NURS 6501 / NURS6501: Advanced Pathophysiology - Module 4 Knowledge Check (Latest 2021 / 2022) Walden University
NURS 6501 - Advanced Pathophysiology
Review Test Submission: Module 4 Knowledge Check
• 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.
Selected SIADH is a condition in which the release of ADH from the
Answer: posterior pituitary is elevated relative to serum sodium
levels, resulting in increased water reabsorption by the
kidneys and fluid overload. Elderly patients on medications
such as metformin, NSAIDs, and antidepressants, cause
SIADH. These drugs either stimulate ADH release, enhance
the physiologic effects of ADH, or have a biologic action
similar to that of ADH.
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.
Response
Feedback:
[None Given]
• 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 patie
nt was taking for her RA secondary to vomiting.
Question:
Explain why the patient exhibited these symptoms?
Selected
Answer:
High levels of glucocorticoids decrease hypothalamic
corticotropin-releasing hormone synthesis and secretion and
also block the trophic and ACTH-secretagogue actions of
CRH on anterior pituitary cells, resulting in loss of ACTH and
its actions on the adrenal gland. The patient exhibited these
symptoms as a result of abrupt withdrawal of exogenous
glucocorticoids.
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 renninangiotensionaldosterone-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.
Response
Feedback:
[None Given]
• 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?
Selected
Answer:
Role of parathyroid hormone in the development of primary
hyperparathyroidism includes the inappropriate excess
secretion of PTH by one or more of the parathyroid glands.
PTH secretion is increased and is not under the usual
feedback control mechanisms.
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.
Response
Feedback: