NURS 6501 Module 4 Knowledge Check Quiz

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 fell once but could ambulate easily. 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 the death of spouse several months ago

Social/family hx

Non-contributory except for a 30-pack/year history of tobacco use.

Meds

Metformin 500 mg PO BID, ASA 81 mg PO QAM, escitalopram (Lexapro) 5 mg PO q am started 2 months ago.

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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 calls endocrinology for a consult to diagnose and manage the syndrome of inappropriate antidiuretic hormone (SIADH).

Question:

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

“SIADH secretion is characterized by high levels of ADH in the absence of normal physiologic stimuli for its release” (McCance et al., 2019, pg. 670). Enhanced water retention in the kidneys causes SIADH. ADH increases renal permeability to water by inducing a water channel protein insertion into the tubular luminal membrane, increasing water reabsorption by the kidneys (McCance et al.., 2019).

This causes ECF volume to expand, causing diluting hyponatremia, hypoosmolarity, and improperly concentrated urine, as the water is being reabsorbed instead of excreted (McCance et al., 2019).

The above patient has some signs that her BUN is elevated, such as confusion. Her sodium level is decreased, and her chloride level is minimally below the normal range. This supports the above paragraph with reabsorbing water instead of being excreted, causing hyponatremia.

NURS 6501 Module 4 Knowledge Check Quiz QUESTION 2

PMH-significant for the 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

A thin, ill-appearing woman is sitting in an 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 is 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.

Hypercortisolism has three different types, primary, secondary, or tertiary. The Primary is Addison disease. It develops due to the inability of the adrenals to produce and secrete adrenocortical hormones. Secondary develops due to inadequate stimulation of the adrenal glands by ACTH.

Tertiary is due to an abrupt withdrawal of exogenous glucocorticoids or as a complication of treatment for Cushing syndrome (McCance et al., 2019). The patient was prescribed prednisone to help decrease her RA symptoms. Prednisone helps with flare-ups. When the patient started having n/v, she was not getting and keeping the prednisone.

Secondary hypocortisolism often results from prolonged administration of exogenous glucocorticoids, which causes suppression of ACTH secretion, causing adrenal atrophy, resulting in inadequate corticosteroidogenesis once the oral, extra glucocorticoids are removed (McCance et al., 2019). Symptoms of secondary hypocortisolism are similar to Addison’s disease, minus hyperpigmentation.

NURS 6501 Module 4 Knowledge Check Quiz QUESTION 3

QUESTION 4

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

QUESTION5

QUESTION 6

QUESTION7

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 workup and management plan. NURS 6501 Module 4 Knowledge Check Quiz

Question 1 of 6:

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

Type I DM, the most common pediatric condition has two distinct types: autoimmune (type IA) and idiopathic or nonimmune (type IB) (McCance et al., 2019). The 3^rd type, type 3c DM, is associated with chronic pancreatitis.

With autoimmune DM, environmental-genetic factors are believed to trigger cell-mediated destruction of pancreatic beta cells (McCance et al., 2019). Type I usually leads to complete insulin deficiency, requiring the patient to take insulin to keep their blood sugars in a healthy range. Otherwise, it would spiral out of control.

With elevated blood glucose levels, water is osmotically attracted from body cells, resulting in intracellular dehydration and hypothalamic stimulation of thirst, causing polydipsia (McCance et al., 2019).

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 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

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

Allergies

None known

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 a local high school works in a fast food store after school and on weekends.

Labs in office

Random glucose 220 mg/dl.

Question 2 of 6:

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QUESTION 10

QUESTION 11

A 17-year-old boy is brought to the pediatrician’s office by his parents. They are concerned about their son’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue 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

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

Allergies

None known

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 a local high school works in a fast food store after school and on weekends.

Labs in office

Random glucose 220 mg/dl.

Question 5 of 6:

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

The fatigue in Type I DM patients results from polydipsia, polyuria, polyphagia, and weight loss. The metabolic changes result in poor use of food products, causing lethargy and fatigue; furthermore, the loss of quality sleep from severe nocturia further causes fatigue (McCance et al., 2019), including a part-time job. He admits to sleeping more and tires very easily. He denies any other symptoms.

PMH

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

Allergies

None known

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 a local high school works in a fast food store after school and on weekends.

Labs in office

Random glucose 220 mg/dl.

Question 6 of 6:

How do genetics and environmental factors contribute to developing Type 1 diabetes?

The genetic predisposition and environmental factors combined cause autoantigens to form on insulin-producing beta cells circulating in the bloodstream and lymphatics. This leads to the processing and presentation of autoantigen by antigen-presenting cells, activating T helper I lymphocytes and T helper 2 lymphocytes (McCance et al., 2019).

The activation of the Th1 lymphocytes causes activation of macrophages with the release of IL-1 and TNF-alpha through interferon-gamma, as well as activation of autoantigen-specific T cytotoxic (CD8) cells through interleukin (McCance et al., 2019).

The T helper 2 lymphocytes cause the activation of B lymphocytes to produce islet cell autoantibodies and anti-glutamic acid decarboxylase antibodies through interleukin (McCance et al., 2019). NURS 6501 Module 4 Knowledge Check Quiz

The activation of the macrophages, autoantigen-specific T cytotoxic cells, and B lymphocytes cause the destruction of beta cells with decreased insulin secretion (McCance et al., 2019, pg. 687).

QUESTION 13

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 developing diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, and growth hormone. Describe how they participate in the development of DKA.

DKA is a severe complication of DM related to a deficiency of insulin and an increase in the insulin counter-regulatory hormones of epinephrine, glucagon, cortisol, and growth hormone (McCance et al., 2019). DKA affects those with Type 1 DM more than type 2. These hormones normally increase glucose production and decrease the body’s use of glucose.

This results in insulin deficiency and decreased glucose uptake, increased fat mobilization with the release of fatty acids, and accelerated gluconeogenesis, glycogenesis, and ketogenesis (McCance et al., 2019, pg. 693). NURS 6501 Module 4 Knowledge Check Quiz

Without insulin, the release of free fatty acids increases ketone bodies’ production in the liver mitochondria. This causes a drop in pH, triggering buffering system with metabolic acidosis. Increased glucagon levels activate gluconeogenic and ketogenic pathways in the liver (McCance et al., 2019).

Ketones are normally used as energy to regenerate bicarbonate, as bicarbonate is lost when the ketone is formed. Hyperketonemia results from impaired ketone use of peripheral tissue. Further bicarbonate buffering does not occur, resulting in metabolic acidosis (McCance et al., 2019).

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QUESTION 20

NURS 6501 Module 4 Knowledge Check Quiz QUESTION 21

A 44-year-old woman presents to the clinic with extreme fatigue, weight gain, decreased appetite, cold intolerance, dry skin, hair loss, and sleepiness. She also admits that she often bursts into tears without 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

Non-contributory.

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, physical exam, and pending laboratory data, the ARNP diagnoses the patient with hypothyroidism.

Question:

What causes hypothyroidism?

Hypothyroidism is caused by the inappropriate production of TH by the thyroid gland. Loss of thyroid function in primary hypothyroidism causes decreased production of TH and increased secretion of TSH and TRH (McCance et al., 2019).

For adults, the most common causes are autoimmune thyroiditis (Hashimoto disease), iatrogenic loss of thyroid tissue after surgery or radioactive treatment, hand and neck radiation therapy, medications, and endemic iodine deficiency (McCance et al., 2019). There may be congenital defects in the pituitary or thyroid glands for infants and children. NURS 6501 Module 4 Knowledge Check Quiz

Secondary hypothyroidism is caused by the pituitary’s failure to synthesize adequate amounts of TSH or a lack of TRH. Pituitary tumors that compress surrounding pituitary cells and possible consequences of treatment are the most common causes. TBI, subarachnoid hemorrhage, or pituitary infarction are other less common causes (McCance et al., 2019).

Subclinical hypothyroidism

Mild thyroid failure is caused by an elevation of TSH level with normal levels of TH.

QUESTION 22

NURS 6501 Module 4 Knowledge Check Quiz QUESTION 23

A 53-year-old woman presents to the primary care clinic complaining 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 tremors, nausea, weakness, anxiety, a sense of doom and dread, epigastric pain, and flank pain. She had one of these spells 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 confirmed the diagnosis.