Pathology of Endocrine SYSTEM of body and diseases associated with it.

4. “Highly integrated and widely distributed
group of organs that provides homeostasis
among various tissues”
 Signaling by Extracellular secreted
molecules:
 Autocrine
 Paracrine
 Endocrine-Hormones

5. “Secretory molecules that act on target cells
distant from their site of synthesis”
Two types:
 Interact with cell surface receptors
a) Peptide hormones i.e. Growth hormone and
insulin
b) Small molecules i.e. epinephrine
 Interact with intracellular receptors
a) Lipd soluble hormones i.e. thyroxine

7.  Bean-shaped structure at base of brain.
 Connected to Hypothalamus through a stalk
called Infundibulum.
 Two lobes:
 Adenohypophysis
 Neurohypophysis
 Release of trophic hormones is under
control of hypothalamic factors i.e either
stimulatory or inhibitory.

9.  Hyperpituitarism
 Excessive secretion of trophic hormone
 Causes:
 Anterior lobe pituitary adenoma
 Hypopituitarism
 Deficiency of trophic hormone
 Causes:
 Ischemic injury
 Surgery or radiation
 Inflammatory reactions

10.  Two bulky lateral lobes connected by isthmus
 Located below or anterior to larynx
 Lobules composed of dispersed follicles
 Follicles- cuboidal to low columnar
epithelium
 Thyroglobulin- presursor protein of thyroid
hormone

12.  Upregulation of carbohydrates and lipid
catabolism
 Stimulation of protein synthesis in wide
variety of cells
 Increase in basal metabolic rate

13.  Hyperthyroidism:
 Thyrotoxicosis due to elevated circulating
levels of free T3 and T4
 GRAVES Disease – autoimmune disease
 Autoantibodies to TSH receptor
 Activate TSH receptors on thyroid epithelial
cells leads to hyperthyroidism
 Hypertrophy and hyperplasia of follicles.
 Ophthalmopathy

14. Sympathetic
overstimulation.
Accumulation of
loose connective
tissue behind
orbits

15.  Inadequate levels of thyroid hormone.
 Cretinism – infants
 Iodine deficiency
 Impaired development of skeletal system and
CNS
 Goiter-impaired synthesis of thyroid
hormone
 Compensatory rise in TSH
 Enlargement of thyroid gland

16.  Pancreatic cells – islets of langerans
 Contain 4 cells
 Alpha cell releasing glucagon
 Beta cell releasing insulin
 Delta cell releasing somatostatin
 PP cells releasing VIP

17.  Group of disorders with a common feature of
hyperlglycemia
 Caused by deficient production or action of
insulin
 Cause secondary damage to vital organs
 Kidneys – end stage renal disease
 Eyes – adult onset blindness
 Nerves – non traumatic lower extremity
amputation
 Blood vessels

18.  Type I – IDDM (20%)
 Type II – NIDDM (80-90%)
 Monogenic forms i.e MODY– rare

19.  Low level of glucose in body
 High levels of glucose in body
 Glucagon secretion
 Insulin secretion

21.  Type-1 diabetes mellitus
 Production of autoantibodies against b cells
of pancreas
 No insulin production
 Hyperglycaemia
 Type-2 diabetes mellitus
 Insulin production is sufficient
 Cells involved in glucose metabolism become
desensitized
 Do not respond to insulin
 Hyperglycaemia

22.  Target tissue fails to response insulin
 Decreased glucose uptake
 Gluconeogenesis
 Decreased glycolosis
 Decreased fatty acid oxidation

23.  Obesity - Increased body fat
 OUTCOMES:
 Insulin resistance
 Diabetes
 Cardiovascular diseases like hypertention and
hyperlipidemia

24.  Excess free fatty acids
 FFA in B cells – release of IL-1B and other pro
inflammatory cytokines – recruit
macrophages and T cells – B cell dysfunction
and insulin resistance
 Adipokines release from adipocyte cause B
cell dysfunction as described above.

25.  FFA and glucose in B cells – release of IL-1B
and other pro inflammatory cytokines –
recruit macrophages and T cells – further
cytokine production
 Amylin or IAPP release IL-IB
 Cause B cell dysfunction and hyperglycemia

26.  Multifactorial but main cause is
hyperglycemia and glucose toxicity
 3 pathways:
 Formation of advanced glycation end
products (AGEs)
 Activation of protein kinase C
 Disturbances in polyol pathways

27.  Diabetic nephropathy
 Retinopathy
 Hypertension
 Peripheral neuropathy
 Microangiopathy
 Macrovascular disease
 Myocardial infarction

28.  Ketoacidosis
 Diabetic coma
 Hyperosmolar non-ketotic coma
 Weakness

29.  Polyuria
 Polydipsia
 Polyphagia
 Ketoacidosis
 Metabolic derangements
 Glucose, fat and protein metabolism
 Glycosuria
 Osmotic diuresis

30.  Proteolysis
 Weightloss
 Muscle weakness
 Ketogenesis
 Ketonemia
 Ketonuria

32.  Polyuria
 Polydipsia
 Obesity
 Weakness
 Weight loss
 Hyperosmolar non-ketotic coma
 Dehydration
 Osmotic diuresis
 Urinary fliud loss

33.  Normal glucose level= 70-120mg/dl
 Random glucose level >200 or =200mg/dl
 Fasting glucose level >126 or =126mg/dl

34.  OGTT – oral glucose tolerance test
>200mg/dl or =200mg/dl
 Euglycemic fasting glucose level
<110mg/dl, OGTT<140mg/dl
 Prediabetes fasting glucose level >110
but<126 mg/dl , OGTT>140 &<200 mg/dl
 Glycaemic control- %age of glycosylated
hemoglobin (HbA1C)
 HbA1C<7 = tight glycaemic control

35.  Medical nutrition therapy
 Oral hypoglycaemic therapy
 Insulin therapy

36.  First line of defense for type-2 diabetics
 Adequate diet – low cholesterol intake
 Excursive
1. Weight reduction
2. Improves insulin sensitivity
3. Lower blood glucose level

37.  Metformin
 Type-2 diabetes
 Reduce hepatic glucose production
 Sulphonylureas
 Tolbutamide
 Tolazamide
 Increase insulin release
 Pramlintide
 Type-1 diabetes

38.  Type-1 diabetes main treatment
 Portable pen injectors
 Subcutaneous injection
 Insulin glargine……..

39.  Blood glucose monitoring
 Body weight monitoring
 Personal hygeine
 Healthy lifestyle
 Reducing excessive salt intake

40.  Paired organs having cortex and medulla
 Synthesize
1. Glucocorticoids
2. Mineralocorticoids
3. Sex steroids

41.  It can be :
 Primary hypoadrenalism
1. Acute adrenocortical insufficiency
2. Chronic adrenocortical insufficiency
 Secondary hypoadrenalism

42.  ADDISON DISEASE:
 Adrenal cortex destruction
 Causes
1. Autoimmune adrenalitis
2. Tuberculosis
3. AIDS
4. Fungal
5. Metastatic cancer

44.  It includes:
 Cushing syndrome
 Hyperaldosteronism
 Adrenogenital syndrome

45.  Elevated glucocorticoid levels
 Causes:
 Exogenous glucocorticoids
 Endogenous causes
-Primary hypothalamic-pituitary diseases
associated with hypersecretion of ACTH
-Secretion of ectopic ACTH by non-pituitary
neoplasm(tumor of thymus gland,
Small cell tumor of Lungs)
-Primary adrenocortical neoplasm (adenoma or
carcinoma)
-Primary cortical hyperplasia

46.  Small cell carcinoma of lungs
 Hypertention
 Weight gain
 Truncal obesity-moon faces (Fat redistribution)
 Buffalo hump(Fat mass at lower cervical and
upper lumbar vertebra)
 Atrophy
 Weakness
 Hyperglycemia
 Glucosuria
 Polydipsia (Excessive thirst)
 Diabetes

47. When you do not succeed in taking giant
steps on the road to your goal,
be satisfied with little steps,
and wait patiently till the time that you are
able to run, or better still, to fly.
Be satisfied to be a little bee in the hive who
will soon become a big bee capable of making
honey…
Thank you …
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