SALALE UNIVERSITY COLLEGE OF HEALTH SCIENCE

DEPARTMENT OF ADULT HEALTH NURSING

Title : Adrenal Disorder

Presented To: Mr Tadele K (Ass’t Prof )
Presented by: Mulunesh Mosisa & Nigussie Wondimu

Sept 2023
11/14/2023 Fiche, Ethiopia 1
 Course Outline
• Objective
• Introduction
• Epidemology
• Causes
• Phatophysiology
• Clinical manifestation
• Complication
• Diagnosis
• Management (nursing& medical )

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 Objective

 At the end of this presentation students will be able to :

 Define adrenal gland disorder

 Identify common adrenal gland disorder

 Describe clinical manifestation of adrenal gland disorder

 Identify cause of adrenal gland disorder

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 Introduction

 Adrenalin gland are also known as suprarenal

glands because it is attached to
upper portion of each kidney.
 The two glands have similar
anatomical structure, functions,
secreted hormones but each gland
has a separate and independent
function.

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 Introduction cont’d

 The adrenal glands consists of two distinct parts:

A) Cortex (outer part, consists of 80%)
 Secretes 3 groups of steroid hormones.
 Mineralocorticoids (eg. Aldostrone).
 Glucocorticoids (eg. cortisol).
 Sex hormones
B) Medulla (inner part, consists of 20%).
 Secretes
 Catecholamine (epinephrine & norepinephrine) which
are responsible for fight or flight response.
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 Adrenal Disorders

Hyperfunction of the Adrenal cortex

 Also known as Cushing’s syndrome.

 It results from excessive adrenocortical activity

(secretion) particularly glucocorticoid & mineralo-

corticoid.

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 Epidemology

 Cushing syndrome may be either corticotropin

(ACTH) dependent or independent. Approximately
80 percent of endogenous Cushing syndrome cases
are ACTH dependent, and approximately 20 percent
are ACTH independent
 Chronic hypercortisolism inhibits both hypothalamic
CRH hormone and V/P.

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 Epidemiology
 Generally considered a rare disease.

 It occurs with an incidence of 1–2 per 100,000

population per year.

 However, it is debated whether mild cortisol excess may

be more prevalent among patients with features of

Cushing’s such as centripetal obesity, type 2 diabetes, and
osteoporotic vertebral fractures, recognizing that these
are relatively nonspecific and common in the population.
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 Cont’d
 Majority of patients with endogenous Cushing’s

syndrome, the underlying cause is an ACTH-producing

corticotrope adenoma of the pituitary, as initially

described by Harvey Cushing in 1912.

 Can be seen at any age, but most common in the third

to sixth decade of life.

 Cushing’s disease more frequently affects women than

men
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 Causes of cushing’s syndrome

 Hyperplasia of the adrenals(functional) due to increased

secretion of ACTH from pituitary in response to stress.
 Adrenal adenoma or carcinoma.
 Pituitary tumor secrete excess ACTH which causes over
production of cortisol by adrenal glands.
 Iatrogenic – due to prolonged use of cortico steroids
such as prednisone to treat severe asthma or arthritis.

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 pathophysiology

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 Clinical manifestations

 Central obesity – redistribution of fat to face (red,

round/moon face), neck, trunk, upper back (buffalo
hump) while the extremities are thin.
 Hypertension - due to renal effects of aldostrone
(V/P).
 Hypertension and heart failure, Sodium and water
retention –edema.
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 C/M cont’d

 DM symptoms– cortisol increases hepatic

glueconeogenesis and decrease peripheral glucose
utilization
 Menstrual irregularities (oligomenorrhea)– excess ACTH
stimulate the adrenal gland to secrete excess androgen.
 Hirsutism (presence of hair on unusual places) due to
excess androgen.
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 C/M cont’d

 Muscle wasting and weakness – due to catabolic

effects of cortisol on muscle protein.
 Osteoporosis before the age of 50 – also due to
increased bone catabolism.
 Poor wound healing due to impaired immune
function, infection and DM.

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 C/M cont’d

 Purple strie (a linear /stretch marks on the abdomen

where the thin, wasted skin is stretched by
underlying fat).
 Psychiatric disturbances. Eg. Depression.
 Pathologic fracture of bone and kidney stones.
 Peptic ulcer – cortisol cause gastric or intestinal
irritation.
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 Complications

 Without treatment, Cushing syndrome can cause

complications, including:
 Bone loss, also called osteoporosis, which can lead to
broken bones.
 High blood pressure, also called hypertension.
 Type 2 diabetes.
 Serious or multiple infections.
 Loss of muscle mass and strength.
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 Diagnostic findings

 Over night dexamethasone suppression test –

administer 1 mg po. at 11 pm midnight and measure
serum cortisol at 8 am. Suppression of cortisol to less
than 5mg/dL indicates normal functioning.

 measurement of serum ACTH & cortisol level.

 Increase of both ACTH & cortisol show pituitary disease

 Decrease of ACTH & increase of cortisol show adrenal

disease.
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 Diagnostic findings

 Elevated blood glucose level due to hepatic

glueconeogenesis.
 CT scan to detect adrenal & pituitary adenomas.
 Blood high sodium and low potassium levels,
elevated glucose.
 X- ray to reveal osteoporosis of bones.

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 Management

 surgical excision of the adrenal glands (adrenalectomy).

 If surgical management is not advisable, drug therapy

may be used to inhibit the synthesis of cortisol in the
adrenal cortex.

 Radiation therapy or transphenoidal hypophysectomy

(remove pituitary) if the cause is pituitary adenoma.

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 Management cont’d

 Pneumonectomy (surgical removal of one lung) if the

cause is adenoma (tumor) of the lung.
 Discontinuance or alteration in administration of
exogenous corticosteroids.

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 Nursing management

 Include foods rich in potassium (orange juice,

bananas, animal foods) and limit sodium content of
the diet to prevent hypertension.
 Administer antacids or cimetidine as prescribed for
the patient with PUD (peptic ulcer disease).

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 Nursing management cont’d

 Prevention of spontaneous fractures because of

osteoporosis by early detecting and prompting
treatment of fractures and providing a diet high in
calcium, vitamin D, and protein.
 Pre-and postoperative care because of glands are
highly vascular, there is an increased risk of
hemorrhage.
 Teach the patient to adjust their corticosteroid
replacement therapy.
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 Hypofunction of Adrenal Cortex

Addison’s disease.
 It is characterized by adrenocortical insufficiency or
inadequate secretion of cortisol to meet the patient
needs.
 Relatively uncommon chronic disorder caused by
deficiency of cortical hormones due to damaged or
atrophied.
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 Causes

 Autoimmune or idiopathic atrophy of the adrenal gland

(80%).
 Surgical removal of both adrenal glands.
 Infection of adrenal glands. Eg. TB, histoplasmosis.
Genetic defects including abnormal adrenal gland
development
 Cancer cells in the adrenal glands

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 Causes cont’d

 Inadequate secretion of ACTH from pituitary gland.

 Therapeutic use of corticosteroids – the adrenal
gland depend on the artificial corticosteroid & will
not produce by itself because of suppression of
hypothalamic pituitary axis by administration of
corticosteroids.

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 Clinical manifestations

 Emaciation (extreme thin), muscle weakness &

fatigue.

 Hypoglycemia due to decreased hepatic

glueconeogenesis secondary to decreased cortisol
hormone.

 Dark skin pigmentation.

 GI disturbances: nausea, vomiting, abdominal pain,

weight loss.
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 C/M cont’d
 Hypotension due to low serum Na secondary to loss
through urine.

 In severe cases, the disturbance of Na & K

metabolism may be marked by depletion of Na &
H2O and severe chronic dehydration which leads to
circulatory shock.

 Can result in Addisonian crisis.

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 complication

 Hyponatremia

 Hyponatremia: causes confusion, fatigue, and

muscle twitches and seizures

 hypercalemia

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 Diagnostic Findings

 Complete history and physical examination

 Low levels of ACTH in the blood or urine.
 Decreased serum cortisol levels.

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 Diagnostic Findings cont’d

 Decreased blood glucose levels due to decreased

hepatic glueconeogenesis.
 Decreased serum sodium levels (hyponatremia) &
increased potassium levels (hyperkalemia).
 Increased WBC (leukocytosis) – infection.

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 Management

 Restore circulatory status—fluids, corticosteroids

 Monitoring V/S and placing the patient in recumbent
position with the legs elevated to decrease
hypotension. Vasopressor (eg. Aldostrone) may be
required if hypotension persists.

 Antibiotics if infection is indicated.

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 Management cont,d

 Life long replacement of corticosteroids to prevent

recurrence of adrenal insufficiency.
 Supplementary dietary intake with added salt to
replace lost fluids.
 Advice diet rich in sodium, carbohydrate and protein.

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 Nursing management

 Monitor electrolyte levels and manage any

imbalance
 Administer hormone replacement therapy
 Monitoring for hypoglycemia and hypotension.

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 Prevention

 Addison's disease can't be prevented, but there are

ways to avoid an addisonian crisis:
 Talk to your health care provider if you always feel
tired or weak or are losing weight without trying.

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 Cont,d

 If you have been diagnosed with Addison's disease,

ask your provider what to do when you're sick. You

may need to learn how to increase your dose of

corticosteroids.

 If you become very sick, especially if you are

vomiting and you can't take your medicine, go to an

emergency room.
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 Disorders of the adrenal medulla

Pheochromocytoma
Is a tumor of adrenal gland (usually benign tumor) that
originate from the chromaffin cells of the adrenal medulla.
One of the condition that causes
 hypersecretion of catecholamine.
Any age but usu. Between 40-50.
Can be familial
Sex: female = male (1:1 ratio)
90% are unilateral & benign
10% are malignant
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 causes

 The causes unknown

 The tumor develops in specialized cells, located in
the center of an adrenal gland. These cells release
hormone epinephrine and nor epinephrine. These
hormone control many body function such as heart
rate, blood pressure and blood sugar

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 Clinical manifestation

 Hypertention as a result of epinephrine and nor

epinephrine

 Headaches as a result of hypertension

 palpitation and tachycardia due to increased

production of catecholamine dilated pupils from

increased production of epinephrine and nor

epinephrine
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 complications

 Stroke
 Heart failure
 Hypertension
 arrhythmias

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 Diagnostic Findings

 Sign of SNS over activity in association with elevation

of BP.

 Associated with 5H’s: hypertension, headache,

hyperhiderosis (excessive sweating), hyperglycemia &
hyper metabolism.
 Serum epinephrine & norepinephrine level is
elevated.
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 Diagnostic Findings cont’d

 Urinary catecholamines and metanephrine tests.

 N.B: Must avoid coffee, tea, bananas, chocolate,
vanilla, nicotine, amphetamines, decongestants
before 24h urine testing.
 Imaging studies: CT scan, MRI & ultrasound to
visualize tumor.

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 Management of pheochromocytoma

 During an episode attack of HTN, place the patient

on bed (bed rest) with head of the bed elevated to
promote an orthostatic decrease in BP.
 Calcium channel blockers and Beta blockers.
 Smooth muscle relaxant to lower BP quickly.

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 Management cont’d

 Adrenalectomy or surgical management

(manipulation of the tumor can cause excessive
release of catecholamines).
 Corticosteroid therapy if adrenalectomy performed.
 Monitor for hypotension and hypoglycemia which
can occur post surgery.

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 Nursing management

 Monitor blood pressure

 Administer medication to control hypertension
 Monitor urine for catecholamine
 Reduce caffeine to lower blood pressure

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 summary
 Adrenal gland disorders are conditions that interfere
with the normal functioning of adrenal glands. It
causes hyperfunction and hypofuctions.
 The adrenal glands consists of two distinct
parts:cortex (outer part ) and Medulla (inner part.
 Some of adrenal disorders are cushing syndrome,
addison disease and pheochromocytoma.

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 Reference
 Harrison 21st Edition

 https://
www.bing.com/search?q=adrenal+gland+disorders+p
pt+slideplay&form=EDGEAR&qs=HS&cvid=77ef8960a
df94c83beb8f6208ad4914b&cc=US&setlang=en-
US&plvar=0

 https://
www.mayoclinic.org/diseases-conditions/cushing-syn48
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 Cont,d

 https://www.uptodate.com/contents/causes-and-
pathophysiology-of-cushing-syndrome

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 THANK YOU

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