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BY:
Habtemariam Mulugeta
College of Medicine and Health Sciences
School of Nursing & Midwifery
Department of Adult Health Nursing
Advanced Nursing Education & Curriculum Development
LESSON PLAN ON: CONN’S SYNDROME
Preparedby:
Name: Habtemariam Mulugeta Abate
ID No: SRSG/398/12
DESSIE, ETHIOPIA
DECEMBER, 2020
I
ACKNOWLEDGEMENT
First, I would like to express my heartfelt gratitude to WU CMHS for giving me this chance
to enhance my knowledge and skill.
Secondly, I would like to thank my instructor Dr. Caridad Sanchez Olis for sharing me his
deep knowledge, experience and expertise.
Last but not least I would like to thank my family and friends in helping me in ideas and
material during my entire work.
1
LESSON PLAN ON: CONN’S SYNDROME
Date: December 14, 2020
Duration: 2 Hour
Instructor name: Habtemariam Mulugeta
Department: Adult Health Nursing
Year of study: 1st Year
Semester: II
1. Unit Title: Conn’s Syndrome
2. Introduction: Conn’s Syndrome also known as primary hyperaldosteronism refers to the
excess production of the hormone aldosterone from the adrenal glands, resulting in low
renin levels. This abnormality is caused by hyperplasia or tumors. Many suffer from
fatigue, potassium deficiency and high blood pressure which may cause poor vision,
confusion or headaches. Symptoms may also include: muscular aches and weakness,
muscle spasms, low back and flank pain from the kidneys, trembling, tingling sensations,
numbness and excessive urination. Complications include cardiovascular disease such as
stroke, myocardial infarction, kidney failure and abnormal heart rhythms. (3 minutes)
3. SessionObjectives
 General Objective: At the end of the topic of Conn’s Syndrome the student will
to have sufficient knowledge about the topic and give effective quality care for
the patient in the aspect of pharmacological and none pharmacological nursing
care for the patient with full confidence independently.
 Specific Objectives:
2
 Define Conn’s Syndrome (Cognitive)
 Discuss physiology adrenal gland & endocrine system (cognitive)
 Understands the clinical symptoms and diagnostic tools of Conn’s
Syndrome (Affective)
 Distinguishes the pharmacological and none pharmacological management
(psychomotor)
4. Required materials and instrument needed
 LCD
 Internet,
 marker,
 White board,
 Paper,
 Pen and marker,
 Lab top,
 Books and handouts
5. Teaching Methods & Activities (Main body of presentation)
a. Teaching methods: Interactive Lecture and Discussion
b. Teaching techniques: LCD Projector and White Board
c. Body: 1:30 minutes
3
d. Content Outline
No. Type of
Disorder
Types of Activities Mechanism of
Management
Assessment
1. Conn’s
Syndrome
Review of Anatomy & Physiology
Definition
Specialty
Epidemiology
Causes
Pathophysiology
Clinical symptoms
Usual onset
Diagnosis
Differential Diagnosis
Complications
Medical management
Nursing management
Surgical management
Prognosis
Depend on the the
Columbia Adrenal
Center,
Hyperaldosteronism
(Conn's Syndrome)
Archived 2011-05-
26 at the Wayback
Machine
Quiz %
questions out
of 5 marks
Conn’s Syndrome
 Review of Anatomy & Physiology:
 The adrenal glands are located on both sides of the body in the retroperitoneum,
above and slightly medial to the kidneys.
4
 In humans, the right adrenal gland is pyramidal in shape, whereas the left is
semilunar or crescent shaped and somewhat larger.
 The adrenal glands measure approximately 3 cm in width, 5.0 cm in length, and
up to 1.0 cm in thickness.
 Their combined weight in an adult human range from 7 to 10 grams. The glands
are yellowish in color.
 The adrenal glands are surrounded by a fatty capsule and lie within the renal
fascia, which also surrounds the kidneys. A weak septum (wall) of connective
tissue separates the glands from the kidneys.
 The adrenal glands are directly below the diaphragm, and are attached to the crura
of the diaphragm by the renal fascia. Each adrenal gland has two distinct parts,
each with a unique function, the outer adrenal cortex and the inner medulla, both
of which produce hormones.
 The adrenal cortex produces three main types of steroid hormones:
mineralocorticoids, glucocorticoids, and androgens. Mineralocorticoids (such as
aldosterone) produced in the zona glomerulosa help in the regulation of blood
pressure and electrolyte balance.
 The glucocorticoids cortisol and cortisone are synthesized in the zona fasciculata;
their functions include the regulation of metabolism and immune system
suppression. The innermost layer of the cortex, the zona reticularis, produces
androgens that are converted to fully functional sex hormones in the gonads and
other target organs.
 The production of steroid hormones is called steroidogenesis, and involves a
number of reactions and processes that take place in cortical cells. The medulla
5
produces the catecholamines, which function to produce a rapid response
throughout the body in stress situations.

 Definition: Conn’s Syndrome is a disease of the adrenal glands that involves an
excessive production of aldosterone.
 Specialty: Endocrinology
 Epidemiology: 10% of people with high blood pressure, about 33% of cases are due to
an adrenal adenoma that produces aldosterone, and 66% of cases are due to an
enlargement of both adrenal glands.
 Causes: Enlargement of both adrenal glands, adrenal adenoma, adrenal cancer, familial
hyperaldosteronism
 Pathophysiology: hyperaldosteronism causes hypernatremia, hypokalemia, and
metabolic alkalosis. Primary hyperaldosteronism is caused by aldosterone-producing
adenomas, bilateral idiopathic adrenal hyperplasia, aldosterone-producing adrenal
6
carcinoma, and familial aldosteronism. The increased amount of aldosterone potentiates
renal sodium reabsorption and water retention, and potassium excretion. The increased
sodium reabsorption by the kidneys results in plasma volume expansion which is the
primary initiating mechanism for hypertension. This may induce tissue inflammation and
heightened sympathetic drive, with subsequent development of fibrosis in vital organs,
such as heart, kidneys, and vasculature. As a result, this may lead to the development of
chronic kidney disease, atrial fibrillation, stroke, ischemic heart disease, and congestive
heart failure. Besides the elevation in sodium, patients often develop hypokalemia and
metabolic alkalosis. Nearly 1/5th of patients with Conn syndrome have impairment in
glucose tolerance which is due to the inhibitory effects of hypokalemia on insulin
secretion.
 Clinical symptoms: High blood pressure, poor vision, headaches, muscular weakness,
muscle spasms
7
 Usual onset: 30 to 50 years old
 Diagnosis:
 Blood test for aldosterone-to-renin ratio used for case detection,
 X-rays, CT scans, and an MRI to confirm the presence of tumors.
 Differential Diagnosis: Hypertension, Metabolic alkalosis, Renal artery stenosis,
Malignant hypertension, Preeclampsia, Licorice intake, Gitelman syndrome, Barter
syndrome, Adrenal carcinoma
 Complications: Stroke, myocardial infarction, kidney failure, abnormal heart rhythms
 Medical management: spironolactone or eplerenone, drugs that block the effect of
aldosterone
 Spironolactone: Drug information
 Dosing: Adult To reduce delay in onset of effect, a loading dose of 2 or 3 times
the daily dose may be administered on the first day of therapy.
 Edema: Oral: 25-200 mg/day in 1-2 divided doses
8
 Hypokalemia: Oral: 25-100 mg daily
 Hypertension (JNC 7): Oral: 25-50 mg/day in 1-2 divided doses
 Diagnosis of primary aldosteronism: Oral: Long test: 400 mg daily for 3-4 weeks;
short test: 400 mg daily for 4 days; maintenance until surgical correction: 100-400
mg/day in 1-2 divided doses
 Heart failure, severe (NYHA class III-IV; with ACE inhibitor and a loop diuretic
± digoxin): 12.5-25 mg/day; maximum daily dose: 50 mg. If 25 mg once daily not
tolerated, reduce to 25 mg every other day was the lowest maintenance dose
possible.
 Note: If potassium >5 mEq/L or serum creatinine >4 mg/dL, discontinue or
interrupt therapy.
 Acne in women (unlabeled use): Oral: 25-200 mg once daily
 Hirsutism in women (unlabeled use): Oral: 50-200 mg/day in 1-2 divided doses
(Koulouri, 2008; Martin, 2008)
 Eplerenone: Drug information
 Dosing: Adult
 Hypertension: Oral: Initial: 50 mg once daily; may increase to 50 mg twice daily
if response is not adequate; may take up to 4 weeks for full therapeutic response.
Doses >100 mg/day are associated with increased risk of hyperkalemia and no
greater therapeutic effect.
 Dose modification during concurrent use with moderate CYP3A4 inhibitors:
Initial: 25 mg once daily
9
 Heart failure (post-MI): Oral: Initial: 25 mg once daily; dosage goal: Titrate to 50
mg once daily within 4 weeks, as tolerated
 Dosage adjustment per serum potassium concentrations for HF (post-MI): <5
mEq/L:
 Increase dose from 25 mg every other day to 25 mg daily or
 Increase dose from 25 mg daily to 50 mg daily
 5-5.4 mEq/L: No adjustment needed
 5.5-5.9 mEq/L:
 Decrease dose from 50 mg daily to 25 mg daily or
 Decrease dose from 25 mg daily to 25 mg every other day or
 Modify dose from 25 mg every other day to withhold medication
 ≥6 mEq/L: Withhold medication until potassium <5.5 mEq/L, then restart at 25
mg every other day
 Nursing management: Health Education about Low Salt Diet
 Surgical management: Laparoscopic surgical removal (adrenalectomy) may be curative
 Prognosis: Conn syndrome is associated with high morbidity and mortality if it is left
untreated. The primary cause of the morbidity is linked to hypertension and hypokalemia,
the latter is known to cause cardiac arrhythmias that can be fatal.
6. Guided Practice/Activities (10minutes): Giving Group Discussion
10
7. Course Schedule Plan:
No. Time Content & Teacher Activity Student Activity Resources
1. 2:30 – 2:55 Review of Anatomy &
Physiology
Definition
Specialty
Interactively &
Attentively follow
Lecture and Hold
Short Notes
Books
Handouts
2. 2:55 – 3:25 Epidemiology
Causes
Pathophysiology
Clinical symptoms
Usual onset
Interactively &
Attentively follow
Lecture and Hold
Short Notes
Books
Handouts
3. 3:25 – 3:35 Break Time Relax & Refresh
4. 3:35 – 4:00 Diagnosis
Differential Diagnosis
Complications
Interactively &
Attentively follow
Lecture and Hold
Short Notes
Books
Handouts
5. 4:00 – 4:30 Medical management
Nursing management
Surgical management
Prognosis
Interactively &
Attentively follow
Lecture and Hold
Short Notes
Books
Handouts
8. Closure:
11
A. Summary (5 Minutes): Revised of the content of the body key terms of Conn’s
Syndrome by the students
B. Assessment/ Evaluation Criterion (15 minutes): Quiz
 5 Multiple Choice Questions
Quiz Instruction: Choose the best answer and encircle the correct answer. (1 mark Each)
1. What hormone is elevated in Conn syndrome?
A. Aldosterone
B. Cortisol
C. Adrenocorticotropic
D. Vasopressin
2. An adult male hypertensive patient in your hospital with the diagnosis of Conn’s
syndrome is more likely to manifest the following clinical indexes EXCEPT?
A. muscle spasms
B. headache
C. hypokalemia
D. acidosis
3. Which one of the following is incorrect statement related to primary
hyperaldosteronism?
A. excess production of the hormone aldosterone from the adrenal glands, resulting in
High renin levels
12
B. Many suffer from fatigue, potassium deficiency and high blood pressure which may
cause poor vision, confusion or headaches.
C. Complications include cardiovascular disease such as stroke, myocardial infarction,
kidney failure and abnormal heart rhythms.
D. About 33% of cases are due to an adrenal adenoma that produces aldosterone
4. Which one of the following is the Incorrect statement about primary
hyperaldosteronism?
A. 66% of cases are due to both adrenal glands hyperplasia.
B. hyperaldosteronism causes hypernatremia, hypokalemia.
C. aldosterone-to-renin ratio is used for case detection of it.
D. usual onset of the disorder is 14 - 20 years age of peoples
5. Which one the following is Incorrect statement about Conn’s Syndrome?
A. Manifestations of muscle cramps due to hyperexcitability of neurons secondary to
low blood calcium
B. muscle weakness due to hypo-excitability of skeletal muscles secondary to
hypokalemia
C. headaches due to low blood potassium or low blood pressure may be seen
D. Secondary hyperaldosteronism is often related to decreased cardiac output which is
associated with elevated renin levels
13
References
1) Brunner and Suddarth’s textbook of medical surgical nursing 14th edition. | Philadelphia:
Wolters Kluwer, [2018]
2) Mary DiGiulio and Donna Jackson Medical-Surgical Nursing Demystified 1st edition.
The McGraw-Hill Companies, Inc 2007
3) https://emedicine.medscape.com/article/127080-overview#showall

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Lesson plan

  • 1. BY: Habtemariam Mulugeta College of Medicine and Health Sciences School of Nursing & Midwifery Department of Adult Health Nursing Advanced Nursing Education & Curriculum Development LESSON PLAN ON: CONN’S SYNDROME Preparedby: Name: Habtemariam Mulugeta Abate ID No: SRSG/398/12 DESSIE, ETHIOPIA DECEMBER, 2020
  • 2. I ACKNOWLEDGEMENT First, I would like to express my heartfelt gratitude to WU CMHS for giving me this chance to enhance my knowledge and skill. Secondly, I would like to thank my instructor Dr. Caridad Sanchez Olis for sharing me his deep knowledge, experience and expertise. Last but not least I would like to thank my family and friends in helping me in ideas and material during my entire work.
  • 3. 1 LESSON PLAN ON: CONN’S SYNDROME Date: December 14, 2020 Duration: 2 Hour Instructor name: Habtemariam Mulugeta Department: Adult Health Nursing Year of study: 1st Year Semester: II 1. Unit Title: Conn’s Syndrome 2. Introduction: Conn’s Syndrome also known as primary hyperaldosteronism refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels. This abnormality is caused by hyperplasia or tumors. Many suffer from fatigue, potassium deficiency and high blood pressure which may cause poor vision, confusion or headaches. Symptoms may also include: muscular aches and weakness, muscle spasms, low back and flank pain from the kidneys, trembling, tingling sensations, numbness and excessive urination. Complications include cardiovascular disease such as stroke, myocardial infarction, kidney failure and abnormal heart rhythms. (3 minutes) 3. SessionObjectives  General Objective: At the end of the topic of Conn’s Syndrome the student will to have sufficient knowledge about the topic and give effective quality care for the patient in the aspect of pharmacological and none pharmacological nursing care for the patient with full confidence independently.  Specific Objectives:
  • 4. 2  Define Conn’s Syndrome (Cognitive)  Discuss physiology adrenal gland & endocrine system (cognitive)  Understands the clinical symptoms and diagnostic tools of Conn’s Syndrome (Affective)  Distinguishes the pharmacological and none pharmacological management (psychomotor) 4. Required materials and instrument needed  LCD  Internet,  marker,  White board,  Paper,  Pen and marker,  Lab top,  Books and handouts 5. Teaching Methods & Activities (Main body of presentation) a. Teaching methods: Interactive Lecture and Discussion b. Teaching techniques: LCD Projector and White Board c. Body: 1:30 minutes
  • 5. 3 d. Content Outline No. Type of Disorder Types of Activities Mechanism of Management Assessment 1. Conn’s Syndrome Review of Anatomy & Physiology Definition Specialty Epidemiology Causes Pathophysiology Clinical symptoms Usual onset Diagnosis Differential Diagnosis Complications Medical management Nursing management Surgical management Prognosis Depend on the the Columbia Adrenal Center, Hyperaldosteronism (Conn's Syndrome) Archived 2011-05- 26 at the Wayback Machine Quiz % questions out of 5 marks Conn’s Syndrome  Review of Anatomy & Physiology:  The adrenal glands are located on both sides of the body in the retroperitoneum, above and slightly medial to the kidneys.
  • 6. 4  In humans, the right adrenal gland is pyramidal in shape, whereas the left is semilunar or crescent shaped and somewhat larger.  The adrenal glands measure approximately 3 cm in width, 5.0 cm in length, and up to 1.0 cm in thickness.  Their combined weight in an adult human range from 7 to 10 grams. The glands are yellowish in color.  The adrenal glands are surrounded by a fatty capsule and lie within the renal fascia, which also surrounds the kidneys. A weak septum (wall) of connective tissue separates the glands from the kidneys.  The adrenal glands are directly below the diaphragm, and are attached to the crura of the diaphragm by the renal fascia. Each adrenal gland has two distinct parts, each with a unique function, the outer adrenal cortex and the inner medulla, both of which produce hormones.  The adrenal cortex produces three main types of steroid hormones: mineralocorticoids, glucocorticoids, and androgens. Mineralocorticoids (such as aldosterone) produced in the zona glomerulosa help in the regulation of blood pressure and electrolyte balance.  The glucocorticoids cortisol and cortisone are synthesized in the zona fasciculata; their functions include the regulation of metabolism and immune system suppression. The innermost layer of the cortex, the zona reticularis, produces androgens that are converted to fully functional sex hormones in the gonads and other target organs.  The production of steroid hormones is called steroidogenesis, and involves a number of reactions and processes that take place in cortical cells. The medulla
  • 7. 5 produces the catecholamines, which function to produce a rapid response throughout the body in stress situations.   Definition: Conn’s Syndrome is a disease of the adrenal glands that involves an excessive production of aldosterone.  Specialty: Endocrinology  Epidemiology: 10% of people with high blood pressure, about 33% of cases are due to an adrenal adenoma that produces aldosterone, and 66% of cases are due to an enlargement of both adrenal glands.  Causes: Enlargement of both adrenal glands, adrenal adenoma, adrenal cancer, familial hyperaldosteronism  Pathophysiology: hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis. Primary hyperaldosteronism is caused by aldosterone-producing adenomas, bilateral idiopathic adrenal hyperplasia, aldosterone-producing adrenal
  • 8. 6 carcinoma, and familial aldosteronism. The increased amount of aldosterone potentiates renal sodium reabsorption and water retention, and potassium excretion. The increased sodium reabsorption by the kidneys results in plasma volume expansion which is the primary initiating mechanism for hypertension. This may induce tissue inflammation and heightened sympathetic drive, with subsequent development of fibrosis in vital organs, such as heart, kidneys, and vasculature. As a result, this may lead to the development of chronic kidney disease, atrial fibrillation, stroke, ischemic heart disease, and congestive heart failure. Besides the elevation in sodium, patients often develop hypokalemia and metabolic alkalosis. Nearly 1/5th of patients with Conn syndrome have impairment in glucose tolerance which is due to the inhibitory effects of hypokalemia on insulin secretion.  Clinical symptoms: High blood pressure, poor vision, headaches, muscular weakness, muscle spasms
  • 9. 7  Usual onset: 30 to 50 years old  Diagnosis:  Blood test for aldosterone-to-renin ratio used for case detection,  X-rays, CT scans, and an MRI to confirm the presence of tumors.  Differential Diagnosis: Hypertension, Metabolic alkalosis, Renal artery stenosis, Malignant hypertension, Preeclampsia, Licorice intake, Gitelman syndrome, Barter syndrome, Adrenal carcinoma  Complications: Stroke, myocardial infarction, kidney failure, abnormal heart rhythms  Medical management: spironolactone or eplerenone, drugs that block the effect of aldosterone  Spironolactone: Drug information  Dosing: Adult To reduce delay in onset of effect, a loading dose of 2 or 3 times the daily dose may be administered on the first day of therapy.  Edema: Oral: 25-200 mg/day in 1-2 divided doses
  • 10. 8  Hypokalemia: Oral: 25-100 mg daily  Hypertension (JNC 7): Oral: 25-50 mg/day in 1-2 divided doses  Diagnosis of primary aldosteronism: Oral: Long test: 400 mg daily for 3-4 weeks; short test: 400 mg daily for 4 days; maintenance until surgical correction: 100-400 mg/day in 1-2 divided doses  Heart failure, severe (NYHA class III-IV; with ACE inhibitor and a loop diuretic ± digoxin): 12.5-25 mg/day; maximum daily dose: 50 mg. If 25 mg once daily not tolerated, reduce to 25 mg every other day was the lowest maintenance dose possible.  Note: If potassium >5 mEq/L or serum creatinine >4 mg/dL, discontinue or interrupt therapy.  Acne in women (unlabeled use): Oral: 25-200 mg once daily  Hirsutism in women (unlabeled use): Oral: 50-200 mg/day in 1-2 divided doses (Koulouri, 2008; Martin, 2008)  Eplerenone: Drug information  Dosing: Adult  Hypertension: Oral: Initial: 50 mg once daily; may increase to 50 mg twice daily if response is not adequate; may take up to 4 weeks for full therapeutic response. Doses >100 mg/day are associated with increased risk of hyperkalemia and no greater therapeutic effect.  Dose modification during concurrent use with moderate CYP3A4 inhibitors: Initial: 25 mg once daily
  • 11. 9  Heart failure (post-MI): Oral: Initial: 25 mg once daily; dosage goal: Titrate to 50 mg once daily within 4 weeks, as tolerated  Dosage adjustment per serum potassium concentrations for HF (post-MI): <5 mEq/L:  Increase dose from 25 mg every other day to 25 mg daily or  Increase dose from 25 mg daily to 50 mg daily  5-5.4 mEq/L: No adjustment needed  5.5-5.9 mEq/L:  Decrease dose from 50 mg daily to 25 mg daily or  Decrease dose from 25 mg daily to 25 mg every other day or  Modify dose from 25 mg every other day to withhold medication  ≥6 mEq/L: Withhold medication until potassium <5.5 mEq/L, then restart at 25 mg every other day  Nursing management: Health Education about Low Salt Diet  Surgical management: Laparoscopic surgical removal (adrenalectomy) may be curative  Prognosis: Conn syndrome is associated with high morbidity and mortality if it is left untreated. The primary cause of the morbidity is linked to hypertension and hypokalemia, the latter is known to cause cardiac arrhythmias that can be fatal. 6. Guided Practice/Activities (10minutes): Giving Group Discussion
  • 12. 10 7. Course Schedule Plan: No. Time Content & Teacher Activity Student Activity Resources 1. 2:30 – 2:55 Review of Anatomy & Physiology Definition Specialty Interactively & Attentively follow Lecture and Hold Short Notes Books Handouts 2. 2:55 – 3:25 Epidemiology Causes Pathophysiology Clinical symptoms Usual onset Interactively & Attentively follow Lecture and Hold Short Notes Books Handouts 3. 3:25 – 3:35 Break Time Relax & Refresh 4. 3:35 – 4:00 Diagnosis Differential Diagnosis Complications Interactively & Attentively follow Lecture and Hold Short Notes Books Handouts 5. 4:00 – 4:30 Medical management Nursing management Surgical management Prognosis Interactively & Attentively follow Lecture and Hold Short Notes Books Handouts 8. Closure:
  • 13. 11 A. Summary (5 Minutes): Revised of the content of the body key terms of Conn’s Syndrome by the students B. Assessment/ Evaluation Criterion (15 minutes): Quiz  5 Multiple Choice Questions Quiz Instruction: Choose the best answer and encircle the correct answer. (1 mark Each) 1. What hormone is elevated in Conn syndrome? A. Aldosterone B. Cortisol C. Adrenocorticotropic D. Vasopressin 2. An adult male hypertensive patient in your hospital with the diagnosis of Conn’s syndrome is more likely to manifest the following clinical indexes EXCEPT? A. muscle spasms B. headache C. hypokalemia D. acidosis 3. Which one of the following is incorrect statement related to primary hyperaldosteronism? A. excess production of the hormone aldosterone from the adrenal glands, resulting in High renin levels
  • 14. 12 B. Many suffer from fatigue, potassium deficiency and high blood pressure which may cause poor vision, confusion or headaches. C. Complications include cardiovascular disease such as stroke, myocardial infarction, kidney failure and abnormal heart rhythms. D. About 33% of cases are due to an adrenal adenoma that produces aldosterone 4. Which one of the following is the Incorrect statement about primary hyperaldosteronism? A. 66% of cases are due to both adrenal glands hyperplasia. B. hyperaldosteronism causes hypernatremia, hypokalemia. C. aldosterone-to-renin ratio is used for case detection of it. D. usual onset of the disorder is 14 - 20 years age of peoples 5. Which one the following is Incorrect statement about Conn’s Syndrome? A. Manifestations of muscle cramps due to hyperexcitability of neurons secondary to low blood calcium B. muscle weakness due to hypo-excitability of skeletal muscles secondary to hypokalemia C. headaches due to low blood potassium or low blood pressure may be seen D. Secondary hyperaldosteronism is often related to decreased cardiac output which is associated with elevated renin levels
  • 15. 13 References 1) Brunner and Suddarth’s textbook of medical surgical nursing 14th edition. | Philadelphia: Wolters Kluwer, [2018] 2) Mary DiGiulio and Donna Jackson Medical-Surgical Nursing Demystified 1st edition. The McGraw-Hill Companies, Inc 2007 3) https://emedicine.medscape.com/article/127080-overview#showall