Nursing Lecture about the Endocrine System: Altered Metabolic Function

Altered Metabolic Function

1. • Lack (<) Endocrine Gland Over (>)
   • Pineal –behind lateral ventricles
   • Diabetes Insipidus Pituitary - SIADH
   • Hypothyroidism Thyroid - Hyperthyroidism
   • pedia: Cretinism Basedow’s/Parry’s
   • adult: Myxedema Coma Grave’s Disease
   • Hypoparathyroidism Parathyroid - Hyperparathyroidism
   • Thymus
   • DM Pancreas
   • Addison’s Disease Adrenals - Cushing’s/Conn’s
   • Gonads (testes / ovaries)
2. • Interaction of endocrine system with aging are inconclusive, however, changes in endocrine glands & target organs occur
   • Loss of self-regulation (autoimmune or immunodeficiency disorders)
   • Target organs lose ability to respond to hormones
   • Hypothalamus & pituitary functions may be altered by changes in neurotransmitter levels
   • Wear out of body structures in time are no longer able to adapt to stressors (theory of stress adaptation)
3. • Inspection:
   • General appearance
   • Weight – √ weight loss but ↑ appetite ; significant weight gain
   • Height – acromegaly, dwarfism, gigantism
   • body size – trunchal obesity
   • Face – moon face
   • Eyes – note for exophthalmus
   • √ Visual acuity
   • Neck area –symmetry & size
   • Midline position of trachea
   • Note thickness/bulging areas over thyroid glands
   • Observe for forceful pulsations in carotid area
   • Palpation:
   • Thyroid gland – anterior &/or posterior approach
   • Normal – non-palpable
   • Pulses – note palpitations
   • Auscultation
   • Auscultate heart rate & rhythm
   • Abdominal bowel sounds
   • Vital signs & history taking
4. • “ diabetes” – going through; “mellitus” – honey/sweet
   • Metabolic disorder characterized by glucose intolerance resulting from an imbalance between insulin supply & demand
   • Involves β -cells if Islet of Langerhans (pancreas) – source of insulin
   • Insulin Functions:
   • Promotes glucose uptake by target cells
   • Prevents fats & glycogen breakdown
   • Inhibits gluconeogenesis
   • Increases protein synthesis
   • Types:
   • Type I = IDDM (insulin dependent diabetes mellitus)/ Juvenile Diabetes
   • Inability to produce adequate insulin (autoimmune) -> lifetime insulin injection
   • Type II = NDDM (non-insulin dependent diabetes mellitus)
   • Impairment in insulin secretion -> oral hypoglycemics
5. • Type I
   • Juvenile onset
   • Abrupt onset
   • Little or no insulin produced
   • within ideal body weight / thin
   • Tx:
   • diet modification
   • Exercise
   • Insulin injection
   • Type II
   • Maturity onset
   • Insidious onset
   • Below normal or normal insulin production (but high demand for it)
   • 80% of clients are obese
   • Tx:
   • diet modification
   • Exercise
   • Oral hyperglycemics (OHA)
6. Genetic predisposition Environmental agents inciting an immune response Autoimmune destruction of β cells Insulin resistance Inability of pancreas to release insulin ↓ glucose utilization Stimulates insulin secretion initially Increased insulin demand Fat & protein mobilization Blood glucose accumulation Uncontrolled increased in blood sugar Diabetes mellitus ↓ insulin response due to exhaustion
7. • Hyperglycemia – increased blood sugar levels (normal = 80-120mg/dL)
   • Glycosuria – (+) glucose in urine
   • Polyuria – excessive urination
   • Polydypsia – excessive thirst
   • Polyphagia – excessive hunger
   • Weight loss despite normal or increased appetite (type I)
   • Loss of body fluids
   • Loss of body tissues
   • Blurring of vision
   • Fatigue / weakness
   • Skin infections
   • Pruritus (candidal infections common among women)
8. • Blood Tests
   • Capillary Blood Glucose (CBG) – use of a drop of capillary blood (lancet & precision strips)
   • - rapid & economical monitoring
   • - self-monitoring
   • Fasting Blood Sugar (FBS)– glucose is measured after 8-12hrs of fasting (normal 70-110mg/dL)
   • - (+) DM > 126mg/dL
   • Glucose Tolerance Test/Oral Glucose Tolerance Test (OGTT) – measures body’s ability to store glucose by removing it from blood
   • - best method for Dx
   • - requires 10-12hrs fasting
   • - client is given 100g glucose then plasma glucose is monitored after 1, 2, or 3hrs
   • - blood glucose should return to normal within 2-3hrs
   • Glycosylated hemoglobin – measures HbA 1c & provides an index of glucose levels over the previous 2-3months
9. • priority = correct deficiency
   • D iet: 50-60%CHO, 10-20%CHON, 20-30%fats (unsaturated)
   • I nsulin
   • A nti-diabetic agents
   • B lood sugar monitoring
   • E xercise
   • T ransplant of pancreas (if indicated)
   • I nsure adequate food intake
   • S crupulous foot care – cut toenails straight
   • - do not use sandpaper or stones
   • - socks = cotton
   • - shoes = snugly
   • - water = tepid
   • - foot powder
   • - dry between toes (after bath)
   • - do not walk on barefoot
10. • Oral Hypoglycemic agents – for type II only
    • C/I: pregnancy, breastfeeding
    • Ex: metformin (Glucophage), glipizide (Glucotrol), acarbose (Precose), glicazide (Diamicron)
    • Insulin – must be stored in cold (not freezing) temp
    • Preparation Onset Duration Peak Route
    • R egular Insulin - 30mins-1hr - 6-8hrs - 2-4hrs SC/IV
    • N PH (isophane) - 1-2hrs - 18-26hrs - 6-12hrs SC
    • U ltralente - 4-6hrs - 14-24hrs - 36hrs SC
    • Subcutaneous injections are absorbed fastest at the abdomen
    • Watch out for signs of hypoglycemia – cold, clammy skin & diaphoresis
    • Instruct client to drink fruit juices (i.e.. Orange juice)
    • Amon g unconscious = D50/50 IV
    • Clien ts taking NPH must have an afternoon snack
11. • Lipodystrophy – loss of fatty tissues
    • Instruct client to rotate injection sites
    • Diabetic Ketoacidosis (DKA) – liver ketone production exceeds cellular use & renal excretion
    • Commonly occurs in type I
    • Often preceded by stress, infection, omission or inadequate insulin use
    • Dx: Blood glucose > 250mg/dL, HCO3 <15meq/l,>
    • Tx goals: improve tissue perfusion & circulatory volume
    • Correct electrolyte imbalances & correct pH
    • Decrease serum glucose
    • Use low-dose insulin therapy (IV)
13. • Function – synthesis of thyroxin (T4) and triiodothyronine (T3)
    • increases metabolism & prot ein synthesis
    • Regulates pituitary feedback mechanism
    • Necessary for brain development (esp. in infants)
    • Bound to thyroid hormone-binding globulin (TBG) for transport in blood
    • T3 = triiodothyronine (active form)
    • T4 = thyroxin (needs to be converted to T3 before manifestation of physiologic action)
    • Secretion is regulated by hypothalamic-pituitary-thyroid feedback (release of thyroid stimulating hormones –TSH)
    • RDA of iodine is 40-50 mcg (infants), 70-120 mcg (children), and 150 mcg (adolescents and adults)
14. Sleep, cold temp, stress hypothalamus Thyroid-releasing hormone (TRH) Anterior pituitary (TSH) Thyroid gland (T3 & T4) Target organs Inhibition
15. • Basal Metabolic Rate – measures O 2 consumption of the body at a given time
    • Thyroid Function Test – immunoassays measuring T 3 , T 4 , & TSH levels
    • Serum TSH - TSH positively regulates thyroid hormone synthesis and release while a a negative feedback exists by thyroid hormone on TSH secretion by the pituitary; only test that can detect small changes of thyroid hormone excess or deficiency
    • Free T4 test (FT4) – measures unbound T4 that is free to enter the cells; total T4 reflects thyroid hormone activity
    • Radioactive iodine uptake test (RAIU) – measures the ability of thyroid gland to remove & concentrate iodine from blood
    • Thyroid scan – used to detect nodules & determine functional activity of thyroid glands
    • CT Scan & MRI – used to demonstrate tracheal compression on neighboring structures
16. • too little thyroid hormone produced, when there is decreased conversion from T4 to T3 , or from Tx of hyperthyroidism
    • Primary – intrinsic disorder in the thyroid gland
    • Congenital (cretinism)
    • Defective hormone synthesis
    • Iodine deficiency – most common cause (Hashimoto’s disease)
    • Result of thyroidectomy
    • Secondary – insufficient stimulation of thyroid hormone by TSH from anterior pituitary gland
    • Tertiary – hypothalamus fails to produce TRH
    • Dx: detailed Hx & physical assessment;
    • low serum T4 & elevated TSH
    • Tx/Nursing Management: Replacement T3 or T4 therapy – FOR LIFE (caution use with MI, HPN, DM, pregnant & elderly)
    • Levothyroxine (Synthroid) – T4
    • Liothyronine (Cytomel) – T3
    • Myxedema Coma – life-threatening end stage expression of the disease
    • Myxedema – non-pitting edema w/periorbital puffiness
    • Coma, hypothermia, cardiopulmonary problems & severe metabolic disorders
    • Aggressive management
18. • Excessive delivery of thyroid hormones
    • Common cause: Grave’s disease (autoimmune) & goiter
    • Ingestion of excessive thyroid hormone replacements
    • Grave’s – abnormal stimulation of thyroid gland by thyroid stimulating antibodies
    • Exophthalmus (bulging of eyeballs) – common manifestation
    • Dx: increased serum T4
    • Tx/ Nursing Management: Anti-thyroids = 2-3wks before effects are seen
    • Propylthiouracil (PTU) – continued during pregnancy but stopped 2-3wks after delivery
    • Methimazole (Tapazole) – inhibits thyroid hormone synthesis
    • SSKI (Lugol’s Solution) – reduces thyroid gland vasculature
    • *Propanolol / Metoprolol – counteracts metabolic rate elevation
    • RAI Therapy
    • Thyroidectomy
    • Thyroid storm/crisis – life-threatening
    • Peripheral cooling is initiated
19. • Hypothyroidism
    • Decreased BMR
    • Myxedematous features
    • Deep voice
    • Impaired growth (child)
    • ↑ cholesterol levels
    • Behavior: mental & physical fatigability; mental retardation (infant)
    • Bradycardia
    • Decreased appetite
    • Weight gain
    • Cold intolerance
    • Hyperthyroidism
    • Increased BMR
    • Exophthalmus
    • Lid lag
    • Fine hand tremors
    • Decreased blinking
    • ↓ cholesterol levels
    • Behavior: restlessness, wakefulness, irritability, anxiety
    • Tachycardia & palpitations
    • Increased appetite
    • Weight loss
    • Heat intolerance
20. • Pre-op: achieve euthyroid state by Lugol’s solution & antithyroid drugs (2-3wks); rest
    • Post-op Care:
    • Bedside: tracheostomy set, suction equipments & calcium gluconate
    • Position: semi-fowler’s with limited head movement, avoid neck hyperextension
    • Monitor for:
    • Bleeding: √dressing & nape area
    • Hypocalcemia: √Chvostek’s & Trousseau’s sign
    • Respiratory distress
    • Thyroid storm – this is medical emergency
    • Laryngeal damage - √hoarseness & loss of voice
21. • also called Radioiodine I-131 therapy
    • for hyperthyroidism
    • I-131(small dose) is swallowed, it is absorbed into the bloodstream in the GI tract and concentrated from the blood by the thyroid gland, where it begins destroying the gland’s cells
    • client simply swallows a single dose (a prepared dose), in capsule or liquid form, and is quickly absorbed
    • effect of this treatment on the thyroid gland usually takes between one and three months to develop, with maximum benefit occurring three to six months after treatment
    • Nearly all the radioactive iodine leaves the body during the first two days following the treatment, primarily through the urine (Small amounts will also be excreted in saliva, sweat, tears, vaginal secretions, and feces)
    • Client will be able to go home after treatment
    • Clients who need to travel immediately after treatment are advised to carry a letter of explanation from physician
22. • Use private toilet facilities, if possible, and flush twice after each use.
    • Bathe daily and wash hands frequently.
    • Drink a normal amount of fluids.
    • Use disposable eating utensils or wash your utensils separately from others.
    • Sleep alone and avoid prolonged intimate contact.
    • Avoid prolonged contacts esp. with pregnant women, infants, & children
    • Launder your linens, towels, and clothes daily at home, separately.
    • Do not prepare food for others that requires prolonged handling with bare hands.
    • C/I: pregnancy (can damage the baby's thyroid gland)
    • breastfeeding mother (unless they are willing to cease breastfeeding their newborn completely)
    • Pregnancy should be delayed until at least 6-12months after treatment (treatment exposes the ovaries to radiation)
    • Women who have not yet reached menopause should fully discuss the use of I-131 with their physician.
    • Inform client that it is highly likely that the entire thyroid gland will be destroyed with this procedure (most clients will need to take thyroid pills for the rest of their life following the procedure.
    • There are essentially no other permanent side effects from the procedure
23. • Parathyroid hormone (PTH) - major regulator of serum calcium & phosphate
    • Serum Ca +2 = 8.5 - 10.5mEq/dL or 4 - 5.5mEq/L
    • Serum PO 4 -3 = 2.5 - 4.5mEq/dL or 1.8 - 2.6mEq/L
    • Parathyroid gland –secretes the hormone
    ↓ serum Ca PTH Kidney- ↓ Ca Elimination & ↑ phosphate elimination ↑ serum Ca Intestine-↑ Ca absorption Bone-release of Ca Activated Vit.D
24. • Blood tests:
    • Serum calcium
    • Serum phosphate
    • Urine calcium & phosphate level determination (PO 4 -3 lost in urine is directly related to PO 4 -3 blood concentrations)
    • Parathyroid hormone by radioimmunoassay
25. • Hypoparathyroidism Hyperparathyroidism
    • Main Problem: - deficiency of Ca +2 in blood - excess Ca +2 in blood ↓Ca +2 in bones
    • S/Sx: - Early = tingling - Recklin-Hensen’s Disease (↑Ca +2 in blood)
    • = Chvostek’s sign - bone pain & destruction
    • = Trousseau's sign
    • Lab: - Ca +2 <>
    • Mgt: - priority = Ca +2 - priority = safety
    • replacement
    • - diet: Broccoli - diet: ↓Ca +2
    • Sardines - ↑oral fluids to prevent stone Spinach formation
    • Tuna - strain urine
    • Meds: - Fosamax - Paracalcitriol – suppress PTH
    • Ca +2 gluconate IV (for acute)
27. • Adrenal glands – found retroperitoneally at the apex of kidneys
    • Medulla = secretes epinephrine & norepinephrine
    • Cortex = secretes:
    • glucocorticoids (cortisol) – response to stress 7 survival
    • Mineralocorticoids (aldosterone) – regulates K + & Na + levels
    • adrenal sex hormones – contributes to pubertal growth
    • Dx:
    • ACTH (Adreno-corticotropic Hormone) Stimulation Test – releases corticosteroids
    • identifies/differentiates Addison’s from Cushing’s
    • *Addison’s = ↓/ (-) corticosteroids; Cushing’s ↑ corticosteroids
    • specimen is brought to the lab immediately
    • Dexamethasone Suppression Test – to identify endogenous depression (within the self, therefore, R/T chemical imbalance
    • 17 Ketosteroid & 17 OHCS (Hydroxycorticosteroids) – same as ACTH
    • * ↓ secretions = Addison’s; ↑ secretions = Cushing’s
28. • CUSHING’S SYNDROME
    • Overproduction of ACTH
    • Cortisol
    • Hyperglycemia
    • CHON deficiency ( ↓ AA)
    • Muscle wasting (appears fat due to edema – trunchal obesity)
    • Poor antibody response
    • Aldosterone
    • hypernatremia & hypokalemia (HPN, weight gain, pitting edema, moon face)
    • Androgen (hirsutism)
    • Mgt: correct electrolyte imbalance = priority
    • prevent infections
    • I&O monitoring & v/s
    • Diet: ↑ CHON & K + ; ↓ Na + & calories
    • Meds: Mitotane (Lysodren) – ↓ cortisol production
    • Adrenalectomy
    • ADDISON’S DISEASE
    • Inadequate production of ACTH
    • Cortisol:
    • Hypoglycemia
    • Hyperpigmentation (inhibits melanocyte stimulating hormone = bronze-skin pigmentation)
    • Aldosterone
    • Hyponatremia & hyperkalemia (dehydration, hypotension, thin)
    • Androgen (lesser pubic hair)
    • Mgt: correct electrolyte imbalance
    • Monitor BP (hypotension & shock)
    • Force fluid intake
    • Reduce stress
    • Diet: ↑ Na + ↓ K + (acute phase); ↑ CHON & carbohydrates
    • Meds: Glucocorticosteroid replacement – FOR LIFE
    • Prednisone, Hydrocortisone (taken with meals/milk)
    • Addisonian Crisis – severe hypotension (coma & shock)
    • CBR, ↓ stimuli, ↑ hydrocortisone doses; treat shock