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PBL Endocrine and Metabolisme System

A 50-year-old man presented with weight loss over the past 3 months, fatigue, lethargy, and frequent sleepiness. Differential diagnoses included diabetes mellitus type 2 and Addison's disease, as the patient's symptoms were consistent with insulin resistance and cortisol deficiency. Appropriate investigations and treatment would depend on the confirmed diagnosis.

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93 views33 pages

PBL Endocrine and Metabolisme System

A 50-year-old man presented with weight loss over the past 3 months, fatigue, lethargy, and frequent sleepiness. Differential diagnoses included diabetes mellitus type 2 and Addison's disease, as the patient's symptoms were consistent with insulin resistance and cortisol deficiency. Appropriate investigations and treatment would depend on the confirmed diagnosis.

Uploaded by

thenightstar_03
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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PBL

ENDOCRINE AND
METABOLISME
SYSTEM
MODUL 1
BY: A3
SCENARIO

A 50 year-old man came with chief


complaint of weight loss since 3 months
ago. He also felt weak, tired and sleepy.
KEYWORDS

 Old man, 50 years old


 Weight loss ( last 3 months )
 Lethargy and fatigue
 Sleepy
QUESTIONS
 Hormones that involve in weight
regulation?
 General mechanism of weight loss?
 Mechanism of lethargy and fatigue?
 Why the patient feels sleepy?
 Differential diagnosis?
 Appropriate investigation?
 Treatment?
ANSWERS

1. Hormones that involve in weight


regulation?
 Insulin
 Glucagon
 Somatostatin
 Thyroid hormone
 Growth Hormone
2. General mechanism of weight loss?
reduced uptake of glucose in tissues and
muscles

Glycogenolysis & lypolisis

Muscle atrophy & lipid pool

Weight loss
3. Mechanism of lethargy and fatigue?
reduce in glucose intake for a period of time

remain glycogen & lipid not enough to provide


sufficient energy

compensation intake of glucose from the


peripheral tissues to vital organs (brain, heart,
etc)

lethargy & fatigue


4. Why the patient feels sleepy?
 sleepiness might indicates loss of awareness,
results from reduced O2 delivery to the brain.
 Without insulin, brain still manage to receive
enough O2 due to high permeability of the
receptor glucose
Lack of energy for a long time

brain dysfunction

Loss of awareness
5. Differential diagnoses?
 DM type II
 Addison’s disease
 Grave’s disease
 Struma goiter
6. Appropriate investigation?
 Anamnesis
 Physical examination
 History (individual, family, medication)
 Sign of infection

7. Treatment?
Depends on DD
DIABETES MELLITUS
TYPE II
DEFENISI

 SYNDROME OF DISORDERED
METABOLISM WITH INAPPROPRIATE
HYPERGLYCAEMIA DUE EITHER TO
AN ABSOLUTE DEFICIENCY OF
INSULIN SECRETION OR A
REDUCTION IN BIOLOGIC
EFFECTIVENESS OF INSULIN (OR
BOTH)
EPIDEMIOLOGY

 AFFLICTS INDIVIDUAL WITH INSULIN


RESISTENCE WHO GENERALLY HAVE
RELATIVE RATHER THAN ABSOLUTE
INSULIN DEFICIENCY
 INDONESIA 1,5 - 2% POPULATION
 PEAK INCIDENCE 40-60 YR OLD
 NIDDM  80% cases
CLINICAL
MANIFESTATION
 POLYDIPSIA
 POLYURIA
 WEIGHT LOSS
OTHER SYMPTOMS

 NUMBNESS
 CHRONIC SKIN INFECTION
 IMPOTENCE
 PRURITUS & SYMPTOM OF VAGINITIS
Insulin resistence

Glucose uptake into cells hyperglycemia

Cell metabolism protein breakdown(gluconeogenesis)


exceed the
renal
ATP production Muscle mass capacity for
glucose
energy reabsorbtion
Weight loss
glycosuria

lethargy Loss of calories Osmotic diuresis


( Intratubular fluid
and solute)
tiredness
H2O absorbed out to
tubule
reabsorbtion of H2O in proximal tubule

Polyuria

dehydration

Thirst

polydipsia
TREATMENT

 DIET
 EXCERCISE
 ANTI DIABETIC DRUGS
 PATIENT EDUCATION & MOTIVATION
COMPLICATION

 STROKE
 VISUAL DISTURBANCES
 CARDIOVASCULAR DISEASE
 RENAL FAILURE
 INFECTION
ADDISON’S
DISEASE
ADDISON’S DISEASE

 1º Adrenocortical Insufficiency
 Destruction of adrenal cortex
 Glucocorticoid and mineralocorticoid
 Rare
 All age group
 F>M; 2.6:1
Etiology
 Autoimmune
 Infectious
 Metastatic malignancy/ lymphoma
 Hemorrhage/ Infarction
 Infiltrative disorders
 Drugs
Clinical Features

Weakness, fatigue, anorexia, weight 100%


loss
Hyperpigmentation 92%
Hypotension 88%
GI disturbances 56%
-Nausea
-Vomitting
-Diarrhoea (<frequent)
PATHOMECHANISM
ALDOSTRONE CORTISOL
Mobilization
Na 2+ ,water reabsorption Glukoneogenesis of lipid and
protein
Body metabolism
Extracelluler fluid volume
Weight loss
Energy
mobilization
Hypotension Hyponatremia

fatigue
INVESTIGATION
 A 0900h plasma ACTH levela high level (>80
ng/L) with low or low-normal cortisol confirms
primary hypoadrenalism.
 Electrolytes and ureasclassically show
hyponatremia, hyperkalemia and high urea
 Adrenal Ab are present in many cases of
autoimmune adrenalitis
 Chest and abdominal x-rayshow evidence of
tuberulosis or calcified adrenals
Treatment
 Long term
 Replacement therapy
 Treat Tb
 Hydrocortisone
 Fludrocortisone
GRAVES
DISEASE
DEFINITION

A KIND OF AUTOIMMUNE DISEASE


WITH SIGNS AND SYMPTOMS;
 Struma diffuse
 Ophtalmopathy
 and sometimes Dermopathy
(pretibial edema)
SIGNS & SYMPTOMS
 Struma diffuse
 Ophtalmopathy
 Loss of weight
 Fatigue
 Sweating
 Heat Resistent
 Miastenia gravis
 Mixedema pretibial
 Increase of lacrimation
PATHOMECHANISM
AUTOIMMUNE DEFECT
↓
ANTIBODY TSH
(TSI)
↓
ATTACHMENT AT TSH RESEPTORS
IN THYRIOD GLAND
↓
HYPERSECRETION OF TIROID HORMONE
EXAMINATION

 Trias Symptoms
 TSHs
 FT4
 FT3
TREATMENT

Pharmacology:
 Karbimazol
 Metimazol
 Propiltiourasil
Iodium radioactive (I131)
Thyrodectomy
Diseases ♂ 50 Weight fatigue lethargy Frequently
yrs old loss sleepy
man
DM Type 2 + + + + +
Addison’s + + + + +
Disease
Graves _ + + + _
Disease
Struma + + + + _
Goiter

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