ENDOCRINE

By: Sonny M. Moreno

Scope 

Physiology  Disorders
ADH ADRENAL GLANDS THYROID PARATHYROID PANCREAS

³The Sequence´ 
Hypothalamus  Pituitary Gland or Hypophysis Anterior or Adenohypophysis Posterior or Neurohypophysis  Target Glands

APG 
       TSH ACTH ICSH FSH LH MSH PROLACTIN GH

PPG 
ADH  OXYTOCIN

TARGET GLANDS 
        Thyroid Adrenal Mammary Skin Bones Ovaries Testes Kidney tubules Uterus

Pancreas 
Alpha ± Glucagon - glucose  Beta ± Insulin - glucose  Delta - Somatostatin ± growth hormone

ADH Abnormality 
SIADH  DI 

  



SIADH Syndrome of Inappropriate Anti Diuretic Hormone Increased secretion of ADH Increased tubular reabsorption = increased blood volume (low Hct, hypoosmolality, edema) Decreased urine output = concentrated urine (high S.G., dark urine) Watch out for manifestations of Fluid Volume Excess Caused: over medication of vasopressin and benign pituitary tumor

Con¶t 
Management:  FVE intervention  Stop vasopressin  Surgery (tumor excision)  Critical conditions:  Pulmonary edema  Cerebral edema  Heart failure  Hypertension  Renal Failure

DI Diabetes Insipidus 

Decreased ADH secretion  Decreased tubular reabsorption = decreased blood volume (high Hct, hyperosmolality, thrombosis)  Increased urine output = diluted urine (low S.G., clear urine)  Watch out for manifestations of Fluid Volume Deficit  Caused: trauma or injury to pituitary gland, resection of hypophysis, insensitivity of kidney to ADH

Con¶t 
Management:  FVD intervention  Synthetic ADH administration (vasopressin)  Critical conditions:  Thrombosis ± thromboembolism ± pulmonary embolism  Ischemia  Infarction  Necrosis (CVA, MI, RF)

ADRENAL GLAND Abnormality 
   
Conn¶s Cushing¶s Disease Cushing¶s Syndrome Addison¶s Disease Pheochromocytoma

Conn¶s Disease or Primary Hyperaldosteronism 
        

Adrenal cortex disorder Over secretion of aldosterone or mineralocorticoid Increased Na and H2O reabsorption=FVE Increased K urinary excretion=hypokalemia Watch out for manifestations of: SIADH Hypervolemia or FVE Hypokalemia (arrhythmias) Caused: tumor and trauma of the adrenal cortex

Con¶t 
     
Management: FVE intervention Stop sodium intake Critical conditions: Arrhythmias Hypertension Same with SIADH

Cushing¶s Disease 
       Adrenal cortex disorder Over secretion of Aldosterone=Na and H2O retention, K excretion Glucocorticoid=hyperglycemia Androgen male:gynecomastia female:hoarseness of voice, hirsutism Steroids=buffalo neck, trunkal obesity

Con¶t 
Management:  FVE intervention  Replace potassium  Insulin administration  Hypertension  Surgery is adrenalectomy  Critical conditions:  Arrhythmias due to hypoK  Hypertensive crisis  Fluid overload  Hyperglycemia

Cushing¶s Syndrome 
Pituitary gland disorder  Same with Cushing¶s Disease  Surgery is hypophysectomy

Addison¶s Disease 
Adrenal cortex disorder  Hyposecretion of:  Aldosterone=Na and H2O excretion, K reabsorption  Glucocorticoid=hypoglycemia  Androgen=decreased libido  o MSH=bronzing of the skin (primary)

Management 
  
FVD intervention Increase potassium excretion Glucagon or simple sugar administration Steroid medication

Critical Conditions 
   
Dehydration Arrhythmias due to hyperK Hypovolemic shock Hypoglycemia Same with DI

Note: 
inc ACTH, inc cortisol = pituitary problem (benign tumor)  normal ACTH, inc cortisol = adrenal problem (benign tumor)  dec ACTH, dec cortisol = atrophy of the pituitary gland  normal ACTH, dec cortisol = atrophy of the adrenal gland

Pheochromocytoma 
  
Hyperfunction of adrenal medulla ocatecholamines (nor E and E) S/sx: HPN, severe headache, osweat, n&v, anorexia, dilated pupuls, cold extremities, CHF and cerebral bleeding.

Dx 
oVMA vanilly mandelic acid (urine specimen)  ocatecholamines (blood specimen)  oblood sugar and glycosuria  (+) tumor  Drug of choice (regetine)  Surgical Intervention (adrenalectomy)

THYROID GLAND Abnormality 
Hypothyroidism  Hyperthyroidism
± Note: ± inc T3, inc T4, dec TSH = thyroid problem ± inc T3, inc T4, inc TSH = pituitary tumor (benign)

Hypothyroidism 
Caused by:  Autoimmune Disease (Hashimoto¶s Thyroiditis)  Use of radioactive iodine  Destruction or removal of thyroid tissue  Dietary iodide deficiency  Overtreatment of antithyroid drug

Manifestations 
      
Fatigue and lethargy Weight gain Cold hands and feet Decreased temp and pulse Cold intolerance Decreased attention span Decreased GIT peristaltic movement Constipation

Con¶t of s/sx 
SQ swelling, putty skin, putty skin, puffy eyelids  Thinning of hair, loss of lateral 1/3 of the eyebrow  Menorrhagia or amenorrhea, decreased libido, abortions  Myxedema = severe complication leads to coma

Management 
      
Symptomatic Thyroid hormone replacement T4 Synthroid, Levothyroid T3 Cytomel T3 & T4 Proloid T3 given NGT, faster than T4 T4 given parenterally (S.E. adrenal insuf.) Note: 3-12 wks S/Sx must disappear 3-

Hyperthyroidism 
Caused by:  Grave¶s Disease
± TSAb thyroid stimulating antibody duplicate ± TSH, which increases thyroid hormone sec. 

Toxic nodular goiter (benign, hot spot)  Overmedication of thyroid hormone 

     

Manifestations: Nervousness, tremors, emotional lability Weight loss, emaciated Flushed skin, warm and moist Increased temp and palpitation to atrial fib Heat intolerance Difficulty in sitting quietly 

Thyroid gland may be palpable and a (+) bruit  Diarrhea  Bulging eyes (exophthalmus), startled expression  Amenorrhea, oligomenorrhea, decreased libido  Delirium, disorientation, extreme nervousness  Arrhythmias  Thyroid storm = hyperpyrexia, diarrhea, dehydration,  tachycardia, arrhythmias, delirium, coma, shock, death 

       

Surgery: SSKI is given preop to dec thyroid vascularity Given with juice to disguise taste Given with straw to prevent staining of teeth Postop: Monitor for bleeding Check for tetany (parathyroid gland is severed) Hoarseness of voice-laryngeal nerve damage voiceWatchout thyroid crisis

Parathyroid Gland Abnormality 
Hypoparathyroidism  Hyperparathyroidism

Hypoparathyroidism 
Caused:  Accidental removal or destruction of parthyroid gland Primary  Thyroidectomy  Radical neck disection  Idiopathic  Autoimmune 

  

Diagnostic: Decreased serum Ca (7.5 mg/100 ml) Decreased PTH Increased PO4 

Manifestation:  Hypocalcemia  Tetany Chvostek¶s sign Trousseau¶s sign Laryngeal spasm  Severe anxiety and apprehension 

Management:  Treat the cause  IV calcium Syringe and ampule of Ca sol. on bed side  Oral Ca with vit D

Hyperparathyroidism 
        Caused: Primary adenoma hyperplasia Diagnostic: Increased vit D Increased PTH Increased serum Ca (11 mg/100 ml) Decreased PO4 

       

Manifestation: Hypercalcemia Decalcification of bone Fracture Deep bone pain Depression of neuromuscular function Generalized fatigue Memory loss Dec LOC, stupor coma 

       

Management: Treat the cause Hydration (IV saline) Diuretics (Ca excretion) Calcitonin (inhibits bone resorption) Dietary Ca restriction Avoid thiazide and vit D (may increase Ca) Dialysis Digitalis is withdrawn (may increase Ca)

Diabetes Mellitus 
DM is a disorder of glucose intolerance caused by a deficiency in insulin production and action resulting in hyperglycemia and abnormal CHO, CHON and fat metabolism.

Types 
Type I or IDDM no insulin diseased pancreas (beta cell)  Type II NIDDM decreased insulin inadequate insulin

IDDM 
   
Genetic and hereditary Zero insulin Coxsackie virus 4 P¶s with weight loss DKA

NIDDM 
    
Adult onset Genetic Insulin resistance Obesity 4 P¶s HHNKS or HONKS 

Diagnostic Evaluation:  Fasting Blood Sugar ± u 126 mg/dl for 2x NPO 8H  2H Postprandial Test ± u 200 mg/dl 75 gm of sugar orally then check after 2H  OGTT -u 200 mg/dl blood is withdrawn every hour (2H after) 

Random Blood Sugar ± u 200 mg/dl + 3 P¶s blood is withdrawn anytime  Glycosylated Hg A1C can detect average serum glucose level over preceding 2-3 months (most reliable) Adult 2.2%-4.0% 2.2%Children 1.8%-4.0% 1.8%-

About Insulin! 
Hyperinsulinism ± tremors, hunger and diaphoresis will manifest  Somogyi Phenomenon ± rebound hyperglycemia after insulin administration (gradual reduction of insulin is the key to manage it)  Insulin Pump ± external battery operated, needle is inserted SQ that delivers regular insulin (monitor hypokalemia)  Site ± abdomen (best site), upper arms, upper buttocks  Route ± SQ, only REGULAR insulin can be given as IV bolus (flush the line first it will absorb insulin) 

Lipodystrophy is a complication if the site of injection is not rotated properly, it can also alter the rate of insulin absorption.  Mixed Insulin ± regular (clear) first to be drawn followed by NPH (cloudy)  Refrigerate after use. 

IV bolus ± mixed with D5W if hypoglycemic, or PNSS ideal for DKA and HONKS  Pinch or 45r for thin patient, 45r 90r 90r for regular client  Good site must be supple skin. 

TYPES OF INSULIN 
  

ONSET PEAK DURATION Immediate Acting 5-25 min, 30-60 min, 5 hour 530Lispro Short Acting 1515-30min, 2-4 hours, 6-8 hours 26Humulin R, Regular, Semilente Intermediate 6060-90min, 4-12 hours, 18 hours 4Acting NPH Lente, Humulin N Long Acting 8 hours, 16-24 hours, 36 hours 16Ultra Lente

END

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