This document discusses disorders of the adrenal cortex. It begins by outlining the learning objectives, which are to understand the etiology, pathophysiology, clinical manifestations, diagnostics, treatment, nursing care, and complications of adrenal cortex disorders. It then provides an overview of adrenal gland disorders in general before focusing specifically on the adrenal cortex and its hormones. Key points covered include the causes, symptoms, diagnostic tests, and treatment of adrenal hypofunction conditions like Addison's disease and adrenal hyperfunction conditions.

1. DISORDER OF
ADRENAL CORTEX
GTJ 320 -- MEDICAL - SURGICAL NURSING III :
(Endocrine & Orthopedic Nursing)

2. LEARNING OBJECTIVE
At the end of this session,
I. Student are able to understand etiology and
pathophysiology of adrenal cortex disorder
II. Identify the clinical manifestation
III. Explain the diagnostic investigation related
IV. Discuss the treatment, intervention and
possible complication
V. Apply nursing art / caring value towards
patient ~ nursing care

3. OVERVIEW OF ADRENAL GLANDS
DISORDER
 It’s condition that interfere with the normal
function of the adrenal glands
 It may cause hyperfunction or hypofunction, and
may be congenital or acquired
 Function of adrenal glands
produces hormones that affect growth
Development and stress
Helps in regulate kidney function
 Consist of 2 parts
 adrenal cortex
Adrenal medulla
Both parts are structurally and
functionally different

4. ADRENAL GLANDS

5. ADRENAL CORTEX
I. Outer part of gland
 Part of hypothalamus – pituitary – adrenal axis
II. Secrete a variety of steriodhormones
 mineralocorticoids : regulate salt and water
balance within the body
 Glucocorticoids (include cortisol) : wide
number of roles within the body
 Androgens : hormones with testosterone
like function

6. ADRENAL MEDULLA
I. Inner part of gland (20% of gland)
 Part of sympathetic nervous system
2. Secrete catecholamine's
 Epinephrine
 Norepinephrine

8. Primary
Regulatory Control
Anatomy Secretory products
Renin-angiotensin Zona
glomerulosa
Aldosterone
ACTH,
hypothalamic CRH
Zona fasciculata Cortisol and sex
hormones
ACTH,
hypothalamic CRH
Zona reticularis Sex hormones (e.g.
androgens)
Preganglionic
sympathetic fibers
Medulla Catecholamines (Epi,
NE)

9. ADRENAL CIRCULATION
• Both the left and right adrenals receive arterial blood
supply in the same fashion
• Paired superior suprarenal arteries - derived from inferior
phrenic arteries
• Paired middle suprarenal arteries - derived directly from
abdominal aorta
• Paired inferior suprarenal arteries - derived from the adjacent
renal arteries
• The left and right adrenals have differing venous
drainage
• The left adrenal venous drainage is through the left adrenal
vein to the left renal vein and finally to the IVC
• The right adrenal venous drainage is through the right
adrenal vein to the IVC
• Recall the same pattern for the left and right gonadal
artery/vein

10. HISTOLOGY OF ADRENAL GLANDS
 Adrenal cortex : Arranged in zonal configuration
Outer zona glomerulosa = small, compact cells
Central zona fasciculata = larger, lipid-rich cells
arranged in radial columns
Inner zona reticularis = compact & pigmented cells
 Adrenal medulla
Thin layers of large chromaffin cells

11. HISTOLOGY OF ADRENAL GLANDS

12. FUNCTION OF ADRENAL GLANDS

13. REGULATION OF ADRENAL GLAND
SECRETION

14. ADRENAL CORTEX

15. ADRENAL CORTEX
• Thelarge cortical cells are arranged into three
layers or zones:
– Thezona glomerulosa,
• Thethin outermost layer
• Constitute about 15%of cortex
– Thezona fasciculata,
• Themiddle and largest portion
• Constitute about 75%of cortex.
– Thezona reticularis,
• Theinnermost zone

16. ADRENAL CORTEX
• Zonaglomerulosa:
– Produce meniralocorticods
– Mainly aldosterone (because it containenzyme
aldosterone synthase)
•Hormones that help control the balance of
minerals (Na+ and K+)and water in theblood

17. ALDOSTERONE SECRETION

18. ALDOSTERONE SECRETION

19. ADRENAL CORTEX
• Zonafasciculata:
– Produce glucocorticods
– Mainly cortisol andcorticosterone
– Thehuman adrenal glands produce the equivalent
of 35–40 mg of cortisone acetate perday
Hormone that play amajor role inglucose
metabolism aswell asin protein and lipid
metabolism
– Thesecretion of these cells is controledby
hypothalamic-pituitary axis viaACTH

20. ADRENAL CORTEX
• Zonareticularis:
– Theinnermost layer of the adrenal cortex, lying
deep to the zonafaciculata and superficial tothe
medulla.
– Thesecells produce androgens

21. ADRENAL CORTEX
• Zonareticularis:
–Theandrogens produced includes
• Dehydroepiandrosterone (DHEA)
• Androstenedione
– Synthesized from cholesterol
• DHEAis further converted to DHEA-
sulfate viaa sulfotransferase

22. ADRENAL CORTEX
• Zonareticularis:
– Theandrogens produced are released into the
blood stream and taken up in the testis and
ovaries to produce testosterone and theestrogens
respectively.

23. DISORDER OF ADRENAL CORTEX
• Patient with adrenal disorders canpresent
with features relatedto:
• HYPOFUNCTIONOFTHEGLAND
• HYPERFUNCTIONOFTHEGLAND

24. TYPES DISORDER OF ADRENAL
CORTEX
Incidentaloma
Primary Hyperaldosteronism
Cushing’s Syndrome
Adrenocortical Carcinoma
Congenital Adrenal Hyperplasia
Adrenal Insufficiency

25. ADRENAL HYPOFUNCTION

26. INTRODUCTION OF ADRENAL
HYPOFUNCTION
 Its a condition in which the adrenal glands are
unable to perform well or function less than what
they normally should.
 The causes of adrenal hypofunction are many and
include a variety of factors including autoimmune
disease.
 The symptoms of adrenal hypofunction need to
be understood well to be able to diagnose and
manage the condition.
 Treatment of adrenal hypofunction is mainly
based on its causes and symptoms.

27. ADRENAL HYPOFUNCTION
• Adrenal insufficiency leads to a reduction in
the output of adrenal hormones
– glucocorticoids and/or mineralocorticoids
• Twotypesof adrenalinsufficiency
• Primaryinsufficiency/ Adrenal hypofunction
• inability of the adrenal glandstoproduce enough
steroid hormones
• Secondaryinsufficiency/ Adrenal hypofunction
• inadequate pituitary or hypothalamic stimulation of
the adrenal glands

28. CAUSES OF PRIMARY ADRENAL
HYPOFUNCTION
 Autoimmune disease
 Genetic diseases
 Infections
 Bleeding in glands
 Surgical removal of adrenal glands

29. CAUSES OF SECONDARY ADRENAL
HYPOFUNCTION
 Condition affecting the pituitary gland can cause
secondary adrenal hypofunction.
The pituitary glands are liable for producing a
hormone which conveys message to adrenal gland to
produce required cortisol for bodily functioning.
If the pituitary gland fails to do this, then no more
cortisol will be produced and this causes secondary
adrenal hypofunction.

30. OTHERS CAUSES OF ADRENAL
HYPOFUNCTION
-Glucocorticoid treatment
– Autoimmune adrenalitis
– Tuberculosis
– Adrenalectomy
– Secondarytumor deposits
– Amyloidosis
– Haemochromatosis
– Histoplasmosis, tuberculosis, CMV, AIDS
– adrenal haemorrhage
COMMON

31. OTHERS CAUSES OF ADRENAL
HYPOFUNCTION
 Metabolic failure in hormone production
•Congenital adrenal hyperplasia e.g. 21-
hydroxylase deficiency, 3-β-hydroxysteroid
dehydrogenase deficiency
•Enzyme inhibition e.g. ketoconazole
•Accelerated hepatic metabolism of cortisol
e.g. phenytoin, barbiturates, rifampicin

32. OTHERS CAUSES OF ADRENAL
HYPOFUNCTION
• Uncommon causes
– ACTH blocking antibodies
– Mutation in ACTH receptor gene
– Adrenal hypoplasia congenita
– Familial adrenal insufficiency

33. SYMPTOMS OF ADRENAL
HYPOFUNCTION
Symptoms of adrenal hypofunction mostly
based on the deficiency of hormone
aldosterone & cortisol
 High / low blood pressure
 Low blood sugar level
 Craving for salty foods
 Excessive sweating

34. SYMPTOMS OF ADRENAL
HYPOFUNCTION
 Unnecessary weight loss
 Fatigue that becomes worse with passing days
 Loss of appetite
 Muscle weakness
 Irregular or no menstruation in females
 Headaches.

35. ROLES OF HORMONE
ALDOSTERONE & CORTISOL
 To maintain immune system
 To regulate blood pressure and blood glucose
level
 To maintain salt and electrolytes balance in
the body
 To ensure heart muscles tone and healthy
bones
 To increase body's response to stress.

36. LAB TEST FOR ADRENAL
HYPOFUNCTION
 Serum level of cortisol, adrenocorticotropic
hormone (ACTH) and Corticotropin-releasing
hormone (CRH)
 ACTH& CRH stimulation test (more specific)
 X-ray
 Ultrasound
 MRI / Ct Scan
Detect any changes /
problems in adrenal
glands or pituitary glands

37. TREATMENT FOR ADRENAL
HYPOFUNCTION
 Cortisol replacement steroids therapy
 Oral replacement (based on height , weight
and medication used)
 Injections (for serious symptoms or adrenal
crisis
o Only prescribed for emergency
situations
 Specialized diet

38. ADDISON’S DISEASE

39. WHAT IS ADDISON’S DISEASE
 Addison's disease is a disorder that occurs
when body produces insufficient amounts of
cortisol and often insufficient levels of
aldosterone as well.
 Also called adrenal insufficiency, Addison's
disease occurs in all age groups and affects
both sexes.
 Addison's disease can be life-threatening.

40. ADRENAL HYPOFUNCTION

41. SYMPTOMS OF ADDISON’S
DISEASE
 Extreme fatigue
 Weight loss & appetite
 Darkening of your skin
(hyperpigmentation)
 Low blood pressure, even
fainting
 Salt craving
 Hypoglycemia
• Nausea, diarrhea or
vomiting
• Abdominal pain
• Muscle or joint pains
• Irritability
• Depression
• Body hair loss or sexual
dysfunction in women
Usually develop slowly , often over several months

42. ADDISON’S DISEASE : CLINICAL
MANIFESTATION
• hyperpigmentation

43. ADDISON’S DISEASE : CLINICAL
MANIFESTATION
• hyperpigmentation

44. ADDISON’S DISEASE : CLINICAL
MANIFESTATION

45. ADDISON’S DISEASE :
INVESTIGATION

46. ADDISON’S DISEASE :
INVESTIGATION
 Others
1. Complete blood count
2. Blood sugar
3. Urine (routine examination)
4. ECG
5. Chest X-ray
6. Serum electrolytes
7. Bone densitometry
8. Serum creatinine

47. ADDISON’S DISEASE : TREATMENT
 Two main treatment
1. Oral corticosteroids
 Hydrocortisone (Cortef), prednisone or cortisone
acetate may be used to replace cortisol. Your
doctor may prescribe fludrocortisone to replace
aldosterone.
2. Corticosteroid injection
 For those not intolerant with oral

48. ADDISON’S DISEASE : TREATMENT
 Replacement of hormones
 glucocorticoid : hydrocortisone 15mg on waking
and 5mg at night
Mineralocorticoid : fludrocortisone 0.05mg to 0.1
mg daily
 Supportive treatment & treatment causes
 if TB : anti-tubercular therapy

49. ADDISON’S DISEASE : TREATMENT
 General advice to the patient
 good nutrition : regular meal,
high carbohydrate : prevent weight gain
sufficient salt : minimize edema and reduce risk for
hypertension
Diabetic diet : glucose intolerant
Administer with meal to prevent ulcer ; When oral
therapy is not possible, injection hydrocortisone
should be taken.
Provide supplementary potassium if possible

50. GLUCOCORTICOID REPLACEMENT

51. EQYUIVALENT DOSES OF
GLUCOCORTICOIDS
1. Hydrocortisone : 20 mg
2. Cortisone acetate : 25 mg
3. Prednisolone : 5 mg
4. Dexamethasone : 0.5 mg

53. ADDISON’S DISEASE :
COMPLICATIONS
 Cardiovascular collapse
 Coma
 Death

54. ADDISONIAN CRISIS
 Its a medical emergency due to acute
adrenocortical insufficientcy

55. ADDISONIAN CRISIS : CAUSES
 Sudden withdrawal of steroid(commonest cause, if pt.
on steroid for long time)
 Following stress e.g.intercurrent disease,trauma,
surgery, severe infection or prolonged fasting in a pt
with latent insufficiency
 Following sudden destruction of pituitary
gland(pituitary necrosis)or when thyroid hormone or
drugs which increase steroid metabolism(e.g.
phenytoin)given to a pt with hypoadrenalism
 Following bilateral adrenalectomy
 Following injury to both adrenals due to
trauma,adrenal vein thrombosis,adrenal haemorrhage
due to meningococcaemia or anticoagulant therapy

56. ADDISONIAN CRISIS : CLINICAL
FEATURES
 Nausea, vomiting, diarrhea
 Abdominal pain
 Diarrhea
 Muscle cramps
 Unexplained fever
 Unconsciousness
 Severe hypotension
 Hyponatraemia, hyperkalaemia, hypoglycaemia,
hypercalcaemia

57. ADDISONIAN CRISIS : TREATMENT
 I/V hydrocortisone 100 mg 6 hrly until GI
symptoms abate then oral therapy
 I/V fluid normal saline and 10% dextrose for
hypoglycaemia
 Precipitating factors should be find out and
treated

61. ADDISONIAN CRISIS : DEATH
 Common causes for death is when patient
developed an acute adrenocortical
insufficiency and died ~ integrated with other
medical problems as example patient may
have subclinical hypoadrenalism – increased
hepatic metabolism by drug induced

62. ADDISON’S DISEASE : NURSING
INTERVENTIONS
1. Physical examination
 Blood pressure (v/sign)
 Body weight
 Edema
 Cataract & glaucoma (3months after treatment)
 Height ( compression degree of axial spine
demineralization)

63. ADDISON’S DISEASE : NURSING
INTERVENTIONS
2. Coping and support
3. Maintain with follow up / appointment with
physician
4. Health education : noted symptoms, make a
list of medication, inform family members

64. ADRENAL
HYPERFUCNTION

65. ADRENAL HYPERFUNCTION
• It is a condition where there is an
overexpression / excessive production of one
or more adrenal hormones (aldosterone,
corticosteroids, androgenic steroids,
epinephrine and norepinephrine).
• The increased adrenal gland activity may be
caused by an adrenal gland tumor or by
excessive stimulation of the gland. Pituitary
hormones stimulate adrenal gland activity.

66. ADRENAL HYPERFUNCTION
There are 3 basic types of corticosteroids
elaborated by the adrenal cortex “
glucocorticoids, mineralocorticoids, and sex
hormone ” and 4 distinctive hyperadrenal
clinical sydromes:
• Cushing syndrome : “ excess cortisol ”
• Hyperaldosteronism : “ excess aldestrone”
• Adrenogenital syndromes : “excess androgen”
• Pheochromocytoma : “ high catecholamine”

67. HYPERALDOSTERONISM
• A medical condition where too much
aldosterone is produced by the adrenal
glands, which can lead to sodium retention
and potassium loss.
• Types:
–Primary hyperaldosteronism
–Secondary hyperaldosteronism

68. PRIMARY HYPERALDOSTERONISM
Also known as hyporninemic
hyperaldosteronism / Conn’s Syndrome

69. PRIMARY HYPERALDOSTERONISM
/ CONN’S SYNDROME
1. Characterized by autonomous excessive
production of aldosterone by adrenal glands
2. Presents with hypertension , hypokalaemic
alkalosis and renal K+ wasting

70. PRIMARY HYPERALDOSTERONISM
/ CONN’S SYNDROME
• Causes:
– Adrenal adenoma
– Bilateral hypertrophy of zona glomerulosa
cells
– Adrenal carcinoma
•Rare cause

71. PRIMARY HYPERALDOSTERONISM
/ CONN’S SYNDROME
• Clinical features:
– Hypertension : aldosterone induced Na
retention with increase in Extra cellular
fluid volume
– Muscle weakness: Due to decrease K+
– Muscle paralysis: severe hypokalaemia
– Latent tetany (continuous tonic spasm of a
muscle; )and paraesthesiae (numbness,
itching, and a feeling of pins and needles on
your skin)
– Polydipsia, polyuria and nocturia: due to
hypokalaemic nephropathy

72. PRIMARY HYPERALDOSTERONISM
/ CONN’S SYNDROME
Investigation
• Electrolyte & blood gasses:
– Hypernatraemia
– Hypokalaemica
– Alkalosis
– Urinary potassium loss, level > 30 mmol
daily during hypokalaemia

73. PRIMARY HYPERALDOSTERONISM
/ CONN’S SYNDROME
Investigation
• Plasma aldosterone : renin activity ratio
– Sensitive screening test
– No need to standardize posture
Ratio Interpretation Action
<800 Diagnosis excluded Seek other cause
>1000,<2000 Diagnosis possible Confirmatory test
>2000 Diagnosis very likely Establish cause

74. SECONDARY ALDOSTERONISM
• Is increased adrenal production of aldosterone
in response to non-pituitary, extra-adrenal
stimuli
• Increase renin secretion
– (hyperreninemic hyperaldosteronism)
• Commoner than primary aldosteronism

75. SECONDARY ALDOSTERONISM
Common
• CCF
• Liver cirrhosis with
ascities
• Nephrotic syndrome
Less common
• Renal artery stenosis
• Sodium – losing
nephritis
• Renin—secreting
tumours

76. CUSHING’S SYNDROME
• Adrenal cortex hyperfunction
• Any condition resulting from overproduction
of primarily glucocorticoid (cortisol)
• Mineralocorticoid and androgen may also be
excessive

78. CAUSES OF CUSHING’S SYNDROME
1. External versus Internal
o effect of corticosteroid treatment
o asthma and rheumatoid arthritis, or in
immunosuppression after an organ transplant.
o Over use of medroxyprogesterone acetate
2. Pseudo-Cushing's syndrome

79. PSEUDO - CUSHING’S SYNDROME
• Appear cushingoid and have some
biochemical abnormalities of true
Cushing’s disease
• Causes
– Severe depression
– Alcoholism
– Obesity
– Polycystic ovarian syndrome

80. PSEUDO - CUSHING’S SYNDROME :
ETIOLOGY
• Excessive cortisol (ACTH dependent)~75%
• Excessive cortisol (ACTH dependent)~25%
• Excess cortisol binding globulin

81. PSEUDO - CUSHING’S SYNDROME :
ETIOLOGY
• Excessive cortisol (ACTH dependent)~75%
–Pituitary disease
• Adenoma (90%)
• Hyperplasia (10 %)
–Ectopic ACTH syndrome
• Malignancy - ( bronchus, thymus,
pancreas, ovary )
–Ectopic CRH syndrome
–Exogenous ACTH administration

82. PSEUDO - CUSHING’S SYNDROME :
ETIOLOGY
• Excessive cortisol (ACTH dependent)~25%
–Adrenal tumour
• Adenoma
• carcinoma
–Nodular hyperplasia
–Exogenous glucocorticoid administration

83. PSEUDO - CUSHING’S SYNDROME :
ETIOLOGY
• Excessive cortisol binding globulin
–Estrogen therapy : Osteoporosis, Oral
Contraceptic Pill
–Pregnancy

84. PSEUDO - CUSHING’S SYNDROME
: CLINICAL FEATURES
• Truncal obesity with deposition of adipose tissue in
characteristic site (moon face, buffalo hump)– exact
mechanism unknown
• Thinning of skin – catabolic response
• Purple striae – catabolic response
• Excessive bruising – catabolic response

85. PSEUDO - CUSHING’S SYNDROME
: CLINICAL FEATURES
• Hirsutism ( esp adrenal carcinoma ) - ↑
adrenal androgen
• Menstrual irregularities - ↑ adrenal androgen
• Skin pigmentation ( ACTH ↑ ) – melanocyte
stimulating activity

86. PSEUDO - CUSHING’S SYNDROME
: CLINICAL FEATURES
• Hypertension – mineralocorticoid effect
→ sodium retention
– Potassium wasting → hypokalamic
alkalosis
• Glucose intolerance - ↑ hepatic
gluconeogenesis and insulin resistance
• Muscle weakness and wasting – catabolic
response in peripheral supportive tissue

87. PSEUDO - CUSHING’S SYNDROME
: CLINICAL FEATURES
• Back pain ( osteoporosis and vertebral
collapse) – inhibit bone formation
• Psychiatric disturbances – euphoria,
mania, depression

89. PSEUDO - CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
 There are two diagnostic steps in the
investigation of patient suspected of having
Cushing's syndrome
 Screening test
for identification of Cushing's syndrome.
the demonstration of high plasma cortisol
level
 Identification of cause

90. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
1. Assessment of circadian rhythm in cortisol
secretion.
 Measure 8 am and 11 pm serum cortisol
level
 Normal : Serum value @ midnight is 50%
less than value @ 8 am
 Cushing’s syndrome : rhythum is loss
 Pseudo-Cushing : normal circadian.

91. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
2. Measuring 24-hour urinary free cortisol
Level (umol /24 h Interpretation
< 300 Normal
300 - 700 Severe depression
Stress
> 700 Diagnostic of Cushing’s
syndrome

92. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
3. Low dose Dexamethasone suppression test :
 0.5 mg Dexametason (oral) given 6 hourly for 2
days
 blood for plasma cortisol collected 6 hour after
last dose
 urine for urine free cortisol test(UFC) is
collected before & on the 2nd day of Dexa

93. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
3. Low dose Dexamethasone suppression test :
RESULT
 UFC suppress by 50% ( < 70nmol/24h Normal
 plasma cortisol suppress < 140 nmol/L
Cushing
Pseudo CS
 no suppression of UFC & Pl. cortisol Cushing’s
Syndrome

94. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
4. High dose Dexamethasone suppression test :
• Normal individuals suppress plasma cortisol
to < 50 nmol/L.
• Patients with Cushing's syndrome fail to show
complete suppression of plasma cortisol
levels. This test is highly sensitive (> 97%).

95. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
5. Plasma Adrenocorticotropic hormone (ACTH)
• Normal < 50 ng/L
• Low – adrenal causes
• Elevated
– Slight – pituitary dependent Cushing’s
– Gross – ectopic secretion of ACTH

96. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
6. Corticotrophin-releasing hormone (CRH )Test
 Differentiate ectopic ACTH secretion and
Cushing’s disease.
 Cushing’s disease – plasma ACTH increases
50% over baseline & cortisol increase by 20%
 Ectopic ACTH or adrenal tumour – no response

97. PSEUDO / CUSHING’S SYNDROME :
LABORATORY INVESTIGATIONS
7. Imaging
 CT scan of adrenal gland:TRO adrenal tumor
 MRI of pituitary gland: majority microadenoma
( < 10mm). MRI reveal lesion in 50 - 60% of
cases
 CT scan/MRI of thorax & abdomen: ectopic
ACTH producing tumor

98. PSEUDO / CUSHING’S SYNDROME :
TREATMENT
• Depend of Cushing's syndrome depends on
the etiology:
– Adrenal adenoma
– Adrenal Carcinoma – resection
– Cushing’s disease - transphenoidal hyposectomy
– Drug ( block cortisol synthesis ) - metyrapone

100. PHEOCHROMOCYTOMA
• Pheochromocytoma is an extremely rare pathological
condition of the adrenal glands where there is
development of benign tumors on the cells present in
the center of the gland causing symptoms.
• The adrenal glands are located at the top of each
kidney and are responsible for producing hormones
which provide instructions to all the organs and tissues
of the body.

101. PHEOCHROMOCYTOMA : CAUSES
• It’s normally develops in the specialized cells
of the adrenal gland called the chromaffin
cells.
• These cells are located right in the center of
the adrenal gland and are responsible for
secreting hormones primarily adrenaline.
• The hormone adrenaline comes to play when
an individual is under stress and calms the
body down.

102. PHEOCHROMOCYTOMA : CAUSES
• This hormone results in an individual having
higher blood pressure readings and a fast
heart rate.
• Pheochromocytoma can causes irregular and
excessive release of adrenaline.
• Rare but treatable

103. PHEOCHROMOCYTOMA : RISK
FACTOR
• Multiple Endocrine Neoplasia - Type II: This is a disorder in
which there is development of tumors in the endocrine
system of the body including the thyroid, parathyroid, lips,
tongue and the gastrointestinal tract.
• Von Hippel-Lindau Disease: This disease can result in
development of tumor in the central nervous system,
endocrine system, pancreas, and kidneys.
• Neurofibromatosis-1: This condition results in
development of tumor in the skin and the optic nerve.

104. PHEOCHROMOCYTOMA :
SYMPTOMS
• Some of the most common symptoms of are:
–Persistent high blood pressure
–Persistent rapid heartbeat
–Excessive sweating
–Severe / persistent headaches
–Tremors
–Having a pale face
–Shortness of breath.

105. PHEOCHROMOCYTOMA :
SYMPTOMS
• Some of the less common symptoms of are:
–Severe anxiety
–Abdominal pain
–Constipation
–Unintentional weight loss.

107. PHEOCHROMOCYTOMA :
COMPLICATIONS
• CNS : stroke secondary to hypertension
• CVS : ischemic heart disease (coronary spasm
& hypertension), cardiomyopathy
(cathecholamines induced myo-necrosis &
hypertension)
• DM due to insulin antaginsm
• Arrhythmia

108. PHEOCHROMOCYTOMA :
COMPLICATIONS
1- Hormone function:
• ECG, ECHO, and blood glucose level.
• Suppressor test: clonidine injection iv 5mg
→ ↓ of BP by 53/25 mmhg for 15 minutes
Due to blockade of alpha-receptors in other
forms of hypertension but not in
Pheochromocytoma.

109. PHEOCHROMOCYTOMA :
COMPLICATIONS
2- Hormone level:
 serum catecholamines level is elevated
(n=2-5mg/L)
 neurophysin serum level is elevated
(secreted in equimolar concentration with
epinephrine)

110. PHEOCHROMOCYTOMA :
COMPLICATIONS
3. Hormone end product:
 24hrs urinary vallinyl mandelic acid (VMA)
is elevated
 Should be collected in acidic medium and
refrigerated).
 The result of the test is falsely high
 In patients taking alpha-methyl dopa,
banana or pine apple (n=2-6 mg/24 hrs).

111. PHEOCHROMOCYTOMA :
COMPLICATIONS
4- Cause:
CT, MRI or sonography of abdomen
iodine 131 -metaiodobenzyl guanidine (MIBG)
scanning, particularly in extra-abdominal
Tumors.
Intravenous pyelogram (IVP) may show
indentation of the upper pole of kidney

113. PHEOCHROMOCYTOMA :
TREATMENT
• Surgical removal of tumour
• Calcium channel blockers control BP
• Sympathetic blocking agents
– Reduce blood pressure
– Reduce symptoms of catecholamine excess
• Beta blockers to reduce dysrhythmias
• Monitor blood sugar/glucose level

114. SUMMARY
• The adrenal glands are small glands located on top of
each kidney and produce hormones that can't live
without, including sex hormones and cortisol.
• In adrenal gland disorders, glands make too much or
not enough hormones. In Cushing's syndrome, there's
too much cortisol, while with Addison's disease, there
is too little. Some people are born unable to make
enough cortisol.