PH 131 - Endocrine Pathophysiology Report

ENDOCRINE SYSTEM HORMONES * HORMONES * HORMONES JANDUSAY * JAVIER * JOVEN * KAMIYA * KALAW LEONG * LLAMZON * LORENZO * LUKBAN

WHAT TO EXPECT: REPORT OBEJECTIVES SHORT REVIEW DISORDERS and DISEASES REPORT SUMMARY

To provide a short review on the Endocrine System To present preventive measures and cures REPORT OBEJECTIVES To discuss common & rare Endocrine diseases & disorders To familiarize students with Endocrine processes To discuss the effects on normal physiology To provide a short summary on the topics discussed REPORT*OBEJECTIVES

REVIEW ENDOCRINOLOGY VS. neurons hormones

REVIEW ENDOCRINOLOGY VS. long-lasting nervous endocrine fast

REVIEW ENDOCRINOLOGY NEGATIVE FEEDBACK MECHANISM

DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

PITUITARY GLAND DWARFISM & GIANTISM DIABETES INSIPIDUS

Pituitary Gland Disorders Diabetes Insipidus

Diabetes Insipidus -(“diabetes”= overflow, “insipidus”= tasteless) -most common abnormality associated with the dysfunction of the posterior pituitary -due to defects in antidiuretic hormone receptors or inability to secrete ADH -can be neurogenic (or central) or nephrogenic

Diabetes InsipidusHow does the normal physiology is disrupted?

Diabetes Insipidus Symptoms: - excretion of large volumes of urine with resulting dehydration and thirst - bed-wetting

How can normal physiology be regained? ,[object Object]

Subcutaneous injection or nasal application of ADH analogs

Restriction of salt in the diet and diuretic drugs,[object Object]

Pancreatic Islet Disorder Hyperinsulinism ,[object Object]

Usually causes Type 2 diabetes

Occurs when there is reduced sensitivity of diabetics who undergo insulin therapy

Can also occur when insulin is injected by non-diabetics. This is usually done by athletes who are trying to enhance their overall anaerobic performances. ,[object Object]

3. Hyperinsulinism How can normal physiology be regained? - immediate intravenous administration of large quantities of glucose - administration of glucagon (or, less effectively of epinephrine) can cause glycogenolysis in the liver and thereby increase blood glucose level extremely rapidly **Permanent damage to the neuronal cells of the nerous system usually occurs when treatment is not given immediately.

THYROID GLAND GOITER HYPERTHYROIDISM HYPOTHYROIDISM

GOITER WHY, YES. THIS IS A…. GOITER? WHAT IS A GOITER? ENLARGEMENT OF THE THYROID.

GOITER SYMPTOMS NORMAL PHYSIOLOGY Thyroid Hormones (T3 & T4) - produced by cells in thyroid gland - regulated by thyroid stimulating hormone (TSH) - produced through the attachment of iodine atoms to ring structures of T3 and T4 AHEM! AHEM! Breathing and swallowing difficulties Coughing and hoarseness

CAUSES TREATMENT POSSIBLE COMPLICATIONS GOITER HYPERTHYROIDISM Surgery- thyroidectomy Lugol’s Iodine Radiocative Iodine HYPOTHYROIDISM

WHAT OVERACTIVE TISSUE IN THE HYPERTHYROIDISM THYROID GLAND PRODUCING T3 TOO MUCH T4 AND TRIIODOTHYRONINE & THYROXINE

CAUSES GRAVE’S DISEASE TOXIC THYROID ADENOMA NORMAL? THYROIDITIS WHAT WHAT WHAT SYMPTOMS? HIGH EXCITABILITY; METABOLISM MILD TO EXTREME WEIGHT LOSS MUSCLE WEAKNESS; TREMORS

DEVELOPMENT OF PROTRUSION OF EYEBALLS exophthalmos EDEMATOUS TISSUES & DEGENERATIVE MUSCLES TREATMENT! SURGICAL REMOVAL OF GLAND LESSEN IODINE INTAKE

HYPOTHYROIDISM T3 T4 TOO LITTLE AND

AUTOIMMUNITY AGAINST THE THYROID =DETERIORATION AUTOIMMUNITY CAUSES ASSOCIATED WITH THYROID GOITER

IODINE DEFICIENT ENDEMIC COLLOID & IDIOPATHIC NONTOXIC GOITER NOT IODINE DEFICIENT THYROID GOITER

SYMPTOMS? FATIGUE; SLEEPINESS; SLUGGISH WEIGHT GAIN; CONSTIPATION FAILURE OF TROPHIC FUNCTIONS myxedema AND TREATMENT! MORE IODINE ORAL MEDICATON

PARATHYROID GLAND HYPOPARATHYROIDISM HYPERPARATHYROIDISM

FUNCTION &NORMAL PHYSIOLOGY PARATHYROID GLAND * control calcium within the blood. * control how much calcium is in the bones, and therefore, how strong and dense the bones are! * As the blood filters through the parathyroid glands, they detect the amount of calcium present in the blood  making more or less parathyroid hormone (PTH). Calcium level in the blood is too low: the parathyroid cells make more parathyroid hormone.

PARATHYROID GLAND …occurs when your parathyroid glands make too much PT and cause you to have too much calcium in the bloodstream. CAUSES OF TOO MUCH PTH: Growth on the parathyroid glands! Enlargement of 2 or more of the parathyroid glands! OR medical conditions (like, lessay, kidney failure and rickets...) HYPOPARATHYROIDISM HYPERPARATHYROIDISM

HYPERPARATHYROIDISM Normally, the amount of calcium going into your bones matches the amount of calcium passing out of your bones. This means that the amount of calcium in your bones should stay about the same all the time. If you have hyperparathyroidism, more calcium is coming out of your bones than is going back in. When this happens, your bones might hurt, ache or become weak. Weak bones break more easily and heal slower than normal bones. PHYSIOLOGY&IMPLICATIONS

HYPERPARATHYROIDISM Feeling weak or tired most of the time General aches and pains Frequent heartburn Nausea & Vomiting; Loss of appetite An increase in bone fractures or breaks Confusion and memory loss Kidney stones; Excessive urination High blood pressure THE SYMPTOMS

HYPERPARATHYROIDISM SURGERY DRINK PLENTY OF WATER LIMIT INTAKE OF CALCIUM AND VITAMIN D DO NOT SMOKE EXERCISE DAILY TREATMENT

HYPOPARATHYROIDISM Hypoparathyroidism is a rare conditionin which your body secretes abnormally low levels of parathyroid hormone (parathormone). This hormone plays a key role in regulating and maintaining a balance of your body's levels of two minerals — calcium and phosphorus. The low production of parathyroid hormone in hypoparathyroidism leads to abnormally low ionized calcium levels in your blood and bones and to an increased amount of phosphorus. PHYSIOLOGY&IMPLICATIONS

HYPOPARATHYROIDISM Tingling or burning (paresthesias) Muscle aches or cramps; Twitching or spasms Fatigue or weakness Painful menstruation Patchy hair loss, such as thinning of your eyebrows Dry, coarse skin; Brittle nails Headaches; Depression, mood swings Memory problems THE SYMPTOMS

HYPOPARATHYROIDISM RESTORE THE CALCIUM AND MINERAL BALANCE IN THE BODY. Treatment involves calcium carbonate and vitamin D supplements, which usually must be taken for life. Blood levels are measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is recommended. TREATMENT

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CUSHING’S SYNDROME CUSHING’S DISEASE ADRENAL GLAND ADDISON’S DISEASE

Characterized by high plasma levels of ACTH and cortisol

Can occur from multiple causes including:Adenomas of the anterior pituitary that secrete large amounts of ACTH Abnormal function of the hypothalamus that causes high levels of corticotrophin-releasing hormone (CRH) “ectopic secretion” of ACTH by a tumor elsewhere in the body Adenomas of the adrenal cortex CUSHING’S

High blood pressure. High blood sugar. Suppressed immunity (and more infections). Insulin resistance Suppressed sex hormones and reduced libido. Suppressed thyroid hormones. - A round, red, full face, often called a "moon" face. - Muscle weakness and thin limbs. - Growth of fine hair on the face, upper back, or arms. - A lump of fat (buffalo hump) on the back of the neck. - Stretch marks over abdomen. CUSHING’S SYMPTOMS

CUSHING’S Cushing's syndrome is treated by restoring a normal balance of hormones. This may involve surgery, radiation treatments or drugs. Tumors on the adrenal glands are removed by surgery. If there is a tumor on just one adrenal gland, the other gland usually shrinks and ceases normal productivity. TREATMENT

Addison's disease results from damage to the adrenal cortex. This damage may be caused by the following: The immune system mistakenly attacking the gland (autoimmune disease) Infections such as tuberculosis, HIV, or fungal infections Hemorrhage, blood loss Tumors Use of blood-thinning drugs (anticoagulants) A disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands. It may be due to : a disorder of the adrenal glands themselves (primary adrenal insufficiency) or inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency) ADDISON’S

Darkening of the skin ; Paleness

Mouth lesions on the inside of a cheek

Slow, sluggish movementSYMPTOMS

ADDISON’S Taking hormones to replace the insufficient amounts being made by your adrenal glands (glucocorticoids (cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone)) TREATMENT

DIABETES MELLITUS PANCREATIC ISLET

PANCREAS retroperitoneal Exocrine gland Endocrine gland -98% of the secreting cells in the pancreas make digestive enzymes -2% of the cells make hormones that are secreted into the portal vein

Normal Physiology Circulating glucose is derived from three sources: 1. intestinal absorption during the fed state 2. glycogenolysis -breakdown of glycogen 3. gluconeogenesis -formation of glucose primarily from lactate and amino acids during the fasting state insulin is the key regulatory hormone of glucose disappearance (hypoglycemic hormone), and glucagon is a major regulator of glucose appearance (extremely potent hyperglycemic agent)

Insulin and glucagon antagonistic interaction humoral stimuli potent regulators of glucose metabolism bi-hormonal definition of diabetes: diabetic state = insulin deficiency + glucagon excess

Diabetes [Mellitus] Pathophysiology

NOTE: TYPE1 – noticeable early symptoms TYPE2 – may occur without or gradual development of symptoms

PH 131 - Endocrine Pathophysiology Report

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PH 131 - Endocrine Pathophysiology Report