MOA OF JAUNDICE

1) The major source of hemeprotein and senescent red blood cells

2) Heme were breakdown into unconjugated bilirubin in the macrophage to reticulo-
endothelial system
3) Unconjugated bilirubin which is lipid soluble transport by albumin to the liver.
4) In the liver, bilirubin is taken up via facilitated diffusion and conjugated with glucuronic acid
which is more water soluble
5) Conjugated bilirubin is send to gallbladder and stored as bile and then secreted into the
small intestine
6) In small intestine, bacteria will remove the glucuronic acid and converted the bilirubin into
urobilinogen.
7) Urobilinogen is oxidized by the intestinal bacteria and eliminate via feces
8) Some of the urobilinogen is reabsorbed from the small intestine and enter the portal blood
of the liver.
9) A portion of urobilinogen in the liver will enter the enterohepatic urobilinogen cycle and the
remaining urobilinogen is transported by blood into the kidney.
10) In the kidney, it is converted into yellow bilirubin and when excreted give the characteristic
to urine colour

Disease of The Endocrine Gland

HYPOSECRETION & HYPERSECRETION

- Adenoma
- Insensitive to hormone
- Genetic defect
- Autoimmune response
- Hyperplasia / infection of the gland

Disease of The Anterior Pituitary

Hyperpituitarism – benign hormone secreting tumor

- Prolactinoma
- Corticotroph cell adenoma
- Gonadaotroph adenoma
- Thyrotroph adenoma
- Growth hormone producing adenoma

ADENOMA HORMONE SECRETED MANIFESTATION

Lactotroph Prolactin Infertility, libido, amenorrhea
Somatotroph Growth hormone Gigantism or acromegaly
Corticotroph ACTH – excess secretion of Cushing’s disease
glucocorticoids by adrenal
cortex
Thyrotroph TSH – increase secretion of Hyperthyroidism
thyroid hormone by throid
 gland
Gonadotroph LH & FSH – little hormonal Neurologic symptom
effect

HYPOPITUITARISM

Factor

- Radiation therapy
- Pituitary infarction
- Nonfunctioning pituitary adenomas

Lack of hormone Manifestations

Prolactin Failure of post – partum lactation
Growth hormone Pituitary dwarfism
ACTH Hypoadrenalism / Addison disease
LH/FSH Decrease libido
TSH Hypothyroidism

Disease of the Posterior Pituitary

Diabetes Insipidus SIADH

About Neurogenic DI  Hypersecretion of ADH
 Hyposecretion of ADH  Secretion of etopic ADH by
 Due to inability to secrete ADH malignant neoplasm
– brain tumour, surgery  Local injury to
inflammation hypothalamus
Nephrogenic DI
- Kidney not respone to ADH
- Kidney damage
Symptoms  High output of dilute urine  Cerebral edema
 Dehydration & thirst  Neurologic dysfunction
 Bed -wetting  Low sodium in blood

THYROID GLAND
 THYROID GLAND PARATHYROID GLAND

HYPERTHYRODISM  Graves’ disease – autoimmune HYPOPARATHYRODISM 

Hyposecretion of PTH
disease – produce TSI that 
Decrease calcium
mimics the action of TSH level
 Functioning adenoma –  Muscle fibre able to
overactive thyroid nodule – depolarize
produce TH independently  Muscle spasm
 Thyroiditis – stored TH leak into Causes
TG - Postsurgical
 Treatment induce - Autoimmune
hyperthyroidism - Postradiation
- Heavy metal
deposition
HYPOTHYROIDISM  Hashimoto’s thyroiditis – HYPERPARATHYRODISM  Overactive parathyroid
autoimmune disorder gland
 Thyroid surgery  High level of PTH
 Radiation therapy  Promote kidney stone
 Pituitary disorder formation.
 Treatment for hyperthyroidism  Promote osteoclast

Primary
hyperparathyroidism
- Overactive PTG
- Causes – adenoma,
hyperplasia of
thyroid gland,
cancer of PTG
Secondary hyperthyroidism
- Causes – kidney
failure, severe
calcium & vit D
deficiency

DISEASE OF THE ADRENAL GLANDS

Cushing’s syndrome Addison’s disease Pheochromocytomas

About  Prolonged exposure to  Adrenal insufficiency  Benign tumors

high level of cortisol  Lack of cortisol or of the
aldosterone chromaffin cells
of adrenal
medulla
Causes  ACTH – dependant  Autoimmune  Hypersecretion
 ACTH – independent adrenalitis of E & NE
 Tuberculosis
  Cancer
 Adrenal haemorrhage
 Amyloidosis
Symptoms  Acne  Hypoglycemia  Prolonged fight-
 Increased facial hair  GI disturbance fight response
 Striae of skin  Weight loss  Paid heart rate
 Easy bruising – skin  Change in distribution  Rapid BP
become thin and of hair  Nervousness
friable  Weakness  Sweating
 Buffalo bump –
accumulation of fat
collects below the
back of the neck
 Muscle weakness

DIABETES MELLITUS

 Hyperglycemia – defects in insulin secretion, insulin action (insulin resistance)

 Classic symptoms
- Polyuria – excessive urine production
- Polydipsia – excessive thirst
- Polyphagia – excessive hunger

TYPE 1 DM TYPE 2 DM
- Juvenile - Adult onset
- Autoimmune destruction of pancreatic - Insulin level normal or elevated but
beta cells there is either a decrease in number of
- Individual has absolute insulin insulin receptors / cells cannot take it
deficiency and no longer produce up
insulin - Arises from combination of insulin
- Depend on exogenous administer resistance and B – cell dysfunction
insulin