Nursing Writing HelpNursing Writing HelpNursing Writing Help
+1 315 633 4181
info@nursingwritinghelp.com
St San Francisco, CA 94109-2967
Nursing Writing HelpNursing Writing HelpNursing Writing Help

Knowledge Check 4

QUESTION 1

  • 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, Cl97 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.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition characterized by high levels of antidiuretic hormone which causes the body to retain a lot of water. In the 67-year old woman in the case study, the condition makes her body to retain water rather than secreting it in the normal way through urine, thereby causing specific levels of electrolytes in the blood to fall below the normal levels. Consequently, the electrolyte balance of the body, particularly sodium gets imbalanced. In the case study patient, depression and Type II diabetes mellitus (DM) are the main cause of SIADH, whereby depression caused overproduction of antidiuretic hormone while Type II diabetes led to low blood sugar level.

QUESTION 2

  • 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? 

The 43-year-old female patient in the case study displayed the symptoms of hypocortisolism due to dependency on steroids and sudden withdrawal. Dependency on steroids resulted in adrenal insufficiency. The patient was on prednisone for some duration, and then stopped taking it. The withdrawal triggered the adrenal gland to decrease the production of cortisol hormone, thereby leading to hypocortisolism. Sudden prednisone withdrawal symptoms incorporate pain in the joints, muscle weakness, nausea, and severe fatigue, which are all displayed by the case study patient.

QUESTION 3

  • 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? 

An increase parathyroid hormone plays a critical role in the development of primary hyperparathyroidism. This increase it causes the bones to release more calcium into the blood, leading to an elevated calcium levels or a condition known as hypercalcemia. Excessive parathyroid hormone symptoms incorporate abdominal pain, excessive urination, or polyuria, as displayed by the patient in the case scenario.

QUESTION 4

  • 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. 

In in patients with hyperparathyroidism, the processes involved in renal stone formation include an overproduction of parathyroid hormone that ultimately led to the release of more calcium into the urine. The excess calcium released in the urine causes the formation of crystal-like substances such as calcium, which cannot be diluted by the fluid in the urine, consequently establishing favorable environment for the formation of renal stones. In the case scenario, the 64-year-old Caucasian female patient passed small stones, a sign that there is overproduction of parathyroid hormone.

QUESTION 5

  • 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.

 A patient with hyperparathyroidism like the 64-year-old Caucasian female is at high risk of bone fracture since her parathyroid glands are overactive and overproduce parathyroid hormone that can further cause her bones to constantly release calcium into her bloodstream. The constant release of calcium into the bloodstream may make her bones to lose their density and hardness and fracture easily

QUESTION 6

  • 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?

 Hypoparathyroidism can have serious consequences such as the development of kidney stones. Patients with hypoparathyroidism risk developing kidney stones especially due to overproduction of parathyroid hormone that raises the calcium level in the urine. The undissolved excess calcium in the urine form crystal-like substances that are responsible for formation of kidney stones, which may require surgery for their removal. For instance, the case scenario patient had a parathyroidectomy to remove the stones that led to hypoparathyroidism. Moreover, the other serious consequence can be intracranial hypertension that can occur due to increased pressure in cerebrospinal fluid in the skull, leading to severe headache and changes in vision.

QUESTION 7

  • 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.”

The pathophysiology of polydipsia is explained by the onset of Type I diabetes which results from an increase in blood glucose levels causing water to be osmotically attracted from the body cells, leading to an intracellular dehydration and hypothalamic stimulation of thirst. The high blood sugar levels exhibited by the onset of diabetes mellitus increases the concentration of blood sugar, thus making an individual to feel thirsty, regardless of amount of water one may drink. For instance, the patient in case scenario has been experiencing unquenchable thirst indicating that there is an imbalance in the osmotic concentration because of the loss of a considerable amount of fluid.

QUESTION 8

  • 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.”

Like polydipsia, the pathophysiology of polyuria can be understood by the factors involved in the onset of Type 1 diabetes that result in osmotic diuresis due to the high glucose levels causing glucose to be excreted in the urine. Afterwards, water follows the glucose concentration passively, leading to an abnormally high output of urine. In most cases, a person with polydipsia urinates more frequent and passes large volumes of urine- more than 3 liters per day compared to the normal urine output in adults of about 1 to 2 liters daily. For instance, patient in this case scenario experienced abnormal frequent urination indicating the presence of polyuria.

QUESTION 9

  • 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.”

Like polydipsia and polyuria, the pathophysiology of polyphagia can be well understood by the factors involved in the onset of uncontrolled Type 1 diabetes, which cause blood glucose levels to persistently remain higher than normal. Consequently, the glucose from the blood are unable to enter the cells because of either a lack of insulin or insulin resistance- so the body is unable to convert the food consumed into energy. The lack of energy leads to an elevated level of hunger leading to weight loss. For instance, the patient in the case scenario gets tired quickly indicating that he has uncontrolled lack of energy due to polyphagia.

QUESTION 10

  • 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.”

The pathophysiology of weight loss results from Type 1 diabetes, which may cause weight loss due to the insufficient insulin, which prevents the body from acquiring glucose from the blood into the cells of the body to convert into energy. As a result, the body starts to the stored burn fat and muscle to obtain energy, thus resulting in a decrease in the overall body weight (muscles and fat are eaten away). For instance, in this case scenario, the patient lost weight despite eating more indicating that there is insufficient insulin, which prevents the body from obtaining the necessary glucose that can be converted to energy.

QUESTION 11

  • 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.”

The pathophysiology of fatigue can be understood by the factors involved in the onset of Tape 1 diabetes, which leads to the inability of the body to obtain sufficient glucose from the blood into body cells to meet the daily energy requirements. Consequently, the person will often experience fatigue, as seen in this case scenario’s patient.

QUESTION 12

  • 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?

Genetic and environmental factors play a crucial role in the development of Type 1 diabetes. For instance, environmental factors like lack of vitamin-D, exposure to enteroviruses, poor diet, polluted air, and damage to immune cells can trigger an autoimmune response that leads to excess blood glucose. Again, obesity that results from a lack of exercise can be accompanied by a decline in muscle mass, thereby inducing insulin resistance. Moreover, stress hormones, such as adrenaline and cortisol, can increase blood sugar. On the other hand, genetic factors such as family history of diabetes increase the chances of an individual to suffer from diabetes. This risk increases with the number of individuals in the family affected because of shared genetic factors like insulin resistance. For instance, in the scenario, 17-year-old boy has a family history of diabetes as seen in his maternal uncle who had some sugar diabetes issues.

QUESTION 13

  • 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. 

The epinephrine hormone participates in the development of KDA by helping the liver to convert stored glycogen to glucose and releases it, thereby increasing blood sugar levels causing KDA. Glucagon hormone participates in the development of KDA by assisting the liver to break down glycogen, leading to elevated ketones and acidosis that are witnessed in KDA. Moreover, cortisol promotes gluconeogenesis, which leads to hyperglycemia seen in KDA. Finally, growth hormone participates enhances the breakdown of triglyceride into free fatty acids and gluconeogenesis, leading to an increase in serum glucose levels noted in KDA. For instance the case scenario, the patient’s blood glucose is higher than the normal level.

QUESTION 14

  • 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 HgA1was 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.

HHNKS or HHS is a condition that results from extremely high blood sugar that is often more than 600 mg /gL. This condition is caused by dysregulation, which leads to the process of ketosis and the deposition of known as diabetic ketoacidosis (DKA). For instance, in the 67-year-old African American male patient in the scenario complained of frequent visits to the bathroom and is very weak. Again, the patient also stated that insulin was too expensive for him to afford, indicating that he had insufficient insulin, implying that he also has Type 2 diabetes as indicated in the patient information.

QUESTION 15

  • 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? 

Cushing’s syndrome can be differentiated from Cushing’s disease in that Cushing’s syndrome is caused by any condition that results in the adrenal gland to overproduce cortisol irrespective of the cause. Cushing’s syndrome is also characterized by facial and torso obesity, high blood, muscle weakness, irritability, excessive hair growth, as noted in the case scenario patient. On the other hand, Cushing’s disease is a particular type of Cushing’s syndrome that is differentiated from Cushing’s syndrome by a pituitary tumor secreting excess ACTH.

QUESTION 16

  • 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? 

Primary hyperaldosteronism is the rennin-independent elevation in the secretion of aldosterone. The pathophysiology begins when the adrenal gland secretes excess aldosterone hormone that lead to an increases in the reabsorption of sodium and loss of hydrogen and potassium ions. This situation causes imbalance making the body to retain too much water, thereby increasing the volume and pressure of blood. For instance, the patient in this scenario had increased blood pressure, hypokalemia, and hypervolemia, which can help to explain the increase in pressure and volume of her blood.

QUESTION 17

  • 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? 

The basic underlying pathophysiology of Type II DM is characterized by the resistance of peripheral insulin, distorted regulation of the production of hepatic glucose, and a decline in functionality of β-cell, ultimately resulting in β -cell failure. Moreover, an impaired insulin secretion results in the decline in responsiveness of glucose. Similarly, the impaired glucose tolerance is induced by a decline in the responsiveness of glucose in the early stages of insulin secretion. The impaired insulin secretion is progressive and entails glucose toxicity and lipo-toxicity that if not treated early enough can lead to a decrease in pancreatic β-cell, thus affecting the long –term blood glucose control that can consequently result in the development of Type II diabetes in the long-run. For instance, the patient in this case scenario begun to display the symptoms of polyuria, polyphagia, polydipsia, and weight loss.

QUESTION 18

  • 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)? 

Diabetes insipidus (DI) results when there are problems with chemical known as vasopressin (AVP), which is also referred to as antidiuretic hormone (ADH) and is produced by the hypothalamus and stored in the pituitary gland. Therefore, in case the pituitary gland or hypothalamus is damaged for instance due to surgery, tumor, head injury, or even any other cause, the patient may suffer from diabetes insipidus because insulin production will be compromised since the normal production, storage, and release of ADH is affected as seen in the case scenario patient.

QUESTION 19

  • 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.

Negative feedback loop controls thyroid levels by causing an increase in thyroid hormones above a specific threshold that inhibit the TRH-secreting neurons located in the hypothalamus and stop their secretion function. As a result, the concentration of the hormone in the blood is sustained. However, the failure of this process may lead to the development of Hyperthyroidism, which is a condition characterized by overproduction of thyroxine hormone that increases metabolism of the body and cause unintentional weight loss and irregular heartbeat, as seen in the above case scenario patient. This patient experienced racing heartbeat that was accompanied by perspiration, hyperactivity, and palpitation indicating that she lacked hormonal control.

QUESTION 20

  • 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? 

The patient in this case scenario developed thyroid storm since she had hyperthyroidism but did not treat the condition as she claimed to have lost the prescription. The condition is characterized by excess production of the two hormones secreted by the thyroid gland. The patient’s factors that led to the development of thyroid storm include hyperthyroidism, and symptoms like racing heartbeat, perspiration, hyperactivity, severe palpitation, and intolerance to heat.

QUESTION 21

  • 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? 

Hypothyroidism is caused by the inability of the body to produce sufficient thyroid hormones, which help in the regulation and utilization of energy. The most common cause of hypothyroidism is an unregulated autoimmune response. The failure of the body to regulate the autoimmune response may lead to the body’s immune system attacking healthy tissues, leading to severe health problems such as hyperactivity, as noted in the patient in this case scenario, who bursts into tears without any reason, experienced a decline in appetite, was depressed, and had sleep issues.

QUESTION 22

  • 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? 

Myxedema coma is caused by a long-lasting, undiagnosed, or untreated hypothyroidism and is mostly triggered by a systemic illness. This disease can result from any cause of untreated hypothyroidism, and the most common cause is chronic autoimmune thyroiditis. For instance, the patient in this case scenario was diagnosed with untreated hypothyroidism, which consequently resulted in myxedema coma.

QUESTION 23

  • 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?

Pheochromocytoma refers to a tumor in the adrenal gland tissue, which causes overproduction of epinephrine and norepinephrine hormones that are important in the regulation of heart rate, blood pressure, and metabolism. This condition led to the classic symptoms present in the case scenario patient, which include overproduction of the epinephrine and norepinephrine hormones that increased the blood pressure, causing the patient to experience severe headache and palpitation.

 

QUESTION 24

  • 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? 

 

The treatment goals for managing pheochromocytoma incorporate removing the tumor and controlling of blood pressure. However, the primary treatment is through surgery to remove the tumor, although it is recommended that prior to the surgery, the patient needs to be given particular blood pressure medications that block the actions of the high-adrenaline hormones to minimize the risk of severe high blood pressure during the surgical procedure.

At vero eos et accusamus et iusto odio digni goikussimos ducimus qui to bonfo blanditiis praese. Ntium voluum deleniti atque.

Melbourne, Australia
(Sat - Thursday)
(10am - 05 pm)
X