PLENARY PRESENTATION

ENDOCRINE AND METABOLIC

SYSTEM

MODULE OF POLYURIA
GROUP X
FACULTY OF MEDICHINE OF MUHAMMADIYAH JAKARTA
UNIVERSITY
 MEMBER OF
GROUP X
Bambang Hady Pratama 2007730024
Bunga Kartika Yunus 2007730134
Cilvina Wulandari 2007730029
Faridah Laili 2007730050
Febbyana Anggun Sari 2007730053
Litta Septina Mahmelia 2007730075
M. Fourta Lasocto 2007730077
Muhammad Barkah 2007730086
Reni Apriyanti 2007730101
Septiana Amelia 2007730113
Vidya Rahmatullah 2007730124
 SCENARIO

A man 50 y.o, come to doctor with

complaint polyuria since 2 months
ago. Patient often get up 4 – 5 time
at night to mixtion. Patient also
complaint always thirsty and
throat feel dry. Around 3 months
ago, patient experience traffic
accident and ever coma 5 days.
 KEYWORD

 A man 50 y.o
 Complaint polyuria since 2 months ago
 Get up 4 – 5 time at night to mixion
 Complaint always thirsty and throat feel dry
 Around 3 months ago, patient experience
traffic accident and ever coma 5 days
 QUESTION
 Explain the anatomy and histology of organ that have a
relation with the case!
 Explain the physiology of urine production!
 Explain the relation polyuria with always thirsty, throat
feel dry and traffic accident!
 Explain the biochemistry of organ that have a relation
with the case!
 What is the mechanism of polyuria in our body?
 What is the diagnose step for this scenario?
 What is the differential diagnose for this scenario?
 How is the therapy from the scenario?
ANATOMY, HISTOLOGY, AND
PHYSIOLOGY of Pituitary
Pituitary

Pars anterior Pars posterior

Pars intermedia
Sisa kantong Rathke
Pituitary Gland
ANTIDEURETIK HORMONE
(ADH) Vasopressin
 ADH

Synthesis at
nerve cell
body in
nucleus
supraoptic
hypothalamu
s
Kidney
 Function of Kidney

 Excretion of metabolic and chemical result

 Regulation of electrolyte and water
concentration
 Regulation of osmolality body fluid and
concentration of electrolyte.
 Regulation of artery pressure .
 Regulation of basa-aci
 Secretion,metabolism and excretion of hormon
 Gluconeogenesis
 Mechanism of Urine
production

iltration in glomerulus

2. Tubulus Secretion

3. Rearbsorpsition
 Excess Fluid Intake
↑ Fluid in body ↓ Secretion ADH
by posterior
hypofisis

Electrolyte Permeability
substance of tubule distal
↓ Urine
Constant & duct coligentes
osmolarity
in reabsorption With water ↓

Water excess Urine

can’t absorption volume ↑
& thin
Trau
ma

POLYURIA
 Kidney Can’t Response
With ADH
e intertisium Medulla formof kidney hyperosmotic

Or failure in tubules distal and duct coligentes

Kidney abnormally

Segment of tubules distal can’t respond with ADH

↑ Urine volume and Th

Mechanism of
Polydipsi

POLYDIPSI
 Anamnesis Question about the especially
symptoms like:

Anore
Polydip xia Lot of
si urine
excretion

Dehydra
tion

Hypernatr
emia
 Physic Examination

 Gastrointestinal: polydipsi, weigh loss

 Cardiovascular: sign of dehydration (tachycardia,
hypotension, etc).
 Respiration: sign of dehydration (tachypneu, pale ).
 Renal: polyuria 5-30 l/day, nocturia.
 Integument: mucosa membrane and dry skin.
 Support Examination

 Water deprivation test

- Dehydration Test until 8 jam.
- Dehydration Test (overnight)
 Pitresin Test
 MRI pituitary and hypothalamus.
 DIFFERENTIAL DIAGNOSIS
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

D Caused by disorderDiabetes mellitus Diabetes mellitus

E of is a long-term is a autoimune
neurohypophyseal- condition where disease that
F renal reflex the body is unable ditentukan secara
I system. Then, to regulate the genetic with
N failure of body amount of glucose destruction
I converting the in the blood imunologic cell
T water, it makes properly. Diabetes that producion
the urine volume develops when hormone insulin,
I over 3 liters a day, the body no so that insulin not
O dehidration, and longer responds formed.
N great thirsty, adequately to the
sometimes great natural hormone
thirsty and great insulin, or when
hunger production of
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

• No significant Prevalence : -
E differentiation 1,4 – 1,6 %
gender in - Often on white
P central diabetes leather among 3
I insipidus and –6%
D nefrogenic
E diabetes
M insipidus
• Same
I prevalence in
O male and female
L • Mortality is rare
O happened in
G adult
Y
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

• Hypothalamus Type 2 diabetes Autoimune that

dysfunction and
produce few
develops when to smash
antidiuretic the body pancreas beta
E hormone becomes cell / idiopatic
T • Hypofisis gland resistant to
release antidiuretic
I hormone into blood
insulin
O stream
• Hyphothalamus
L destruction or
O hypofisis gland
caused by operative
G • Brain trauma
Y (especially fracture
on basis cranial)
• Tumor
• Sarcoidosis or
tuberculosis
• Aneurism or artery
occlusion that going
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

• Polyuria (2-40  Increased  Poliury

L/day) production of  Polidypsi
• Polidypsia urine  Nocturia
S • Nocturia  Unusual thirst  Fatigue
Y • Weight loss  Tiredness
M • Dehydration  Loss of weight
P • Orthostatic  Blurred vision
T hypotension  Infections such
• Lethargy as thrush or
O irritation of the
M genitals
S
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

P A. Central Diabetes Initially resistance - Defektive cell

Insipidus caused insulin is still beta so that
A by haven't caused happening
T - Releasing clinical diabetes. insulopenia and
H Antidiuretic Upon that pancreas metabolic.
Hormone (ADH) beta cell is still get - Insulin to
O failure compensation this decrease caused
M - Disorder of situation and efisiency function
E transportation happening a glucose in perifer
ADH hyperinsulinemia and to increase as
C and blood glucose is production
H B. Nefrogenic still normal or new glucose, so that
A Diabetes few increased. Then glucose plasma
Insipidus after happening to increase 300 -
N - Renal produce pancreas beta cell is 1200mg/100ml.
I liquid excessive not equal, new will This increasing
S urine because happen mellitus will arise
failed give diabetes clinical confluence in all
M respond to ,one that marked by body.
antidiuretic its increasing
hormone and happening titrates
DD DIABETES DIABETES MELITUS
INSIPIDUS Diabetes type 2 Diabetes type 1

• Commonly NIDDM ( non- IDDM ( insulin

P good insulin dependent dependent
• Depend on diabetes melitus ) diabetes
R kind of disease have long live melitus ) have to
O and the basic same with non live expectant
G disease diabetic, may be sekitar 75% from
N just several year non-diabetic
O shorter that can
relation with
S cardiovascular
I disease and c
S erebrovasculer
 THERAPY
DIABETES INSIPIDUS
 Therapy of diabetes insipidus
must be adapted for symptom
 Nothing therapy for the patient
have a symptom like nocturia and
polyuria if the symptom don’t
disturb daily activity. But, the
patient with trouble at thirsty
center, must therapy with tight
observation to prevent the
happening of dehydration.
 Non Pharmacology
 rest
 Diet
 To prevent dehydration,must take enough fluid when
thirsty

 Pharmacology :
- In the complete DIS need hormonal
replacement.
- DDAVP(1-DESAMINO-8-D-ARGININE
vassopresin) is main drug of choice for DIS.
Dose: 5 – 10 meg

Side effect
Little side effect and pressor effect, and allergy is
rarely.
Adjuvant Therapy
Thyazide diuretic
 Mechanism of drug :
be a natriuresys temporary, mild ECF
deflation and decreasing GFR.
this problem cause increasing of
reabsorption Na+ and water at nephron
which more procsimal, so causes
decreasing of water enter to tubule distal
and collecting duct.

 Dose: 50 – 100 mg/day.

 Side effects
orthostatic hypotension, but can be used at
DIS and DIN
Clorpropamide
 Mechanism of Drug
Increases effect ADH to kidney tubule,
Can increase to releasing ADH from this pituitary
so this drug no usable at complete DIS or DIN

 Dose:250 – 750 mg/day

 Side effects :
Hypoglycemia, combine with thyazide to get
maximal effect
There isn’t not sulfonylurea which more effective
and less toxically is compared to clorpropamid
for drug DIS.
Clofibrat
 Mechanism of drug
like clorpropamid, clofibrat to increase releasing
ADH endogen.

 Dose: 250 – 500 mg/ (every 6 – 8 hour)

 Indication
lacking of klofibrat compared to klorpropamid
it is must be given 4x 0ne day, but don’t arise
hypoglycemia.

 Side effects :
Trouble gastrointestinal, miositis, liver function.