HANDOUT KEPERAWATAN MEDIKAL BEDAH II

JURUSAN S1 KEPERAWATAN

SEKOLAH TINGGI ILMU KESEHATAN WIRA MEDIKA BALI

2019

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 ENDOKRINOLOGI
Anatomy Of Endocrine System

 Fungsi tubuh  sistem saraf dan sistem endokrin/hormonal

 Sistem saraf  sistem hormonal Sekresi Kel. medula adrenal dan kel. Hipofisis 
respon terhadap rangsang saraf
 Hormon  zat kimia yang disekresikan ke dalam cairan tubuh oleh satu atau sekelompok sel
dan mempunyai efek pengaturan fisiologis thd sel-sel tubuh lain
 Hormon dari Hipofisis Anterior
Growth hormon  pertumbuhan hampir di seluruh sel dan jaringan tubuh
Adrenokortikotropin (ACTH)  korteks adrenal  hormon adrenokortikal
Hormon perangsang tiroid (TSH)  kel. Tiroid  tiroksin dan triiodotironin
Hormon perangsang folikel (FSH)  pertumbuhan folikel dlm ovarium sblm ovulasi dan
peningkatan pembentukan sperma di dlm testis
Hormon Lutein (LH)  menimbulkan proses ovulasi, sekresi hormon kelamin ♀ oleh
ovarium dan testosteron oleh testis
Prolaktin  meningkatkan perkembangan payudara dan sekresi air susu

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 Hormon dari Hipofisis Posterior
Hormon antidiuretik (vasopresin)  retensi air  jumlah air dlm tubuh ↑  jika
konsentrasi ↑  vasokontriksi PD & me↑ TD
Oksitosin  uterus berkontraksi selama proses persalinan, membuat sel-sel mioepitelial
dlm payudara berkontraksi  air susu keluar saat bayi menghisap
 Thyroid Gland
Thyroxine and Triiodothyronine  me↑ kec. Reaksi kimia hampir diseluruh sel tubuh 
me↑ met. Tubuh secara umum
Calcitonin  memacu pengendapan kalsium di tulang  me↓ konsentrasi Ca dalam CES
 Parathyroid Gland
Parathormone  mengatur konsentrasi ion kalsium  dengan cara: absorbsi kalsium dari
usus, pe↓ ekskresi kalsium oleh ginjal, pelepasan kalsium dari tulang
 Adrenal Cortex
Mineralocorticoids (Aldosterone)  me↓ ekskresi Na, me↑ ekskresi K  kadar Na ↑ dan
kadar K ↓
Glucocorticoids (Cortisol)  me ↑ kadar gula darah (met. Protein, karbohidrat, lemak),
inhibiting inflammation and immune response
 Adrenal Medulla
Epinefrin  bekerja pada otot jantung, otot polos, dan kel (fu/ emergency)  increases
HR, BP, blood flow to skeletal, blood glucose level
Norepinefrin  organ-organ yang dipersarafi oleh sis. Saraf simpatis
 Pancreas (Islets of Langerhans)
Insulin  target tissue: general but especially liver, skeletal muscle, adipose  memacu
masuknya glukosa ke dalam sel
Glucagon  target tissue: liver  meningkatkan sintesis dan pelepasan glukosa dari hati
ke sirkulasi tubuh
 Testes
Testosteron  Maturation and maintenance of male reproductive organs (♂), secondary
sex characteristics
 Ovaries
Estrogens  merangsang perkembangan organ kelamin ♀, payudara, dan berbagai sifat
kelamin sekunder
Progesteron  merangsang sekresi “cairan uterus” untuk kel. Endometrium (prepare
uterus for pregnancy), membantu meningkatkan perkembangan aparatus sekretorik
payudara, menstrual cycle

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 Pineal Gland
Melatonin  target tissue: Hypothalamus  inhibits gonadotropin-releasing hormone,
which consenquently inhibits reproductive function; regulates daily rhytms, such as
sleep and wakefulness
 Thymus
Thymosin  target tissue: tissue involved in immune response  immune system
development and function
 Plasenta
Human Chorionic Gonadotropin (HCG)  meé pertumbuhan korpus luteum & sekresi
estrogen dan progesteron oleh korpus luteum
Estrogen  me é pertumbuhan organ kelamin ibu & beberapa jaringan janin
Progesteron  perkemb. Endometrium uterus  persiapan implantasi
Human Somatomammotropin  perkemb. Jaringan janin & perkemb. payudara

TYROID DISORDER

1. HIPOTIROID

Insufficient circulating thyroid hormon → destruction of thyroid tissue, devective

hormon synthesis, decrease TSH secretion

Hypothyroidism  occur in infancy  cretinism

Clinical manifestation:

 Infant – devective physical development & metal retardation

 Childhood – intelectual development normal mentaly sluggish, mucle

hypertrophy, eruption of permanen teeth, delayed sexual maturation

 Adult – slowing of body processes, fatique, lethargic, mental changes :

impaired memory, slow speech, cold intolerance, hair loss, dry skin, muscle

weakness, constipation, weight gain and menorrhagia

Diagnostic : T3, T4 – Low

Collaborative care

 Hormon Replacement Therapy

Synthetic Oral Thyroxine - Levothyoxine

 Adulth – Low Caloric Diet To Promote Weight Los

Nursing Management

1. Nursing Diagnoses

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
  Hypothermia – Cold Intolerence

 Altered nutrition – More Body requirement – hypometabolism

 Consipation – Gastrointestinal Hypomitility

 Activity Intolerance – Decrease Metabolic Rate

 Thought Processes – disminished Cerebral Blood Flow - CO↓

2. Nursing Implementation

 Health Promotion

 Acute Intervention – Hospital Setting

 Home Care

Health Promotion

 Detection Of Hypotyhroidism

 Maintain Thyroid Function – Adequate Dietary Intake of Iodine

Acute Intervention

 Complication of hypothyroid – myxedema coma

 Characterized by: hypotension, subnormal temp, hypoventilation – mental

sluggishehness, drowsiness, lethargycoma, medical emergency

 Precipatated by: infection, drugs (Tranguilizers, narcotic, barbitura tes),

trauma, cold exposures.

 Needs support: vital function & IV thyroid hormon

Home Care

 Health Education – Written Instruction

 Life long Drug Therapy – stressed

 Sign & Simptom Over Dose : Dyspnea, Orthopnea, Palpitation, Rapid HR,

Nervousness, Insomnia

Contact Clinician Immediately

2. HIPERTIROIDISME

Thiroxine (T4) dan triiodotironin (T3) adalah bentuk aktif hormon tiroid 

berfungsi u/ mengatur regulasi energi metabolisme pertumbuhan &

perkembangan

Hipertiroid adlh peningkatan sintesis dan pelepasan hormon tiroid oleh kelenjar

tiroid  tirotoksikosis  hipermetabolisme

Hipertiroidisme & Tiroroksikosis  Grave’s disease

by: Ns. Theresia Anita Pramesti,
S.Kep., M.Kep.
 Etiologi : Goiter toksika, Tirotoksikosis, peny. Grave

Insidensi :

♀ 4 – 10x >>> ♂

30 – 50 th

Defisiensi iodine

Penyakit tiroid yang lain : tiroiditis, goiter

Grave’s disease : diffuse toxic goiter  multisistem, peny autoimun ditandai o/:

pembesaran diffus tiroid, peningkatan prod hormon tiroid, opthalmopathy

 etiologi : tdk jelas  fa/ resiko : insuffisiensi iodine

Manifestasi Klinis :

pe↑ metabolisme

pe↑ sensitivitas jaringan (m’stimulasi saraf simpatis):

 Cardiovaskuler: TD sistol me↑, HR ↑, cardiac contraction me↑,

aritmia (AF), cardiac output me↑, palpitasi, angina  saat T3 & T4 >>> 

edema paru

 Respiratory: RR me↑, dyspnea on mild exertion

 GIT: nafsu makan me↑, kehausan, pe↓ BB, peristaltik me↑, diare,

hepatomegali & splenomegali

 Integumen: hangat, kulit halus dan lembab, rambut rontok, fine

silky hair

 Persarafan: gugup, tremor halus pd jari, restlessness, depresi,

delirium, stupor, koma

 Muskuloskeletal: fatigue, lemah otot

 Reproduksi: menstruasi irregular, amenore, libido ↓↓,

gynecomastia, fertility me↓

 Lain-lain: intoleransi thd panas, exophtalmus, suhu basal me↑,

bicara cepat, retraksi kelopak mata

Komplikasi: krisis tiroktosin (badai tiroid), infeksi, trauma, perdarahan

 Manifestasi: tachicardia, heart failure, shock, temperatur

me↑, restlessness, nyeri abdomen, nausea, vomiting, diare, delirium, coma

Manajemen: me↓ hormon tiroid dlm darah

me↓ suhu

mengganti cairan tubuh

by: Ns. Theresia Anita Pramesti,
S.Kep., M.Kep.
 menghilangkan stressor

radioimmunoassay

Collaborative care:

a. terapi bedah

b. obat anti tiroid (OAT): propylthiouracil (PTU), metimazole, penghambat

sintesis hormon tiroid

iodine block release thiroid hormon to circulation

β adrenergik blocker : propanolol

c. Iodine radioaktif: membatasi sekresi hormon tiroid dng menghancurkan

jaringan tiroid

d. Terapi nutrisi: diet tinggi kalori 4000 – 5000 kkal/hari

Makan 6x/hari & snack tinggi protein

Mineral, vit. A, thiamin, B6, C, susu

Hindari makanan berbumbu & berserat ↑

Hindari cafein, cola dan teh

Nursing care

a) Diagnosa :

intoleransi aktivitas → fatigue, exhaustion, heat intolerens

Resiko injury → ulcerasi kornea, tremor otot

Kelainan nutrisi → hipermetabolisme

Kecemasan

Hipertermi

b) Implementasi

Health promotion

Preventive relapse

Intervensi akut: restfull, calm & quite room

Placing client in cool room

Light linen

Latihan otot besar

Batasi pengunjung

Establish supportive relationship

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
3. GOITER DISEASE

 Pembesaran kelenjar tiroid akibat sekresi hormon tiroid yang berlebihan.

 Peradangan pada kelenjar tiroid yang menyebabkan kemunduran pada kelenjar

itu dan hasil akhirnya adalah berkurangnya atau tidak adanya sekresi hormon

tiroid

 Etiologi

 Goiter dapat menyertai hipotiroidisme atau hipertiroidisme, tetapi tidak selalu

ada pada kedua keadaan tersebut

 Adanya stimulasi terhadap kelenjar tiroid oleh TSH atau TSI

 Hipotiroidisme

kegagalan kelenjar tiroid

kekurangan iodium

 Hipertiroidisme

defek hipotalamus atau hipofisis anterior

grave’s disease

konsumsi zat goitrogenik dlm jml besar (iodium / litium)

Gangguan Akibat Kekurangan Yodium (GAKY)

 Insidens

 Saat ini diperkirakan 1.6 miliar penduduk dunia mempunyai risiko

kekurangan yodium

 300 juta menderita gangguan mental akibat kekurangan yodium.

 Kira-kira 30.000 bayi lahir mati setiap tahun

 lebih dari 120.000 bayi kretin, yakni retardasi mental, tubuh pendek, bisu tuli

atau lumpuh.

 Kebutuhan Yodium

 Kebutuhan yodium setiap hari di dalam makanan yang dianjurkan

50 mikrogram untuk bayi (12 bulan pertama)

90 mikrogram untuk anak (usia 2-6 tahun)

120 mikrogram untuk anak usia sekolah (usia 7-12 th)

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 150 mikrogram untuk dewasa (diatas usia 12 tahun)

200 mikrogram untuk ibu hamil dan meneteki

 Akibat GAKI pada manusia ?

 Tiroksin : pada masa pertumbuhan penting pada perkembangan fisik dan

syaraf (otak)

 Penting saat masa fetus, masa kehamilan, masa bayi, masa anak,

masa remaja.

 Dampak kekurangan :

1. Kretin endemik

2. Kretin neurologik

 Gambaran klinis kretinisme

Kretin endemik dan Kretin neurologik :

Lahir di daerah kekurangan yodium, dng dua atau lebih dari :

1. Gangguan kecerdasan

2. Tuli simetrik tipe sensorik

3. Kelainan saraf (gangguan jalan, gangguan bicara, refleks patologik kelambatan

jalan)

 Keduanya irreversibel, permanen, tidak dapat diperbaiki dengan obat apapun.

 Spektrum Gaki

Fetus Anak dan remaja

Abortus Gondok

Lahir mati Hipotiroidisme juvenil

Anomali congenital Ggn fungsi mental

Kematian perinatal Ggn perkembangan fisik

Kematian anak

Kretin endemic

Kretin miksedematosa

Defek psikomotor
Neonatus Dewasa

Gondok neonatus Gondok dng akibatnya

Hipotiroidisme neonatus Hipotiroidisme

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 Gangguan fungsi mental

 Survey Epidemiologi

KRITERIA PEREZ, 1960

GRADE MANIFESTASI
0 tidak teraba
1 teraba dan terlihat dengan kepala ditengadahkan
1a tidak teraba / jika teraba tidak lebih besar dari tiroid normal
1b jelas teraba dan membesar, umumnya tidak terlihat walau kepala tengadah
2 mudah dilihat dengan posisi biasa
3 terlihat dari jarak tertentu

Table.2. Symptomatology of endemic cretinism from Sengi and Papua New Guinea (in%)
Sengi Papua
A. Hearing loss 93 93.6
Deaf-mutism 12 79.9
B. Mental retardation 95 >90
C. Neuromotor abnormalities 76 79.9
Impaired speech 37 13.7
Specific gait 46
Elevated reflexes 29 40
Babinsky sign 5
Squint 2 25.5
Later walker 22
D. Clinical hypothyroidism 29 0
Short stature 29 10-50
E. Goiter 70 10-50
Djokomoeljanto 1974, Pharoah 1972.

4. GRAVE’S DISEASE

 Suatu penyakit autoimun yang biasanya ditandai oleh produksi auto antibodi

yang memiliki kerja mirip TSH pada kelenjar tiroid

 Faktor predisposisi :

usia 20 – 30 tahun

wanita >>> pria

 Gejala serta tanda hipertiroidisme pada penyakit Graves

Tanda dan Gejala tidak tahan hawa panas, Hiperkinesis, capai, berat badan

Secara Umum menurun, percepatan pertumbuhan, Drug tolerance,

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 youthfulness
Sistem Tanda & Gejala Sistem Tanda & Gejala
Gastrointestinal hiperdefekasi, Susunan saraf pusat labil, intitabel,

kelaparan, makan psikosis, tremor,

banyak, haus, nervositas, periodic

muntah paralysis
Muskular rasa lemah Cardiorespirasi dyspnoea,

hipertensi, aritmia,

palpitasi, gagal

jantung
Genitourinaria oligomenoroe, Darah / limfatik limfositosis, anemia,

amenoroe, Libido Splenomegali,

menurun pembesaran

kelenjar limfe leher

Integumen rambut rontok, Skeletal Osteoporosis, kulit

berkeringat basah, onycholysis,

epifisis cepat

menutup, nyeri

tulang
Spesifik untuk Optalmopati (50%)  udema pretibial, kemosis, proptosis,

penyakit Graves, diplopia, visus < ulkus kornea

ditambah : Dermopati (0.5-4%)

Akropaki ( 1 % )
Sumber McDougall.1991.

 Diagnosis of Graves’ Disease

Clinical signs Laboratory tests

diffuse goitre
eye signs thyroid-stimulating antibodies (TSAb)
acropachy thyroglobulin antibodies (TgAb) (anti-Tg Ab)
vitiligo
family history microsomal antibodies (anti-M Ab)

Indication for Medical Treatment Antithyroid Drugs

patient preference carbimazole

small goitre methimazole

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
mild disease propylthiouracil (PTU)

other disease potassium perchlorate

children lithium

pregnancy iodides

opthalmopathy proppanolol

pre-operative sodium ipodate

pre-radioiodine

thyrotoxic crisis

relapse after thyroidectomy

Indication for Medical Treatment in Graves’ disease

Table of anthithyroid drugs. Carbimazole is the drug of choice in Europe. Some

clinicians add thyroxine to the carbimazole in a blocking-replacement regime, once the

patient is clinically euthyroid. Carbimazole is rapidly converted to methimazole (10 mg

carbimazole = 6 mg methimazole)

5. DISORDERS OF THE PARATHYROID GLANDS

 Production and secretion of the hormone parathormone from parathyroids is

regulated by the plasma calcium level.

 A low calcium level will stimulate the release of parathormone, which increase

the level of calcium in the plasma  a high calcium level will inhibit the release of

parathormone

 Parathormone raises tha calcium level in the plasma by acting on the renal

tubules to increase the excretion of phosphorus in the urine and the reabsorption

of calcium. It also the release of calcium from the bone into the bloodstream

5.1. HYPOPARATHYROIDISM

 Caused by atrophy or traumatic injury to the parathyroid glands.

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
  This can occur as a result of accidental removal or destruction of parathyroid

tissue during a thyroidectomy or irradiation of the thyroids or from idiopathic

atrophy of the glands

 Signs and Symptoms

 A drop in serum calcium levels and an increase in phosphorus levels 

tetany

 Muscular twitching and spasms accur because of extreme irritability of

neuromuscular tissue

 If the calcium level continues to fall  convulsions, cardiac arrhytmias, and

spasms of the larynx

 Treatment

 Oral or parenteral administration of calcium salt  acute phase

 Restoring and maintaining normal level calcium in the blood  chronic

phase

5.2. HYPERPARATHYROIDISM (Von Recklinghausen’s Disease)

 Occurs most often in postmenopausal women

 Occur as a result of benign enlargenet of parathyroid glands (adenoma) or

hyperplasia of two or more glands

 Signs and Symptoms

 Hypercalcemia (above 10,5 mg/dl)  dehydration, confusion, lethargy,

anorexia, nausea, vomiting, weight loss, constipation, thirst, frequent

urination, and hypertension

 Hypercalcemia  thinning of the bone and bone cysts  a fracture often

occur

6. DIABETES INSIPIDUS

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
  Diabetes Insipidus (DI) is a disorder in which there is an abnormal increase in

urine output, fluid intake and often thirst. It causes symptoms such as urinary

frequency, nocturia (frequent awakening at night to urinate) or enuresis

(involuntary urination during sleep or "bedwetting").

 the urine is pale, colorless or watery in appearance and the measured

concentration (osmolality or specific gravity) is low.

 Sometimes diabetes insipidus is referred to as "water" diabetes

 Types of Diabetes Insipidus

Diabetes Insipidus is divided into four types, each of which has a different

cause and must be treated differently.

The most common type of DI is caused by a lack of vasopressin, a hormone

that normally acts upon the kidney to reduce urine output by increasing the

concentration of the urine.

Such as:

a. Pituitary DI also known as Central or Neurogenic

DI

Due to the destruction of the back or "posterior" part of the pituitary gland

where vasopressin is normally produced

The posterior pituitary can be destroyed by a variety of underlying diseases

including tumors, infections, head injuries, infiltrations, and various

inheritable defects

Pituitary DI is usually permanent and cannot be cured but the signs and

symptoms (i.e. constant thirst, drinking and urination) can be largely or

completely eliminated by treatment with various drugs including a modified

from of vasopressin known as desmopressin or DDAVP.

b. Gestagenic or Gestational DI

a lack of vasopressin can also develop during pregnancy if the pituitary is

slightly damaged and/or the placenta destroys the hormone too rapidly

treatable with DDAVP but, in this case, the deficiency and the DI often

disappear 4 to 6 weeks after delivery at which time the DDAVP treatment can

usually be stopped

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
 c. Nephrogenic DI

is caused by an inability of the kidneys to respond to the "antidiuretic effect"

of normal amounts of vasopressin

can result from a variety of drugs or kidney diseases including heritable

genetic defects

cannot be treated with DDAVP

relieve the signs and symptoms of nephrogenic DI.

d. Primary Polydipsia

occurs when vasopressin is suppressed by excessive intake of fluids

most often caused by an abnormality in the part of the brain that regulates

thirst (daerah sepanjang dinding anteroventral dari vebtrikel ke-3 dan

anterolateral dari nutrieus preoptik)

Such as:

Dipsogenic DI

Difficult to differentiate from pituitary DI particularly since the two

disorders can result form many of the same brain diseases

Excessive urination but, unlike pituitary DI, it does not completely

eliminate the increased thirst and fluid intake

Results in water intoxication, a condition associated with symptoms such

as headache, loss of appetite, lethargy and nausea and signs such as an

abnormally large decrease in the plasma sodium concentration

(hyponatremia).

Pyschogenic Polydipsia

The other subtype of primary polydipsia is due not to abnormal thirst but

to psychosomatic causes

cannot be treated at present.

 What is considered "excessive" urination?

 An adult who urinates more than 50mL/kg body weight per 2 hours is

generally considered to have a higher than normal output

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
  What is considered "excessive thirst ?

 An adult who drinks more than 4 quarts (1 gallon) or approximately 12

glasses (144 oz) of beverages per day would have a higher than normal

intake.

 Summary

Type of DI Identification
Neurogenic DI also known as central, hypothalamic, pituitary or

neurohypophyseal is caused by a deficiency of the

antidiuretic hormone, vasopressin.

Nephrogenic DI also known as vasopressin-resistant. It is caused by

insensitivity of the kidneys to the effect of the antidiuretic

hormone, vasopressin.
Gestagenic DI also known as gestational. It is caused by a deficiency of

the antidiuretic hormone, vasopressin, that occurs only

during pregnancy.
Dipsogenic DI is a form of primary polydipsia. It is caused by abnormal

thirst and the excessive intake of water or other liquids

7. ADDISON’S DISEASE

Disorder that result in your body producing insufficient amount of certain

hormones produced by your adrenal glands

In this condition, overall decrease fuction of the adrenal cortex leads to a deficit in

all three hormones secreted by the adrenal cortex  related to insufficiencies of the

mineralocorticoids and the glucocorticoids

Most common in people ages 30 – 50.

Treatment : taking hormones to replace the insufficient amount being made by

your adrenal glands

Etiologi

 Primary Insufficiency

A disorder affecting the adrenal cortex itself  idiophatic atrophy,

inflammation, infection, and nonsecreting tumors of the adrenal cortex

Causes

by: Ns. Theresia Anita Pramesti,

S.Kep., M.Kep.
  The failure of adrenal glands, result of the bady attacking itself

(autoimmune)

 Tuberculosis

 Other infections of adrenal glands

 Spread of cancer to adrenal glands

 Bleeding into the adrenal glands

 Asthma

 Arthritis

 Secondary Insufficiency

A disorder affecting the pituitary gland that stimulates adrenal secretion 

failure of the pituitary gland to secrete corticotropin (ACTH).

This can occur because the pituitary is underfunctioning or the gland was

surgically removed (hypophysectomy) or because of certain pituitary tumors

and abrupt withdrawal of steroid therapy

Signs And Symptons

 Muscle weakness and fatigue

 Weight loss and decrease appetite

 Darkening of your skin(hyperpigmentation)

 Low blood sugar

 Nausea, diarrhea, vomiting

 Irritability

 Depression

 Orthosthatic Hypotension

Addisonian Crisis

 Pain in your low back, abdoment or leg

 Severe vomiting and diarrhea, leading to dehydration

 Severe symptoms associated with fluid and electrolyte imbalance

(hyponatremia & hyperkalemia) and hypoglycemia

 Low blood pressure

 Loss of consciousness

8. CHUSING SINDROME
by: Ns. Theresia Anita Pramesti,
S.Kep., M.Kep.
 Chusing’s syndrome is rare disorder.

Symptoms typical of chusing’s sundrome are manifestations of excess

levels of hormones from the adrenal cortex.

Can be caused by:

 Excessive secretion of corticotrophin (ACTH) by the pituitary

gland  release of corticotrophin-releasing factor (CRF) from the

hypothalamus

 A secreting tumor of the adrenal certex

 Ectopic production of corticotrophin by tumor outside the

pituitary, most commonly lung carcinoma, medullary thyroid carcinoma, and

thymoma.

 Iatrogenic chusing’s syndrome due to overzealous use of

exogenous steroid therapy

Symptoms and signs:

 Painful fatty swellings in the intrascapular speace (buffalo hump)

and the facial area (moon face)

 An enlarged abdomen with thin extremitas

 Bruising following even minor traumas

 Impotence

 Amenorrhea

 Hypertension

 General weakness due to abnormal protein metabolism with loss

muscle mass

Unusual growth of body hair (hirsutism) can be occur in women, and

streaked purple markings in the abdominal area can occur due to collections of

body fat

Patients with chusing’s syndrome who have a familial predisposition to

diabetes mellitus frequently develop insulin dependent diabetes mellitus as aresult

of the antiinsulin, diabetogenic properties of cortisol

Treatment

 Microsurgical procedures on the pituitary gland

 Using steroidsadrenalectomy  if chusing’s syndrome is arising

from an adrenal tumor

by: Ns. Theresia Anita Pramesti,
S.Kep., M.Kep.
 by: Ns. Theresia Anita Pramesti,
S.Kep., M.Kep.