Session Slides NURS 232 Session 18

NURS 232 MEDICAL CONDITIONS OF THE
INTEGUMENTARY, GASTROINTESTINAL
AND ENDOCRINE SYSTEMS
Session Eighteen Disorders of

the Adrenal Gland
Lecturer: Dr. Kwadwo Ameyaw Korsah, UG, SON
Contact Information: kakorsah@ug.edu.gh
College of Education
School of Continuing and Distance Education
2014/2015 2016/2017
Session Overview
Disorders of the adrenal gland are discussed
including Cushings syndrome, aldosteronism,
Adissons disease and Pheocromocytoma.
The pathophysiology of these conditions are well
noted.
Dr. Kwadwo Ameyaw Korsah, UG, SON
Slide 2
Session Objectives
At the end of the session, the student should be
able to:
Apply their previous knowledge in anatomy and
physiology to explain the pathophysiology of
conditions associated with the adrenal gland.
Recognize possible clinical signs and symptoms
of these conditions.
Identify predisposing factors related to these
conditions.
Render appropriate nursing care to patients with
these conditions.
Slide 3
Session Outline
The key topics to be covered in the session are as
follows:
Topic One - Cushings syndrome
Topic Two - Adissons disease
Slide 4
Topic One
CUSHINGS SYNDROME
Slide 5
Background of Cushings
Syndrome
From your Previous Knowledge (PK)
Adrenal gland is also called Suprarenal
Gland. Adrenal are paired glands located
on top of the kidney. Each of the adrenal
glands has 2 parts. These are:
1. Inner part which is Adrenal Medulla.
2. Outer part also called Adrenal Cortex.
. The two function as separate endocrine
glands.
Background of Cushings Syndrome

Contd.
Adrenal Medulla:
Principal Hormones released by the
medulla are:
1. Epinephrine or Adrenalin
2. Small amount of Nor-epinephrine.
. These are released in response to
stimulation by the sympathetic nervous
system. Thus they become active when a
person is physically excited.

Contd.
They are referred to as fight-or-flight

hormones because they prepare the
body for vigorous physical activity.
Some effects of these hormones are:
1. Increase the heart rate and Blood
Pressure.
2. Increase metabolic rate of tissues
especially skeletal muscles, cardiac
muscle and nervous tissues.
3. Dilate the bronchioles and this allows air
to move in and out of the lung with
greater ease, Etc.

Contd.
Adrenal Cortex:
It releases steroid hormones. Three
classes of steroid hormones secreted are:
1. Glucocorticoids
2. Mineralocorticoids
3. Androgens and Oestrogens (sex
Hormones)

Contd.
Glucocorticoids: The major glucocorticoids
is Cortisol (Hydrocortisone) which raises
blood sugar level by reducing glucose
utilization and also by promoting glucose
formation from protein and fat
(gluconeogenesis) among so many
functions.
Cortisol also suppresses the inflammatory
reactions at multiple sites in the body.
10

Contd.
Mineralocorticoids: They regulate
electrolyte and water balance by
promoting absorption of sodium and
excretion of potassium by the renal
tubules. Example is Aldosterone (a major
hormone of this class). It acts mainly on
the kidneys but it can affects other organs
in the body.
11

Contd.
Helps to retain Na+ (ions) and water in the
body and helps elimination of K+ (ions)
from the body.
Low BP Release of a Protein (Renin) from
the kidney.
Renin causes blood protein
Angiotensinogen to be converted to
Angiotensin I Angiotensin II (active
protein). Angiotensin II acts on the adrenal
cortex to increase aldosterone secretion
(causing retention of sodium and water)
and it constricts blood vessels. Together
these effects help to raise blood pressure.
12

Contd.
Androgen and Oestrogens: (Sex
Hormones). Small quantities of these are
produced for sexual development and
growth.
Androgen is required by both sexes for
normal pubertal and skeletal development.
13

Contd.
The adrenal production of glucocorticoids
and sex hormones is controlled by Pituitary
Adrenocorticotrophic Hormone (ACTH) or
corticotrophin.
14

Contd.
ACTH binds to receptors on cells in the
cortex of the adrenal glands. ACTH
increases the secretion of a hormone from
the adrenal cortex called Cortisol.
15

Contd.
ACTH is also required to keep the adrenal
cortex from degenerating.
Again, ACTH binds to Melanocytes in the
skin and increases skin pigmentation.
16

Contd.
One symptom of too much ACTH secretion
is the darkening of the skin.
The rate of ACTH secretion is controlled by
a releasing hormone from the
hypothalamus called corticotrophinreleasing hormone (CRH).
17

Contd.
Clinical Disturbances of Adrenal Cortical
Function.
Adrenal cortical dysfunction
abnormalities of both glucocorticoids and
mineralocorticoids.
Cushings Syndrome was described by an
American, Dr. Harvey Cushing in 1932.
Cushings Syndrome = Hypercortisolism =
Hyperadrenocorticism.
18
CUSHINGS SYNDROME
Cushings syndrome is a chronic disorder
in which hyperfunction of the adrenal
cortex produces excessive amount of
circulating cortisol.
In other words, this condition results from
high levels of cortisol or other
corticosteroids in the blood and is
associated with various changes in the
body including the development of
obesity, hypertension, diabetes, and
osteoporosis.
It is relatively rare and most commonly
affects adults aged 20 50.
19
CUSHINGS SYNDROME
Cushing's syndrome occurs when the
body's tissues are exposed to excessive
levels of cortisol for long periods of time.
Many people suffer the symptoms of
Cushing's syndrome because they take
glucocorticoid hormones such as
prednisone for asthma, rheumatoid
arthritis, and inflammatory diseases etc.
20
CUSHINGS SYNDROME
The prolonged use or abuse (especially by
women for cosmetic reasons) of oral or
topical corticosteroids such as
prednisolone, dexamethasone,
hydrocortisone or cortisone, or
preparations containing any of these
drugs, is also a cause.
21
CUSHINGS SYNDROME
Others develop Cushing's syndrome
because of overproduction of cortisol by
the body. Normally, the production of
cortisol follows a precise chain of
events. First, the hypothalamus, a part of
the brain which is about the size of a small
sugar cube, sends corticotropin releasing
hormone (CRH) to the pituitary gland.
22
CUSHINGS SYNDROME
CRH causes the pituitary to secrete ACTH
(adrenocorticotropin), a hormone that
stimulates the adrenal glands. When the
adrenals, which are located just above the
kidneys, receive the ACTH, they respond
by releasing cortisol into the blood stream.
23
CUSHINGS SYNDROME
Cortisol performs vital tasks in the body. It
reduces the immune system's
inflammatory response etc.
24
CUSHINGS SYNDROME
When the amount of cortisol in the blood is
adequate, the hypothalamus and pituitary
release less CRH and ACTH. This ensures
that the amount of cortisol released by the
adrenal glands is precisely balanced to
meet the body's daily needs.
However, if something goes wrong with
the adrenals or their regulating switches in
the pituitary gland or the hypothalamus,
cortisol production can go awry or its
production will happen in a way not
planned.
25
CUSHINGS SYNDROME
26
Classification
This disorder may be classified as
primary, secondary, or iatrogenic,
depending on the etiologic origin.
1. Primary Cushings syndrome is the result
of a benign or malignant adrenal tumour
that causes an increased production of
cortisol.
27
Classification contd.
2. Secondary Cushings syndrome is the
result of one of the following conditions:
(a). A pituitary or hypothalamic disorder that
causes increased release of ACTH; this
disorder is called Cushings disease.
Cushings disease refers to one specific
cause, namely adenoma in the pituitary
gland that produces large amounts of
ACTH which in turn elevates cortisol.
28
(b). An ectopic disorder that produces ACTH
(for example, bronchogenic (carcinoma or
malignant neoplasm of the lung which
cause over 50% of these cases) or
pancreatic carcinoma; this disorder is
called ectopic Cushings syndrome.
In either case, the increased ACTH
stimulation results in hyperplasia of the
adrenal cortex with increased cortisol
production.
29
3. Iatrogenic Cushings syndrome is the
result of long term glucocorticoid therapy
(an excess cortisol levels). Clients who
take steroids over long periods of time
( for example, for the treatment of
arthritis, after an organ transplant, or as
an adjunct to chemotherapy) are at
increased risk for developing iatrogenic
form of the disorder.
The most common iatrogenic Cushings
may be due to Drs treatment.
30
Clinical Manifestations
1. In many instances, patients may be
treated for the secondary metabolic
dysfunction such as diabetes mellitus
before a diagnosis of Cushings syndrome
is considered.
31
contd.
Increased hepatic gluconeogenesis and
impaired insulin utilization result in
postpriandial hyperglycemia and
occasionally frank diabetes mellitus with
all signs and symptoms. Patients with
concurrent diabetes mellitus may
experience worsening hyperglycemia.
Thus cortisol raises blood sugar levels by
reducing glucose utilization and also by
promoting glucose formation from protein
and fat.
32
contd.
In other words, cortisol counteracts insulin,
contributing to hyperglycaemia by
stimulus of hepatic gluconeogenesis and
inhibiting utilization of glucose.
33
contd.
2. Again in many instances, patients may be
treated for hypertension before a
diagnosis of Cushings syndrome is
considered. Hypertension occurs as
sodium and water are retained at the
distal tubule of the nephron due to
excessive aldosterone production.
34
contd.
Sodium and water retention may
accentuate body weight increase, may
cause edema, and may expand blood
volume. Hypertension is found in almost
every patient with excessive cortisol and
may be caused by increased volume or
increased sensitivity of arterioles to
circulating catecholamines.
35
contd.
Catecholamines are hormones made by
adrenal glands. They are released into
blood during times of physical activity or
emotional stress. They are norepinephrine
and epinephrine.
36
contd.
3. Altered protein metabolism: Excessive
catabolism of proteins results in loss of
muscle mass, causing the following
symptoms:
(a). Proximal muscle wasting (in the
extremities) and weakness, which may be
characterized by difficulty getting up from
low chairs, difficulty climbing stairs, or
generalized weakness and fatigue.
37
contd.
(b). Depletion of protein matrix of bone,
resulting in osteoporosis, compression
fractures of spine, backache, bone pain,
and pathologic fractures.
(c). Loss of collagen support of skin,
resulting in thin, fragile skin that bruises
easily, and purple striae (stretch marks).
(d). Poor/slow wound healing and infection.
38
contd.
4. Altered Fat Metabolism: Changes in fat
metabolism (increase in fat mobilization)
result in fat deposits (abnormal deposition
of fat) in the abdominal region, fat pads
under the clavicle, a buffalo hump over
the upper back, and a round moon face.
Redistribution of fat with these
characteristic features may be seen in
patients without overt obesity. Body
weight is usually increased.
39
contd.
5. Alteration in Inflammatory and Immune
Response: Cortisol excess results in
decreased lymphocytes, particularly T
lymphocytes, decreased cell mediated
immunity, and altered antibody activity.
These changes make persons particularly
vulnerable to viral and fungal infections.
40
contd.
Depression in inflammatory and immune
responsiveness results in opportunistic
infections such as Pneumocystis carinii
(parasite transitional between fungus and
protozoan) or other fungal infections. Poor
wound healing may also be related to
infections.
41
contd.
6. Excessive Androgen Activity: If excessive
androgens are present, female patients
exhibit virilization (development of male
sexual characteristics in a woman), which
includes the following signs:
(a). Hirsutism (excessive facial hair in
particular) manifested initially as fine,
downy coat of hair on face and body
(neck, chest, abdomen, and thighs).
42
contd.
(b). Changes in menstrual cycle, varying
from irregularities to oligomenorrhea to
amenorrhea.
(c). Men have decreased fertility with
diminished or absent desire for sex.
(d). Children tend to be obese with slowed
growth rates.
43
contd.
7. Hyperpigmentation of the skin and
mucous membrane may be present and
indicates elevation of ACTH, which may be
from an ectopic site or the pituitary. ACTH
which has melanotrophic activity levels are
higher and therefore hyperpigmentation is
more common and significant from ectopic
sources than from the pituitary. Please
read on other related clinical
manifestations like alterations in
emotional stability e.g. Anxiety,
severe depression etc.
44
Complications
1. Hyperglycemia
2. Hypertension
3. Hypernatremia
4. Hypokalemia
Please read on these complications
45
Diagnosis
Cushings syndrome is diagnosed through
physical examination and a variety of
tests, including serum measurement of
cortisol and urine tests for cortisol. The
most important initial diagnostic test in
the patient with suspected Cushings
syndrome is confirmation of excess
glucocorticoid production.
46
Diagnosis contd.
1. Physical appearance may suggest the
condition e.g. fat deposits (abnormal
deposition of fat) in the abdominal region,
fat pads under the clavicle, a buffalo
hump over the upper back, and a round
moon face., wasting of the tissues at the
extremities and hyperpigmentation of the
skin.
47
Diagnosis contd.
The following laboratory tests may be
ordered:
2. Measurement of plasma cortisol
levels:
Normal values taken at 8am: 6 23
micrograms/deciliter. Higher result may
indicate or suggest:
1. Adrenal Tumour
2. Cushings Syndrome
3. Ectopic ACTH producing tumour.
4. Pituitary Cushings or Cushings Disease
48
Diagnosis contd.
Lower than normal level will mean
1. Addisons Disease
2. Hypopituitarism.
49
Diagnosis contd.
3. Measurement of ACTH level to
determine the etiologic origin of the
syndrome. Normally, plasma ACTH levels
are highest from 7am to 10am and lowest
from 7pm to 10pm. In secondary Cushing's
syndrome, ACTH is elevated; in primary
Cushings syndrome, ACTH is decreased.
50
Diagnosis contd.
4. A 24-hour urine tests to measure free
cortisol and androgens; these hormones
are increased in Cushings syndrome.
5. A low dose dexamethasone suppression
test may be conducted in which a low dose
dexamethasone, a potent synthetic
glucocorticoid, is administered and plasma
cortisol and urine 17-hydroxycorticosteroid
levels are obtained.
51
Diagnosis contd.
In patients with normal adrenal function,
even low doses of the glucocorticoid will
produce decreased cortisol and 17hydroxycorticosteroid levels. In patients
with bilateral adrenal hyperplasia or
adrenal tumours, there will be no decrease
in these levels.
52
Diagnosis contd.
6. Diagnosis of this syndrome includes an
increase in serum sodium and blood
glucose levels and decreased
concentration of potassium and
disappearance of lymphoid tissues.
7. Skull films, chest x-ray studies, CT
scanning are used to localize tumours in
suspected organs including the pituitary.
53
Treatment
Treatment modalities include surgery,
irradiation, pharmacologic therapy, or a
combination of these three approaches.
Although there are no ideal treatments,
attempts are made to normalize cortisol
secretion, prevent insufficiencies, and
minimize risks and continued need for
medication.
54
Treatment contd.
1. Pharmacologic therapies are used, often
in combination with irradiation. Central
agents to treat pituitary Cushings disease
include cyproheptadine (Periactine)
(starting dose 4mg x 3 dly, then increase
to 4mg to 20mg x 3 dly) that inhibits ACTH
secretion, and bromocriptine (Parlodel).
Few patients respond to these drugs, and
relapse are common after drug
withdrawal.
55
Treatment contd.
2. Adrenal enzyme inhibitors may be used in
conjunction with irradiation or in
preparation for surgery. These drugs block
certain enzymatic reactions required for
cortisol synthesis. Look at these examples
below:
56
Treatment contd.
The drugs most commonly used are
aminoglutethimide (Elipten), metyrapone
(Metopirone), mitotane (Lysodren) directly
suppresses activity of the adrenal cortex
and decreases peripheral metabolism of
corticosteroids and ketoconazole (Nizoral).
Adrenal cortical insufficiency is a common
drug side effect and possible Addisonian
crisis.
57
Treatment contd.
3. Surgical Treatment:
(a). Surgical removal of the pituitary gland
(hypophysectomy) is indicated when
Cushings syndrome is the result of a
pituitary disorder. The gland is removed
either by a transsphenoidal route or by a
craniotomy.
58
Treatment contd.
In transsphenoidal surgery, instruments
are inserted into part of the brain by going
through the nose and the sphenoidal bone
to remove tumour of the pituitary gland.
59
Treatment contd.
A common, often preferred treatment of
pituitary tumour is the transsphenoidal
surgical removal of the microadenoma.
The surgery has a remission rate of 60
85%, but recurrences are possible.
60
Treatment contd.
(b). Unilateral adrenalectomy is the
treatment of choice for unilateral adrenal
adenomas. Bilateral adrenalectomy is
indicated for adrenal carcinoma or
bilateral nodular hyperplasia of the
adrenal glands. (Please read on all the
above surgical operations).
(c). Ectopic ACTH-secreting tumours are
removed surgically if possible.
61
Treatment contd.
4. Irradiation is another therapeutic option
that can cause complete or partial
pituitary gland destruction. If the pituitary
gland is destroyed by irradiation, life-long
replacement of pituitary hormone is
necessary.
62
Nursing Care
The nurse caring for the client with
Cushings syndrome must take a holistic
approach to plan and implement
interventions for a wide variety of
responses, including problems related to
fluid and electrolyte balance, injury,
infection, and body image etc.
63
Nursing Care contd.

The nurse must also note that treatment is
dependent on the cause and requires
specialized investigations.
The nurse must remember to manage
hypertension and diabetes mellitus along
standard lines or should be based on
specific hospital protocol.
64
Nursing Care contd.

The nurse must also refer all suspected
cases to an Endocrinologist or Specialist
Physician in a Regional or Teaching
Hospital for appropriate investigations and
management.
It can be managed at a district/municipal
hospital level provided required personnel
and facilities are available.
65
Nursing Care contd.

Fluid Volume Excess:
The excess cortisol secretion associated
with Cushings syndrome results in sodium
and water reabsorption, causing fluid
volume excess. The client will have weight
gain, edema, and hypertension. Therefore
nursing interventions follow:
1. Weigh the client at the same time each
day with the same scale and record the
results.
66
Nursing Care contd.

2. Record accurate intake and output on
each shift. An analysis of the intake and
output ratio necessary for assessing the
risk of fluid imbalance.
67
Nursing Care contd.

3. Monitor blood pressure, rate and rhythm
of pulse, respiratory rate, and breath
sounds. Assess for peripheral edema and
jugular vein distension. Extracellular fluid
volume excess resulting from sodium and
water retention is manifested by
hypertension and a bounding, rapid pulse.
In addition there may be crackles and
wheezes in the lung field during
auscultation.
68
Nursing Care contd.

4. Teach the client and the family the
reasons for restricting fluid and the
importance of limiting fluid if ordered.
Restricting fluid can help decrease the risk
of fluid volume excess. Involving the client
and family in the plan of care and teaching
the rationale for interventions facilitates
achieving goals.
69
Nursing Care contd.

Risk for Injury:
The client with Cushings syndrome is at risk
for injury from several causes. Excess
cortisol causes increased demineralization
of bones, resulting in osteoporosis and risk
of pathologic fractures. Muscle weakness
and fatigue are common, increasing the
potential for accidental falls.
70
Nursing Care contd.

1. Maintain a save environment by keeping
unnecessary equipment out of the way
and off the floor.
2. Ensure adequate lighting especially at
night.
3. Assist the client to walk if necessary
4. Monitor for signs of fatigue (increased
pulse and respiration); and plan rest
periods.
71
Nursing Care contd.

Risk for Infection:
Elevated cortisol levels impair the immune
response and put the client with Cushings
syndrome at increased risk for infection.
Increased cortisol also affects protein
synthesis, causing delayed wound healing,
and inhibits collagen formation, which
results in epidermal atrophy, further
inhibiting resistance to infection.
72
Nursing Care contd.
In addition, impaired blood flow to

edematous tissue results in altered
cellular nutrition, which increases
potential for infection.
1. Use principles of medical asepsis and
sterile asepsis when caring for the client,
conducting procedures, or providing
wound care. An impaired immune
response increases the risk of infection.
73
Nursing Care contd.
Impaired skin and tissues make aseptic

techniques even more necessary to
decrease this risk. Intact skin is the first
line of defense against infection; if
invasive procedures are performed or a
wound is present, this defense is lost.
74
Nursing Care contd.

2. If wounds are present, assess the colour,
odor, and consistency of wound drainage.
Also assess for increased pain in and
around the wound. Cortisol excess also
delays wound healing and closure.
3.Teach the client to increase intake of
protein and vitamins C and A. Protein,
vitamin C, and vitamin A are necessary to
collagen formation; collagen helps support
and repair body tissues.
75
Nursing Care contd.

4. Monitor the clients vital signs and
verbalizations of her physical state.
Increased body temperature and pulse are
systemic indicators of infection. However,
because Cushings syndrome impairs the
normal inflammatory response, the usual
indicators of inflammation may not be
present. A generalized feeling of malaise
may be the primary manifestation of
infection.
76
Nursing Care contd.

Body Image Disturbance:
The client with Cushings syndrome has
obvious physical changes in appearance.
The abnormal fat distribution, moon face,
buffalo hump, striae and facial hair (in
women) all contribute to disruptions in the
way clients with this disorder perceive
themselves.
77
Nursing Care contd.

1. Encourage the client to express feelings
and to ask questions about the disorder
and its treatment. The loss of ones normal
body image may prompt feelings of
hopelessness, powerless, anger, and
depression. Understanding the disease
and adapting to changes from that disease
are the first steps in regaining control of
ones own body (Coping Strategies),
accepting the condition, avoiding
confrontation, adhering to treatment
protocols, and then utilization of health
education from health staff and resource
78
Nursing Care contd.

2. Ask the client to discuss strengths and
previous coping strategies. Enlist the
support of family or significant others in
reaffirming the clients worth.
Disturbances in body image are often
accompanied by low self-esteem.
79
Nursing Care contd.

3. Discuss signs of progress in controlling
symptoms, for example, decreased facial
edema. Many of the physical changes from
cortisol excess disappear with treatment.
The nurse should clearly communicate this
fact, because the client may believe the
changes are permanent.
80
Nursing Care contd.

Client and Family Teaching:
The client with Cushings syndrome requires
education about self-care at home specific
to the type of treatment given. Discharge
planning focuses on safety measures if
fatigue, weakness, and osteoporosis are
present; on taking medications as
prescribed; and on having regular health
assessments to maximize wellness.
81
Nursing Care contd.

Clients often require medications for the rest
of their lives, and dosage changes are
highly likely. Although all clients should
have access to information and health
resources, the older client may especially
require referrals to social services or
community health services because of
complexity of the treatment and care
required.
82
Topic Two
ADISSONS DISEASE
Slide 83
ADDISONS DISEASE
Addisons disease (also known as chronic
adrenal insufficiency, hypocortisolism or
hypocortism is a rare endocrine disorder in
which the adrenal gland produces
insufficient amounts of steroid hormones
glucocorticoids and mineralocorticoids.
84
Addisons Disease contd.
These hormones are important for

certain bodily functions. The condition
may develop in children as well as adults
and affects men and women equally.
Although it is more common in adults
under the age of 60.
85

The condition was named after
Dr. Thomas Addison, a British
physician, who described the
condition in his 1855
publication On the
Constitutional and Local
Effects of Disease of the
Suprarenal Capsules.
86

Types
There are 2 main types of adrenal
insufficiency. These are:
1. Primary adrenal insufficiency (Addisons
disease). This is due to the destruction of
the layers of the adrenal cortex by e.g.
autoimmune disorder, infectious diseases
etc.
87
Types contd.
With loss of glandular tissue, chronic low
levels of cortisol secretion is developed
with elevated levels of
Adrenocorticotropic Hormone (ACTH)
because the pituitary produces normal
level of ACTH but the adrenal cortex
cannot utilize it due to tissue destruction.
2. Secondary adrenal insufficiency is caused
by an ACTH deficit resulting from
pituitary tumours, irradiation, pituitary
surgery etc.
88
Causes of Addisons Disease
It may occur as the result of a large

number of underlying causes.
1. In about 70% of all cases, are caused by
autoimmune disorders.
2. In about 20% of all cases, destruction of
the adrenal cortex is caused by
tuberculosis. Patients with acquired
immune deficiency syndrome (AIDS) are
also at risk. The pathogens responsible
for either disease can infiltrate and
destroy adrenal tissues.
89

contd.
3. It is also caused by fungal infection e.g.
histoplasmosis (infectious disease
caused by inhaling the microscopic spore
of a fungus histoplasma capsulatum
characterized by fever, anaemia, and
emaciation) which affects the adrenal
gland by producing destructive tumourlike masses called granulomas, or a
disease called amyloidosis in which a
starchy substances is deposited in places
throughout the body, interfering with the
function of whatever structure it is
present within.
90

contd.
In children certain bacterial infections e.g.
meningococcus.
4. Sudden cessation of corticosteroid
therapy after prolonged use can also lead
to adrenal insufficiency.Example in women
who abuse corticosteroids for cosmetic
reasons e.g. for skin bleaching or weight
gain.
91
Significant symptoms are not noted until

90% of adrenal cortex has been
destroyed. In about 75% of all patients, it
is gradual, slowly developing disease.
Aldosterone deficiency affects the ability
of the distal tubules of the nephron to
conserve sodium hence sodium is lost
and potassium is retained.
92
contd.
1. Extracellular fluid becomes depleted due
to dehydration.
2. Blood volume is decreased.
3. Hypotension and syncope (faint) are

common.
93
contd.
4. Hypovolemic shock may occur.
5.Darkened (pigmented) skin because of
excess ACTH production.
6. Hypoglycemia because cortisol
insufficiency causes decreased hepatic
glyconeogenesis.
94
contd.
7. Hyponatremia, due to loss of production
of hormone aldosterone as aldosterone
deficiency affects the ability of the distal
tubules of the nephron to conserve
sodium. Hence sodium is lost in urine.
8. Hyperkalemia (raised blood potassium
levels) also due to loss of production of
hormone aldosterone.
95
contd.
9. As dehydration becomes more blood
pressure will continue to drop and patient
will feel increasing weak.
10. As time goes on skin continues to
appear severely darkened, around nipple,
vagina, mouth and rectum because of
increasing ACTH levels
(hyperpigmentation in about 98% of
clients with Addisons disease).
96
contd.
1.
2.
3.
4.
Other Associated Clinical Manifestations

Include:
Easily Fatigue due to reduced sugar level
Loss of energy
Muscle weakness
Weight loss
97
contd.
Metabolic acidosis (increased blood
acidity), also due to loss of the hormone
aldosterone. Na lost in urine and H+
retained in plasma
98
contd.
Low levels of aldosterone stimulation of
the renal distal tubule leads to sodium
wasting in the urine and H+ retention in
the serum. Metabolic acidosis will lead to
other clinical problems like:
1. Anorexia
2. Nausea and Vomiting
99
contd.
3. Abdominal pains
4. Weakness
5. Warm, flushed skin
6. Altered mental status
7.Decreasing levels of consciousness
100
Diagnosis
Many patients do not recognize the slow
progression of symptoms and disease is
ultimately identified when a physician
notices the area of increased pigmentation
of the skin.
101
Diagnosis contd.
Tests to Confirm Diagnosis
1. Patients are given a testing dose of
(ACTH)- synthetic type may be given(tetracosactide IM/IV). ACTH
administration leads to increased cortisol
production. In Addisons disease this will
not occur due to the destruction and or
shrinking of the adrenal cortex.
102
Diagnosis contd.
2. Level of cortisol in blood can also be
checked.
3. To distinguish between primary
adrenocortical insufficiency (Addisons
disease) and secondary adrenocortical
insufficiency caused by failure of the
pituitary to produce enough ACTH, levels
of ACTH in blood are examined.
103
Diagnosis contd.
Normal or high levels of ACTH indicate that
the pituitary is working properly, but the
adrenal cortex is not responding normally
to the presence of ACTH. This confirms the
diagnosis of Addisons disease.
104
Diagnosis contd.
Other diagnostic procedures:
4. Medical imaging, usually in the form of
ultrasound or CT scans of the head: These
identify any intracranial problem
impinging on the pituitary gland.
105
Other suggestive features

include:
1. Hypoglycemia, low blood sugar (worse in
children) because cortisol insufficiency
causes decreased hepatic glycogeneosis.
2. Hyponatremia (low blood sodium levels),
due to loss of production of hormone
aldosterone as aldosterone deficiency
affects the ability of the distal tubules of
the nephron to conserve sodium. Hence
sodium is lost in urine, potassium is
retained.
106

include contd.
3. Hyperkalemia (raised blood potassium
levels) also due to loss of production of
hormone aldosterone.
107

include contd.
4. Metabolic acidosis (increased blood
acidity), also due to loss of the hormone
aldosterone because sodium reabsorption
in the distal tubule is linked with
acid/hydrogen irons (H+) secretion. Low
levels of aldosterone stimulation of the
renal distal tubule leads to sodium wasting
in the urine and H+ retention in the
serum.
108
Treatment
Therapeutic objectives are:
To correct fluid and electrolyte imbalance
To replace corticosteroids
To identify and treat any precipitating
factor.
109
Treatment contd.
1. The client with Addison disease requires
early diagnosis and treatment. Medical
treatment is based on replacing low level
of cortisol. In the case of Addison crisis
(acute adrenal insufficiency), this will be
achieved by injecting high dosage steroid
intravenous (IV). Unfortunately, this can
induce Cushings disease.
110
Treatment contd.
2. Dehydration and loss of salt will also be
treated by administering carefully
balanced solutions through IV.
3. Steroid preparation (Hydrocortisone) and
replacement of Aldosterone by mouth.
4. When the patient has any kind of infection
or injury, the normal dose of
hydrocortisone need to be doubled.
5. Increase sodium in diet
111
Treatment contd.
Non-Pharmacological Treatment centres on
monitoring Blood Pressure, fluid
input/output and electrolytes regularly.
Pharmacological Treatment
Intravenous Fluid Replacement:
Adults: 0.9% Sodium Chloride, 5%
Dextrose, or Dextrose Saline, 1 litre 4 to
6hourly in acute phase.
112
Treatment contd.
Children: 0.45% Sodium Chloride IV, and
5% Glucose IV, according to total fluid
requirement.
Intravenous Hydrocortisone:
Adults: 200mg, IV stat, then 100mg IV, 6
hourly until condition is stable.
Children:
1-5 years: 50mg 6 hourly
6-12 years: 100mg 6 hourly
113
Treatment contd.
Treat infection
(e.g.malaria,pneumonia,UTI), if present or
suspected, with appropriate medication.
When the patients condition is stable go
on to maintenance therapy.
Note that IV hydrocortisone therapy may
be required for several days. Do not rush
to change to maintenance therapy.
114
Treatment contd.
Maintenance:
Adults: Prednisolone, oral, 5mg morning
and 2.5mg evening each day or
hydrocortisone, oral, 20mg morning and
10mg evening each day.
Children: Prednisolone 140micrograms/kg
body weight in two (2) divided doses or
hydrocortisone 560micrograms/kg body
weight in 2 divided doses.
115
Treatment contd.
Long-term corticosteroid therapy requires
specialist supervision so patients should
report to hospital if they become ill.
All patients, including children suspected
to have adrenal insufficiency should be
referred to endocrinologist or specialist
physician.
116
Treatment contd.
In addition to treatment, the doctor may
prescribe Fludrocortisone (Florinef) which
replaces aldosterone and controls bodys
sodium and pottassium needs and keep BP
normal.
The doctor may recommend treating
androgen deficiency with an androgen
replacement therapy called
Dehydroepiandrosterone.
117
Treatment contd.
Some studies indicate that, for women
with Addisons disease, androgen
replacement therapy may improve overall
sense of well-being, libido and sexual
satisfaction.
118
Addisonian Crisis
Addisonian crisis also known as acute
adrenal insufficiency occurs in both men
and women of all age groups. Because in
adrenal insufficiency symptoms usually
progress slowly, they are usually ignored
until a stressful event like an illness cause
them to become life-threatening in which
the condition is called a crisis.
119
Addisonian Crisis contd.

Addisonian crisis may also occur in clients
who are abruptly withdrawn from
glucocorticoid medications or who have
hemorrhage into the adrenal glands from
either septicemia or anticoagulant therapy.
120
Addisonian Crisis contd.

Signs and Symptoms of Addisonian
Crisis. The client with Addisonian crisis
may have any of the symptoms of
Addisons disease, but the primary
problems are severe:
1. Dehydration
2. Low Blood Pressure (hypotension)
3. Loss of Consciousness
4. Circulatory Collapse
5. Shock and Coma
If left untreated can be fatal and lead to
death
121
Nursing Management of Addisons

Disease
The client with Addisons disease requires
nursing care for a variety of responses to
the decrease in cortisol levels.
In the client with Addisons disease, fluid
volume deficit results from loss of water
and sodium, as well as from vomiting and
diarrhea. Extracellular fluid volume deficit,
decreased cardiac output, hypotension,
and hypovolemic shock may occur,
especially in crisis situations.
122

Disease contd.
Therefore, we need to monitor intake and
output and assess for signs of
dehydration: E.g.
Dry mucous membrane e.g. oral mucosa
Thirst
Poor skin turgor
Sunken eyeballs
Scanty, dark urine
Weight loss
Etc.
123

Disease contd.
Encourage the client to maintain liberal
fluid intake by mouth.
An increase in dietary sodium can
decrease the hyponatremia characteristic
of adrenal insufficiency.
Weigh the client daily at the same time
and in the same clothing.
124

Disease contd.
Teach the client to sit and stand slowly,
and provide assistance as necessary.
Extracellular fluid volume deficit causes
hypotension, dizziness, and possible loss
of consciousness. These manifestations
increase the risk of injury from fall.
125

Disease contd.
Monitor cardiovascular status: take and record
vital signs, BP, assess the character of pulse and
pattern of respiration.
Try to establish baseline data including mental
status, neurological function etc.
Administer all forms of the drug with food to
minimize its ulcerogenic effect.
Encourage regular follow-ups and monitoring for
other health problems which is very necessary
Etc.
126
Summary
1.
2.
3.
4.
5.
In Addison disease:
Serum cortisol levels are decreased in adrenal
insufficiency
Blood glucose levels are decreased in adrenal
insufficiency
Serum sodium levels are decreased in adrenal
insufficiency
Serum potassium levels are increased in
adrenal insufficiency
Plasma ACTH levels are increased in primary
adrenal insufficiency but decreased in
secondary adrenal insufficiency
127
Reading Assignment
Please read on Aldosteronism and
pheochromacytoma.
Slide 128
Reference
Van De Graff, K. M., Fox, S. I., & Lafleur, K. M. (1997). Synopsis
of Anatomy and Physiology, WCB McGraw-Hill, New York.
Philips, W. J., Monahan, F. D., Sand, J.K., Marek, J.F., &
Neighbors, M.(2003). Medical Surgical Nursing: Health and
Illness Perspectives, 7th Ed., Mosby, London.
Lemone, P. &Burke, K. M. (1996). Medical Surgical Nursing:
Critical Thinking in Clients Care. Addison Wesley, Menlo
Park.
Mercks Medical Manual, 2002.
Vander, A., Sherman, J., & Luciano, D. (1998).Human
Physiology: The mechanisms of body function, 7th Ed., WBC
McGraw-Hill, New York.
129

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NURS 232 MEDICAL CONDITIONS OF THE

Session Eighteen Disorders of

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

They are referred to as fight-or-flight

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Background of Cushings Syndrome

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON

Dr. Kwadwo Ameyaw Korsah, UG, SON