This document discusses endocrine glands and their hormones and functions. It provides information on various endocrine glands including the pituitary gland, adrenal glands, thyroid gland, parathyroid gland, pancreas, ovaries and testes. It discusses hormone regulation through negative feedback mechanisms and case studies on conditions affecting the endocrine system.

1. PSYCHO
ENDOCRINOLOGY
Dr. James M. Alo, RN,MAN,MAP.PHD

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

5. ENDOCRINE GLANDS
ENDOCRINE HORMONE FUNCTION
GLAND
ADRENAL EPINEPHRINE Increase heart rate & BP
Bronchodilation,
MEDULLA NOR-
Glycogenolysis
EPINEPHRINE
Stress hormone

7. 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

8. 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

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?

15. PLANNING
HEALTH PROMOTION
l IODIZED SALT
l CONTROLLING WEIGHT
HEALTH MAINTENANCE &
RESTORATION
l STEROID THERAPY

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

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

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

25. ANTERIOR PITUITARY
DISTURBANCES
HYPOPITUITARISM
HYPERPITUITARISM

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

30. POSTERIOR PITUITARY
DISTURBANCES
DIABETES INSIPIDUS
SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE

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

35. Mission possible

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

40. HYPOTHYROIDISM HYPERTHYROIDISM
SERUM
CHOLESTEROL:
INCREASED DECREASED
BMR:
DECREASED INCREASED
SKIN:
THICK, PUFFY, DRY WARM, MOIST, FLUSHED
HAIR:
SOFT, SILKY
DRY, BRITTLE

41. HYPOTHYROIDISM HYPERTHYROIDISM
NERVOUS SYSTEM:
APATHETIC HYPERACTIVE
LETHARGIC LABILE MOOD
MAYBE HYPERSENSITIVE
HYPERIRRITABLE TENSED
SLOW CEREBRATION
WEIGHT:
INCREASED DECREASED
APPETITE:
DECREASED INCREASED

42. MANAGEMENT
HYPOTHYROIDISM HYPERTHYROIDISM
MEDICAL: MEDICAL:
HORMONE REST
REPLACEMENT ANTITHYROID
DESSICATED THYROID DRUGS:
THYROGLOBULIN LUGOL’S SOLUTION
Na LEVOTHYROXINE THIOUREA DERIVATIVES
Na LYOTHYRONINE RADIOACTIVE IODINE
BETA-BLOCKERS
SURGICAL:
SUBTOTAL
THYROIDECTOMY

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

47. THYROID STORM / CRISIS
S/SX: MANAGEMENT:
HYPERTHERMIA DECREASE TEMP
> 41C ANTITHYROID
TACHYCARDIA DRUGS
APPREHENSION GLUCOSE
RESTLESSNESS DIGITALIS
IRRITABILITY STEROIDS TO
DELIRIUM DECREASE ACTH
COMA

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

49. VARIANTS OF
HYPERTHYROIDISM
GRAVE’S DSE
THYROIDITIS
GOITER

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

54. GOITER
ENLARGEMENT OF THE THYROID GLAND.
TYPES:
TOXIC NODULAR
NONTOXIC

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

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

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

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

69. 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

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

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

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

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

76. ADRENAL CORTEX
DISORERS
ADRENAL INSUFFICIENCY
ADRENAL CRISIS
CUSHING’S SYNDROME
ALDOSTERONISM

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

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

80. ADRENAL CRISIS
S/SX:
HYPOTENSION
FLUID LOSS
HYPONATREMIA

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

88. ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE
PRIMARY – CONN’S SYNDROME
SECONDARY

89. CONN’S SYNDROME
PRIMARY ALDOSTERONISM
CAUSE:
ADRENAL ADENOMA
S/SX:
HYPOKALEMIA
FATIGUE
HYPERNATREMIA, HPN, TETANY
MANAGEMENT:
SURGERY
ALDACTONE – ALDOSTERONE ANTAGONIST

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

91. ADRENAL MEDULLA
HORMONES : EPINEPHRINE
NOREPINEPHRINE
EFFECTS

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

94. PHEOCHROMOCYTOMA
MANAGEMENT:
SURGERY
MEDICAL : ADRENERGIC BLOCKING
AGENTS: PHENTOLAMINE
NURSING CARE:
MONITOR BP IN SUPINE & STANDING
MONITOR URINE FOR GLUC & ACETONE

95. PANCREAS
HORMONES:
INSULIN BY BETA CELLS
GLUCAGON BY ALPHA CELLS

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

97. DIABETES MILLETUS
PATHOPHYSIOLOGY
REDUCED /NO INSULIN
OSMOTIC
DEHYDRATION HYPERGLYCEMIA
GLUCOSURIA LIPOLYSIS CELLULAR
HUNGER
OSMOTIC
DIURESIS
WEIGHT LOSS
POLYPHAGIA
POLYURIA
POLYDIPSIA

98. DIABETES MILLETUS
S/SX:
3 – P’s
WEIGHT LOSS
STAGES:
PREDIABETES
SUSPECTED
CHEMICAL
CLINICAL / OVERT

99. DIABETES MILLETUS
PREDIABETES / POTENTIAL:
CONCEPTION
EVIDENCE OF GLUCOSE METABOLISM
ALTERATION

100. DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETES
NO STRESS STRESS
NORMAL GLUCOSE OVERT DIABETES
METABOLISM

101. DIABETES MILLETUS
CHEMEICAL:
SUBCLINICAL
GTT IS ABNORMAL
NO STRESS STRESS
ASYMPTOMATIC SYMPTOMATIC

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

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

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

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

114. SURPRISE!!!

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

116. D.K.A.
PATHOPHYSIOLOGY
NO INSULIN
OSMOTIC
DEHYDRATION MARKED HYPERGLYCEMIA
GLUCOSURIA LIPOLYSIS
CELLULAR
HUNGER
OSMOTIC
DIURESIS WEIGHT
LOSS KETOACIDOSIS
POLYPHAGIA
POLYURIA
POLYDIPSIA

117. 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

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

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