatigue, poor concentration, and menstrual irregularity in addition to muscle weakness. Given her physical appearance and history, a tentative diagnosis of hypercortical function was made. Diagnostics included serum and urinary cortisol and serum adrenocorticotropic hormone (ACTH). MRI revealed a pituitary adenoma.

Question:

How would you differentiate Cushing’s disease from Cushing’s syndrome?

Correct Answer:
Cushing’s syndrome is a rare disease that is caused by the over production of cortisol by the adrenal glands. This can be caused by a tumor of the adrenal glands, the lungs, or the pituitary gland. When the tumor produces too much ACTH, it causes over production of cortisol by the adrenal glands. If the source is the pituitary, it is called Cushing’s disease. Cushing’s disease occurs more often in women than men and more often occurs between the ages of 20 and 40.

ACTH dependent hypercortisolism, the excess ACTH stimulates excess production of cortisol and loss of the negative feedback control of ACTH secretion. People with Cushing’s syndrome do not have diurnal or circadian secretion patterns of ACTH and cortisol, and they do not increase ACTH and cortisol secretion in response to stressors.

Question 16
Needs Grading

A 47-year-old female is referred to the endocrinologist for evaluation of her chronically elevated blood pressure, hypokalemia, and hypervolemia. The patient’s hypertension has been refractory to the usual medications such as beta blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors. After a full work up including serum and urinary electrolyte levels, aldosterone suppression test, plasma aldosterone to renin ratio, and MRI which revealed an autonomous adenoma, the endocrinologist diagnoses the patient with primary hyper-aldosteronism.

Question:

What is the pathogenesis of primary hyper-aldosteronism?

Correct Answer:
Primary hyperaldosteronism can be caused by either hyperactivity in one adrenal gland (unilateral disease) or both (bilateral disease). Unilateral disease is usually caused by an aldosterone producing adenoma (benign tumor) and less commonly by adrenal cancer or hyperplasia (when the whole gland is hyperactive). Excessive autonomous secretion of aldosterone without its principle regulator, angiotension II, causes hypokalemia and induces insulin resistance; promotes inflammation, endothelial dysfunction, and cardiovascular remodeling (increased left ventricular wall and carotid intima thickness. It also affects adipose tissue differentiation and function. Therefore, primary hyperaldosteronism can influence the features of metabolic syndrome, including hypertension, obesity, dyslipidemia, insulin resistance and hyperglycemia.

Question 17
Needs Grading

A 47-year-old African American male presents to the clinic with chief complaints of polyuria, polydipsia, polyphagia, and weight loss. He also said that his vison occasionally blurs and that his feet sometimes feel numb. He has increased hunger despite weight loss and admits to feeling unusually tired. He also complains of “swelling” and enlargement of his abdomen.

Past Medical History (PMH) significant for HTN fairly well controlled with and ACE inhibitor; central obesity, and dyslipidemia treated with a statin, Review of systems negative except for chief complaint. Physical exam unremarkable except for decreased filament test both feet. Random glucose in office 290 mg/dl. The APRN diagnoses the patient with type II DM and prescribes oral medication to control the glucose level and also referred the patient to a dietician for dietary teaching.

Question:

What is the basic underlying pathophysiology of Type II DM?

Correct Answer:
There are very complex interactions that result in the development of Type II diabetes. The pathophysiology of type 2 diabetes mellitus is characterized by peripheral insulin resistance, impaired regulation of hepatic glucose production, and declining β-cell function, eventually leading toβ -cell failure. Type 2 diabetes mellitus consists of a constellation of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. It is often associated with obesity.

Question 18
Needs Grading

A 21-year-old male was involved in a motorcycle accident and sustained a closed head injury. He is waking up and interacting with his family and medical team. He complained of thirst that doesn’t seem to go away no matter how much water he drinks. The nurses note that he has had 3500 cc of pale-yellow urine in the last 24 hours. Urine was sent for osmolality which was reported as 122 mOsm/L. A diagnosis of probable neurogenic diabetes insipidus was made.

Question:

What causes diabetes insipidus (DI)?

Correct Answer:
Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). There are 2 major forms: Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized by decreased secretion of antidiuretic hormone (ADH; also referred to as arginine vasopressin [AVP]). Nephrogenic DI characterized by decreased ability to concentrate urine because of resistance to ADH action in the kidney. AVP is the primary determinant of free water excretion in the body. Its main target is the kidney, where it acts by altering the water permeability of the cortical and medullary collecting tubules. Water is reabsorbed by osmotic equilibration with the hypertonic interstitium and returned to the systemic circulation. Question 19 Needs Grading A 43-year-old female patient presents to the clinic with complaints of nervousness, racing heartbeat, anxiety, increased perspiration, heat intolerance, hyperactivity and palpitations. She states she had had the symptoms for several months but attributed the symptoms to beginning to care for her elderly mother who has Alzheimer’s Disease. She has lost 15 pounds in the last 3 months without dieting. Her past medical history is significant for rheumatoid arthritis that she has had for the last 10 years well controlled with methotrexate and prednisone. Physical exam is remarkable for periorbital edema, warm silky feeling skin, and palpable thyroid nodules in both lobes of the thyroid. Pending laboratory diagnostics, the APRN diagnoses the patient as having hyperthyroidism, also called Graves’ Disease. Question: Explain how the negative feedback loop controls thyroid levels. Correct Answer: Hyperthyroidism is a set of disorders that involve excessive synthesis and secretion of thyroid hormones T3 and T4. This unregulated release causes a hypermetabolic state that can lead to a serious condition called thyrotoxicosis. The thyroid gland is regulated by thyroid stimulating hormone (TSH) from the pituitary gland, which, in turn, is regulated by the hypothalamus via a negative feedback loop. Calcitonin, a hormone that affects blood calcium levels, is also secreted by the thyroid gland. Hyperthyroidism is known as Graves’ Disease. Genetic factors interacting with the environment triggers play an important role in the pathogenesis. It is classified as an autoimmune disease and often goes along with other autoimmune diseases. It results from a failure of the feedback system. Normally, the secretion of thyroid hormone is controlled by a complex feedback mechanism involving the interaction of stimulatory and inhibitory factors (see the image below). Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the pituitary to release TSH. In Graves’ disease, a circulating autoantibody against the thyrotropin receptor provides continuous stimulation of the thyroid gland. This stimulatory immunoglobulin has been called long-acting thyroid stimulator (LATS), thyroid-stimulating immunoglobulin (TSI), thyroid-stimulating antibody (TSab), and TSH-receptor antibody (TRab). These antibodies stimulate the production and release of thyroid hormones and thyroglobulin. Question 20 Needs Grading A 43-year-old female patient with known Graves’ Disease presents to the clinic with complaints of nervousness, racing heartbeat, anxiety, increased perspiration, heat intolerance, hyperactivity and severe palpitations. She states she had been given a prescription for propylthiouracil, an antithyroid medication but she did not fill the prescription as she claims she lost it. She had been given the option of thyroidectomy which she declined. She also notes that she is having trouble with her vision and often has blurry eyes. She states that her eyes seem “to bug out of her face”. She has had recurrent outs of nausea and vomiting. She was recently hospitalized for pneumonia. Physical exam is significant for obvious exophthalmos and pretibial myxedema. Vital signs are temp 101.2˚F, HR 138 and irregular, BP 160/60 mmHg. Respirations 24. Electrocardiogram revealed atrial fibrillation with rapid ventricular response. The APRN recognizes the patient is experiencing symptoms of thyrotoxic crisis, also called thyroid storm. The patient was immediately transported to a hospital for critical care management. Question: How did the patient develop thyroid storm? What were the patient factors that lead to the development of thyroid storm? Correct Answer: Thyroid storm is a hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis. Individuals may be undiagnosed or undertreated when they develop the symptoms. The symptoms are caused by the sudden release and action of thyroxine (T4) and triiodothyronine (T3) that exceeds metabolic demands. Symptoms must be rapidly treated in order to prevent life threatening complications such as high output heart failure, hyperthermia, delirium and hypovolemia from excessive vomiting. Question 21 Needs Grading A 44-year-old woman presents to the clinic with complaints of extreme fatigue, weight gain, decreased appetite, cold intolerance, dry skin, hair loss, and sleepiness. She also admits that she often bursts into tears without any reason and has been exceptionally forgetful. Her vision is occasionally blurry, and she admits to being depressed without any social or occupational triggers. Past medical history noncontributory. Physical exam Temp 96.2˚F, pulse 62 and regular, BP 108/90, respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted. Based on the clinical history and physical exam, and pending laboratory data, the ARNP diagnoses the patient with hypothyroidism. Question: What causes hypothyroidism? Correct Answer: Patients with primary hypothyroidism have elevated TSH levels and decreased free hormone levels. Patients with elevated TSH levels (usually 4.5- 10.0 mIU/L) but normal free hormone levels or estimates are considered to have mild or subclinical hypothyroidism. The most common cause of hypothyroidism is autoimmune thyroiditis known as Hashimoto’s disease. Primary hypothyroidism is essentially the only disease that is characterized by sustained rises in TSH levels. As the TSH level increases early in the disease, conversion of T4 to T3 increases, maintaining T3 levels. In early hypothyroidism, TSH levels are elevated, T4 levels are normal to low, and T3 levels are normal. Question 22 Needs Grading A 44-year-old woman is brought to the clinic by her husband who says his wife has had some mental status changes over the past few days. The patient had been previously diagnosed with hypothyroidism and had been placed on thyroid replacement therapy but had been lost to follow-up due to moving to another city for the husband’s work approximately 4 months ago. The patient states she lost the prescription bottle during the move and didn’t bother to have the prescription filled since she was feeling better. Physical exam revealed non-pitting, boggy edema around her eyes, hands and feet as well as the supraclavicular area. The APRN recognizes this patient had severe myxedema and referred the patient to the hospital for medical management. Question: What causes myxedema coma? Correct Answer: In a patient with underlying hypothyroidism, inciting factors responsible for developing myxedema coma are numerous and include infection, trauma, cold exposure, or medications such as sedatives and anesthetics. Although most individuals are not comatose, they are at risk for significant cardiovascular and pulmonary complications. Patients will exhibit severe hypothermia without shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis ad coma. Question 23 Needs Grading A 53-year-old woman presents to the primary care clinic with complaints of severe headaches, palpitations, high blood pressure and diaphoresis. She relates that these symptoms come in clusters and when she has these “spells”, she also experiences, tremor, nausea, weakness, anxiety, and a sense of doom and dread, epigastric pain, and flank pain. She had one of these spells when she was at the pharmacy and the pharmacist took her blood pressure which was recorded as 200/118. The pharmacist recommended that she immediately be evaluated for these symptoms. Past medical history significant for a family history of neurofibromatosis type 1 (NF1). Based on the presenting symptoms and family history of NF1, the APRN suspects the patient has a pheochromocytoma. Laboratory data and computerized tomography of the abdomen confirms the diagnosis. Question 1 of 2: What is a pheochromocytoma and how does it cause the classic symptoms the patient presented with? Correct Answer: Pheochromocytoma is an endocrine tumor of the adrenal gland that continuously secretes catecholamines (epinephrine and norepinephrine) in an uncontrolled fashion. Hypertension results from increase peripheral vascular resistance and may be sustained or paroxysmal. Because of excessive catecholamine secretion, pheochromocytomas may precipitate life-threatening hypertension or cardiac arrhythmias. Hypermetabolism and sweating are related to chronic activation of sympathetic receptors in adipocytes, hepatocytes and other tissue. Glucose intolerance may happen because of catecholamine induced inhibition of insulin release by the pancreas. Catecholamines produced by pheochromocytomas are metabolized within chromaffin cells. Norepinephrine is metabolized to normetanephrine and epinephrine is metabolized to metanephrine. Because this process occurs within the tumor, independently of catecholamine release, pheochromocytomas are best diagnosed by measurement of these metabolites rather than by measurement of the parent catecholamines. Question 24 Needs Grading A 53-year-old woman presents to the primary care clinic with complaints of severe headaches, palpitations, high blood pressure and diaphoresis. She relates that these symptoms come in clusters and when she has these “spells”, she also experiences, tremor, nausea, weakness, anxiety, and a sense of doom and dread, epigastric pain, and flank pain. She had one of these spells when she was at the pharmacy and the pharmacist took her blood pressure which was recorded as 200/118. The pharmacist recommended that she immediately be evaluated for these symptoms. Past medical history significant for a family history of neurofibromatosis type 1 (NF1). Based on the presenting symptoms and family history of NF1, the APRN suspects the patient has a pheochromocytoma. Laboratory data and computerized tomography of the abdomen confirms the diagnosis. Question 2 of 2: What are the treatment goals for managing pheochromocytoma?