ENDOCRINE

SYSTEM

BY: MARC ANTHONY LIAO

RN
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTIONS
GLAND
PITUITARY TSH Thyroid to release
hormones
ANTERIOR
LOBE
ACTH Adrenal cortex to release
hormones
FSH,LH Growth, maturation &
function of sex organs
GH/ Growth of body tissues &
bones
SOMATOTROPIN
PROLACTIN/ Development of mammary
glands & lactation
LTH
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
PITUITARY ADH Regulates water metabolism

POSTERIOR
LOBE
OXYTOCIN Stimulate uterine contractions
release of milk
INTERMEDIATE MSH Affects skin pigmentation
LOBE
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION
GLAND
ADRENAL ALDOSTERONE Fluid & electrolyte balance;
Na reabsorption;
CORTEX
K excretion
CORTISOL Glycogenolysis;
Gluconeogenesis
Na & water reabsorption
Antiinflammatory
Stress hormone
SEX Promotes secondary sex
HORMONES characteristics
Protein Anabolism
 ENDOCRINE GLANDS

ENDOCRINE HORMONE FUNCTION

GLAND
ADRENAL EPINEPHRINE Increase heart rate & BP
Bronchodilation,
MEDULLA NOR-
Glycogenolysis
EPINEPHRINE
Stress hormone
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
THYROID T3 & T4’ Regulate metabolic rate
P,C,F metabolism
Regulate physical & mental
growth & development
THYRO- Decrease serum Ca by
increasing bone deposition
CALCITONIN

PARA PTH Increase serum calcium by

promoting bone decalcification
THYROID
 ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND

PANCREAS INSULIN Decrease blood glucose by:

Glucose diffusion across cell
BETA membrane;
CELLS Converts glucose to glycogen

ALPHA GLUCAGON Increase blood glucose by:

Gluconeogenesis
CELLS Glycogenolysis
 ENDOCRINE GLANDS
ENDOCRINE HORMONES FUNCTION
GLAND
OVARIES ESTROGEN & Development of secondary sex
charac in female
PROGES-
Maturation of sex organs
TERONE
Sexual functioning
Maintenance of pregnancy
TESTES TESTOS- Development of secondary sex
TERONE 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)
 ANTERIOR PITUITARY
DISTURBANCES

HYPOPITUITARISM
HYPERPITUITARISM
PANHYPOPITUITARISM (SIMMOND’S DSE)
 HYPERPITUITARISM
ANTERIOR LOBE
EOSINOPHILIC TUMOR
 INCREASED GROWTH HORMONE AND
PROLACTIN
BASOPHILIC TUMOR
 INCREASED TSH, FSH, LH, MSH,
 INCREASED ACTH (CUSHING’S DSE)
CHROMOPHOBE TUMOR
 INCREASED ACTH & GROWTH HORMONE
 PITUITARY ANTERIOR LOBE
HORMONE HYPO FXN HYPER FXN
GH Dwarfism – young Gigantism – young
Cachexia – adult Acromegaly – adult
ACTH Atrophy of adrenal Cushing’s dse
cortex
TSH Atrophy & depressed Grave’s dse
thyroid fxn
GSH Atrophy & infertility
Exaggerated fxn of sex
organs
PROLACTIN Underdevelopment of Galactorrhea
mammary glands
 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: S/SX:
TUMOR POLYURIA
TRAUMA 15-29L/ DAY
VASCULAR DSE POLYDIPSIA
INFLAMMATION SG OF URINE IS
PITUITARY SURGERY <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
INCREASE FLUIDS
MONITOR I&O
MAINTAIN FLUID & ELECTROLYTE BALANCE
 SYNDROME OF
INAPPROPRIATE ADH
ELEVATED ADH

CAUSES:
 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:
 Diuretics
 Demeclocycline (declamycin) – a tetracycline
analogue that interferes with the action of ADH on
the collecting tubules
 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, GRAVE’S DSE or

young children Exophthalmic goiter
HYPOTHYROIDISM
WITHOUT MYXEDEMA-
atrophy/ 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 of Increase use of F & P
WATER as fuel
HYPOTHYROIDISM HYPERTHYROIDISM
SERUM
CHOLESTEROL:
INCREASED DECREASED
BMR:
DECREASED INCREASED
SKIN:
THICK, PUFFY, DRY WARM, MOIST, FLUSHED
HAIR:
SOFT, SILKY
DRY, BRITTLE
HYPOTHYROIDISM HYPERTHYROIDISM

NERVOUS SYSTEM:
APATHETIC HYPERACTIVE
LETHARGIC LABILE MOOD
MAYBE HYPERSENSITIVE
HYPERIRRITABLE TENSED
SLOW CEREBRATION

WEIGHT:
INCREASED DECREASED

APPETITE:
DECREASED INCREASED
 MANAGEMENT
HYPOTHYROIDISM HYPERTHYROIDISM
MEDICAL: MEDICAL:
HORMONE ANTITHYROID DRUGS:
REPLACEMENT •LUGOL’S SOLUTION
•THYROGLOBULIN •RADIOACTIVE IODINE
•Na LEVOTHYROXINE •BETA-BLOCKERS
•Na LYOTHYRONINE SURGICAL:
•SUBTOTAL
THYROIDECTOMY
 THYROID STORM / CRISIS
S/SX: MANAGEMENT:
HYPERTHERMIA DECREASE TEMP
> 41C ANTITHYROID
TACHYCARDIA DRUGS
APPREHENSION DIGITALIS
RESTLESSNESS STEROIDS
IRRITABILITY
DELIRIUM
COMA
 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
GRAVE’S DSE
THYROIDITIS
GOITER
 GRAVE’S 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
(DALRYMPLE’S 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, HASHIMOTO’S
 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
COMMON IN TREATMENT:
IODIZED OIL IM
WOMEN:
ADOLESCENT IODINE TABLETS

PREGNANT SALT FORTIFICATION

LACTATING WITH IODINE

EDUCATE ABOUT
MENOPAUSE
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
 CHVOSTEK’S, TROUSSEAU’S
CHRONIC HYPOCALCEMIA
 FATIGUE, WEAKNESS
 LOSS OF TOOTH ENAMEL, DRY SCALY SKIN
 CARDIAC ARRHYTHMIA
HYPOPARATHYROIDISM
XRAY: INCREASED BONE DENSITY
MANAGEMENT:
Ca SUPPLEMENT
VIT D SUPPLEMENT – LIQ FORM: WITH WATER,
JUICE OR MILK, pc
SEIZURE precaution
STRIDOR OR HOARSENESS
 LISTEN FOR

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

FRACTURES
 TUBULAR CALCIUM DEPOSITS - KIDNEY STONES,
RENAL COLIC
 MUSCLE WEAKNESS
 CARDIAC ARRHYTHMIAS,

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
FOR STONES
 STRAIN URINE
CARE FOR PARATHYROIDECTOMY
 ADRENAL GLAND
STIMULATED BY ACTH

HORMONE PRECURSOR:
 CHOLESTEROL

SECRETES:
 CORTISOL
 ALDOSTERONE
 SEX HORMONES : ANDROGEN, ESTROGEN
 ADRENAL GLAND
HORMONE FUNCTION
ALDOSTERONE Renal : Na & Cl reabsorption; K
excretion
GI : Na absorption
GLUCO Increase 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

CUSHING’S SYNDROME

ALDOSTERONISM
 ADRENAL INSUFFICIENCY
ADDISON’S 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 ADDISON’S

DISEASE
 ADRENAL CRISIS
PRECIPITATING CAUSES:
ABDOMINAL DISCOMFORT
INFECTION
TRAUMA
HIGH TEMP
EMOTIONAL UPSET
 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
 CUSHING’S SYNDROME
CAUSE:
SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM
ACTH BY PITUITARY TUMOR
EXCESSIVE GLUCORTICOID ADMINISTRATION
 CUSHING’S 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
 CUSHING’S SYNDROME
PURPLE STRIAE – FROM THINNING OF SKIN
ECHYMOSIS FROM SLIGHT TRAUMA
ANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISM
GYNECOMASTIA
HYPERTENSION FROM S. Na
 CUSHING’S SYNDROME
TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORT
PREVENT INFECTION – INFLAM & IMMUNE
RESPONSE ARE SUPPRESSED
PROMOTE SAFETY
SURGERY – SUB/TOTAL ADRENALECTOMY
 ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME

SECONDARY
 CONN’S 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
 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
TYPES: TYPE II –
TYPE I  MATURITY ONSET
 AFTER AGE 40
 JUVENILE ONSET
 OBESE
 BEFORE 15 YO
 REDUCED INSULIN
 LEAN/ NORMAL
RECEPTOR
WEIGHT
 NONINSULIN DEPENDENT
 ABSOLUTE INSULIN
 PRONE TO HHONK
DEFICIENCY
 INSULIN -DEPENDENT
 PRONE TO DKA
 DIABETES MILLETUS
DIAGNOSTIC EXAMS: URINE TESTS:
FBS/ OGTT  BENEDICT’S

2 HR- POSTPRANDIAL CLINITEST TAB

 ACETONE TEST
GLYCOSYLATED HGB
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:
CLIENT’S 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:
SITE OF INJECTION:
 ABDOMEN
 ANTERIOR THIGH
 ARM
 UPPER BACK
 BUTTOCKS
 DIABETES MILLETUS
INSULIN THERAPY
REACTIONS:
LOCAL: GENERALIZED:
 STNGING  HIVES
 INDURATION  URTICARIA
 ITCHING  ANTIHISTAMINES 30
LIPODYSTROPHY MIN B4
 DESENSITIZATION
 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
 ACUTE COMPLICATIONS OF
DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR,
NONKETOTIC (HHONK) COMA

SOMOGYI EFFECT
 D.K.A.
S/SX:
 S/SX OF DM +
 KETONURIA
 METABOLIC ACIDOSIS
 KUSSMAUL’S 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 SYMPATHETIC
 HUNGER  IRRITABILITY
 NAUSEA  SWEATING
 HYPOTENSION  TREMBLING
 BRADYCARDIA  TACHYCARDIA
CEREBRAL  PALLOR
 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
 CHRONIC COMPLICATIONS OF
DIABETES MILLETUS
DEGENERATIVE CHANGES IN THE VASCULAR
SYSTEM
 ATHEROSCLEROSIS
NEUROPATHY FROM:
 VASCULAR INSUFFICIENCY
 HYPERGLYCEMIA
EYE COMPLICATIONS FROM ANOXIA
 CATARACT
 DIABETIC RETINOPATHY- BLINDNESS
 CHRONIC COMPLICATIONS OF
DIABETES MILLETUS
NEPHROPATHY
 DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE
KIDNEY
HEART DISEASE
 MI FROM ATHEROSCLEROSIS
SKIN CHANGES
 DIABETIC DERMOPATHY – HYPERPIGMENTED & SCALY
PRETIBIAL AREAS
LIVER CHANGES
 ENLARGEMENT & FATTY INFILTRATION
 THANK YOU FOR LISTENING

“DON’T CHASE SUCCESS PURSUE EXCELLENCE”

-3 IDIOTS