Documentos de Académico
Documentos de Profesional
Documentos de Cultura
Anatomi
Korteks Adrenal
Bagian luar kelenjar adrenal
Dari mesoderm
Menghasilkan steroid hormon
(glucocorticoid, mineralocorticoid,
sex steroids)
Medula Adrenal
Bagian dalam kelenjar adrenal
Dari sel krista neural
Menghasilkan hormon epinephrine
dan norepinephrine
Vena:
V.suprarenalis dextra V.cava inferior
V.suprarenalis sinistra + V.phrenica inferior
V.renalis sinistra
Persarafan:
Plexus coeliacus & abdominopelvic
LO 2
Histologi
Korteks Adrenal
Zona
Medula Adrenal
Terdiri atas deretan sel kromafin, dengan sinusoid
venosa lebar diantaranya.
Terdapat sekelompok kecil sel saraf
Menghasilkan adrenalin & nor adrenalin
Sitoplasma mengandung banyak vesikel berisikan
sekret ini.
Sel tersusun dalam deretan setebal satu sel pada
tepi sinusoid venosa.
LO 3
Faal
HORMON
KORTEKS
ADRENAL
Pengaruh Mineralokortikoid
~aldosteron
Aktivitas utama tubulus distal ginjal retensi Na+ &
eliminasi K+
Retensi Na+ memicu retensi osmotik H2O volume
CES>> tekanan darah >>
Sangat esensial tanpa aldosteron meninggal
akibat syok sirkulasi
Stimulasi aldosteron
SRAA (o/ krn penurunan Na+ & tekanan darah)
Peningkatan konsentrasi K+ plasma
Pengaruh Glukokortikoid
~kortisol
Efek metabolik
Merangsang glukoneogenesis hati
Menghambat penyerapan glukosa o/ banyak jaringan
kecuali otak
Merangsang penguraian protein di banyak jaringan
terutama otot
asam amino bebas > glukoneogenesis
Meningkatkan lipolisis
asam lemak bebas > sumber bahan bakar pengganti
glukosa
Efek permisif
Kortisol hrs adekuat agar katekolamin dapat
memicu vasokonstriksi
Hipersekresi
androgen adrenal
Pseudohermafroditis
me wanita
Pseudopubertas
prekoks
Insufisiensi adrenokorteks
Primer (Addison disease)
Destruksi autoimun atrofi idiopatik kelenjar adrenal
sekresi hormon adrenal <<
Sekunder
Kelainan hipofisis / hipotalamus ACTH <<
kortisol<< ; aldosteron normal
Gejala gejala defisiensi kortisol penurunan respon
thdp stres, hipoglikemia, hiperpigmentasi akibat sekresi
berlebihan ACTH
Gejala gejala addison hiperkalemia & hiponatremia
ggg irama jantung; vol CES < hipotensi
HORMON
MEDULA
ADRENAL
Efek metabolik
Glukoneogenesis & glikogenolisis di hati
Lipolisis > asam lemak bebas >
Laju metabolisme >
Efek lain
Keadaan terjaga & kewaspadaan SSP
Keringat > pengeluaran panas
Membesarkan pupil, mendatarkan lensa mata
Stimulasi katekolamin
Dikontrol o/ masukan simpatis;
peningkatan impuls simpatis ke kelenjar
Faktor2 utama yg mengontrol
Kondisi stres
Trauma fisik atau psikologis, perdarahan,
penyakit, olahraga, hipoksia (O2 arteri rendah),
pajanan dingin, hipoglikemia
LO 4
Biokimia
CATECHOLAMINES
Family of bioamines and are secretory
products of the sympathoadrenal system
Epinephrine (8085% of stored
catecholamines) is synthesized primarily in
the cells of the adrenal medulla, whereas
Norepinephrine (1520% of stored
catecholamines) is synthesized and stored
not only in the adrenal medulla but also in
various areas of the central nervous system
Biosynthesis of cathecolamines
Secretion of cathecolamines
Stimulators
pain, hemorrhage, exercise, hypoglycemia, and
hypoxia
Hormon release
Stress nerve impulses emanating from
adrenergic nuclei in the hypothalamus release of
the neurotransmitter acetylcholine from
preganglionic neurons that innervate the
adrenomedullary cells rapid entry of extracellular
calcium (Ca ) into the cytosol synthesis and
release of epinephrine and norepinephrine from the
chromaffin granules
2
Physiological effects
Inactivation of
cathecolamines
Renin-angiotensin-aldosteron
system
GLUCOCORTICOIDS
Cortisol (hydrocortisone) is the major
physiologic glucocorticoid (GC) in
humans, although corticosterone also
has some glucocorticoid activity
LO 5
Kelainan kelenjar adrenal
Cushings syndrome
Etiology
Adrenal hyperplasia
Secondary to pituitary ACTH overproduction
Pituitary-hypothalamic dysfunction
Pituitary ACTH-producing micro- or macroadenomas
Adrenal neoplasia
Adenoma
Carcinoma
Clinical signs
Diagnostic tests
Radiologic test
CT scan of the abdomen adrenal tumors and for
diagnosing bilateral hyperplasia
Diagnosis
DD
Pseudo-cushings syndrome
obesity, chronic alcoholism, depression, and
acute illness of any type abnormalities in
steroid output:
elevated urine cortisol
blunted circadian rhythm of cortisol levels
resistance to suppression using the overnight
dexamethasone test
Treatment
Adrenal neoplasm
resected using laparoscopic techniques
mitotane (o,p'-DDD), an isomer of the
insecticide DDT Mitotane suppresses
cortisol production and decreases plasma
and urine steroid levels
receive long-term glucocorticoid maintenance
therapy, and, in some, mineralocorticoid
replacement is appropriate
Bilateral hyperplasia
surgical removal ACTH- or CRH-producing
tumors
Aldosteronism
Primary Aldosteronism with an
Adrenal Tumor
Primary Aldosteronism without an
Adrenal Tumor
Secondary Aldosteronism
Pathophysiology
Laboratory findings
Hypokalemia may be severe (<3
mmol/L)
Hypernatremia is infrequent
alkalosis is perpetuated by potassium
deficiency
overnight concentration test impaired
ability to concentrate the urine,
probably secondary to the hypokalemia
Evaluation
Diagnosis
1. diastolic
hypertension
without edema
2. hyposecretion of
renin
3. hypersecretion
of aldosterone
that does not
suppress
appropriately in
response to
volume
expansion
DD
Treatment
surgical excision of the adenoma
administration of an aldosterone
antagoniste.g., spironolactone (25
100 mg every 8 h)
Eplerenone (50150 mg every 8 h)
idiopathic bilateral hyperplasia
surgery is indicated only when
significant, symptomatic hypokalemia
cannot be controlled with medical
therapy
Secondary aldosteronism
increased production of aldosterone in response to
activation of the renin-angiotensin system
aldosterone is often higher in patients with secondary
aldosteronism
accelerated phase of hypertension or on the basis of
an underlying edema disorder
e/
primary overproduction of renin (primary reninism)
overproduction of renin secondary to a decrease in renal
blood flow and/or perfusion pressure
renin-producing tumors (primary reninism)
Pathophysiolog
y
Most etiology
Congenital
adrenal
hyperplasia
(21-Hydroxylase
Deficiency) ->
Neonate with
ambiguous
genitalia
Etiology
Signs &
symptoms
Laboratory findings
serum sodium, chloride, and
bicarbonate levels are reduced, and the
serum potassium level is elevated
extravascular sodium loss depletes ECFV
and accentuates hypotension
Elevated plasma vasopressin and
angiotensin II levels may contribute to
the hyponatremia by impairing free
water clearance
Diagnosis
Treatment
Hydrocortisone (cortisol) is the mainstay of
treatment (2030 mg/d)
maintain an ample intake of sodium (34 g/d)
mineralocorticoid supplementation
administration of 0.050.1 mg fludrocortisone
per day PO
female patients with adrenal insufficiency,
androgen levels are also low 2550 mg of
DHEA PO
Secondary Adrenocortical
Insufficiency
e/ ACTH deficiency
Signs & symptoms
primary disease but are not hyperpigmented
near-normal level of aldosterone secretion
Tests
low-dose (1 g) ACTH test for suspected secondary ACTH deficiency
laboratory findings
low blood cortisol and ACTH levels
Treatment
Glucocorticoid
Adrenal crisis
rapid and overwhelming intensification of chronic
adrenal insufficiency, usually precipitated by sepsis
(Pseudomonas or meningococcemia (WaterhouseFriderichsen syndrome)) or surgical stress
Signs & symptoms
Nausea, vomiting, and abdominal pain may become
intractable
Fever may be severe or absent
Lethargy deepens into somnolence, and hypovolemic
vascular collapse ensues
mineralocorticoid secretion is usually preserved
Treatment
IV infusion of 5% glucose in normal
saline solution should be started with a
bolus IV infusion of 100 mg
hydrocortisone followed by a continuous
infusion of hydrocortisone at a rate of 10
mg/h
Vasoconstrictive agents (such as
dopamine) may be indicated in extreme
conditions as adjuncts to volume
replacement
Hypoaldosteronism
Isolated aldosterone deficiency
accompanied by normal cortisol
production occurs in association with
hyporeninism
Features
unexplained hyperkalemia, which is often
exacerbated by restriction of dietary sodium
intake
deficiency in renin production
Tests
Low renin and aldosterone levels hyporeninemic
hypoaldosteronism
high renin levels and low aldosterone levels biosynthetic
defect or a selective unresponsiveness to angiotensin II
Treatment
administration of 0.050.15 mg fludrocortisone PO daily
should restore electrolyte balance if salt intake is adequate
(e.g., 150200 mmol/d)
Hyperenimic hypoaldosteronims higher doses of
mineralocorticoid to correct hyperkalemia
LO3.
Definisi, epidemiologi,
etiologi, patofisiologi, tanda dan
KELAINAN
PADA
gejala, diagnosis, pemeriksaan fisik, pemeriksaan
tatalaksana, komplikasi, prognosis.
MEDULApenunjang,
ADRENAL
Pheochromocytoma
catecholamine-producing tumors derived from
the sympathetic (pheochromocytomas) or
parasympathetic nervous system
(paragangliomas)
Epidemiology
28 out of 1 million persons per year, and about 0.1%
of hypertensive patients harbor a pheochromocytoma
"rule of tens
10% are bilateral, 10% are extraadrenal, and 10% are
malignant
Clinical
features
zellbalen appearance in
microscopic
Diagnosis
Treatment
Complete tumor removal is the ultimate therapeutic goal
-Adrenergic blockers (phenoxybenzamine) should be initiated
at relatively low doses (e.g., 510 mg orally three times per day)
Oral prazosin or intravenous phentolamine can be used to
manage paroxysms while awaiting adequate alpha blockade
Before surgery blood pressure should be consistently below
160/90 mmHg
Beta blockers (e.g., 10 mg propranolol three to four times per
day)
Other antihypertensives, such as calcium-channel blockers or
angiotensin-converting enzyme inhibitors
laparoscopy, using either a transperitoneal or retroperitoneal
(for bilateral adrenalectomy)