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ENDOCRINE,[object Object],SYSTEM,[object Object],HORMONES * HORMONES * HORMONES,[object Object],JANDUSAY * JAVIER * JOVEN * KAMIYA * KALAW,[object Object],LEONG * LLAMZON * LORENZO * LUKBAN,[object Object]
WHAT TO EXPECT:,[object Object],REPORT OBEJECTIVES,[object Object],SHORT REVIEW,[object Object],DISORDERS and DISEASES,[object Object],REPORT SUMMARY,[object Object]
To provide a short review on the Endocrine System,[object Object],To present preventive measures and cures,[object Object],REPORT OBEJECTIVES,[object Object],To discuss common & rare Endocrine diseases & disorders,[object Object],To familiarize students with Endocrine processes,[object Object],To discuss the effects on normal physiology,[object Object],To provide a short summary on the topics discussed,[object Object],REPORT*OBEJECTIVES,[object Object]
REVIEW,[object Object]
REVIEW,[object Object],ENDOCRINOLOGY,[object Object],VS.,[object Object],neurons,[object Object],hormones,[object Object]
REVIEW,[object Object],ENDOCRINOLOGY,[object Object],VS.,[object Object],long-lasting,[object Object],nervous,[object Object],endocrine,[object Object],fast,[object Object]
REVIEW,[object Object],ENDOCRINOLOGY,[object Object],NEGATIVE,[object Object],FEEDBACK,[object Object],MECHANISM,[object Object]
Hormone Summary,[object Object],ENDOCRINOLOGY,[object Object]
DISEASES,[object Object],AND,[object Object],DISORDERS,[object Object]
DISEASES&DISORDERS,[object Object],PITUITARY GLAND,[object Object],THYROID GLAND,[object Object],PARATHYROID GLAND,[object Object],ADRENAL GLAND,[object Object],PANCREATIC ISLET,[object Object],SEX HORMONES,[object Object]
PITUITARY GLAND,[object Object],DWARFISM & GIANTISM,[object Object],DIABETES INSIPIDUS,[object Object]
PITUITARY GLAND,[object Object],DWARFISM & GIANTISM,[object Object],DIABETES INSIPIDUS,[object Object]
Pituitary Gland Disorders ,[object Object],Diabetes Insipidus,[object Object]
Diabetes Insipidus,[object Object],-(“diabetes”= overflow, “insipidus”= tasteless),[object Object],-most common abnormality associated with the dysfunction of the posterior pituitary,[object Object],-due to defects in antidiuretic hormone receptors or inability to secrete ADH,[object Object],-can be neurogenic (or central) or nephrogenic,[object Object]
Diabetes InsipidusHow does the normal physiology is disrupted?,[object Object]
Diabetes Insipidus,[object Object],Symptoms:,[object Object],	- excretion of large volumes of urine with resulting dehydration and thirst,[object Object],	- bed-wetting,[object Object]
How can normal physiology be regained?,[object Object],[object Object]
Subcutaneous injection or nasal application of ADH analogs
Restriction of salt in the diet and diuretic drugs,[object Object]
Pancreatic Islet Disorder,[object Object],Hyperinsulinism,[object Object],[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,[object Object]
3. Hyperinsulinism,[object Object],How can normal physiology be regained?,[object Object],	- immediate intravenous administration of large quantities of glucose,[object Object],- administration of glucagon (or, less effectively of epinephrine) can cause glycogenolysis in the liver  and thereby increase blood glucose level extremely rapidly,[object Object],**Permanent damage to the neuronal cells of the nerous system  usually occurs when treatment is not given immediately.,[object Object]
DISEASES&DISORDERS,[object Object],PITUITARY GLAND,[object Object],THYROID GLAND,[object Object],PARATHYROID GLAND,[object Object],ADRENAL GLAND,[object Object],PANCREATIC ISLET,[object Object],SEX HORMONES,[object Object]
THYROID GLAND,[object Object],GOITER,[object Object],HYPERTHYROIDISM,[object Object],HYPOTHYROIDISM,[object Object]
GOITER,[object Object],WHY, YES. THIS IS A….,[object Object],GOITER?,[object Object],WHAT IS A GOITER?,[object Object],ENLARGEMENT,[object Object],OF THE,[object Object],THYROID.,[object Object]
GOITER,[object Object],SYMPTOMS,[object Object],NORMAL PHYSIOLOGY,[object Object],Thyroid Hormones (T3 & T4) ,[object Object],- produced by cells in thyroid gland,[object Object],- regulated by thyroid stimulating hormone (TSH),[object Object],- produced through the attachment of ,[object Object],iodine atoms to ring structures of T3 and T4,[object Object],AHEM! AHEM!,[object Object],Breathing and swallowing difficulties,[object Object],Coughing and hoarseness,[object Object]
CAUSES,[object Object],TREATMENT,[object Object],POSSIBLE COMPLICATIONS,[object Object],GOITER,[object Object],HYPERTHYROIDISM,[object Object],Surgery- thyroidectomy ,[object Object],Lugol’s Iodine,[object Object],Radiocative Iodine ,[object Object],HYPOTHYROIDISM,[object Object]
WHAT,[object Object],OVERACTIVE,[object Object],TISSUE IN THE,[object Object],HYPERTHYROIDISM,[object Object],THYROID GLAND,[object Object],PRODUCING,[object Object],T3,[object Object],TOO MUCH,[object Object],T4,[object Object],AND,[object Object],TRIIODOTHYRONINE,[object Object],& THYROXINE,[object Object]
CAUSES,[object Object],GRAVE’S DISEASE,[object Object],TOXIC THYROID ADENOMA,[object Object],NORMAL?,[object Object],THYROIDITIS,[object Object],WHAT,[object Object],WHAT,[object Object],WHAT,[object Object],SYMPTOMS?,[object Object],HIGH EXCITABILITY; METABOLISM,[object Object],MILD TO EXTREME WEIGHT LOSS,[object Object],MUSCLE WEAKNESS; TREMORS,[object Object]
DEVELOPMENT OF,[object Object],PROTRUSION OF EYEBALLS,[object Object],exophthalmos,[object Object],EDEMATOUS,[object Object],TISSUES &,[object Object],DEGENERATIVE,[object Object],MUSCLES,[object Object],TREATMENT!,[object Object],SURGICAL REMOVAL OF GLAND,[object Object],LESSEN IODINE INTAKE,[object Object]
HYPOTHYROIDISM,[object Object],T3,[object Object],T4,[object Object],TOO LITTLE,[object Object],AND,[object Object]
AUTOIMMUNITY,[object Object],AGAINST THE ,[object Object],THYROID,[object Object],=DETERIORATION,[object Object],AUTOIMMUNITY,[object Object],CAUSES,[object Object],ASSOCIATED WITH,[object Object],THYROID GOITER,[object Object]
IODINE DEFICIENT,[object Object],ENDEMIC COLLOID &,[object Object],IDIOPATHIC NONTOXIC,[object Object],GOITER,[object Object],NOT IODINE DEFICIENT,[object Object],THYROID GOITER,[object Object]
SYMPTOMS?,[object Object],FATIGUE; SLEEPINESS; SLUGGISH,[object Object],WEIGHT GAIN; CONSTIPATION,[object Object],FAILURE OF TROPHIC FUNCTIONS,[object Object],myxedema,[object Object],AND,[object Object],TREATMENT!,[object Object],MORE IODINE,[object Object],ORAL MEDICATON,[object Object]
DISEASES&DISORDERS,[object Object],PITUITARY GLAND,[object Object],THYROID GLAND,[object Object],PARATHYROID GLAND,[object Object],ADRENAL GLAND,[object Object],PANCREATIC ISLET,[object Object],SEX HORMONES,[object Object]
PARATHYROID GLAND,[object Object],HYPOPARATHYROIDISM,[object Object],HYPERPARATHYROIDISM,[object Object]
FUNCTION &NORMAL PHYSIOLOGY,[object Object],PARATHYROID GLAND,[object Object],* control calcium within the blood. ,[object Object],* control how much calcium is in the bones, ,[object Object],and therefore, how strong and dense the bones are!,[object Object],* As the blood filters through the parathyroid glands, ,[object Object],they detect the amount of calcium present in the blood ,[object Object], making more or less parathyroid hormone (PTH).  ,[object Object],Calcium level in the blood is too low: the parathyroid cells make more parathyroid hormone. ,[object Object]
PARATHYROID GLAND,[object Object],…occurs when your parathyroid glands make too much PT,[object Object],and cause you to have too much calcium in the bloodstream. ,[object Object],CAUSES OF TOO MUCH PTH:,[object Object],Growth on the parathyroid glands! ,[object Object],Enlargement of 2 or more of the parathyroid glands!,[object Object],  OR medical conditions (like, lessay, kidney failure and rickets...),[object Object], ,[object Object],HYPOPARATHYROIDISM,[object Object],HYPERPARATHYROIDISM,[object Object]
HYPERPARATHYROIDISM,[object Object],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.,[object Object],PHYSIOLOGY&IMPLICATIONS,[object Object]
HYPERPARATHYROIDISM,[object Object],Feeling weak or tired most of the time,[object Object],General aches and pains,[object Object],Frequent heartburn ,[object Object],Nausea & Vomiting; Loss of appetite,[object Object],An increase in bone fractures or breaks,[object Object],Confusion and memory loss,[object Object],Kidney stones; Excessive urination,[object Object],High blood pressure,[object Object],THE SYMPTOMS,[object Object]
HYPERPARATHYROIDISM,[object Object],SURGERY,[object Object],DRINK PLENTY OF WATER,[object Object],LIMIT INTAKE OF CALCIUM AND VITAMIN D,[object Object],DO NOT SMOKE,[object Object],EXERCISE DAILY,[object Object],TREATMENT,[object Object]
HYPERPARATHYROIDISM,[object Object]
PARATHYROID GLAND,[object Object],HYPOPARATHYROIDISM,[object Object],HYPERPARATHYROIDISM,[object Object]
HYPOPARATHYROIDISM,[object Object],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.,[object Object],The low production of parathyroid hormone in hypoparathyroidism leads to abnormally ,[object Object],low ionized calcium levels in your blood and bones ,[object Object],and to an increased amount of phosphorus.,[object Object],PHYSIOLOGY&IMPLICATIONS,[object Object]
HYPOPARATHYROIDISM,[object Object],Tingling or burning (paresthesias) ,[object Object],Muscle aches or cramps; Twitching or spasms ,[object Object],Fatigue or weakness,[object Object],Painful menstruation,[object Object],Patchy hair loss, such as thinning of your eyebrows,[object Object],Dry, coarse skin; Brittle nails,[object Object],Headaches; Depression, mood swings,[object Object],Memory problems,[object Object],THE SYMPTOMS,[object Object]
HYPOPARATHYROIDISM,[object Object],RESTORE THE CALCIUM ,[object Object],AND MINERAL BALANCE IN THE BODY.,[object Object],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.,[object Object],TREATMENT,[object Object]
HYPOPARATHYROIDISM,[object Object]
HEP!,[object Object],HEP!,[object Object],HEP!,[object Object],HAVE YOO BEEN LISTENING? ,[object Object],Test your knowledge and try your luck…,[object Object],With our game!,[object Object]
DISEASES&DISORDERS,[object Object],PITUITARY GLAND,[object Object],THYROID GLAND,[object Object],PARATHYROID GLAND,[object Object],ADRENAL GLAND,[object Object],PANCREATIC ISLET,[object Object],SEX HORMONES,[object Object]
CUSHING’S SYNDROME,[object Object],CUSHING’S DISEASE,[object Object],ADRENAL GLAND,[object Object],ADDISON’S DISEASE,[object Object]
SYNDROME,[object Object],CUSHING’S,[object Object]
[object Object]
Characterized by high plasma levels of ACTH and cortisol
Another name hypercortisolism
Can occur from multiple causes including:Adenomas of the anterior pituitary that secrete large amounts of ACTH,[object Object],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,[object Object],Adenomas of the adrenal cortex,[object Object],CUSHING’S,[object Object]
High blood pressure.,[object Object],High blood sugar.,[object Object],Suppressed immunity (and more infections).,[object Object],Insulin resistance ,[object Object],Suppressed sex hormones and reduced libido.,[object Object],Suppressed thyroid hormones.,[object Object],  - 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.,[object Object],CUSHING’S,[object Object],SYMPTOMS,[object Object]
CUSHING’S,[object Object],DISEASE,[object Object]
CUSHING’S,[object Object],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.,[object Object],TREATMENT,[object Object]
ADDISON’S,[object Object],DISEASE,[object Object]
Addison's disease results from damage to the adrenal cortex.,[object Object], This damage may be caused by the following:,[object Object],The immune system mistakenly attacking the gland (autoimmune disease),[object Object],Infections such as tuberculosis, HIV, or fungal infections,[object Object],Hemorrhage, blood loss,[object Object],Tumors,[object Object],Use of blood-thinning drugs (anticoagulants) ,[object Object],A disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands.  ,[object Object],It may be due to :,[object Object],a disorder of the adrenal glands themselves (primary adrenal insufficiency) or ,[object Object], inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency),[object Object],ADDISON’S,[object Object]
ADDISON’S,[object Object],[object Object]
Chronic diarrhea
Darkening of the skin ; Paleness
Extreme Weakness
Unintentional weight loss
Mouth lesions on the inside of a cheek
Nausea and vomiting
Salt craving
Slow, sluggish movementSYMPTOMS,[object Object]
ADDISON’S,[object Object],Taking hormones to replace the insufficient amounts being made by your adrenal glands (glucocorticoids (cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone)),[object Object],TREATMENT,[object Object]
DISEASES&DISORDERS,[object Object],PITUITARY GLAND,[object Object],THYROID GLAND,[object Object],PARATHYROID GLAND,[object Object],ADRENAL GLAND,[object Object],PANCREATIC ISLET,[object Object],SEX HORMONES,[object Object]
DIABETES MELLITUS,[object Object],PANCREATIC ISLET,[object Object]
PH 131 - Endocrine Pathophysiology Report
PANCREAS,[object Object],retroperitoneal,[object Object],Exocrine gland,[object Object],Endocrine gland,[object Object],-98% of the secreting cells in the pancreas make digestive enzymes ,[object Object],-2% of the cells make hormones that are secreted into the portal vein,[object Object]
Pancreatic Hormones,[object Object]
Normal Physiology,[object Object], Circulating glucose is derived from three sources:,[object Object],1.  intestinal absorption during the fed state,[object Object],	2.  glycogenolysis -breakdown of glycogen,[object Object],	3.  gluconeogenesis -formation of glucose primarily from 	lactate and amino acids during the fasting state,[object Object],insulin is the key regulatory hormone of glucose disappearance (hypoglycemic hormone), and glucagon is a major regulator of glucose appearance (extremely potent hyperglycemic agent),[object Object]
PH 131 - Endocrine Pathophysiology Report
Disruptions on Physiology,[object Object]
Insulin and glucagon ,[object Object],antagonistic interaction,[object Object],humoral stimuli   ,[object Object],potent regulators ,[object Object],of glucose metabolism,[object Object],bi-hormonal ,[object Object],definition of diabetes:,[object Object],diabetic state = insulin deficiency ,[object Object],+ glucagon excess,[object Object]
Diabetes [Mellitus] Pathophysiology,[object Object]
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
NOTE:,[object Object],TYPE1 – noticeable early ,[object Object],symptoms,[object Object],TYPE2 – may occur without  ,[object Object],or gradual development of symptoms,[object Object]

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