2. 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 &
LTH lactation
3. ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
PITUITARY ADH Regulates water metabolism
POSTERIOR
LOBE
OXYTOCIN Stimulate uterine contractions
release of milk
INTERME- MSH Affects skin pigmentation
DIATE LOBE
4. 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 Slightly significant
HORMONES
9. 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
charac in male
TERONE
Maturation of sex organs
Sexual functioning
10. 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)
11. 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 & RELEASE HORMONE
(e.g. Thyroid gland release of Thyroxine)
RETURN OF THE NORMAL
CONCENTRATION OF HORMONE
12. 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
13. 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
14. CASE STUDY
She claimed history of goiter since her
30’s but no follow-up was done.
What are your nursing plans?
16. STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO
REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & ADRENAL ATROPHY
RELEASE BY ADRENAL MEDULLA
17. 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
18. STEROID THERAPY
ASSESSMENT:
BASELINE STEROID LEVEL IS
ASSESSED BEFORE PROLONGED THERAPY IS
STARTED TO DETERMINE THE DOSE REQUIRED
STEROID WITHDRAWAL (LOW STRESS
TOLERANCE)
l EXHAUSTION
l WEAKNESS
l LETHARGY
19. STEROID THERAPY
ASSESSMENT:
ACUTE ADRENAL CRISIS
l RESTLESSNESS
l WEAKNESS
l HEADACHE
l DHN
l N/V
l FALLING BP TO SHOCK
PSYCHOLOGICAL CXS
l MOOD ELEVATION,
l FRANK EUPHORIA
l THEN, DEPRESSION
20. STEROID THERAPY
IMPORTANT FACTS:
MAJOR UNTOWARD EFFECTS:
l MASKS INFECTION
l DEFENSE AGAINST INFECTION FROM
LYMPHOPENIA
l SLOW WOUND HEALING FROM ITS
ANTIINFLAMMATORY EFFECT
l P.U.D. ACTIVATION/ REACTIVATION
l SERUM SODIUM
l SERUM POTASSIUM
22. STEROID THERAPY
IMPORTANT FACTS:
PROBLEMS OF LONG TERM THERAPY:
l GROWTH RETARDATION
l OBESITY
l GASTRITIS TO P.U.D.
l OSTEOPOROSIS
l HPN
l RENAL CALCULI
l ADRENAL ATROPHY
23. STEROID THERAPY
STEROID LEVELS
PITUITARY GLAND IS INHIBITED TO
REALEASE ACTH
ENDOGENOUS CORTISOL
PRODUCTION & ADRENAL ATROPHY
RELEASE BY ADRENAL MEDULLA
24. 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
26. HYPOPITUITARISM
ANTERIOR LOBE
PANHYPOPITUITARISM
(SIMMOND’S DSE)
l DECREASED SECRETION OF ALL
ANTERIOR LOBE HORMONES
27. HYPERPITUITARISM
ANTERIOR LOBE
EOSINOPHILIC TUMOR
l INCREASED GROWTH HORMONE AND
PROLACTIN
BASOPHILIC TUMOR
l INCREASED TSH, FSH, LH, MSH,
l INCREASED ACTH (CUSHING’S DSE)
CHROMOPHOBE TUMOR
l INCREASED ACTH & GROWTH
HORMONE
28. 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 & Grave’s dse
depressed thyroid fxn
FSH Atrophy & infertility Exaggerated fxn of
sex organs
PROLACTIN Underdevelopment Decreased milk
of mammary glands production
29. MANAGEMENT
HYPOPITUITARISM
l SURGICAL REMOVAL / IRRADIATION
l REPLACEMENT THERAPY
l THYROID HORMONES
l STEROIDS
l SEX HORMONES
l GONADOTROPINS (restore fertility)
HYPERPITUITARISM
l SURGICAL REMOVAL / IRRADIATION
l MONITOR FOR HYPERGLYCEMIA &
CARDIOVASCULAR PROBLEMS
31. 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 <1.010
SURGERY S/SX OF DHN
SHOCK
32. DIABETES INSIPIDUS
ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN
MANAGEMENT
HORMONAL REPLACEMENT – FOR LIFE
l VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR
NASAL SPRAY
NON-HORMONAL THERAPY
l CHLORPROPRAMIDE – INCREASE RESPONSE OF THE
BODY TO DECREASED VASOPRESSIN
SALT & P RESTRICTED DIET, INCREASE
FLUIDS
MONITOR I&O
MAINTAIN FLUID & ELECTROLYTE
BALANCE
33. SYNDROME OF
INAPPROPRIATE ADH
ELEVATED ADH
CAUSES:
BRONCHOGENIC CA
NONENDOCRINE TUMORS
S/SX:
DECREASED SERUM SODIUM
l CX IN LOC TO UNCONSCIOUSNESS
l SEIZURES
WATER INTOXICATION
l N/V
l MENTAL CONFUSION
34. SYNDROME OF
INAPPROPRIATE ADH
MANAGEMENT:
WATER INTAKE RESTRICTION
ADMINISTER AS ORDERED:
l NaCl
l Diuretics
l Demeclocycline (declamycin) – a
tetracycline analogue that interferes with
the action of ADH on the collecting tubules
36. THYROID GLAND
STIMULATED BY THYROID STIMULATING
HORMONE (TSH)
NEEDS IODINE TO SYNTHESIZE HORMONE
SECRETES:
l THYROXINE (T4)
l TRIIODOTHYRONINE (T3)
37. 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:
l T3 RED CELL UPTAKE
l RADIOACTIVE IODINE UPTAKE (I131
l THYROID SCAN
38. THYROID DISTURBANCES
HYPOTHYROIDISM HYPERTHYROIDISM
CRETINISM- infants, GRAVE’S DSE or
young children Exophthalmic goiter
HYPOTHYROIDISM
WITHOUT MYXEDEMA-
atrophy/ destruction of
thyroid gland
MYXEDEMA –adults
39. 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
43. ANTITHYROID MEDICATIONS
LUGOL’S SOLUTION
(POTASSIUM IODIDE)
l DECREASE THYROID VASCULARITY
l INHIBIT IODINE RELEASE
l DILUTED IN MILK / JUICE
l STAINS THE TEETH- USE STRAW
THIOUREA & DERIVATIVES
(PTU,METHIMAZOLE)
l BLOCK THYROID HORMONE RELEASE
l TOXIC SIGNS: FEVER, SORETHROAT, LEUKOPENIA
RADIOACTIVE IODINE
l PATIENT IS ISOLATED FOR 3 DAYS
BETA BLOCKERS
l PROPANOLOL
44. SUBTOTAL THYROIDECTOMY
REMAINING TISSUE PROVIDES ENOUGH HORMONES FOR
NORMAL FXN
PRE OP NURSING CARE:
PATIENT EDUCATION ON POST OP:
l LITTLE HOARSENESS
l DIFFICULTY OF SWALLOWING
POST OP NURSING CARE:
SEMIFOWLER’S
AVOID HYPEREXTENSION OF THE NECK
BE ASKED TO SPEAK @ 40 MIN INTERVAL –
ASSESS RECURRENT NERVE INJURY
WATCH OUT FOR COMPLICATIONS.
45. SUBTOTAL THYROIDECTOMY
COMPLICATIONS:
RECURRENT LARYNGEAL NERVE INJURY
l HOARSENESS
HEMORRHAGE
l 12-24 HRS POST OP
l OBSERVE FOR IRREGULAR BREATHING, CHOKING
SIGNS
l TRACHEOSTOMY SET @ BEDSIDE
TETANY
RESPIRATORY OBSTRUCTION
THYROID STORM
46. TETANY
DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS
REMOVED
S/SX:
1ST – TINGLING TOES & FINGERS
2ND – CHEVOSTEK’S SIGN (TAPPING THE FACIAL
MUSCLES)
3RD – TROUSSEAU’S SIGN (CARPO-PEDAL SPASM
WITH OCCLUSION OF CIRCULATION WITH A BP CUFF)
MANAGEMENT:
CALCIUM REPLACEMENT: CaGluconate IV
48. 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
50. GRAVE’S DISEASE
CAUSE:
UNKNOWN
AUTOIMMUNE WITH LONG-ACTING
THYROID STIMULATOR
S/SX: TRIAD OF SYMPTOMS:
HYPERTHYROIDISM
OPHTHALMOPATHY
DERMOPATHY
51. OPHTHALMOPATHY
EXOPHTHALMOS – ACCUMULATION OF
FLUID IN THE FAT PADS BEHIND HE EYEBAL
LID LAG – PROMINENT PALPEBRAL FISSURE
WHEN THE PATIENT LOOKS DOWN
THYROID STARE
(DARYMPLE’S SIGN) – INFREQUENT EYE
BLINKING
52. DERMOPATHY
PRETIBIAL MYXEDEMA
@ THE DORSUM OF THE LEG
RAISED, THICKENED, PRURITIC,
HYPERPIGMENTED SKIN
CLUBBING OF FINGERS & TOES
OSTEOARTHROPATHY
53. THYROIDITIS
CLASSIFICATION:
SUBACUTE, NONSUPPURATIVE
l UNKNOWN CAUSE
l ASSOC. WITH VIRAL URT INFECTIONS
CHRONIC, HASHIMOTO’S
l IMMUNOLOGICAL FACTORS
l PRESENCE OF IMMUNOGLOBULINS &
ANTIBODIES DIRECTED AGAINST THE
THYROID
55. TOXIC NODULAR
GOITER
COMMON IN ELDERLY
FROM LONG STANDING SIMPLE
GOITER
NODULES
l FUNCTIONING TISSUE
l SECRETES THYROXINE
AUTONOMOUSLY FROM TSH
56. NON-TOXIC GOITER
(SIMPLE/ COLLOID/ EUTHYROID)
CAUSE :
IODINE DEFICIENCY
INTAKE OF GOITROGENIC SUBSTANCES/
DRUGS:
l CASSAVA,
l CABBAGE,
l CAULIFLOWER,
l CARROTS
l RADDISH
l TURNIPS
l RED SKIN OF PEANUTS
l IODINE
l COBALT
l LITHIUM
57. 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
58. NON-TOXIC GOITER
TREATMENT:
IODIZED OIL IM
COMMON IN
IODINE TABLETS
WOMEN:
SALT
ADOLESCENT
FORTIFICATION
PREGNANT WITH IODINE
LACTATING EDUCATE ABOUT
MENOPAUSE INTAKE OF:
l SEAWEEDS
l SHELLFISH
l FISH- TAMBAN, HITO,
DALAG
59. MYXEDEMA COMA
MEDICAL EMERGENCY
OCCURS IN SEVERE & UNTREATED
MYXEDEMA
HIGH MORTALTY RATE
S/SX:
INTENSIFIED HYPOTHYROIDISM
NEUROLOGIC IMPAIRMENT COMA
61. MYXEDEMA COMA
MANAGEMENT:
IV THYROID HORMONES
CORRECTION OF HYPOTHERMIA
MAINTAIN VITAL FXNS
TREAT PRECIPITATING CAUSES
62.
63. PARATHYROID GLAND
4 GLANDS
SECRETES PARATHORMONE (PTH) IN
RESPONSE TO SERUM Ca & Ph LEVELS
REGULATE CALCIUM & PHOSPHORUS
METABOLISM
ORGANS AFFECTED:
BONES - RESORPTION
KIDNEYS
l Ca REABSORPTION
l Ph EXCRETION
GIT – ENHANCES Ca ABSORPTION
64. PARATHYROID DISORDERS
DIAGNOSTIC TESTS:
HEMATOLOGICAL
l SERUM CALCIUM
l SERUM PHOSPHORUS
l SERUM ALKALINE PHOSPHATASE
URINARY STUDIES
l URINARY CALCIUM
l URINARY PHOSPHATE - TUBULAR
REABSORPTION OF PHOSPHATE
65. HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION
HYPOCALCEMIA
CALCIUM IS:
l DEPOSITED IN THE BONE
l EXCRETED
CAUSE:
HEREDITARY
IDIOPATHIC
SURGICAL
66. HYPOPARATHYROIDISM
S/SX:
ACUTE HYPOCALCEMIA
l TINGLING OF THE FINGERS
l CHEVOSTEK’S, TROUSSEAU’S
CHRONIC HYPOCALCEMIA
l FATIGUE, WEAKNESS
l PERSONALITY CHANGES
l LOSS OF TOOTH ENAMEL, DRY SCALY SKIN
l CARDIAC ARRHYTHMIA
l CATARACT
67. 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
68. HYPERPARATHYROIDISM
INCREASED PTH PRODUCTION
HYPERCALCEMIA
HYPOPHOSPHATEMIA
PRIMARY – TUMOR OR HYPERPLASIA OF THE
PARATHYROID GLAND
SECONDARY – COMPENSATORY OVERSECRETION
OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:
l CHRONIC RENAL DSE
l RICKETS
l MALABSORPTION SYNDROME
l OSTEOMALACIA
70. 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
71. ADRENAL GLAND
STIMULATED BY ACTH
HORMONE PRECURSOR:
l CHOLESTEROL
SECRETES:
l CORTISOL
l ALDOSTERONE
l SEX HORMONES : ANDROGEN, ESTROGEN
72. 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
77. ADRENAL INSUFFICIENCY
ADDISON’S DISEASE
INCAPABILITY OF THE ADRENAL
CORTEX TO PRODUCE
GLUCOCORTICOIDS IN RESPONSE
TO STRESS
78. ADRENAL CRISIS
ACUTE EPISODES FROM STRESS
THAT TAXES THE ADRENAL
CORTICAL FUNCTION BEYOND ITS
CAPABILITIES
POSSIBLE COMPLICATION OF
ADDISON’S DISEASE
81. ADRENAL CRISIS
LAB:
SERUM ELEC: DECREASED Na
INCREASED K
S. BUN :
S. GLUCOSE:
ADRENAL HORMONE ASSAY :
HYDROXYCORTICOID & 17 KETOSTEROID IN 24-
HR URINE DET.
82. ADRENAL CRISIS
GOALS OF CARE:
TO REVERSE SHOCK
RESTORE BLOOD CIRCULATION
REPLENISH NEEDED STEROID
83. ADRENAL CRISIS
TREATMENT:
D5NSS
ADRENAL CORTICAL HORMONE
REPLACEMENT: INJECTABLE
NEOSYNEPHRINE - SHOCK
HIGH SALT DIET
ANTIBIOTICS
84. CUSHING’S SYNDROME
CAUSE:
SUSTAINED OVER-PRODUCTION OF
GLUCOCORTICOIDS BY ADRENAL GLAND FROM
ACTH BY PITUITARY TUMOR
EXCESSIVE GLUCORTICOID
ADMINISTRATION
85. 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
86. CUSHING’S SYNDROME
PURPLE STRIAE – FROM THINNING
OF SKIN
ECHYMOSIS FROM SLIGHT TRAUMA
ANDROGENIC EFFECTS:
OLIGOMENORRHEA
HIRSUTISM
GYNECOMASTIA
HYPERTENSION FROM S. Na
87. CUSHING’S SYNDROME
TREATMENT & NURSING CARE:
PSYCHOLOGICAL SUPPORT
PREVENT INFECTION – INFLAM &
IMMUNE RESPONSE ARE SUPPRESSED
PROMOTE SAFETY
SURGERY – SUB/TOTAL ADRENALECTOMY
92. PHEOCHROMOCYTOMA
TUMOR OF ADRENAL MEDULLA
SECRETES INCREASED AMOUNT OF CATECHOLAMINES
S/SX:
HPN
HYPERGLYCEMIA
CARDIAC ARRHYTHMIA & CHF
DIAGNOSTIC TEST :
VMA IN 24H URINE
93. VMA IN 24H URINE
END PRODUCT OF CATECHOLAMINE
METABOLISM
DRUGS & FOOD TO BE WITHHELD
24H B4 THE TEST:
l COFFEE & TEA
l BANANA
l VANILLA
l CHOCOLATES
103. DIABETES MILLETUS
TYPES:
TYPE I TYPE II –
l JUVENILE ONSET l MATURITY ONSET
l BEFORE 15 YO l AFTER AGE 40
l LEAN/ NORMAL l OBESE
WEIGHT l REDUCED INSULIN
l ABSOLUTE INSULIN RECEPTOR
DEFICIENCY l NONINSULIN
l INSULIN -DEPENDENT DEPENDENT
l PRONE TO DKA l PRONE TO HHONK
104. DIABETES MILLETUS
DIAGNOSTIC DEXTROSTRIP
EXAMS: URINE TESTS:
FBS l BENEDICT’S
2 HR- l CLINITEST TAB
POSTPRANDIAL l ACETONE TEST
OGTT
GLYCOSYLATED
HGB
105. 2 HR POSTPRANDIAL
BLOOD SUGAR
INTAKE OF 100GM GLUCOSE, 2 HRS
BEFORE THE TEST
TEST FOR ABILITY TO DISPOSE
GLUCOSE LOAD
106. 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
107. GLYCOSYLATED
HEMOGLOBIN
MEASURES GLUCOSE METABOLISM
FOR THE PAST 3 MONTHS
USEFUL TO CHECK:
l COMPLIANCE WITH THERAPY
l HISTORY OF SUBCLINICAL OR
CHEMICAL DIABETES
108. DIABETES MILLETUS
PLANNING & IMPLEMENTATION:
CLIENT’S ACTIVITY
DIET : C,F,P – 50, 30, 20 LOW SATURATED FATS,
HIGH FIBER
DRUGS:
l ORAL HYPOGLYCEMICS
l BIGUANIDE
l SULFONYLUREAS
l CONTRAINDICATED - PREGNANCY
l INSULIN
109. 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
111. DIABETES MILLETUS
INSULIN THERAPY
REACTIONS:
LOCAL: GENERALIZED:
l STNGING l HIVES
l INDURATION l URTICARIA
l ITCHING l ANTIHISTAMINES
LIPODYSTROPHY 30 MIN B4
l DESENSITIZATION
112. LIPODYSTROPHY
CAUSE:
FAULTY TECHNIQUE
TRAUMA
INJECTION OF REFRIGERATED
INSULIN
MANAGEMENT:
ROTATING SITES: 1 AREA IS NOT USED
MORE THAN ONCE EVERY 3 WKS
113. INSULIN THERAPY &
HORMONAL ACTIVITY
GLUCORTICOIDS & EPINEPHRINE
CAUSES HYPERGLYCEMIA DURING:
l PHYSICAL TRAUMA
l STRESS
l INFECTION
l ANXIETY
l ANGER
l FEAR
l CHANGE IN LIFESTYLE
INCREASE IN INSULIN DOSE IS NEEDED
119. INSULIN SHOCK
LOW BLOOD SUGAR
CAUSE:
OVERDOSE OF EXOGENOUS INSULIN
EATING LESS
OVEREXERTION WITHOUT ADDITIONAL
CALORIE INTAKE
120. INSULIN SHOCK
S/SX:
PARASYMPATHETIC SYMPATHETIC
l HUNGER l IRRITABILITY
l NAUSEA l SWEATING
l HYPORTENSION l TREMBLING
l BRADYCARDIA l TACHYCARDIA
CEREBRAL l PALLOR
l LETHARGY,
l YAWNING
l SENSORIUM CX
121. 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
122. HHONK
PATHOPHYSIOLOGY
Very insufficient INSULIN
SEVERE
OSMOTIC
DEHYDRATION MARKED HYPERGLYCEMIA
LIPOLYSIS
GLUCOSURIA Without
CELLULAR
KETOSIS
HUNGER
OSMOTIC
DIURESIS
WEIGHT
LOSS POLYPHAGIA
POLYURIA
POLYDIPSIA
123. HHONK
S/SX:
S/SX OF DKA WITHOUT:
l KAUSMAUL’S BREATHING
l ACETONE BREATH
l METABOLIC ACIDOSIS
l KETONURIA
124. LACTIC ACIDOSIS
SEVERE TISSUE ANOXIA
LACTIC ACID PRODUCTION
AGGRAVATION OF EXISTING
METABOLIC ACIDOSIS
125. SOMOGYI EFFECT
TOO MUCH INSULIN
HYPOGLYCEMIA
GLUCAGON IS RELEASED
REBOUND
HYPERGLYCEMIA
+
LIPOLYSIS KETOSIS
GLUCONEOGENESIS
GLYCOGENOLYSIS
126. CHRONIC COMPLICATIONS
OF DIABETES MILLETUS
DEGENERATIVE CHANGES IN THE
VASCULAR SYSTEM
l UNDERNOURISHMENT
l ATHEROSCLEROSIS
NEUROPATHY FROM:
l VASCULAR INSUFFICIENCY
l VIT B DEFICIENCY
l HYPERGLYCEMIA
EYE COMPLICATIONS FROM ANOXIA
l CATARACT
l DIABETIC RETINOPATHY
l RETINAL DETACHMENT
127. CHRONIC COMPLICATIONS
OF DIABETES MILLETUS
NEPHROPATHY
l DAMAGE & OBLITERATION OF CAPILLARIES
SUPPLYING THE KIDNEY
HEART DISEASE
l MI FROM ATHEROSCLEROSIS
SKIN CHANGES
l DIABETIC DERMOPATHY – HYPERPIGMENTED &
SCALY PRETIBIAL AREAS
LIVER CHANGES
l ENLARGEMENT & FATTY INFILTRATION
128. Ms A, 45 y.o., has a simple goiter. She’s
being seen by the community health nurse
for teaching & follow-up regarding nutritional
deficiencies related to her goiter. Ms A’s
problem is almost associated with what
nutritional deficiency?
a. Calcium
b. Iodine
c. Iron
d. Sodium
