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ENDOCRINE SYSTEM
ENDOCRINE GLAND
ENDOCRINE GLANDS
HORMONES FUNCTIONS
Thyroid to release hormones Adrenal cortex to release hormones Growth, maturation & function of sex organs
PROLACTIN/ LTH
ENDOCRINE GLANDS
ENDOCRINE GLAND HORMONE ADH FUNCTION
Regulates water metabolism
ENDOCRINE GLAND
ENDOCRINE GLANDS
HORMONES FUNCTION
ALDOSTERONE Fluid & electrolyte balance; Na reabsorption; K excretion Glycogenolysis; Gluconeogenesis Na & water reabsorption Antiinflammatory Stress hormone Slightly significant
ADRENAL CORTEX
CORTISOL
SEX HORMONES
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 Decrease serum Ca by increasing bone deposition Increase serum calcium by promoting bone decalcification
THYROID
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
ENDOCRINE GLANDS
ENDOCRINE HORMONES GLAND FUNCTION
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)
INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine) PITUITARY GLAND IS INHIBITED TO
RELEASE STIMULATING HORMONE (e.g. TSH)
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
THERAPY
STEROID THERAPY
STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
ADRENAL ATROPHY
STEROID THERAPY
PHARMACOLOGIC CONSIDERATIONS: PEPTIC ULCER IN SHORT TERM, HIGH
DOSE STEROID TX
PALLIATIVE EFFECT
STEROID THERAPY
ASSESSMENT: BASELINE STEROID LEVEL IS
ASSESSED BEFORE PROLONGED THERAPY IS STARTED TO DETERMINE THE DOSE REQUIRED
STEROID THERAPY
PSYCHOLOGICAL CXS
MOOD ELEVATION, FRANK EUPHORIA THEN, DEPRESSION
STEROID THERAPY
IMPORTANT FACTS: MAJOR UNTOWARD EFFECTS: MASKS INFECTION DEFENSE AGAINST INFECTION FROM
LYMPHOPENIA
SLOW P.U.D.
ANTIINFLAMMATORY EFFECT
ACTIVATION/ REACTIVATION
STEROID THERAPY
IMPORTANT FACTS: MINOR UNTOWARD EFFECTS:
PIGMENTATION ACNE FACIAL
HAIR MOON-FACIE
IMPORTANT FACTS:
STEROID THERAPY
RETARDATION
STEROID THERAPY
STEROID LEVELS PITUITARY GLAND IS INHIBITED TO REALEASE ACTH
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
HYPOPITUITARISM HYPERPITUITARISM
HYPOPITUITARISM
ANTERIOR LOBE
HYPERPITUITARISM
ANTERIOR LOBE
EOSINOPHILIC TUMOR
INCREASED
PROLACTIN
BASOPHILIC TUMOR
INCREASED
CHROMOPHOBE TUMOR
INCREASED
HORMONE
MANAGEMENT
HYPOPITUITARISM
SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY
HYPERPITUITARISM
SURGICAL REMOVAL / IRRADIATION MONITOR FOR HYPERGLYCEMIA & CARDIOVASCULAR PROBLEMS
DIABETES INSIPIDUS
S/SX: POLYURIA
15-29L/ DAY
DIABETES INSIPIDUS
IM OR
NON-HORMONAL THERAPY
SALT & P RESTRICTED DIET, INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE BALANCE
WATER INTOXICATION
Mission possible
THYROID GLAND
STIMULATED BY THYROID STIMULATING HORMONE (TSH) NEEDS IODINE TO SYNTHESIZE HORMONE SECRETES:
THYROXINE
THYROID DISTURBANCES
DIAGNOSTIC TESTS:
B.M.R.- AMT OF O2 USED BY A PERSON @ A GIVEN
TIME
SERUM THYROXINE (T4), SERUM TRIIODOTHYRONINE (T3), SERUM TSH BLOOD SERUM CHOLESTEROL
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 of Increase use of F & P WATER as fuel
BMR:
DECREASED
SKIN:
THICK, PUFFY, DRY
HAIR:
DRY, BRITTLE
HYPERTHYROIDISM
HYPERACTIVE LABILE MOOD HYPERSENSITIVE TENSED
WEIGHT:
INCREASED DECREASED
APPETITE:
DECREASED INCREASED
MANAGEMENT
SURGICAL:
SUBTOTAL THYROIDECTOMY
ANTITHYROID MEDICATIONS
LUGOLS SOLUTION
(POTASSIUM IODIDE)
DECREASE THYROID VASCULARITY INHIBIT IODINE RELEASE DILUTED IN MILK / JUICE STAINS THE TEETH- USE STRAW
RADIOACTIVE IODINE
BETA BLOCKERS
SUBTOTAL THYROIDECTOMY
REMAINING TISSUE PROVIDES ENOUGH HORMONES FOR NORMAL FXN
SUBTOTAL THYROIDECTOMY
COMPLICATIONS:
RECURRENT LARYNGEAL NERVE INJURY
HOARSENESS 12-24 HRS POST OP OBSERVE FOR IRREGULAR BREATHING, CHOKING SIGNS TRACHEOSTOMY SET @ BEDSIDE
HEMORRHAGE
TETANY
DEPENDS UPON THE NUMBER OF PARATHYROID GLANDS REMOVED
S/SX: 1ST TINGLING TOES & FINGERS 2ND CHEVOSTEKS SIGN (TAPPING THE FACIAL
MUSCLES)
MANAGEMENT:
DECREASE TEMP ANTITHYROID DRUGS GLUCOSE DIGITALIS STEROIDS TO DECREASE ACTH
CAUSES:
EMOTIONAL STRESS PHYSICAL STRESS
VARIANTS OF HYPERTHYROIDISM
GRAVES DSE THYROIDITIS GOITER
GRAVES DISEASE
CAUSE:
UNKNOWN AUTOIMMUNE WITH LONG-ACTING THYROID STIMULATOR
OPHTHALMOPATHY
EXOPHTHALMOS ACCUMULATION OF
FLUID IN THE FAT PADS BEHIND HE EYEBAL
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
CHRONIC, HASHIMOTOS
IMMUNOLOGICAL FACTORS PRESENCE OF IMMUNOGLOBULINS & ANTIBODIES DIRECTED AGAINST THE THYROID
GOITER
ENLARGEMENT OF THE THYROID GLAND.
TYPES:
TOXIC NODULAR NONTOXIC
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
NON-TOXIC GOITER
TREATMENT: COMMON IN WOMEN:
ADOLESCENT PREGNANT LACTATING MENOPAUSE IODIZED OIL IM IODINE TABLETS SALT FORTIFICATION WITH IODINE EDUCATE ABOUT INTAKE OF:
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
PARATHYROID DISORDERS
DIAGNOSTIC TESTS: HEMATOLOGICAL
SERUM
URINARY STUDIES
URINARY
HYPOPARATHYROIDISM
DECREASED PTH PRODUCTION HYPOCALCEMIA CALCIUM IS:
DEPOSITED IN THE BONE EXCRETED
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
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
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
HORMONE
ADRENAL GLAND
FUNCTION
Renal : Na & Cl reabsorption; K excretion GI : Na absorption increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS Blocks inflammation Counteracts effect of histamine Physiologically insignificant Becomes useful during menopause in women
ALDOSTERONE
GLUCOCORTICOIDS
SEX HORMONE
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 INSUFFICIENCY
ADDISONS DISEASE
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
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
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
ALDOSTERONISM
HYPERSECRETION OF ALDOSTERONE
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
& TEA
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
PATHOPHYSIOLOGY
REDUCED /NO INSULIN REDUCED /NO INSULIN HYPERGLYCEMIA HYPERGLYCEMIA OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION GLUCOSURIA GLUCOSURIA OSMOTIC OSMOTIC DIURESIS DIURESIS POLYURIA POLYURIA
DIABETES MILLETUS
DIABETES MILLETUS
S/SX: 3 Ps WEIGHT LOSS STAGES: PREDIABETES SUSPECTED CHEMICAL CLINICAL / OVERT
DIABETES MILLETUS
PREDIABETES / POTENTIAL:
CONCEPTION CONCEPTION
DIABETES MILLETUS
SUSPECTED/ SUBCLINICAL/ LATENT:
PREDIABETES PREDIABETES
NO STRESS
STRESS STRESS
DIABETES MILLETUS
CHEMEICAL:
SUBCLINICAL GTT IS ABNORMAL NO STRESS NO STRESS ASYMPTOMATIC ASYMPTOMATIC STRESS STRESS SYMPTOMATIC SYMPTOMATIC
DIABETES MILLETUS
CLINICAL / OVERT:
CHEMICAL CHEMICAL PERSISTENT INCREASED FBS PERSISTENT INCREASED FBS WITH OR WITHOUT STRESS WITH OR WITHOUT STRESS
SYMPTOMATIC
DIABETES MILLETUS
TYPES: TYPE I
TYPE II
JUVENILE ONSET BEFORE 15 YO LEAN/ NORMAL WEIGHT ABSOLUTE INSULIN DEFICIENCY INSULIN -DEPENDENT PRONE TO DKA
MATURITY ONSET AFTER AGE 40 OBESE REDUCED INSULIN RECEPTOR NONINSULIN DEPENDENT PRONE TO HHONK
DIABETES MILLETUS
DIAGNOSTIC EXAMS: FBS 2 HRPOSTPRANDIAL OGTT GLYCOSYLATED HGB DEXTROSTRIP URINE TESTS:
BENEDICTS CLINITEST TAB ACETONE TEST
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
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 ARM UPPER
THIGH
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
SURPRISE!!!
ACUTE COMPLICATIONS
OF DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA) INSULIN SHOCK HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA SOMOGYI EFFECT
D.K.A. PATHOPHYSIOLOGY
NO INSULIN NO INSULIN OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION MARKED HYPERGLYCEMIA MARKED HYPERGLYCEMIA
LIPOLYSIS LIPOLYSIS
KETOACIDOSIS KETOACIDOSIS
POLYDIPSIA 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
PATHOPHYSIOLOGY
SEVERE SEVERE OSMOTIC OSMOTIC DEHYDRATION DEHYDRATION GLUCOSURIA GLUCOSURIA OSMOTIC OSMOTIC DIURESIS DIURESIS POLYURIA POLYURIA
Very insufficient INSULIN Very insufficient INSULIN MARKED HYPERGLYCEMIA MARKED HYPERGLYCEMIA LIPOLYSIS LIPOLYSIS Without Without KETOSIS KETOSIS
HHONK
POLYPHAGIA POLYPHAGIA
POLYDIPSIA POLYDIPSIA
HHONK
S/SX: S/SX OF DKA WITHOUT:
KAUSMAULS
LACTIC ACIDOSIS
SEVERE TISSUE ANOXIA SEVERE TISSUE ANOXIA
SOMOGYI EFFECT
TOO MUCH INSULIN HYPOGLYCEMIA GLUCAGON IS RELEASED
UNDERNOURISHMENT ATHEROSCLEROSIS VASCULAR INSUFFICIENCY VIT B DEFICIENCY HYPERGLYCEMIA CATARACT DIABETIC RETINOPATHY RETINAL DETACHMENT
NEUROPATHY FROM:
DAMAGE & OBLITERATION OF CAPILLARIES SUPPLYING THE KIDNEY MI FROM ATHEROSCLEROSIS DIABETIC DERMOPATHY HYPERPIGMENTED & SCALY PRETIBIAL AREAS ENLARGEMENT & FATTY INFILTRATION
HEART DISEASE
SKIN CHANGES
LIVER CHANGES
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?
a. b. c. d.