Cushing syndrome results from excessive cortisol secretion and is characterized by central obesity, muscle wasting, hyperglycemia, and hypertension. It can be caused by prolonged glucocorticoid use or tumors that secrete cortisol or ACTH. Diagnosis involves testing for cortisol levels, and treatment focuses on treating the underlying cause and managing complications through lifestyle changes and medications. Nursing care aims to prevent injuries and infections while promoting skin integrity and a healthy body image and thought processes.

1. College of nursing
madras medical college, Chennai
medical surgical nursing
cushing syndrome
Presented by
Edwin jose .l
Msc(n) I year

2. INTRODUCTION
 Cushing syndrome is an endocrine disease with multiple etiologies
and is characterized by a constellation of clinical manifestations that
result from excessive concentrations of circulating cortisol (i.e.,
hypercortisolism).
 The syndrome is named after Harvey Cushing, an American surgeon
who first reported the condition in 1912.

3. DEFINITION
Cushing syndrome is a clinical condition that results from chronic
exposure to excess corticosteroids, particularly glucocorticoids.

4. PREVALENCE
 The prevalence is estimated to be nearly 40 per million, and the incidence
ranges from 1.2 to 2.4 per million per year, according to several population-
based studies
 Among adults, CS affects women 3-times more frequently than men, and
symptoms commonly appear between the third and sixth decade of life.
 It has been reported that CS appears at a younger age and with a more severe
clinical presentation in men than in women .
 In older adults, a lack of difference in the prevalence of CS between men and
women has been reported

5. NORMAL PHYSIOLOGY
 Under normal physiological conditions (circadian rhythm, where
cortisol levels peak in early morning and late at night), systemic
inflammation (cytokine), or stress (physiological or psychological),
corticotropin-releasing hormone (CRH) is released from the
paraventricular hypothalamic nucleus via the median eminence.
From the median eminence, CRH is transported in the hypophyseal
portal venous system to the pituitary gland, where it binds to the
CRH receptor-1 (CRH-R1) on pituitary corticotroph cells.
CRH binding to CRH-R1 receptors activates adenylate cyclase and
stimulates proopiomelanocortin (POMC) gene expression in the
corticotroph cells.

6.  Proopiomelanocortin preprohormone is processed into and b-lipotropin .
Products of b-lipotropin include b-endorphin and a-lipotropin.
 ACTH is secreted into the systemic circulation and binds to receptors in the
adrenal cortex, where it stimulates production and secretion of
glucocorticoids, including cortisol.
 Under normal conditions, circulating cortisol provides physiological control
of this endocrine axis by its negative feedback inhibition on hypothalamic
CRH and pituitary ACTH secretion

8. causes
Causes of Cushing syndrome are typically divided into two basic categories
 Adrenocorticotropic hormone (ACTH) dependent i.e., hypercortisolism is the
result of elevated serum ACTH concentrations
 ACTH-independent
 The majority of cases are the result of administering supra-physiologic doses
of corticosteroid drugs for various health conditions (e.g., autoimmune
disease).
 Common corticosteroids prescribed include prednisone, prednisolone, and
methylprednisolone. This type of Cushing syndrome is often referred to as
iatrogenic Cushing syndrome and is a reversible form of the disorder.

9.  hypersecretion of ACTH by a small, benign pituitary tumor known as an
adenoma. This is commonly known as Cushing disease and is the most
common cause of pathologic Cushing syndrome.
 hypersecretion of ACTH by non-pituitary tumors (e.g., small cell lung
carcinoma). This is known as ectopic Cushing syndrome because the source
of ACTH technically lies outside of the neuroendocrine system.
 hypersecretion of cortisol from either a benign or a cancerous tumor
(carcinoma) of the adrenal gland
 hypersecretion of corticotropin-releasing hormone (CRH) by a benign tumor
of the hypothalamus.
 Excessive circulating CRH causes excessive secretion of ACTH by the
pituitary and, ultimately, elevates serum cortisol levels.

11. pathophysiology

12. Clinical manifestations
Metabolic Syndrome:
1. visceral obesity
 Centripetal (visceral) fat deposition ,Truncal obesity,
 face (moon face)
 dorsocervical (buffalo hump)
 supraclavicular fat pads
 Weight gain but not definitive
Usually resolves after normalization of cortisol levels

13. 2. protein-wasting symptoms
 skin thinning,
 wide purple striae,
 proximal muscle wasting, due to the protein wasting effect of cortisol
 Skin becomes fragile to minor trauma, leading to frequent bruising,
ulcerations, and infections
 Muscle wasting, especially in the lower limbs leads to atrophy, fatigue,
weakness, and gait disturbance
 Bone wasting caused by hypercortisolism leads to general osteoporosis.
 Trabecular bone, particularly the vertebral body, is the most frequently
affected part, and spinal compression fractures are observed in around half
of patients with CD.

14. 3. Hyperglycemia :
Chronic excessive cortisol secretion leads to muscle, liver, and
adipocyte insulin resistance.
Nearly half of patients with Cushing disease are affected by
diabetes mellitus
4. Dyslipidemia.
nearly half of patients with Cushing disease have lipid
abnormalities

15. Cardiovascular Disease:
 Arterial Atherosclerosis and Hypertension
 Common features in Cushing syndrome
 Common in nearly 50% of Cushing syndrome
 Arterial and Venous Thrombosis
 caused by lipid and coagulation disturbances
 Hypercoagulability

16. Opportunistic Infections:
 Increased susceptibility to infection is caused by the direct
immunosuppression effect of hypercortisolemia .
 Extremely high cortisol levels are associated with an increased risk of
serious infections.
 The risk of fungal infections depends on the degree of cortisol excess.
Neuropsychiatric Disorders:
 depression
 irritability
 anxiety
 sleep disturbance

17. Cognitive Impairments:
 Short-term memory and cognition impairment
 Loss of brain volume, particularly hippocampal atrophy, is induced by
chronic hypercortisolemia
Other Clinical Features:
 Systemic edema - common symptom and is caused by increased
permeability rather than congestive heart failure.
 Renal stones are seen in nearly half of patients
 hirsutism and hypogonadism- excess of adrenocortical androgens
 Most women experience dysmenorrhea, and infertility
 Loss of libido is also frequent in men

18. Diagnostic evaluation
History collection - drug taking history to exclude
exogeneous glucocorticoid exposure is necessary
Physical examination
Routine Laboratory Analysis- increased neutrophil and
decreased lymphocyte and eosinophil counts; hypokalemia;
metabolic alkalosis; hyperglycemia; and
hypercholesterolemia, and may be useful for the follow-up
of treated patients.

19. Initial Biochemical Tests for the Screening of CS
24 h urinary free cortisol (UFC; at least two measurements)
late-night salivary and serum cortisol (two measurements)
1-mg overnight dexamethasone suppression test (DST)
 longer low-dose DST (2 mg/d for 48 h)
Other Examination:
Hair cortisol levels
segmental hair cortisol levels

20. Biochemical Examinations to Diagnose CD:
 Plasma ACTH Levels
 High-Dose Dexamethasone Suppression Test (HDDST)
 CRH Test
 Desmopressin Test
Imaging Studies to Diagnose CD:
 Pituitary Magnetic Resonance Imaging (MRI)
 fluorodeoxyglucose-positron emission tomography
 IPSS

21. variants
 Cyclic CS (Periodic CS)
Cyclic Cushing's syndrome (CS) is a rare disorder, characterized by repeated episodes
of cortisol excess interspersed by periods of normal cortisol secretion. The so-called
cycles of hypercortisolism can occur regularly or irregularly with intercyclic phases
ranging from days to years
 Hypercortisolic States without CS (“Pseudo-Cushing”)
 Pseudo-Cushing’s syndrome (PCS) constitutes a group of physiological or non-
physiological medical conditions that mimic Cushing’s syndrome (CS) clinical
features along with a mild biochemical hypercortisolaemia which remains under a
physiological feedback hormonal control.
 Physiological conditions such as pregnancy, surgical or emotional stress, severe
illness, intense chronic exercise, and non-physiological as chronic alcoholism,
obesity, metabolic syndrome, poorly controlled diabetes mellitus, major
depression, malnutrition, anorexia nervosa represent a PCS.

22. treatment
CS treatment includes
 normalization of cortisol hypersecretion,
 reversal of the clinical features associated with CS such as diabetes mellitus,
hypertension, muscle atrophy, enhanced cardiovascular risk, depression,
memory impairment, and decreased QoL,
 prevention of or recovery from concomitant comorbidities while restoring life
expectancy and QoL to those in the general population,
 long-term disease control without tumor recurrence
 reversal of optic chiasm compression in cases of pituitary macro-tumor, if
present.

23. Pharmacotherapy:
Tumour directed drugs
Cabergoline
Pasireotide
Steroidogenesis Inhibitors
Metyrapone
Ketoconazole
 mitotane
 etomidate

24. Combination Therapy
Glucocorticoid Receptor Antagonists
 Mifepristone

25. Surgical management
 Pituitary Tumor excision - by transsphenoidal hypophysectomy
 Adrenalectomy – for primary adrenal hypertrophy
 Radiation therapy – for residual tumor

26. complications
Diabetes mellitus
Hypertension
Dyslipidemia
Osteoporosis
Electrolyte abnormalities
Prevention and treatment of thromboembolic
disease
Coronary heart disease
Infection

27. Nursing management
 Decreasing risk for injury
 Decreasing risk for infection
 Preparing the patient for surgery
 Encouraging rest and activity
 Promoting skin integrity
 Improving body image
 Improving thought processes
 Monitoring and managing potential complications

28. NURSING DIAGNOSIS
 Risk for injury related to weakness
 Risk for infection related to altered protein metabolism and inflammatory
response
 Self-care deficit related to weakness, fatigue, muscle wasting, and altered
sleep patterns Impaired skin integrity related to edema, impaired healing, and
thin and fragile skin
 Disturbed body image related to altered physical appearance, impaired sexual
functioning, and decreased activity level
 Disturbed thought processes related to mood swings, irritability, and
depression