Endocrine System Revised

7/27/2019 Endocrine System Revised

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ENDOCRINE SYSTEM2011 COVERAGE ANATOMY AND PHYSIOLOGY PITUITARY DISORDERS ADH DISORDERS ADRENAL GLANDS DISORDERS THYROID GLAND DISORDERS PARATHYROID GLANDS DISORDERS DIABETES MELLITUS PITUITARY DISORDERS1. HYPERPITUITARISM2. HYPOPITUITARISM ADH DISORDERS1. SYNDROME OF INAPPROPRIATE ADH2. DIABETES INSIPIDUS ADRENAL GLANDS DISORDERS1. CONNS DISEASE2. CUSHINGS DISEASE3. ADDISONS DISEASE4. PHEOCHROMOCYTOMA THYROID GLAND DISORDERS1. GOITER2. HYPERTHYROIDISM3. HYPOTHYROIDISM

PARATHYROID GLANDS DISORDERS

1. HYPERPARATHYROIDISM2. HYPOPARATHYROIDISM DIABETES MELLITUS


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1. TYPE I2. TYPE II3. GESTATIONAL DM WHAT IS ENDOCRINE SYSTEM? IT IS A SYSTEM COMPOSED OF DIFFERENT ENDOCRINE ORGANS. RELEASES HORMONES INTO THE BLOOD STREAM. ITS A DUCTLESS SYSTEM HORMONES ARE CHEMICAL SUBSTANCES PRODUCED OR RELEASED BY AN ENDOCRINE ORGANS, ALSO KNOWN

AS THE MESSENGER.

ANATOMY AND PHYSIOLOGY HYPOTHALAMUS-PITUITARY AXIS

HYPOTHALAMUS PITUITARY GLAND

ANTERIOR PG OR ADENOHYPOPHYSIS TSH THYROID GLAND THYROID HORMONES ACTH ADRENAL CORTEX CORTISOL (AGA) GH BONES AND MUSCLES, GLUCAGON MSH SKIN - MELANIN FSH OVARY- ESTROGEN SPERM PRODUCTION LH GRAAFIAN FOLLICLE PROGESTERONE SPERM MATURATION PROLACTIN - BREAST MILK PRODUCTION

POSTERIOR PG OR NEUROHYPOPHYSIS ADH KIDNEYS (DCT) WATER REABSORPTION OXYTOCIN BREAST AND UTERUS - CONTRACTION HOW DOES IT WORK?

H

POSITIVE FEEDBACK ESTROGEN


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PROGESTERONE INHIBITORY FEEDBACK PROLACTIN OXYTOCIN NEGATIVE FEEDBACK MSH ADH GH ACTH TSH HYPOTHALAMUS - SPIN SENSOR OF HORMONAL FLUCTUATION POSITIVE FEEDBACK INHIBITORY FEEDBACK NEGATIVE FEEDBACK PITUITARY DISORDERS HYPOPITUITARISM HYPERPITUITARISM HYPOPITUITARISM CAUSE

SIMMONDS, SHEEHANS CHROMOPHOBIC PITUITARY TUMOR

DX USE THE S/SX MRI

S/SX OXY & PROLACTIN (GALACTORRHEA) FSH & LH (AMENORRHEA)


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MSH (ALBINISM) ACTH (ADDISONS) GH (DWARFISM) ADH (DI) TSH (HYPOTHYROIDISM) MX BROMOCRIPTINE TO LOWER PROLACTIN SANDOSTATIN TO REDUCE THE TUMOR SURGERY: TRANS SPHENOIDAL HYPOPHYSECTOMY HORMONE REPLACEMENT THERAPY SOMATOTROPIN TO REPLACE GH LEVOTHYROXINE TO REPLACE TH HYDROCORTISONE TO REPLCE CORTISOL VASOPRESSIN TO REPLACE ADH

HYPERPITUITARISM CAUSE

BASOPHILIC PIT. TUMOR ACIDOPHILIC PIT. TUMOR

DX USE THE S/SX MRI

S/SX FSH & LH (AMENORHEA) OXY & PROLACTIN (GALACTORRHEA) MSH (SKIN PIGMENTATION) ACTH (CUSHINGS) GH (GIGANTISM OR ACROMEGALY) ADH (SIADH)


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TSH (HYPERTHYROIDISM) MX BROMOCRIPTINE TO LOWER PROLACTIN AND GH SANDOSTATIN TO REDUCE THE TUMOR SURGERY: TRANSSPHENOIDAL HYPOPHYSECTOMY ACROMEGALY

ARTHRITIS CARPAL TUNNEL SYNDROME OSTEOPOROSIS KYPHOSIS HYPERTENSION ARTERIOSCLEROSIS HEART ENLARGEMENT HEART FAILURE AN ENLARGED JAW THICKENED TONGUE ENLARGED AND WEAKENED HANDS COARSENED FACIAL FEATURES OILY OR LEATHERY SKIN PROMINENT SUPRAORBITAL RIDGE PITUITARY DISORDERS HYPOPITUITARISM S/SX

OXY & PROLACTIN (GALACTORRHEA) FSH & LH (AMENORRHEA) MSH (ALBINISM) ACTH (ADDISONS) GH (DWARFISM)


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ADH (DI) TSH (HYPOTHYROIDISM)

HYPERPITUITARISM S/SX

) FSH & LH (AMENORHEA) OXY & PROLACTIN (GALACTORRHEA) MSH (SKIN PIGMENTATION) ACTH (CUSHINGS) OR ACROMEGALY) GH (GIGANTISM ADH (SIADH) TSH (HYPERTHYROIDISM

STEREOTAXIC HYPOPHYSECTOMY STEREOTAXIS IS A THREE-DIMENSIONAL AIMING TECHNIQUE USING X RAYS OR SCANS FOR GUIDANCE. INSTRUMENTS CAN BE PLACED IN THE BRAIN WITH PINPOINT ACCURACY THROUGH TINY HOLES IN THE SKULL. STEREOTAXIS IS ALSO USED TO DIRECT RADIATION WITH SIMILAR PRECISION USING A GAMMA KNIFE TRANSSPHENOIDAL HYPOPHYSECTOMY HYPOPHYSECTOMY IS A PROCEDURE TO ACCESS AND REMOVE THE PITUITARY GLAND (A). TO ACCESS IT, AN INCISION IS MADE BENEATH THE PATIENT'S UPPER LIP TO ENTER THE NASAL CAVITY (B). A SPECULUM IS INSERTED, AND SPECIAL FORCEPS ARE USED TO REMOVE THE PITUITARY TUMOR (C). TRANSSPHENOIDAL HYPOPHYSECTOMY PREOP DRUG:

BROMOCRIPTINE (PARLODEL) TO LOWER GH AND PROLACTIN OCTREOTIDE (SANDOSTATIN) TO REDUCE TUMOR

POSTOP CARE HEAD ELEVATION FOR 2 WEEKS NASAL PACKING, MOUTH CARE INCREASE ICP PRECAUTIONS OBSERVE FOR CSF LEAKAGE (HALO SIGN)


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WATCHOUT DIABETES INSIPIDUS-POLYURIA REHAB: LIFELONG SUPPLEMENT OF HORMONES, MAC ADH ABNORMALITY

DI

SIADH

DIABETES INSIPIDUS CAUSE: SURGERY, TRAUMA, TUMOR ADH S/SX FVD, HYPERNATREMIA

POLYURIA URINE OUTPUT, URINE SG BV, FVD, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD) THIRST

MANAGEMENT LIFE TIME PITRESSIN OR VASOPRESSIN FLUID RESUSCITATION

SYNDROME OF INAPPROPRIATE ANTI DIURETIC HORMONE CAUSE: TUMOR, DRUGS ADH S/SX FVE, HYPONATREMIA

OLIGURIA URINE OUTPUT, URINE SG BV, FVE, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD)

MANAGEMENT TRANSSPHENOIDAL HYPOPHYSECTOMY RESTRICT FLUIDS


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COMPARISONDI

CAUSE: SURGERY, TRAUMA, TUMOR ADH-POLYURIA S/SX FVD, HYPERNATREMIA

POLYURIA URINE OUTPUT, URINE SG BV, FVD, THIRST , HCT AND PLASMA OSMOLALITY SODIUM (BLOOD) MANAGEMENT LIFE TIME PITRESSIN OR VASOPRESSIN FLUID RESUSCITATION

SIADH

CAUSE: TUMOR, DRUGS ADH-OLIGURIA S/SX FVE, HYPONATREMIA

OLIGURIA URINE OUTPUT, URINE SG BV, FVE, HCT AND PLASMA OSMOLALITY SODIUM (BLOOD)

MANAGEMENT TRANSSPHENOIDAL HYPOPHYSECTOMY RESTRICT FLUIDS

ADRENAL GLANDSABNORMALITY

CONNS DISEASE CUSHINGS

PRIMARY (DISEASE) SECONDARY (SYNDROME)


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ADDISONS DISEASE PRIMARY SECONDARY

PHEOCHROMOCYTOMA CONNS DISEASE CAUSE:

PRIMARY (ADENOMA) HYPERSECRETIONS OF ALDOSTERONE ONLY

DX: SERUM ELECTROLYTES (NA, K) URINE ( ALDOSTERONE) IMAGING (MRI)

CONNS DISEASE S/SX AND INTERVENTION:

HYPERNATREMIA: NEUROLOGIC (SEIZURE)INTERVENTION: RESTRICT NA, NEUROLOGIC ASSESSMENT, SEIZURE PRECAUTIONS

FVE: HPN, EDEMA, CHFINTERVENTION: I&O, RESTRICT WATER, KVO, DIURETICS (K SPARER)

HYPOKALEMIA: INVERTED T WAVE, ARRHYTHMIAS, CARDIAC ARREST, CONSTIPATION, MUSCLEWEAKNESS

INTERVENTION: GIVE ORAL SUPPLEMENT, KALIUM DURULE (TABLET), IV KCL (INCORPORATED TO 1 L OF

PNSS), CARDIAC MONITOR,

CONNS DISEASE SURGERY:

BILATERAL ADRENALECTOMY (SCOPIC) POSTOP: WATCHOUT ADDISONS DISEASE S/SX REHAB: LIFETIME STEROIDS, MEDIC ALERT CARD (MAC), WATCHOUT ADDISONS AND CUSHINGS

CUSHINGS DISEASE CAUSE

PRIMARY: TUMOR AT THE ADRENAL CORTEX


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SECONDARY : TUMOR AT THE PITUITARY GLAND DX: DX: 24 HOUR URINE CORTISOL,

PLASMA CORTISOL,

DEXAMETHASONE SUPPRESSION ( ACTH: 2 C.D.)

S/SX CORTISOL - CATABOLISM ALDOSTERONE NA, H20, K GLUCOCORTICOID - HYPERGLYCEMIA ANDROGEN FEMALES ARE AFFECTED

MX PRIMARY: ADRENALECTOMY SECONDARY: HYPOPHYSECTOMY

ADDISONS DISEASE CAUSE

PRIMARY: ADRENAL CORTEX ATROPHY SECONDARY: PIT. GLAND ATROPHY

DX: 24 HOUR URINE CORTISOL, PLASMA CORTISOL,

ACTH STIMULATION TEST ( CORTISOL 1 A.D.)

S/SX CORTISOL - WEAKNESS ALDOSTERONE - NA, H20,K GLUCOCORTICOID - HYPOGLYCEMIA ANDROGEN MALES ARE AFFECTED

MX SYPMTOMATIC LIFETIME STEROIDS ADDISONIAN CRISIS

COMPARISON CUSHINGS DISEASE CAUSE


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PRIMARY: TUMOR AT THE ADRENAL CORTEX SECONDARY : TUMOR AT THE PITUITARY GLAND


DEXAMETHASONE SUPPRESSION

( ACTH: 2 C.D.)

S/SX CORTISOL ALDOSTERONE GLUCOCORTICOID ANDROGEN

MX PRIMARY: ADRENALECTOMY SECONDARY: HYPOPHYSECTOMY

ADDISONS DISEASE CAUSE

PRIMARY: ADRENAL CORTEX ATROPHY SECONDARY: PIT. GLAND ATROPHY


ACTH STIMULATION TEST

( CORTISOL 1 A.D.)

S/SX CORTISOL ALDOSTERONE GLUCOCORTICOID ANDROGEN

MX SYPMTOMATIC LIFETIME STEROIDS


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CUSHINGS DISEASE CAUSE DX S/SX CX MX MEDICAL MANAGEMENT:

1. MITOTANE ADRENAL CYTOTOXIC 2, METYRAPONE REDUCE HYPERADRENALISM CAUSED BY ECTOPIC ACTH 3. AMINOGLUTETHIMIDE (CYTADREN) ADRENAL STEROID INHIBITOR, ANTINEOPLASTIC

INSTRUCTION IN USING STEROIDS TAKEN IN THE MORNING INCREASED THE DOSE DURING HIGH LEVEL OF STRESS HIGHLY INDIVIDUALIZE (DOSING) WATCHOUT FOR SIDE EFFECTS:

CUSHINGOID (TRUNKAL OBESITY, MOON FACIE, BUFFALO HUMP) HIRSUTISM OR VIRILISM PANCYTOPENIA, GLAUCOMA, CORNEAL ULCERATION NOTE: S/SX OF CUSHINGS DISEASE STEROIDS SIDE EFFECTS

HYPERTENSION, THROMBOEMBOLISM WEIGHT GAIN, MOON FACE, TRUNKAL OBESITY, BUFFALO HUMP PRONE TO INFECTION GI BLEEDING GLAUCOMA, CORNEAL ULCERATION MUSCLE WASTING, POOR WOUND HEALING OSTEOPOROSIS HYPERGLYCEMIA


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ACNE VIRILIZATION (MUSCULINE EFFECT IN WOMEN) ADDISONS DISEASE PHEOCHROMOCYTOMA CAUSE: TUMOR IN THE ADRENAL MEDULLA DX: EPI AND NOR-E (BLOOD), CATECHOLAMINES - FROM E AND NOR-E (BLOOD), VANILLYL MANDELIC ACID VMA (URINE-24H COLLECTION) REFLECTION OF CATECHOLAMINES METANEPHRINE (24 H URINE) REFLECTION OF EPINEPHRINE PHEOCHROMOCYTOMA S/SX:

RELATED TO HIGH LEVEL OF EPINEPHRINE AND NOREPINEPHRINE HYPERTENSION, TACHYCARDIA, ARRHYTHMIAS (SYMPATHETIC RELATED ALSO), BLOOD SUGAR AND GLYCOSURIA

INTERVENTION: ER CASE DRUG OF CHOICE (REGETINE), SURGERY: BILATERAL ADRENALECTOMY

THYROID GLAND DISORDERS1. GOITER2. HYPERTHYROIDISM3. HYPOTHYROIDISM GOITER CAUSE:

IODINE DEFICIENT (40 FG/DAY OF IODINE) HYPOTHYROIDISM (COMPENSATORY ENLARGEMENT) HYPERTHYROIDISM (HYPERTROPHY)


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RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (COLD SPOT, N.T.N.G.) PBI, T3, T4

S/SX: BMR, MYXEDEMA COMA MX:

SYMPTOMATIC LIFE TIME SUPPLEMENT OF SYNTHETIC T3 AND T4

HYPERTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (GRAVES DISEASE) DX: RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (HOT SPOT, T.N.G.) PBI, T3, T4

S/SX: BMR, THYROID STORM MX:

SYMPTOMATIC ANTI-THYROID DRUGS RADIOACTIVE IODINE (HIGH) SURGICAL THYROIDECTOMY

HYPOTHYROIDISM CAUSE: AUTOIMMUNE DISEASE (HASHIMOTOS THYROIDITIS) DX: RADIOACTIVE IODINE UPTAKE (UPTAKE) THYROID SCAN (COLD SPOT, N.T.N.G.) PBI, T3, T4

S/SX: BMR, MYXEDEMA COMA MX:

SYMPTOMATIC


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LIFE TIME SUPPLEMENT OF SYNTHETIC T3 AND T4

HYPERTHYROID & HYPOTHYROID MANIFESTATIONS HYPERTHYROIDISM ANTI-THYROID DRUGS THIONAMIDES (PROPYLTHIOURACIL) METHIMAZOLE (TAPAZOLE), CARBIMAZOLE AXN: DEC SYNTHESIS OF THYROID HORMONES, MAY TAKE SEVERAL WEEKS TO TAKE EFFECT LIFETIME MEDS, 3X/DAY SIDE EFFECT:

AGRANULOCYTOSIS (REPORT SORE THROAT) LIVER DISEASE (JAUNDICE, ABDL PAIN)

RADIOACTIVE IODINE 123-I OR 131-I AXN: DESTROY THYROID TISSUE DISADVANTAGE: DESTRUCTION OF THE THYROID GLAND CAN NOT BE CONTROLLED AND IT MIGHT LEAD TO

SEVERITY OF THE ENTIRE GLAND

AVOID CONTACT WITH FECES AND URINE (FLUSH TOILET 2-3X) RADIOACTIVE IODINE PAINLESS PROCEDURE, 1 OR MORE CAPSULES TAKEN PO (LEAD CONTAINER) LIQUID FORM IS ALSO AVAILABLE RADIATION EMITTED IS ABLE TO REDUCE THE SIZE OF THE THYROID WASTES ARE EXCRETED VIA FECES, URINE, SWEAT, BREAST MILK AND SALIVA (RADIATION HAZARD) SAFETY PRIVATE ROOM (2-5 DAYS ISOLATION) SURGICAL THYROIDECTOMY SSKI SATURATED SOLUTION OF POTASSIUM IODIDE (LUGOLS) IS GIVEN PREOP TO DECREASE THYROID VASCULARITY GIVEN WITH JUICE TO DISGUISE TASTE, GIVEN WITH STRAW TO PREVENT STAINING OF TEETH SE: SIALORRHEA

IODISM OR IODINE TOXICITY (SWELLING OF BUCCAL MUCOSA, SALIVATION, CORYZA, SKIN ERUPTION)


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POSTOP: THYROIDECTOMY AIRWAY PATENCY MONITOR BLEEDING WATCHOUT THYROID CRISIS CHECK FOR TETANY (PARATHYROID GLAND IS SEVERED) HOARSENESS OF VOICE-LARYNGEAL NERVE DAMAGE POSITION: SUPINE OR SEMI FOWLERS, NO HYPERFLEXION AND HYPEREXTENSION OF THE NECK, HEAD

MIDLINE, NO PILLOW!!!

HYPOTHYROIDISM SYNTHETIC THYROID HORMONES LIFETIME MEDS, 3X/DAY T4 SYNTHROID, LEVOTHYROID T3 CYTOMEL T3 & T4 PROLOID T3 GIVEN NGT, FASTER THAN T4 T4 GIVEN PARENTERALLY SIDE EFFECT: ADRENAL INSUFFICIENCY NOTE: 3-12 WEEKS OF MEDICATIONS BEFORE SIGNS AND SYMPTOMS DISAPPEAR HYPERCALCEMIA CAUSE: HYPERPARATHYHROIDISM S/SX:

DEEP BONE PAIN

LITHIASIS FORMATION

HYPOPHOSPHATEMIA (LOW ENERGY STORE)

SHORTENED QT INTERVAL

MNGMT: PARATHYROIDECTOMY, HYDRATION, PREVENT FRACTURE REDUCE CA INTAKE, DIALYSIS HYPOCALCEMIA CAUSE: HYPOPARATHYHROIDISM S/SX:

TETANY: TINGLING, TROUSSEAU, CHVOSTEK AND LARYNGEAL SPASM


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HYPERPHOSPHATEMIA (WIDE CALCIFICATION)

LENGTHENED QT INTERVAL (TORSADES DE POINTES)

MNGMT: ORAL, TABLET AND IV )CALCIUM GLUCONATE)RESPIRATORY SUPPORT FOR LARYNGEAL SPASM

COMPARATIVELY HYPERCALCEMIA CAUSE: HYPERPARATHYHROIDISM S/SX:

DEEP BONE PAIN

LITHIASIS FORMATION

HYPOPHOSPHATEMIA (LOW ENERGY STORE)

SHORTENED QT INTERVAL

MNGMT: PARATHYROIDECTOMY, HYDRATION, PREVENT FRACTURE REDUCE CA INTAKE, DIALYSIS HYPOCALCEMIA CAUSE: HYPOPARATHYHROIDISM S/SX:

TETANY: TINGLING, TROUSSEAU, CHVOSTEK AND LARYNGEAL SPASM

HYPERPHOSPHATEMIA (WIDE CALCIFICATION)

LENGTHENED QT INTERVAL (TORSADES DE POINTES)

MNGMT: ORAL, TABLET AND IV )CALCIUM GLUCONATE)RESPIRATORY SUPPORT FOR LARYNGEAL SPASM

HYPOCALCEMIA

PARATHYROID GLANDS DISORDERS

1. HYPERPARATHYROIDISM2. HYPOPARATHYROIDISM DIABETES MELLITUS1. TYPE I2. TYPE II3. GESTATIONAL DM PHYSIOLOGY ALPHA CELL

GLUCAGON (GLYCOGENOLYSIS)


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BLOOD SUGAR BETA CELL-

INSULIN (GLYCOGENESIS) BLOOD SUGAR

DELTA CELL- SOMATOSTATIN INHIBITORY TO GH AND TSH

PHYSIOLOGY OF GLUCAGON PHYSIOLOGY OF INSULIN TERMINOLOGIES GLYCOGENESIS: GLUCOSE TO GLYCOGEN (INSULIN) GLYCOGENOLYSIS: GLYCOGEN TO GLUCOSE (GLUCAGON) GLUCONEOGENESIS: GENERATION OF GLUCOSE FROM NON-CHO ( FATS AND PROTEIN) LIPOGENESIS: GLUCOSE TO FATTY ACIDS LIPOGENOLYSIS: BREAKDOWN OF FATS (GOOD-EXERCISE) KETOGENESIS: BREAKDOWN OF FATS (BAD-DM)

FORMATION OF KETONE BODIES-DKA DM COVERAGE1. CAUSE2. DX3. S/SX4. CX5. MX COMPARISON

NIDDM-TYPE II

ADULT ONSET (40Y/O) DECREASED INSULIN TO NORMAL GENETIC, HEREDITARY


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INSULIN RESISTANT (CELL)(SUGAR)

OBESITYIDDM-TYPE I

JUVENILE ONSET ZERO INSULIN

(SUGAR)

GENETIC, HEREDITARY AUTOIMMUNE

(COXSACKIE VIRUS)

VIRALWHAT WILL HAPPEN IF YOU HAVE GLUCOSE INTOLERANCE?

PATHOPHYSIOLOGY

OF

DIABETES MELLITUS

(TYPE I AND II)

HYPERGLYCEMIA S/SX: 4 PS

POLYURIA POLYDIPSIA POLYPHAGIA PARESTHESIA

POOR WOUND HEALING RECURRENT INFECTIONS HYPOGLYCEMIA S/SX: ADRENERGIC - HR, RR, BP, SWEATING, TREMORS, PALPITATIONS, NERVOUSNESS AND PALLOR NEUROLOGIC HEADACHE, LIGHT HEADEDNESS, SLURRED SPEECH, AND LOC

IF CONSCIOUS GIVE 10-15 GM OF SIMPLE SUGAR, 5-6 PCS. OF CANDIES, 3 GLUCOSE TABLET OR 4 OZ OFJUICE

IF UNCONSCIOUS GIVE 1 MG OF GLUCAGON SQ OR IM, 50% OF DEXTROSE SOLUTION IV BOLUS


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POLYPHAGIA HOW TO DETECT GLUCOSE INTOLERANCE? 2-HOUR POSTPRANDIAL TEST (AFTER MEAL)

NPO 8-12 HOURS BLOOD EXTRACTION (BASELINE AND FBS) 75 GM OF SUGAR (ORAL) BLOOD EXTRACTION AFTER 2 HOURS 200 MG/DL (+)

HOW TO DETECT GLUCOSE INTOLERANCE? OGTT ORAL GLUCOSE TOLERANCE TEST

NPO 8-12 HOURS BLOOD EXTRACTION (BASELINE AND FBS) 75 GM OF SUGAR (ORAL) BLOOD EXTRACTION EVERY HOUR (1ST, 2ND, 3RD, 4TH) 200 MG/DL (+)

HOW TO DETECT GLUCOSE INTOLERANCE? FASTING BLOOD SUGAR

NPO 8-12 HOURS 110 MG/DL NPO 8H (+)

HOW TO DETECT GLUCOSE INTOLERANCE AND COMPLIANCE? GLYCOSYLATED HEMOGLOBIN A1C (HBA1C)

NO SPECIAL PREP GLUCOSE MOLECULES REACT WITH HEMOGLOBIN

(GLYCATED HB-120 DAYS)

6.5% INDICATES POOR CONTROL OF BLOOD GLUCOSE LEVELS HAVE BEEN ASSOCIATED WITH

CARDIOVASCULAR DISEASE, NEPHROPATHY AND


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RETINOPATHY. DIAGNOSTIC EVALUATION

1. RANDOM BLOOD SUGAR (NO NPO)2. 2H POSTPRANDIAL TEST (NPO)3. OGTT (NPO)4. FASTING BLOOD SUGAR (NPO)5. GLYCOSYLATED HBA1C (NO NPO) INTERVENTIONS

NIDDM TYPE II

MANAGEMENT:

DIET EXERCISE WEIGHT REDUCTION ORAL HYPOGLYCEMIC AGENT (OHA) BIDS (INSULIN AND OHA) INSULIN HHNKS OR HONKS

DEHYDRATION IV FLUIDS (ISOTONIC, PNSS) HYPERGLYCEMIA INSULIN IV DRIP (REGULAR INSULIN ONLY) NO KETOACIDOSIS

IDDM TYPE I

MANAGEMENT:

DIET EXERCISE MAINTAIN WEIGHT NO OHA INSULIN DKA


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DEHYDRATION IV REPLACEMENT HYPERGLYCEMIA INSULIN IV DRIP (REGULAR INSULIN ONLY) KETOACIDOSIS TREAT WITH INSULIN IF SEVERE GIVE NAHCO3 (CSF ACIDOSIS, HYPOKALEMIA)

DIET (AVOID SIMPLE SUGAR, EXCHANGE LIST) 50%, 30%, 20% (CHO, FATS, CHON) NON DIABETIC 50%,20%,30% (CHO, FATS, CHON) DIABETIC 4/9/4 KCAL/GM (CHO, FATS, CHON) 2,800 KCAL/DAY RDA

SIMPLE SUGAR OR MONOSACCHARIDES CAKES, COOKIES, CANDIES AND ICE CREAM USUALLY CONTAIN WHITE TABLE SUGAR MILK (GALACTOSE)-DAIRY PRODUCTS HONEY FRUITS MOLASSESARNIBAL PUTANGBENGE!!! SIMPLE VS COMPLEX CARB SIMPLE CARBOHYDRATES OR SIMPLE SUGARS THESE CARBS ARE BROKEN DOWN AND DIGESTED VERY

QUICKLY, BUT MOST SIMPLE CARBS CONTAIN REFINED SUGARS AND VERY FEW ESSENTIAL VITAMINS AND

MINERALS.

EXAMPLES INCLUDE TABLE SUGAR, FRUIT JUICE, MILK, YOGURT, HONEY, MOLASSES, MAPLE SYRUP AND BROWNSUGAR.

COMPLEX CARBOHYDRATES THE COMPLEX CARBS TAKE LONGER TO DIGEST AND ARE PACKED WITH FIBER,VITAMINS AND MINERALS.

EXAMPLES INCLUDE VEGETABLES, WHOLE GRAIN BREADS, OATMEAL, LEGUMES, BROWN RICE AND WHEATPASTA.

DRUGS THAT CAN CONTROL BLOOD SUGAR. ORAL HYPOGLYCEMIC AGENT (OHA) INSULIN ORAL HYPOGLYCEMIC AGENTS1. SULFONYLUREAS - STIMULATES INSULIN SECRETIONS AND INCREASES TISSUE SENSITIVITY TO INSULIN


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2. BIGUANIDES DECREASES INTESTINAL UPTAKE AND HEPATIC PRODUCTION OF GLUCOSE AND INCREASESTISSUE SENSITIVITY

3. ALPHA GLUCOSIDASE INHIBITOR SLOWS CARBOHYDRATE ABSORPTION4. THIAZOLIDINEDIONES INSULIN SENSITIZER, INCREASES TISSUE SENSITIVITY TO INSULIN ORAL HYPOGLYCEMIC AGENTS1. SULFONYLUREAS,GLIPIZIDE, EUGLUCON

SE: HYPERSENSITIVITY, HEADACHE, GI UPSET

2. BIGUANIDES, GLUCOPHAGE, METFORMINSE: LACTIC ACIDOSIS, GI UPSET, METALLIC TASTE, TAKE B12 AND FOLIC ACID

3. ALPHA GLUCOSIDASE INHIBITOR, GLUCOBAYSE: FLATULENCE, GI UPSET

4. THIAZOLIDINEDIONES, AVANDIASE: LIVER DISEASE

TYPES OF INSULIN1. IMMEDIATE ACTING

HUMALOG (LISPRO)2. SHORT ACTING

REGULAR SEMILENTE HUMULIN R NOVOLIN R

3. INTERMEDIATE ACTING

LENTE NPH OR NEUTRAL PROTAMINE HAGEDORN HUMULIN N NOVOLIN N

4. LONG ACTING

ULTRA LENTE FACTS ABOUT INSULIN


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PINCH OR 45 FOR THIN PATIENT 90 FOR REGULAR CLIENT FACTS ABOUT INSULIN MIXED INSULIN 70/30 REGULAR (CLEAR) FIRST TO BE DRAWN FOLLOWED BY NPH (CLOUDY) FACTS ABOUT INSULIN TUBERCULIN SYRINGE 1ML INSULIN SYRINGE 100 UNITS FACTS ABOUT INSULIN INSULIN SLIDING SCALE USE REGULAR INSULIN ONLY PRIME TUBING FIRST (100 U INSULIN) INCORPORATED TO PNSS CHECK HYPOK DRILL: ADMISTER 300 UNITS OF REGULAR INSULIN IN 500 ML OF PNSS. DELIVER 28 UNITS/HOUR. HOW MANY

DROPS/MINUTE? DF 60.

HOW MANY HOURS TO CONSUME? FORMULA: ML/HOUR

300 U INSULIN:500ML PNSS :: 28 U INSULIN/H : X ML/H (300X )= (500X28) 300X = 14,000 X = 14,000/300 X = 46.66ML/H OR 46.66 GTTS/MIN

DURATION IN HOUR TVI/ML PER HOUR


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500/46.66 10.7 HOURS

FACTS ABOUT INSULIN INSULIN PUMP EXTERNAL BATTERY OPERATED NEEDLE IS INSERTED SQ THAT DELIVERS REGULAR INSULIN,

1 UNIT/HOUR (DAYTIME)

FAST ACTING (LISPRO) FREQUENT BLOOD GLUCOSE MONITORING IS ADVISED $ 5K US FACTS ABOUT INSULIN LIPODYSTROPHY IS A COMPLICATION IF THE SITE OF INJECTION IS NOT ROTATED PROPERLY, IT CAN ALSO ALTER

THE RATE OF INSULIN ABSORPTION.

GOOD SITE MUST BE SUPPLE SKIN. FACTS ABOUT INSULIN HYPERINSULINISM TREMORS, HUNGER AND

DIAPHORESIS WILL MANIFEST

DAWN PHENOMENON COMMON IN TYPE I, HYPERGLYCEMIA IN THE MORNING SOMOGYI PHENOMENON REBOUND HYPERGLYCEMIA

AFTER INSULIN ADMINISTRATION

(GRADUAL REDUCTION OF INSULIN IS THE KEY TO MANAGE IT AND GIVE A SNACK )

THANK YOU

FUNDA LECTURE CENTRAL VENOUS CATHETERS SWAN GANZ OR PULMONARY CATHETERS IV KCL THORACENTESIS PERICARDIOCENTESIS


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PARACENTESIS URINARY CATHETERS REMINDERS DIABETIC KIT FOOT CARE S/SX OF CX: (VISUAL, URINE, LOC, BP, DYSPNEA ETC.) MAC BGM REGULAR CHECK UP LAB EXAMS DIET (AVOID SIMPLE SUGAR, EXCHANGE LIST)

50/30/20 (CHO, FATS, CHON) NON DIABETIC 50/20/30 (CHO, FATS, CHON) DIABETIC 4/9/4 KCAL/GM (CHO, FATS, CHON) 2,800 KCAL/DAY RDA

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HYPOTHALAMUS-PITUITARY AXIS PITUITARY DISORDERS1. PITUITARY TUMOR2. HYPERPITUITARISM3. HYPOPITUITARISM4. DIABETES INSIPIDUS (DI)5. SYNDROME OF INAPPROPRIATE ADH (SIADH) PITUITARY TUMOR CAUSE:

BASOPHILICCUSHINGS SYNDROME EOSINOPHILIC OR ACIDOPHILIC

GIGANTISM OR ACROMEGALY

CHROMOPHOBIC HYPOPITUITARISM


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DX: SCAN AND S/SX S/SX: INCREASED ICP, HEADACHE, PAPILLEDEMA (VISUAL DISTURBANCE), OTHER S/SX IS DEPENDENT ON THE

TYPE OF TUMOR

CX: HORMONE IMBALANCES MX: HYPOPHYSECTOMY

BROMOCRIPTINE (PARLODEL) TO LOWER GH AND PROLACTIN OCTREOTIDE (SANDOSTATIN) TO REDUCE TUMOR

COMPARISON HYPERPITUITARISM CAUSE:

BASOPHILICCUSHINGS SYNDROME EOSINOPHILIC OR ACIDOPHILIC GIGANTISM OR ACROMEGALY

DX: SCAN AND S/SX S/SX: FSH, LH, OXY, PRO (FLOP)

TSH, ADH, GH, MSH ACTH (TAGMA)

CX: RELATED TO HORMONE IMBA. MX: HYPOPHYSECTOMY HYPOPITUITARISM CAUSE

CHROMOPHOBIC HYPOPITUITARISM SHEEHANS SYNDROME SIMMONDS DISEASE

DX: SCAN AND S/SX S/SX: FSH, LH, OXY, PRO (FLOP)TSH, ADH, GH, MSH ACTH (TAGMA) CX: RELATED TO HORMONE IMBA. MX: HYPOPHYSECTOMY AND SUPPLEMENT OF HORMONES HYPERPITUITARISM CAUSE


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DX S/SX CX MX HYPOPITUITARISM NURSING PROBLEMS DECREASED TISSUE PERFUSION (BRAIN, HEART, KIDNEYS) SECONDARY TO HYPEROSMOLALITY ALTERATION IN ELIMINATION INCREASED URINARY OUTPUT SECONDARY TO HYPEROSMOLALITY RISK FOR FLUID VOLUME DEFICIT SECONDARY TO INCREASED URINARY OUTPUT AND HYPEROSMOLALITY ALTERATION IN ADL SECONDARY TO POLYURIA AND PARESTHESIA RISK FOR SKIN BREAKDOWN SECONDARY TO PARESTHESIA AND NEUROPATHY NURSING PROBLEMS RISK FOR CARDIOVASCULAR DISEASES SECONDARY TO HYPERLIPIDEMIA ALTERATION IN METABOLISM (FATS AND PROTEIN CATABOLISM) SECONDARY TO CELLULAR HYPOGLYCEMIA FLUIDS, ELECTROLYTES AND ACID BASE IMBALANCES SECONDARY BODY COMPENSATION ALTERATION IN BREATHING PATTERN SECONDARY TO DKA SENSORY PERCEPTION DEFICIT SECONDARY TO CATARACT, RETINOPATHY, NEUROPATHY NURSING PROBLEMS DISTURBANCE IN BODY IMAGE SECONDARY TO CACHEXIA KNOWLEDGE DEFICIT SECONDARY TO ILLNESS PROGRESSION ANXIETY RELATED TO PROGNOSIS OF THE DISEASE SEXUAL ACTIVITY DISTURBANCE RELATED TO NEUROPATHY, HYPERLIPIDEMIA (ERECTILE DYSFUNCTION) NURSING PROBLEMS ALTERED NUTRITION BALANCE SECONDARY TO DIETARY CHANGES NONCOMPLIANCE SECONDARY LIFESTYLE CHANGES, DISEASE PROGRESSION, DIETARY REGIMEN ETC CAREGIVER STRAIN

Date post:	02-Apr-2018
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Endocrine System Revised

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