METABOLISM

ENDOCRINE SYSTEM

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONES FUNCTIONS
Thyroid to release hormones Adrenal cortex to release hormones Growth, maturation & function of sex organs

PITUITARY TSH ANTERIOR ACTH LOBE

FSH,LH

Growth of body tissues & GH/ bones SOMATOTROPIN

PROLACTIN/ LTH

Development of mammary glands & lactation

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE ADH FUNCTION
Regulates water metabolism

PITUITARY POSTERIOR LOBE

OXYTOCIN MSH INTERMEDIATE LOBE

Stimulate uterine contractions release of milk Affects skin pigmentation

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONES
ALDOSTERONE

FUNCTION
Fluid & electrolyte balance; Na reabsorption; K excretion
Glycogenolysis; Gluconeogenesis Na & water reabsorption Antiinflammatory Stress hormone

ADRENAL CORTEX

CORTISOL

SEX HORMONES

Slightly significant

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE EPINEPHRINE NOREPINEPHRINE FUNCTION
Increase heart rate & BP Bronchodilation, Glycogenolysis Stress hormone

ADRENAL MEDULLA

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE
T3 & T4

FUNCTION
Regulate metabolic rate P,C,F metabolism Regulate physical & mental growth & development

THYROID

THYROCALCITONIN
PTH PARATHYROID

Decrease serum Ca by increasing bone deposition

Increase serum calcium by promoting bone decalcification

ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE FUNCTION
Decrease blood glucose by: Glucose diffusion across cell membrane; Converts glucose to glycogen Increase blood glucose by: Gluconeogenesis Glycogenolysis

PANCREAS INSULIN BETA CELLS ALPHA CELLS

GLUCAGON

ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION GLAND OVARIES ESTROGEN & Development of secondary sex charac in female PROGESMaturation of sex organs TERONE Sexual functioning
Maintenance of pregnancy

TESTES

TESTOSTERONE

Development of secondary sex charac in male Maturation of sex organs Sexual functioning

HORMONE REGULATION
NEGATIVE FEEDBACK MECHANISM CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE) RHYTHMIC PATTERNS OF SECRETION
(e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)

AUTONOMIC & C.N.S. CONTROL

(PITUITARY-HYPOTHALAMIC AXIS, ADRENAL MEDULLA HORMONES)

NEGATIVE FEEDBACK MECHANISM

DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLAND
RELEASE OF STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TO PRODUCE &

(e.g. RELEASE HORMONE Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

NEGATIVE FEEDBACK MECHANISM

INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLAND IS INHIBITED TO
RELEASE STIMULATING HORMONE (e.g. TSH)

DECREASED PRODUCTION & SECRETION

OF TARGET ORGAN OF THE HORMONE (e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

CASE STUDY
Katie, an elderly, came in because of palpitations. VS revealed: 37.9o , 120, 25, 140/ 90 She expressed hyperactivty, sweating, increased appetite & weight loss

CASE STUDY
She claimed history of goiter since her 30s but no follow-up was done. What are your nursing plans?

PLANNING
HEALTH PROMOTION
IODIZED SALT CONTROLLING WEIGHT

HEALTH MAINTENANCE & RESTORATION

STEROID THERAPY

STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH

ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

STEROID THERAPY
PHARMACOLOGIC CONSIDERATIONS: PEPTIC ULCER IN SHORT TERM, HIGH DOSE STEROID
TX

ADMINISTER DRUG: HIGHER DOSE IN THE

MORNING, TAPERING TO LOWER ONES IN THE AFTERNOON

LAST DOSE @ MEAL TIME TO AVOID INSOMNIA PALLIATIVE EFFECT

STEROID THERAPY
ASSESSMENT: BASELINE STEROID LEVEL IS ASSESSED BEFORE
PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED

STEROID WITHDRAWAL (LOW STRESS TOLERANCE)

EXHAUSTION WEAKNESS LETHARGY

STEROID THERAPY
ASSESSMENT: ACUTE ADRENAL CRISIS
RESTLESSNESS WEAKNESS HEADACHE DHN N/V FALLING BP TO SHOCK

PSYCHOLOGICAL CXS
MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION

STEROID THERAPY
IMPORTANT FACTS:

MAJOR UNTOWARD EFFECTS: MASKS INFECTION DEFENSE AGAINST INFECTION FROM

LYMPHOPENIA

SLOW WOUND HEALING FROM ITS

ANTIINFLAMMATORY EFFECT P.U.D. ACTIVATION/ REACTIVATION

SERUM SODIUM SERUM POTASSIUM

STEROID THERAPY
IMPORTANT FACTS: MINOR UNTOWARD EFFECTS:
PIGMENTATION ACNE FACIAL HAIR MOON-FACIE

STEROID THERAPY
IMPORTANT FACTS:

PROBLEMS OF LONG TERM THERAPY:

GROWTH RETARDATION OBESITY GASTRITIS TO P.U.D. OSTEOPOROSIS HPN RENAL CALCULI ADRENAL ATROPHY

STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO REALEASE ACTH

ENDOGENOUS CORTISOL PRODUCTION & RELEASE BY ADRENAL MEDULLA

ADRENAL ATROPHY

STEROID THERAPY
IMPLEMENTATION
DECREASE Na IN THE DIET CALORIC RESTRICTION FOODS HIGH IN POTASSIUM GIVE MEDS WITH ANTACIDS OR WITH FOOD TEST STOOLS OR EMESIS FOR BLOOD REPORT ANY EVIDENCE OF GI BLEEDING LYMPHOPENIC PRECAUTION

ANTERIOR PITUITARY DISTURBANCES

HYPOPITUITARISM HYPERPITUITARISM

HYPOPITUITARISM
ANTERIOR LOBE

PANHYPOPITUITARISM (SIMMONDS DSE)

DECREASED SECRETION OF ALL ANTERIOR LOBE HORMONES

HYPERPITUITARISM
ANTERIOR LOBE
EOSINOPHILIC TUMOR
INCREASED GROWTH HORMONE AND PROLACTIN

BASOPHILIC TUMOR
INCREASED TSH, FSH, LH, MSH, INCREASED ACTH (CUSHINGS DSE)

CHROMOPHOBE TUMOR
INCREASED ACTH & GROWTH HORMONE

PITUITARY ANTERIOR LOBE

HORMONE GH ACTH HYPO FXN Dwarfism young Cachexia - adult Atrophy of adrenal cortex HYPER FXN Gigantism young Acromegaly - adult Cushings dse

TSH
FSH PROLACTIN

Atrophy & depressed thyroid fxn Atrophy & infertility

Underdevelopment of mammary glands

Graves dse
Exaggerated fxn of sex organs Decreased milk production

MANAGEMENT
HYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY
THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)

HYPERPITUITARISM
SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS

POSTERIOR PITUITARY DISTURBANCES

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

DIABETES INSIPIDUS ABSOLUTE / PARTIAL

DEFICIENCY OF VASOPRESSIN

CAUSE: TUMOR TRAUMA VASCULAR DSE INFLAMMATION PITUITARY SURGERY

S/SX: POLYURIA
15-29L/ DAY

POLYDIPSIA SG OF URINE IS <1.010 S/SX OF DHN SHOCK

DIABETES INSIPIDUS ABSOLUTE / PARTIAL

DEFICIENCY OF VASOPRESSIN

MANAGEMENT HORMONAL REPLACEMENT FOR LIFE

VASOPRESSIN (PITRESSIN TANNATE IN OIL) IM OR NASAL SPRAY

NON-HORMONAL THERAPY
CHLORPROPRAMIDE INCREASE RESPONSE OF THE BODY TO DECREASED VASOPRESSIN

SALT & P RESTRICTED DIET, INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE BALANCE

SYNDROME OF INAPPROPRIATE ADH

ELEVATED ADH
CAUSES: BRONCHOGENIC CA NONENDOCRINE TUMORS S/SX: DECREASED SERUM SODIUM
CX IN LOC TO UNCONSCIOUSNESS SEIZURES

WATER INTOXICATION
N/V MENTAL CONFUSION

SYNDROME OF INAPPROPRIATE ADH

MANAGEMENT:
WATER INTAKE RESTRICTION ADMINISTER AS ORDERED: NaCl Diuretics Demeclocycline (declamycin) a tetracycline analogue that interferes with the action of ADH on the collecting tubules

Mission possible

THYROID GLAND
STIMULATED BY THYROID STIMULATING HORMONE (TSH) NEEDS IODINE TO SYNTHESIZE HORMONE SECRETES:
THYROXINE (T4) TRIIODOTHYRONINE (T3)

THYROID DISTURBANCES
DIAGNOSTIC TESTS:
B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN TIME PBI MEASURE IODINE LIBERATED IN THE BLOOD WITH THYROID
DAMAGE

SERUM THYROXINE (T4), SERUM TRIIODOTHYRONINE (T3), SERUM TSH BLOOD SERUM CHOLESTEROL

RADIOACTIVE IODINE TESTS:

T3 RED CELL UPTAKE RADIOACTIVE IODINE UPTAKE (I131 THYROID SCAN

THYROID DISTURBANCES
HYPOTHYROIDISM HYPERTHYROIDISM
CRETINISM- infants, GRAVES DSE or young children Exophthalmic goiter HYPOTHYROIDISM WITHOUT MYXEDEMAatrophy/ destruction of thyroid gland MYXEDEMA adults

EFFECTS
HYPOTHYROIDISM HYPERTHYROIDISM
Reduction in HEAT Increase heat PRODUCTION Failure of MENTAL & PHYSICAL GROWTH increased storage of Deranged C C, P & F metabolism, glycosuria Abnormal collection Increase use of F & of WATER P as fuel

HYPOTHYROIDISM HYPERTHYROIDISM SERUM CHOLESTEROL:

INCREASED DECREASED

BMR:
DECREASED INCREASED
WARM, MOIST, FLUSHED SOFT, SILKY

SKIN:
THICK, PUFFY, DRY

HAIR:
DRY, BRITTLE

HYPOTHYROIDISM
NERVOUS SYSTEM:
APATHETIC LETHARGIC MAYBE HYPERIRRITABLE SLOW CEREBRATION

HYPERTHYROIDISM

HYPERACTIVE LABILE MOOD HYPERSENSITIVE TENSED

WEIGHT:
INCREASED DECREASED

APPETITE:
DECREASED INCREASED

MANAGEMENT
HYPOTHYROIDISM HYPERTHYROIDISM

MEDICAL: HORMONE REPLACEMENT

DESSICATED THYROID THYROGLOBULIN Na LEVOTHYROXINE Na LYOTHYRONINE

MEDICAL: REST ANTITHYROID DRUGS:

LUGOLS SOLUTION THIOUREA DERIVATIVES RADIOACTIVE IODINE BETA-BLOCKERS

SURGICAL:
SUBTOTAL THYROIDECTOMY

ANTITHYROID MEDICATIONS
LUGOLS SOLUTION
(POTASSIUM IODIDE)
DECREASE THYROID VASCULARITY INHIBIT IODINE RELEASE DILUTED IN MILK / JUICE STAINS THE TEETH- USE STRAW

THIOUREA & DERIVATIVES

(PTU,METHIMAZOLE)
BLOCK THYROID HORMONE RELEASE TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA

RADIOACTIVE IODINE
PATIENT IS ISOLATED FOR 3 DAYS

BETA BLOCKERS
PROPANOLOL

SUBTOTAL THYROIDECTOMY
REMAINING TISSUE PROVIDES ENOUGH HORMONES FOR NORMAL FXN

PRE OP NURSING CARE: PATIENT EDUCATION ON POST OP:

LITTLE HOARSENESS DIFFICULTY OF SWALLOWING

POST OP NURSING CARE:

SEMIFOWLERS AVOID HYPEREXTENSION OF THE NECK BE ASKED TO SPEAK @ 40 MIN INTERVAL ASSESS RECURRENT NERVE INJURY WATCH OUT FOR COMPLICATIONS.

SUBTOTAL THYROIDECTOMY
COMPLICATIONS:
RECURRENT LARYNGEAL NERVE INJURY
HOARSENESS

HEMORRHAGE
12-24 HRS POST OP OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS TRACHEOSTOMY SET @ BEDSIDE

TETANY RESPIRATORY OBSTRUCTION THYROID STORM

TETANY
DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVED

S/SX: 1ST TINGLING TOES & FINGERS 2ND CHEVOSTEKS SIGN (TAPPING THE FACIAL MUSCLES) 3RD TROUSSEAUS SIGN (CARPO-PEDAL SPASM WITH
OCCLUSION OF CIRCULATION WITH A BP CUFF)

MANAGEMENT: CALCIUM REPLACEMENT: CaGluconate IV

THYROID STORM / CRISIS

S/SX:
HYPERTHERMIA > 41C TACHYCARDIA APPREHENSION RESTLESSNESS IRRITABILITY DELIRIUM COMA

MANAGEMENT:
DECREASE TEMP ANTITHYROID DRUGS GLUCOSE DIGITALIS STEROIDS TO DECREASE ACTH

THYROID STORM / CRISIS

INCREASED AMOUNT OF THYROID HORMONES

POST OP AFTER RADIOACTIVE IODINE ADMINISTRATION TOO SHORT PERIOD OF PRE OP TX

CAUSES:
EMOTIONAL STRESS PHYSICAL STRESS

VARIANTS OF HYPERTHYROIDISM
GRAVES DSE THYROIDITIS GOITER

GRAVES DISEASE
CAUSE:
UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR

S/SX: TRIAD OF SYMPTOMS:

HYPERTHYROIDISM OPHTHALMOPATHY DERMOPATHY

OPHTHALMOPATHY
EXOPHTHALMOS ACCUMULATION OF FLUID IN THE
FAT PADS BEHIND HE EYEBAL

LID LAG PROMINENT PALPEBRAL FISSURE WHEN THE

PATIENT LOOKS DOWN

THYROID STARE
(DARYMPLES SIGN) INFREQUENT EYE BLINKING

DERMOPATHY
PRETIBIAL MYXEDEMA

@ THE DORSUM OF THE LEG

RAISED, THICKENED, PRURITIC, HYPERPIGMENTED SKIN CLUBBING OF FINGERS & TOES OSTEOARTHROPATHY

THYROIDITIS
CLASSIFICATION:
SUBACUTE, NONSUPPURATIVE
UNKNOWN CAUSE ASSOC. WITH VIRAL URT INFECTIONS

CHRONIC, HASHIMOTOS
IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID

GOITER
ENLARGEMENT OF THE THYROID GLAND.

TYPES:
TOXIC NODULAR
NONTOXIC

TOXIC NODULAR GOITER

COMMON IN ELDERLY FROM LONG STANDING SIMPLE GOITER NODULES
FUNCTIONING TISSUE SECRETES THYROXINE AUTONOMOUSLY FROM TSH

NON-TOXIC GOITER
(SIMPLE/ COLLOID/ EUTHYROID)

CAUSE :
IODINE DEFICIENCY INTAKE OF GOITROGENIC SUBSTANCES/ DRUGS:
CASSAVA, CABBAGE, CAULIFLOWER, CARROTS RADDISH TURNIPS RED SKIN OF PEANUTS IODINE COBALT LITHIUM

NON-TOXIC GOITER
IODINE DEFICIENCY OR INTAKE OF GOITROGENIC SUBSTANCES

IMPAIRED THYROID HORMONE SYNTHESIS

SERUM THYROXINE PITUITARY SECRETE TSH

THYROID GLAND ENLARGES

TO COMPENSATE FOR THE REDUCED LEVEL OF THYROXINE

NON-TOXIC GOITER
TREATMENT: COMMON IN WOMEN:
ADOLESCENT PREGNANT LACTATING MENOPAUSE IODIZED OIL IM IODINE TABLETS SALT FORTIFICATION WITH IODINE EDUCATE ABOUT INTAKE OF:
SEAWEEDS SHELLFISH FISH- TAMBAN, HITO, DALAG

MYXEDEMA COMA
MEDICAL EMERGENCY OCCURS IN SEVERE & UNTREATED MYXEDEMA HIGH MORTALTY RATE

S/SX:
INTENSIFIED HYPOTHYROIDISM NEUROLOGIC IMPAIRMENT COMA

MYXEDEMA COMA
PRECIPITATING FACTORS:
FAILURE TO TAKE MEDS INFECTION TRAUMA EXPOSURE TO COLD USE OF SEDATIVES, NARCOTICS, ANESTHETICS

MYXEDEMA COMA
MANAGEMENT:
IV THYROID HORMONES CORRECTION OF HYPOTHERMIA MAINTAIN VITAL FXNS TREAT PRECIPITATING CAUSES

PARATHYROID GLAND
4 GLANDS

SECRETES PARATHORMONE (PTH) IN RESPONSE TO

SERUM Ca & Ph LEVELS

REGULATE CALCIUM & PHOSPHORUS METABOLISM

ORGANS AFFECTED: BONES - RESORPTION

KIDNEYS
Ca REABSORPTION Ph EXCRETION

GIT ENHANCES Ca ABSORPTION

PARATHYROID DISORDERS
DIAGNOSTIC TESTS: HEMATOLOGICAL
SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE PHOSPHATASE

URINARY STUDIES
URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION HYPOCALCEMIA CALCIUM IS:
DEPOSITED IN THE BONE EXCRETED

CAUSE: HEREDITARY IDIOPATHIC SURGICAL

HYPOPARATHYROIDISM
S/SX: ACUTE HYPOCALCEMIA
TINGLING OF THE FINGERS CHEVOSTEKS, TROUSSEAUS

CHRONIC HYPOCALCEMIA
FATIGUE, WEAKNESS PERSONALITY CHANGES LOSS OF TOOTH ENAMEL, DRY SCALY SKIN CARDIAC ARRHYTHMIA CATARACT

HYPOPARATHYROIDISM
XRAY: INCREASED BONE DENSITY

MANAGEMENT:
Ca SUPPLEMENT VIT D SUPPLEMENT LIQ FORM: WITH WATER, JUICE OR
MILK, pc

SEIZURE prec LISTEN FOR STRIDOR OR HOARSENESS TRACHEOSTOMY SET @ BEDSIDE CaGLUCONATE @ BEDSIDE

HYPERPARATHYROIDISM
INCREASED PTH PRODUCTION HYPERCALCEMIA HYPOPHOSPHATEMIA

PRIMARY TUMOR OR HYPERPLASIA OF THE PARATHYROID

GLAND

SECONDARY COMPENSATORY OVERSECRETION OF PTH IN

RESPONSE TO HYPOCALCEMIA FROM: CHRONIC RENAL DSE RICKETS MALABSORPTION SYNDROME OSTEOMALACIA

HYPERPARATHYROIDISM
S/SX:
BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRUCTURES TUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIA MUSCLE WEAKNESS PERSONALITY CX, DEPRESSION CARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISM
MANAGEMENT:
TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC
TISSUE

IV PNSS 5L/ DAY WITH DIURETICS CRANBERRY JUICE (ACID-ASH) LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSES STRAIN URINE FOR STONES CARE FOR PARATHYROIDECTOMY

ADRENAL GLAND
STIMULATED BY ACTH HORMONE PRECURSOR:
CHOLESTEROL

SECRETES:
CORTISOL ALDOSTERONE SEX HORMONES : ANDROGEN, ESTROGEN

ADRENAL GLAND
HORMONE
ALDOSTERONE

FUNCTION

Renal : Na & Cl reabsorption; K excretion GI : Na absorption GLUCOincrease serum glucose by CORTICOIDS gluconeogenesis & glycogenolysis esp during STRESS Blocks inflammation Counteracts effect of histamine SEX HORMONE Physiologically insignificant Becomes useful during menopause in women

SYMPTOMATOLOGY
ALDOSTERONE DEFICIENCY
DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON HYPOTENSION TO SHOCK INCREASED K METABOLIC ACIDOSIS

SYMPTOMATOLOGY
CORTISOL DEFICIENCY
ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY HYPOGLYCEMIA HYPOTENSION INCREASED K, WEAK PULSE PIGMENTATION IMPAIRED STRESS TOLERANCE

SYMPTOMATOLOGY
SEX HORMONE DEFICIENCY
LOSS OF BODY HAIR LOSS OF LIBIDO OR IMPOTENCE MENSTRUAL & FERTILITY DISORDER

ADRENAL CORTEX DISORERS

ADRENAL INSUFFICIENCY ADRENAL CRISIS CUSHINGS SYNDROME ALDOSTERONISM

ADRENAL INSUFFICIENCY

ADDISONS DISEASE
INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO STRESS

ADRENAL CRISIS
ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES POSSIBLE COMPLICATION OF ADDISONS

DISEASE

ADRENAL CRISIS
PRECIPITATING CAUSES: ABDOMINAL DISCOMFORT INFECTION TRAUMA HIGH TEMP EMOTIONAL UPSET ANTICOAGULANT DRUGS

ADRENAL CRISIS
S/SX: HYPOTENSION FLUID LOSS HYPONATREMIA

ADRENAL CRISIS
LAB:
SERUM ELEC: DECREASED Na
INCREASED K

S. BUN : S. GLUCOSE: ADRENAL HORMONE ASSAY :

HYDROXYCORTICOID & 17 KETOSTEROID IN 24-HR URINE
DET.

ADRENAL CRISIS
GOALS OF CARE:
TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

ADRENAL CRISIS
TREATMENT:
D5NSS ADRENAL CORTICAL HORMONE REPLACEMENT: INJECTABLE NEOSYNEPHRINE - SHOCK HIGH SALT DIET ANTIBIOTICS

CUSHINGS SYNDROME
CAUSE:
SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID ADMINISTRATION

CUSHINGS SYNDROME
S/SX:
TRUNCAL OBESITY BUFFALO HUMP MOON-FACIE WT GAIN SODIUM RETENTION THINNING OF EXTREMITIES FROM LOSS OF
MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHINGS SYNDROME
PURPLE STRIAE FROM THINNING OF SKIN ECHYMOSIS FROM SLIGHT TRAUMA ANDROGENIC EFFECTS:
OLIGOMENORRHEA HIRSUTISM GYNECOMASTIA

HYPERTENSION FROM

S. Na

CUSHINGS SYNDROME
TREATMENT & NURSING CARE:
PSYCHOLOGICAL SUPPORT PREVENT INFECTION INFLAM & IMMUNE RESPONSE
ARE SUPPRESSED

PROMOTE SAFETY SURGERY SUB/TOTAL ADRENALECTOMY

ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE

PRIMARY CONNS SYNDROME SECONDARY

CONNS SYNDROME
PRIMARY ALDOSTERONISM

CAUSE:
ADRENAL ADENOMA

S/SX:
HYPOKALEMIA FATIGUE HYPERNATREMIA, HPN, TETANY

MANAGEMENT:
SURGERY ALDACTONE ALDOSTERONE ANTAGONIST

SECONDARY ALDOSTERONISM
THE PROBLEM IS OUTSIDE THE ADRENAL GLAND: e.g. RENIN ANGIOTENSIN SYSTEM

ADRENAL MEDULLA
HORMONES : EPINEPHRINE NOREPINEPHRINE

EFFECTS

PHEOCHROMOCYTOMA
TUMOR OF ADRENAL MEDULLA SECRETES INCREASED AMOUNT OF CATECHOLAMINES

S/SX:
HPN HYPERGLYCEMIA CARDIAC ARRHYTHMIA & CHF

DIAGNOSTIC TEST :
VMA IN 24H URINE

VMA IN 24H URINE

END PRODUCT OF CATECHOLAMINE METABOLISM

DRUGS & FOOD TO BE WITHHELD 24H B4 THE TEST:

COFFEE & TEA BANANA VANILLA CHOCOLATES

PHEOCHROMOCYTOMA
MANAGEMENT:
SURGERY MEDICAL : ADRENERGIC BLOCKING AGENTS: PHENTOLAMINE

NURSING CARE:
MONITOR BP IN SUPINE & STANDING MONITOR URINE FOR GLUC & ACETONE

PANCREAS
HORMONES:
INSULIN BY BETA CELLS GLUCAGON BY ALPHA CELLS

DIABETES MILLETUS
CAUSE: INSUFFICIENCY OF INSULIN LACK OF INSULIN EFFECT: HYPERGLYCEMIA

DIABETES MILLETUS

PATHOPHYSIOLOGY
REDUCED /NO INSULIN OSMOTIC DEHYDRATION GLUCOSURIA OSMOTIC DIURESIS POLYURIA HYPERGLYCEMIA

LIPOLYSIS

CELLULAR HUNGER

WEIGHT LOSS POLYDIPSIA

POLYPHAGIA

DIABETES MILLETUS
S/SX: 3 Ps WEIGHT LOSS STAGES: PREDIABETES SUSPECTED CHEMICAL CLINICAL / OVERT

DIABETES MILLETUS
PREDIABETES / POTENTIAL:

CONCEPTION

EVIDENCE OF GLUCOSE METABOLISM ALTERATION

DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETES

NO STRESS

STRESS

NORMAL GLUCOSE METABOLISM

OVERT DIABETES

DIABETES MILLETUS
CHEMEICAL:
SUBCLINICAL GTT IS ABNORMAL

NO STRESS

STRESS SYMPTOMATIC

ASYMPTOMATIC

DIABETES MILLETUS
CLINICAL / OVERT:
CHEMICAL PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS

SYMPTOMATIC

DIABETES MILLETUS
TYPES: TYPE I
JUVENILE ONSET BEFORE 15 YO LEAN/ NORMAL WEIGHT ABSOLUTE INSULIN DEFICIENCY INSULIN -DEPENDENT PRONE TO DKA

TYPE II
MATURITY ONSET AFTER AGE 40 OBESE REDUCED INSULIN RECEPTOR NONINSULIN DEPENDENT PRONE TO HHONK

DIABETES MILLETUS
DIAGNOSTIC EXAMS: FBS 2 HR- POSTPRANDIAL OGTT GLYCOSYLATED HGB DEXTROSTRIP URINE TESTS:
BENEDICTS CLINITEST TAB ACETONE TEST

2 HR POSTPRANDIAL BLOOD SUGAR

INTAKE OF 100GM GLUCOSE, 2 HRS BEFORE THE TEST TEST FOR ABILITY TO DISPOSE GLUCOSE LOAD

OGTT
CONFIRMATORY, WHEN OTHER BLOOD TESTS ARE BORDERLINE 3 DAYS OF NORMAL ACITIVITY & 150MG OF CARB DIET NPO 10-12HRS BEFORE THE TEST BASELINE BLOOD SUGAR TAKEN GLUCOSE LOAD IS GIVEN, P.O. OR IV BLOOD & URINE SPECS TAKEN 30 MIN, 1HR, 2HRS, 3 HRS, AFTER GLUCOSE LOADING

GLYCOSYLATED HEMOGLOBIN
MEASURES GLUCOSE METABOLISM FOR THE PAST 3 MONTHS USEFUL TO CHECK:
COMPLIANCE WITH THERAPY HISTORY OF SUBCLINICAL OR CHEMICAL DIABETES

DIABETES MILLETUS
PLANNING & IMPLEMENTATION: CLIENTS ACTIVITY DIET : C,F,P 50, 30, 20 LOW SATURATED FATS, HIGH FIBER DRUGS:
ORAL HYPOGLYCEMICS
BIGUANIDE SULFONYLUREAS CONTRAINDICATED - PREGNANCY

INSULIN

DIABETES MILLETUS
INSULIN THERAPY DISPENSED IN U/ml : eg 100, 80 REFRIGERATE GIVEN @ ROOM TEMP GENTLY ROTATED, NOT SHAKEN ROUTE : SQ (MTC); IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND

DIABETES MILLETUS
INSULIN THERAPY: SITE OF INJECTION:
ABDOMEN ANTERIOR THIGH ARM UPPER BACK BUTTOCKS

DIABETES MILLETUS
INSULIN THERAPY REACTIONS: LOCAL:
STNGING INDURATION ITCHING

GENERALIZED:
HIVES URTICARIA ANTIHISTAMINES 30 MIN B4 DESENSITIZATION

LIPODYSTROPHY

LIPODYSTROPHY
CAUSE:
FAULTY TECHNIQUE TRAUMA INJECTION OF REFRIGERATED INSULIN MANAGEMENT: ROTATING SITES: 1 AREA IS NOT USED MORE THAN
ONCE EVERY 3 WKS

INSULIN THERAPY & HORMONAL ACTIVITY

GLUCORTICOIDS & EPINEPHRINE CAUSES HYPERGLYCEMIA DURING:
PHYSICAL TRAUMA STRESS INFECTION ANXIETY ANGER FEAR CHANGE IN LIFESTYLE

INCREASE IN INSULIN DOSE IS NEEDED

SURPRISE!!!

ACUTE COMPLICATIONS OF
DIABETIC KETO-ACIDOSIS (DKA) INSULIN SHOCK HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA SOMOGYI EFFECT

DIABETES MILLETUS

D.K.A. PATHOPHYSIOLOGY
NO INSULIN OSMOTIC DEHYDRATION MARKED HYPERGLYCEMIA

GLUCOSURIA OSMOTIC DIURESIS

LIPOLYSIS
WEIGHT LOSS

CELLULAR HUNGER
POLYPHAGIA

KETOACIDOSIS

POLYURIA

POLYDIPSIA

D.K.A.
S/SX:
S/SX OF DM + KETONURIA METABOLIC ACIDOSIS KUSSMAULS RESPIRATION ACETONE BREATH DHN FLUSHED FACE TACHYCARDIA CIRCULATORY COLLAPSE COMA

DEATH

D.K.A.
MANAGEMENT: ADEQUATE VENTILATION FLUID REPLACEMENT INSULIN RAPID ACTING ECG ELEC IMB

INSULIN SHOCK
LOW BLOOD SUGAR

CAUSE:
OVERDOSE OF EXOGENOUS INSULIN

EATING LESS
OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE

INSULIN SHOCK
S/SX: PARASYMPATHETIC
HUNGER NAUSEA HYPORTENSION BRADYCARDIA

SYMPATHETIC
IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR

CEREBRAL
LETHARGY, YAWNING SENSORIUM CX

INSULIN SHOCK
CLINICAL FINDING :
BLOOD GLUCOSE BELOW 55-60 mg%

TREATMENT:
GLUCOSE PO ( SUGAR, ORANGE JUICE OR CANDY) or IV ADMINISTRATION OF GLUCAGON IM, IV OR SQ

HHONK
PATHOPHYSIOLOGY
Very insufficient INSULIN

SEVERE OSMOTIC DEHYDRATION

GLUCOSURIA OSMOTIC DIURESIS POLYURIA

MARKED HYPERGLYCEMIA

LIPOLYSIS Without KETOSIS

CELLULAR HUNGER

WEIGHT LOSS

POLYPHAGIA

POLYDIPSIA

HHONK
S/SX: S/SX OF DKA WITHOUT:
KAUSMAULS BREATHING ACETONE BREATH METABOLIC ACIDOSIS KETONURIA

LACTIC ACIDOSIS
SEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING

METABOLIC ACIDOSIS

SOMOGYI EFFECT
TOO MUCH INSULIN

HYPOGLYCEMIA

GLUCAGON IS RELEASED

LIPOLYSIS GLUCONEOGENESIS GLYCOGENOLYSIS

REBOUND HYPERGLYCEMIA + KETOSIS

CHRONIC COMPLICATIONS OF DIABETES MILLETUS SYSTEM DEGENERATIVE CHANGES IN THE VASCULAR

UNDERNOURISHMENT ATHEROSCLEROSIS
VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA

NEUROPATHY FROM:

EYE COMPLICATIONS FROM ANOXIA

CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT

CHRONIC COMPLICATIONS OF DIABETES MILLETUS NEPHROPATHY

DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY
MI FROM ATHEROSCLEROSIS

HEART DISEASE

SKIN CHANGES
DIABETIC DERMOPATHY HYPERPIGMENTED & SCALY PRETIBIAL AREAS

LIVER CHANGES
ENLARGEMENT & FATTY INFILTRATION

Ms A, 45 y.o., has a simple goiter. Shes being seen by the community health nurse for teaching & follow-up regarding nutritional deficiencies related to her goiter. Ms As problem is almost associated with what nutritional deficiency?
Calcium Iodine Iron Sodium

a. b. c. d.