MS Nursing Notes PDF

lOMoARcPSD|46770072 Scribd - MS NURSING NOTES Nursing (Catanduanes State University) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university Downloaded by Pipit Lim ([email protected]) ...

lOMoARcPSD|46770072 Scribd - MS NURSING NOTES Nursing (Catanduanes State University) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 MEDICAL SURGICAL NURSING (CANTUBA) NOTE: STUDY DIABETIS MELLITUS and ACUTE HEMORRHAGIC PANCREATITIS STRESS RESPONSE / SMR (SYMPATHOMEDULLAR RESPONSE) / SAMR (SYMPATHOADRENALMEDULLARY RESPONSE)  stressor → HYPOTHALAMUS → responses to injury:  sympatho-adrenal medullary response o WHEN STRESSED → diaphoresis, increased BP, PR, depth & rate of respiration, pallor, cold, clammy skin, weight loss, myalgia, anorexia, diarrhea/constipation, oliguria/anuria, transient hyperglycemia, increase visual acuity o given a stressor will stimulate the hypothalamus and activate a sympatho-adrenal medullary response → adrenal medulla secretes catecholamines (epinephrine, norepinephrine)  epinephrine is both a vasodilator (coronary artery, cerebral artery, per) & vasoconstrictor (peripheral vascular arteries)  if coronary is dilated → increased myocardial blood flow → increased (longer) myocardial contraction → INCREASED PR → tachycardia  if pulmonary vein dilates, relaxation of smooth muscle of bronchi/bronchioles → bronchial dilation → increased rate & depth of respirations → hyperpnea  peripheral arterioles constricted → increased peripheral resistance → increased BP  arteriole supply in skin & mucous membrane constricted → decreased blood supply → pallor  promotes glycogenolysis (breakdown of glycogen to glucose in the liver) → transient hyperglycemia  norepinephrine → vasoconstrictor o AUTONOMIC NERVOUS SYSTEM → SYMPATHETIC & PARASYMPATHETIC  sympathetic - adrenergic - derived from the word adrenaline; the effects of SNS resembles the effects of epinephrine; the effect is rapid & manifested once it is stimulated (meanwhile, the effects of epinephrine only occur when the levels of epinephrine start to elevate in your blood)  symptoms that are highly sympathetic in origin (as opposed to medullary)  SN → sweat w/ stimulation → diaphoresis → cold, clammy skin  GIT → SN supply in GI tract → decreased gastric secretion & decreased motility → constipation, anorexia  sympathetic nerve supplying the urinary bladder muscle will cause the bladder muscle to relax & urinary sphincter to close → no urine → oliguria or anuria  SN nerve in pupils → pupil dilation → increase in visual acuity  parasympathetic - cholinergic o when stressor is removed, SN activity is normalized & epinephrine is within normal levels o to cope up w/ stressor, this first response is activated. if failed, the adrenocortical response is activated  adrenocortical response o glucocorticoid/steroids (cortisol, cortisone) - an anti-inflammatory agent, also promotes gluconeogenesis (formation of glucose from fats and protein)  anabolism - building up/constructive phase  catabolism - breaking down/destructive phase  STRESS → more cortisol produced → increased gluconeogenesis → increased protein catabolism → state of negative nitrogen balance → weight loss, body weakness  our intake of protein = energy consumption/energy expenditure  if intake is greater than expenditure, anabolism > catabolism → positive nitrogen balance  if intake is lesser than expenditure, anabolism > catabolism → negative nitrogen balance o mineralocorticoid (aldosterone) - fluid & sodium retention, potassium excretion → oliguria, anuria  neurohypophyseal response Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 o hypophysis cerebri / pituitary gland located in the base of the brain @ the sella turcica  anterior pituitary (adenohypophysis) → glandular  TSH (thyroid stimulating hormone)  ACTH (adrenocorticotropic hormone)  FSH (follicle stimulation hormone)  LH (luteinizing hormone)  MSH (melanocyte stimulating hormone)  SH (somatotropin hormone)  GH (growth hormone)  posterior pituitary (neurohypophysis) → extension of the hypothalamus → activated by stress  ADH (vasopressin) → fluid retention → oliguria, anuria  oxytocin → uterine contractions (if mother is stressed, premature uterine contractions)  if all mechanisms fails, end of the system → death will ensue o parasympathetic response will occur → the very opposite of the symptoms will take place o if symptoms are highly sympathetic → good coping mechanism o if symptoms are parasympathetic → poor coping mechanism ENDOCRINE  two possible pathophysiological processes o HYPOACTIVITY / HYPOSECRETION  congenital absence of gland → e.g. one lobe of thyroid gland or two parathyroid glands  surgical removal of the gland → total thyroidectomy, parathyroidectomy, adrenalectomy  idiopathic atrophy of the gland (decrease in size due to unknown cause) o HYPERACTIVITY / HYPERSECRETION  tumor within or outside the gland  failure of the kidneys to excrete the hormone  failure of the liver to deactivate (detoxifying) the hormone ANTERIOR PITUITARY HYPOSECRETION  PIT. DWARFISM o height is twice of that a newborn, short arms and legs  FROHLICH'S SYNDROME o dwarfism + obesity + genital atrophy (loss of reproductive ability) + mental retardation  SIMMOND'S DISEASE / PITUITARY CACHEXIA o appearance of a "wizened old man" + premature senility + mental lethargy, dry skin, hair & teeth start to fall, amenorrhea, absence of spermatogenesis  administer commercially prepared growth hormones → somatotropin, somatrem/protropin, humatrope ANTERIOR PITUITARY HYPERSECRETION  GIGANTISM o symptoms appear before the closure of the epiphyseal line o hyperactivity of anterior pituitary → rapid growth of the long bones → prolongation / elongation of the long bones  ACROMEGALY o symptoms appear after the closure of the epiphyseal line  increase in bone thickness & hypertrophy of the soft tissue (no longer get taller bc epiphyseal lines are closed), enlargement of the cartilages (nose, ears, larynx → deepening of the voice)  prognathism/protrusion of the jaw  thickening of the lips & oral mucous membrane  lengthening of the chin Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  overgrowth of the mandible → separation of the lower teeth  broad hands, spade-like fingers  abdomen → enlargement of the visceral organs (splenomegaly, hepatomegaly) o management - suppress production of the hormone o removal of the anterior pituitary gland (hypophysectomy) o drugs to inhibit the production of the GH  somatostatin, sandostatin, octreotide  epiphyseal line closes at 18-20 years old POSTERIOR PITUITARY GLAND DIABETES INSIPIDUS (DI)  disorder in water metabolism due to the decreased supply of ADH  symptoms o prevent the renal tubules from reabsorbing the water → polyuria (5-29 L/day) → polydipsia & diluted urine (→ decreased urine specific gravity) & increased serum osmolarity (bc of hyponatremia)  management - administer commercially prepared ADH (vasopressin tannate, pitressin tannate, desmopressin acetate, lypressin acetate, clofibrate) o nursing responsibilities  vasopressin & pitressin → oily preparation → DEEP IM  can cause lipodystrophy (rotate the site of administration)  potent vasoconstrictor → monitor BP (can cause hypertension)  desmopressin & lypressin → nasal spray  first priority nursing responsibility → ensure clear airway passages before spraying  clofibrate (Atromid, Clo 5) → antilipidemic drug & also has an antidiuretic effect SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)  hyperactive posterior pituitary gland → increased ADH → o → fluid retention (→ increased intravascular volume → hypervolemia → increased BP) o → fluid retention → electrolyte dilution → dilutional hyponatremia → fluid movement into the cell → cellular overhydration → movement of fluid into brain tissue → cerebral edema → increased ICP o → increased intravascular volume → increased renal perfusion → increased GFR → increased URINE → no leg edema  management - suppress the gland o surgical (hypophysectomy) o cobalt therapy (destruction of gland) o drugs - demeclocycline/Declomycin (oral) → antimicrobial (tetracyline) → inhibits ADH PARATHYROID GLANDS  parathormone → reabsorption of calcium by the renal tubules & excretion of phosphorus, essential for blood coagulation, regulates cardiac rhythmicity HYPOPARATHYROIDISM / HYPOCALCEMIA / TETANY  tetany - uncontrolled spasm, hyperirritability, positive Chvostek (tapping the facial nerve - just below the temple and in front of the ear; positive if there is unilateral spasm) / Trosseau (occlude the blood flow of the extremity for 1-2 mins using a tourniquet or BP cuff; positive if when the blood flow has been occluded, there is carpopedal spasm) o hypocalcemia - normal 8-11 mg/dL, 4.5-5.5 mEq/L  advise seafood/seashells  hypocalcemia → hyperphosphopatamia  hypercalcemia → hypophosphopatemia  milk, cheese, dairy products, egg yolk → high in phosphorus  cabbage & broccoli & tofu → high in calcium, low in phosphorus Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  commercially prepared calcium o calcium carbonate, calcium lactate, calcium chloride 10%, calcium gluconate o best time to take an oral calcium preparation → after meals (any calcium preparation → stimulate the release of gastrin → HCl production / prevents GI upset) o give with vit. D/Tachysterol (dihydrotachysterol/Hytakerol, calciferol [ergo-, chole-], calcifediol, calcitriol/Rocaltrol) to increase reabsorption of calcium o vitamin A - retinol o vitamin C - ascorbic acid o vitamin D - tachysterol o vitamin E - tocopherol o vitamin K - menadione / Phytonadione  HYPERPARATHYROIDISM / HYPERCALCEMIA ADRENAL GLANDS CUSHING'S SYNDROME  hyperactive adrenal cortex → increased cortisol o increase in SSS hormones → SUGAR, SALT, SEX o adrenal cortex releases glucocorticoids → gluconeogenesis (sugar) →  → increased lipolysis → abnormal fat distribution → moon facies & buffalo hump  → increased protein catabolism → tissue starvation, muscle wasting → negative nitrogen balance → truncal obesity  → reduce fibroblastic activity → loss of collagen & connective tissue → thinning / stretching of the skin → abdominal (purple) striae (stretch marks) o adrenal cortex releases mineralocorticoids (aldosterone) → fluid & sodium retention (salt) →  → increase intravascular volume → hypervolemia → increased BP (hypertension)  → hypernatremia, hypokalemia o adrenal releases androgens (sex) →  → virilism, mascunalization, hirsutism  can be caused by prolonged steroidal therapy  moon face (facies; face is round, oily, with acne), virilism (masculinization), hirsutism (excessive hair growth), buffalo hump (as a result of fatty deposits on the neck & supraclavicular area)  management - suppression o adrenalectomy o cortisol inhibitors (aminoglutethimide) o trilostane o metyrapone o mitotane ADDISON'S DISEASE  hypoactive adrenal cortex → decreased cortisol  decrease in SSS hormones → SUGAR, SALT, SEX  decrease in sugar hormone - hypoglycemia o anterior pituitary gland stimulated by decreased steroid to release ACTH (increase) → melanocyte stimulating effect → tan complexion / bronze skinned individual  decrease in salt hormone o intravascular volume decreased → hypovolemia → decreased BP o hyponatremia, hyperkalemia (→if level below 2.5 & above 7 → myocardial irritability → dysrhythmias → cardiac arrest)  decrease in sex hormone → loss of axillary and pubic hair  management - supplement o administer steroids (prednisolone, dexamethasone, hydrocortisone, betamethasone) → gastric irritation → take it on a full stomach or after meals  cause hyperglycemia → monitor blood sugar level  causes fluid & salt retention → limit sodium & fluid intake, monitor I&O, monitor body weight once a day  prolonged used to steroid → can cause osteoporosis → increase calcium intake Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 increase capillary fragility → ecchymosis → avoid any form of trauma or injury / avoid contact sports  suppress immune response → avoid any possible sources of infection (crowded, congested areas, avoid contact w/ people with infections), placed in reverse isolation if on prolonged steroid therapy  taper the dose (withdraw gradually) to prevent Addisonian crisis o administer aldosterone (fludrocortisone/Florinef)  ADDISONIAN CRISIS o can occur if doses not tapered o hypoglycemia, hypotension, hyperkalemia, hyponatremia → cardiac arrest CONN'S DISEASE (PRIMARY ALDOSTERONISM)  results from an adenoma (benign tumor) of the adrenal cortex → increased aldosterone o fluid retention, sodium retention, hypervolemia PHEOCHROMOCYTOMA  results from an adenoma (benign tumor) of the adrenal medulla → increased catecholamines (epinephrine, norepinephrine) o 5 Hs  hypertension  headache  hyperglycemia  hypermetabolic  hyperhidrosis o VMA test → vanillylmandelic acid test  evaluates the level of catecholamines in the blood (0.2-0.9 mg/dL) and in the urine (0.2- 7 mg/24 hours)  collect a 24-hour urine specimen  management - adrenalectomy THYROID GLANDS  anterior aspect of the neck → left and right lobes of thyroid gland which are connected by an isthmus → secretes T3 (triiodothyronine), T4 (thyroxine), thyrocalcitonin  ingested iodine oxidized to plasma iodide (which enters the thyroid gland) + tyrosin (amino acid/protein) = thyroglobulin (storage form of the thyroid hormone) → when released into the circulation → T3 & T4 o FEEDBACK MECHANISM:  anterior pituitary gland → trophic hormones (any hormone capable of stimulating a target organ) → TSH (thyroid stimulating hormone) → thyroid gland (target organ) → T3 & T4  if the level of T3 & T4 is decreased → messages to anterior pituitary gland → RELEASE TSH  if the level of T3 & T4 is increased → anterior pituitary gland to INHIBIT the production of TSH  anterior pituitary gland → ACTH (adrenocorticotropic hormone) → adrenal cortex → SSS  T3 & T4 - needed for growth & development TESTS DONE TO DIAGNOSE THYROID DISORDERS:  PBI (PROTEIN BOUND IODINE) o evaluates the amount of iodine attached to the protein molecule of the blood o 4-8 ug (micrograms)%  below 4 - hypothyroidism  higher 8 - hyperthyroidism o no food (seafood, enriched bread) / drugs (cough syrup, ASA, estrogenic preparations like contraceptives, dyes) containing iodine 2-3 days before the blood test Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  T3T4 o evaluates the level of T3 & T4 in the blood; directly proportional to thyroid function (if increased, hyperthyroidism; if decreased, hypothyroidism) o T3 - 70-170 ug% → very reliable (more potent than T4, T3 will not bind with iodine [can readily enter and penetrate a cell to influence cellular metabolism]) o T4 - 4.7-11 ug% o no NPO required  TSH o evaluates the level of TSH in the blood; inversely proportional to thyroid function bc of the negative feedback mechanism (if increased, hypothyroidism; if decreased, hyperthyroidism) o 0.6 - 4.7 ug/ml o no NPO required  BMR (BASAL METABOLIC RATE DETERMINATION) o evaluates O2 consumption when the client is at rest o the night before, place on NPO for 12 hours; ensure client has had a good night sleep;  when client has not done an activity/ate, clamp the nostrils, client will be breathing to a tube connected to an O2 tank w/ a machine that evaluates O2 function  TBMR (THEORETICAL BASAL METABOLIC RATE DETERMINATION) o pulse pressure + pulse rate/min - 111 o normal value: 20-30 o not definitive because there are many factors that influence BP and pulse rate; it is a mere rough estimate  RAIU (RADIOACTIVE IODINE UPTAKE) o evaluates the amount of radioactive RAI131 accumulated by the thyroid gland and excreted by the kidneys o uptake = 15-40% o urine = 40-80% o no food/drugs containing iodine prior to procedure o on the day of test, administer per orem "RAI131 cocktail" (liquid form, unpleasant, brassy taste + flavoring is added; therefore, it became a cocktail) and right after, start collecting 24-hour urine specimen → 24 hours after → scanner/geiger counter  EXAMPLE: 12 noon (administered RAI131 cocktail @ 8 millicuries) → teach patient how to collect 24-hour urine specimen → 12 noon of the following day, expose the thyroid gland to the scanner  if normal, result of the scanner → thyroid should have stored (reuptake) 1.2-3.2 millicuries (15-40% of the original)  if less than 1.2 (15%) → hypothyroidism  if more than 3.2 (40%) → hyperthyroidism  urine should contain 3.2-6.4 millicuries out of the 8 (40-80%)  if less than 3.2 (40%) → hyperthyroidism  if more than 6.4 (80%) → hypothyroidism  reuptake is directly proportional and urine inversely proportional to thyroid function  NOTE: normal values depend on the amount of RAI131 cocktail administered o hyperthyroidism - increased reuptake, decreased excretion o hypothyroidism - decreased reuptake, increased excretion  THYROID SCAN o evaluates the amount of RAI131 stored by the thyroid gland to determine the size, shape, and function of the thyroid gland o only measures what the gland can store, RAI131 is given per orem HYPOTHYROIDISM  decreased T3 & T4 → decreased activity of sebaceous & sweat glands → accumulation of mucopolysaccharide subcutaneously → mucinous facies or myxedema (exhibited by non-pitting edema, thickened skin, enlarged tongue, dry, waxy edema, deepening of the voice)  according to onset of symptoms o CRETINISM - symptoms appear during childhood o MYXEDEMA - symptoms appear during adulthood  according to cause Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 o PRIMARY - failure of the thyroid gland to secrete T3 & T4 o SECONDARY - failure of the anterior pituitary gland to secrete TSH  dwarfism → secondary hypothyroidism bc of an hypoactive anterior pituitary gland  stunted growth (bc T3 & T4 → growth & development), delayed puberty, hypometabolic → below normal VS, poor memory, mental sluggishness, decreased O2 for metabolism (unable to tolerate extreme cold weather), weight gain (T3 & T4 → needed for metabolism)  management - supplement o commercially prepared thyroid preparations (thyroxine/Levothyroxine/Liothyronine), proloid (thyroglobulin [storage form]), cytomel, synthroid, euthroid, thyrolar, thyrax, thydin, eltroxin HYPERTHYROIDISM  grave's disease / basedow / parry's disease / thyrotoxicosis / toxic goiter  two theories of cause o LATS - gamma globulin in the blood known as long acting thyroid stimulator (LATS) → iodine accumulation & thyroid hyperplasia → manifests goiter o EPS - anterior pituitary gland releases an exophthalmos producing substance → eye signs o TRIAD SYMPTOMS  goiter - enlargement of the thyroid gland  eye signs - exophthalmos (protrusion of the eye ball), proptosis (downward displacement of the eyeball), lid lag, infrequent blinking, fixed stare, periorbital edema, von graefe's sign (failure of the eyelids to follow the movement of eyes when the patient looks down)  infrequent blinking & fixed stare → dalrymple's sign  hyperthyroidism (brought brought by elevated T3 & T4)  hyperactive, hypermetabolic (vital signs above normal, increased appetite but no weight gain, over excitability of SNS (tremors, diaphoresis, palpitations, nervousness,  most common GI problem in GRAVE'S DISEASE → diarrhea  most common GI problem in uncontrolled advanced grave's disease → constipation (bc SNS has been stimulated)  simple goiter / goiter due to iodine deficiency / endemic goiter (mountainous area) / non-toxic goiter - enlarged thyroid gland but no exophthalmos, or tremors  if T3 & T4 elevated → toxic goiter / grave's disease o goiter is simply the enlargement of thyroid gland (there can be a goiter with a normal, below level, or above level T3 & T4) o a non-toxic goiter can be toxic anytime → if exposed to stress, infection, or has an unexpected pregnancy, or prolonged exposure to cold weather, there can be an elevation T3 & T4  treatment o anti-thyroid preparation → prevents the synthesis of T3 & T4 by blocking the utilization of iodine  tapazole/methimazole, PTU - propylthiouracil, Neomercazole /carbimazole  observe for adverse effects → most common (with the prolonged use of anti-thyroid preparations) → agranulocytosis (decreased neutrophils, eosinophils, basophils)  parameter to evaluate → differential count; if no differential count, CBC o iodine preparation → reduce the vascularity (henceforth, given before surgery to lessen bleeding), increase the firmness of the gland; also promotes the storage of T3 & T4  lugole solution, KISS (potassium iodide saturated solution) / SSKI (saturated solution of potassium iodide) o adrenergic blocking agent → to control the symptoms brought about by SN over excitation (decreases BP, tremors, etc)  propanolol, Inderal, betaloc, atenenolol, Naldol o RAI131 → to reduce the size of the gland  isotopes are capable of destroying a gland → reduces the size of the gland  risk of congenital abnormalities, genetic mutations  surgery - thyroidectomy o sistrunk - removal of thyroglossal cyst o right/left thyroid lobectomy - removal of left or right thyroid o isthmusectomy - removal of the connection between thyroids Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 o radical/total thyroidectomy - 5/6 of the gland is removed (1/6 is left intact to prevent hypothyroidism; unless thyroid gland is cancerous)  to prevent hypothyroidism after a total thyroidectomy → thyroglobulin (storage form of thyroid hormone) for life o nursing responsibilities  PRIORITY - establishment of a patent airway → semi-fowlers position to ensure full lung expansion & promote adequate oxygenation  NOTE: NO HIGH FOWLERS POSITION → causes strain on the neck muscle → tension on suture line → bleeding  incision site → collar line / curvilinear  anterothoracotomy → lobectomy  lumbotomy incision / flank incision → nephrectomy, uro, pyelolithotomy  suprapubic → bladder  sternal stripping → heart  cough exercises, turn client from side to side  evaluate cardiopulmonary functioning → monitor VS until its stable  promote adequate nutrition and fluid & electrolyte balance  foods can be given if fully awake AND gag reflex has returned  check for gag reflex → tongue depressor, touch / tickle the posterior pharynx  positive gag reflex → palate will elevate, contraction of the pharyngeal muscle  promote adequate elimination  expect ALL post-op patients to urinate about 6-8 hours after anesthesia → restoration of normal bladder tone  if after 6-8 hours no urine, palpate and check if bladder is distended then stimulate urination  encourage early ambulation → shorten recovery period, to boost patient's morale, prevent post-op complications  allow them to get out of bed as soon as VS are stable; while ambulating, support head & nape of the neck → to prevent undue flexion & sudden hyper-distention  monitor signs & symptoms for post-op complications  tetany → results from the accidental removal of parathyroid glands  accidental removal of one gland, there will be no signs  if two, mild tetany  if three or four, positive Chvostek & Trosseau's sign  calcium preparation and Vitamin D  hoarseness & aphonia (no voice) → two recurrent laryngeal nerves that control vocal chords & are responsible for voice production  if one recurrent laryngeal nerves are accidentally removed → hoarseness  if trauma to the nerves/edema of glottis → hoarseness  if both were accidentally removed → aphonia  bleeding → can be caused by failure to administer lugole solution & KISS or failure to tie/ligate the bleeders → pt. will be brought back to OR, ligate the bleeders  failure to ligate the bleeders → continuous oozing of blood → hematoma can occlude the trachea → airway obstruction  check bleeding → slip hand under the nape to check for dampness, client may feel tightness around the neck or a "choking" sensation, evaluate VS (rapid, weak, feeble & thready pulse, decreased BP, rapid but shallow respirations)  respiratory obstruction → secondary to bleeding (hematoma → trachea)  laryngospasm, laryngeal edema (results from surgical trauma, anesthesia, hypocalcemia) → emergency tracheostomy (to establish an airway)  THYROID CRISES/STORM  anxiety pre-op may cause thyroid storm post-op  post-op infection from wound may cause thyroid storm  before surgery, T3 & T4 elevated → antithyroid medications administered → euthyroid state (state of normal thyroid function) → operation for thyroid Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 surgery → post-op bc of stress or wound infection, the remaining thyroid gland is compensating → produces elevated T3 & T4  essentially, it is an hyperthyroidism post-op bc of stress or infection  earliest manifestation of thyroid crisis post-op → fever with tachycardia  management for thyroid crisis post-op → same as hyperthyroidism  NOTE: tracheostomy set must be at bedside → to establish an artificial airway  health teachings o diet rich calories (high in carbohydrates, protein, some amount of unsaturated fats) → to satisfy the increased appetite, to restore the lost glycogen reserve o avoid stimulants in the diet (no colas, no caffeinated beverages) o increase fluid intake → bc of diaphoresis o get body weight o provide physical & mental rest → reduces metabolism o provide quiet, calm, and restful environment bc of the SN over excitability o eye signs  exophthalmos (result of the fatty deposit around the eyeball which is pushing the eyeball forward) → exposed to environmental stimuli → corneal dryness → corneal ulceration → blindness  instill saline to moisten the eye  use of dark glasses o periorbital edema (bc of fluid accumulation behind the eyeball) → promote drainage → elevate head on several pillows o no amount of medical surgical treatment can regress the eye signs DIABETES MELLITUS  DIAGNOSTICS o FPG - fasting plasma glucose → fasting blood sugar o RBS - random blood sugar (no NPO required) o PPBS - post prandial blood sugar determination  NPO 2 hours after giving a diet consisting of at least 100 g of carbohydrates o Hgt - hemoglucotest or CBG (capillary blood glucose) o OGTT - oral glucose tolerance test o BT, CT - Benedict's test & Climistert test for glycosuria o ACETATE - test for ketonuria → ketone bodies in the urine  acetest tablet which is creamy white → instill 1 or 2 drops of urine → if it becomes purple/lavender, ketonuria; if no changes, negative for ketonuria o Hgb A1C → glycosylated hemoglobin test; to evaluate for the amount of glucose attached to the Hgb of the blood for the previous 120 days (life span of the Hgb of the RBC)  diagnoses the compliance to medical management after being treated continuously for about 3-4 months  TYPE 1 / JUVENILE / INSULIN DEPENDENT / BRITTLE DIABETES / LABILE DIABETES o there is absolute insulin deficiency o 15-30 years old o slender o more prone to DKA (diabetic ketoacidosis) o best way to control blood sugar → insulin  TYPE 2 / NON-INSULIN DEPENDENT / MATURITY ONSET DIABETES / ADULT ONSET DIABETES o there is relative insulin deficiency (bc of insulin resistance) o after 40 years old o obese o more prone to HHNS (hyperglycemia hyperosmolar nonketotic syndrome) o best way to control blood sugar → oral hypoglycemic agent, maintain ideal weight, regular exercise, dietary regimen  SYMPTOMS o tissue starvation → polyphagia, weight loss o failure of the cell to utilize the glucose for energy → weakness, hyperglycemia o hyperosmolarity brought about hyperglycemia → polyuria, glycosuria o extracellular fluid dehydration → polydipsia Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  INSULIN MANAGEMENT SLOW ACTING / LONG RAPID ACTING SHORT ACTING INTERMEDIATE ACTING ACTING onset: 10-15 mins onset: 30 mins-1 hr onset: 2-4 hours onset: 6-8 hours peak: 30 mins-1 hr peak: 2-4 hours peak: 6-12 hours peak: 18-24 hours duration: 3 hours duration: 6 hours duration: 24 hours duration: 36 hours color: depends on color: clear & colorless color: clear & colorless color: turbid & cloudy type examples: humulin R, examples: NPH (neutral examples: humulin U, examples: humalog, novolog, regular insulin, Semi- protamine hagedorn), ultra lente, lantus, Lispro, Aspart Lente, velosulin, MC humulin N, lente, monotard, glargine, PZI - actrapid, novalin r novalin L, globin protamine zinc i note: best given 60-90 mins before a meal (so physiologic note: given 3 times a day note: given only once a day note: effect of insulin will parallel (before the 3 meals) the absorption of glucose)  other responsibilities o administration of insulin → SUBCUTANEOUS, IM, IV  proteinase (gastric enzyme) destroys insulin → not administered oral  most common insulin given incorporated into IV bottle - humulin R, crystalline zinc insulin, regular insulin  D5W + insulin → increase reuptake of K → treatment for hyperkalemia o observe client for symptoms for hypoglycemia HYPOGLYCEMIA / HYPERINSULINISM / INSULIN SHOCK DKA / HYPERGLYCEMIA / DIABETIC COMA insulin overdose, prolonged NPO & vomiting, long interval missed dose of insulin, infection & stress from the time insulin given & serving of the food complains of thirst, dim vision, flushed skin, warm to complains of hunger pangs, double vision, pallor, cold touch, cherry red lips, increased temp, BP is below clammy skin, profuse perspiration, decreased temp, BP is normal, kussmaul air hunger respiration, fruity normal, tremors acetone breath  MANAGEMENT o KETOACIDOSIS  administer rapid-acting insulin  DKA = rapid acting insulin is needed but regular insulin IV > rapid acting insulin IM o HYPOGLYCEMIA  initially, 10-15 g of carbohydrate (give 4-8 oz of soft drinks or fruit juice; 1 tbsp of sugar or 5 ml of honey/karo syrup/maple syrup; 4-6 pieces of candies or 2-3 slices of graham crackers)  if w/ altered LOC, open the mouth, place 1 tablespoon of sugar inside the oral cavity & it will be absorbed  if not corrected w/ 10-15 g of carbs (if blood sugar is below 50 mg/dL), adminsiter epinephrine (1:1,000 SQ), glucagon (1-2 mg IM), IV glucose in water  DAWN PHENOMENON o patient slept with normal/below normal blood sugar; however, counterregulatory hormones (thyroxine, epinephrine) released at 2-3 am  consider the insulin & peak of action  do not attempt to give a midnight snack  SOMOGYI Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 o patient goes to sleep with normal blood sugar; rebound effect occurs around 2-3 am (blood sugar goes down then up, etc)  OHA (ORAL HYPOGLYCEMIC AGENT) o contraindications to OHA - pregnancy, infection, surgery, under stress, signs of allergy, kidney, liver diseases → switched to INSULIN despite being non-insulin dependent o onset - 1-3 hours after administration o peak - 4-8 hours after administration o duration - 12-24 hours administration o SULFONYLUREAS  stimulates the beta cells of the islets of Langerhans to secrete indogenous insulin  diabinese/chlorpropamide, euglucon/glibenclamide, dymelor/acetohexamide, orinase/tolbutamide, tolinase/tolazamide, diamicron/gliclazide  most common adverse effect → headache, body weakness, GI upset, paresthesia (numbess/partial loss of sensation), tinnitus o BIGUANIDE  increases the uptake of glucose by the cells  metformin, phenformin, glucophage o ALPHA GLUCOSIDASE INHIBITORS  delays the absorption of glucose  acarbose/precose, gliset o THIAZOLILIDIONE  fosters/enhances the effect of insulin at the receptor site without increasing the release of insulin by the beta cells  pioglitazone/actos, rosiglitazone/avandia o COMBINATION OF BIGUANIDE & THIAZOLILIDIONE (ACTOSMET)  HEALTH TEACHINGS o DIETARY REGIMEN  carbohydrates (45-65%)  simple → fruits, sugar → immediate effect (increase in sugar)  complex → rice, starch, bread, noodle, pasta → more preferred for DM clients bc the rate of absorption is lower than simple carbohydrates  protein (15-20%)  fat (10-15%) - the fat content of any food item will delay the absorption of glucose  REGULAR EXERCISE o when muscles are working, the functioning muscle is using the stored glucose for energy (so you don't need a transport vehicle, insulin, to use glucose for energy) o diabetic client with regular exercise → take snacks in between exercises (to prevent hypoglycemia) NEUROLOGY ASSESSMENT  LEVEL OF CONSCIOUSNESS o causes of an altered level of consciousness  center for consciousness is located @ both cerebral hemispheres  the center for wakefulness is reticular activating system @ center of brain stem  any structural lesion that compresses the brain stem or both cerebral hemispheres will cause an altered LOC  tumor  hematoma  brain abscess  for the brain cell to survive, it requires blood, glucose, electrolytes, oxygen  any metabolic depression on brain stem or both cerebral hemispheres can cause an altered LOC (e.g. hypoglycemia, hypoxia, fluid & electrolyte imbalance, effects of toxic drugs/chemicals) o GLASGOW COMA SCALE (GCS)  assesses - eye opening, verbal response, motor response Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  decerebrate → affectation of brain stem (diencephalon, medulla oblongata) → respiratory arrest  decorticate → affectation of  a client can experience both if they have a diseases of the pons, midbrain, or brain herniation  if experiencing both, give a score of 2  below 7 = coma  5-6 = coma  3-4 = deep coma o center that regulates the rate & depth of respiration → medulla oblongata o center that regulates the rhythm of respiration → pons o motor and speech center → broca's → left hemisphere, frontal lobe o sensory center → wernicke's  LOBES o parietal - pain, pressure, touch, temperature o occipital - vision o temporal - hearing, balance, memory o frontal - voluntary movements, memory, speech, emotions, attitudes, abstraction o APHASIA  motor expressive aphasia - unable to talk or write → affectation @ frontal lobe  sensory receptive aphasia - unable to understand both written and spoken words → visual receptive aphasia (occipital lobe), auditory receptive aphasia (temporal lobe)  global aphasia - combination of motor & sensory aphasia → affectation both of the broca's and wernicke's area o SYMPTOMS MAY BE  ipsilateral symptoms - symptoms are on the side of the lesion  contralateral symptoms - opposite the side of the lesion  EXAMPLE: if there is right sided lesion/tumor  focal symptoms may be ipsilateral or contralateral which depends on the criss crossing of the nerves in the pyramidal tract (controls fine, voluntary movement)  ipsilateral → puffiness of the right eyelid, saliva will drool to the right, right shoulder will sag  contralateral → paresis (weakness)/plegia (paralysis) of left side of the body  extrapyramidal tract (controls coarse voluntary movement)  basal ganglia is the center for coordination and is part of the extrapyramidal tract  visual deficit is contralateral bc the supply is from the optic nerve in the optic chiasm (which crisscrosses)  right sided affectation → if there is anisocoria → ipsilateral bc compression of the oculomotor nerve  GAIT o ataxic gait - unable to remain steady with feet together → seen w/ affectation of the cerebellum o dystonic gait - irregular non-directive movement → seen in clients w/ muscle atony o dystrophic/waddling gait - with feet apart, the body will move to the sides → seen in clients w/ muscle dystrophy where there is a weakness in the pelvic girdle & client's w/ hip dislocation o hemiplegic gait - foot dragging → affectation in pyramidal tract o scissoring/scissors gait - short, slow steps with the legs alternating, crossing each other → seen in spastic paralysis o steppage gait - high exaggerated steps → affectation in the lower motor neuron  REFLEXES o superficial & pathological reflexes o knee-jerk / patellar o bicep - arm flexion o tricep - arm extension o babinski - stroke the sole of the foot in an inverted J  normal response: flexion of the toes Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  pathological: extension of the big toe, fanning of the other toes o gordon's & chaddocks - modification of the babinski  gordon's - try to press/squeeze the calf muscle → observe for the dorsiflexion of the big toe (if positive, pathological)  chaddock's - stroke the inner aspect of the leg → observe for the dorsiflexion of the big toe (if positive, pathological) o kernig's - flex and extend the lower extremity → observe for the pain and spasm in the hamstring muscle o cremasteric - stroke the inner aspect of the thigh → observe if the testes will rise or if the scrotum will elevate  use a tongue depressor in testing for this reflex o brudzinski - flex or bend the head towards the chest → observe for the flexion of the ankle, knee, thigh (if positive, pathological) o binda - turn the head to one side → observe if the opposite shoulder turns upward and inward o strongest muscle → flexor stronger than extensor, adductor stronger than abductor  COORDINATION o romberg's test - tell the client to stand with feet together, eyes closed → observe if the client falls or swings to one side (if positive, indicates ataxia or disequilibrium, disease of the cerebellum)  CRANIAL NERVES DIAGNOSTIC TESTS GENERAL GUIDELINES FOR DIAGNOSTIC TESTS  blood test → know if NPO or not  radioactive → know if there's a need for contrast medium or not if there is a need, nursing interventions arise all contrast mediums are considered nephrotoxic → lab test to evaluate serum creatinine and GFR  lumbar puncture / spinal tap o done both for diagnostic (for examination of CSF) and therapeutic purposes (to reduce the ICP by withdrawal of CSF, administration of analgesics in subarachnoid space) o responsibilities  secure a consent; prepare local anesthetic agent (lidocaine/xylocaine 1-2%, novocaine, tetracaine HCl, marcaine)  inform the client about the mild shooting pain while the needle is being introduced into the subarachnoid spaces  empty the bladder prior to the procedure  position (fetal position, C position, prawn position, side lying position with the head pressed to the chest and the knees flexed to the chest), the client and cleanse the site to be punctured (between L3L4, L4L5, L5S bc anatomically the spinal cord ends before L1 → spinal cord injury is prevented)  needle is connected to a spinal manometer which registers the CSF pressure  evaluate the color, volume, transparency of the CSF aspirated  normal volume = 90-150 ml → aspirated only about 5-10 ml  normal color = colorless (if yellowish → xanthochromia → indicates an old blood clot inside the skull (the platelet of the old blood clot gives the yellowish color))  normal transparency = clear  CSF protein = 15-45 mg% (if elevated, tumor, multiple sclerosis, GBS)  CSF glucose = 50-80 mg% → glycorrhachia (glucose in CSF)  CSF chloride = 118-132 mEq/L (if decreased, CNS infection)  WBC = 0-8 ml (if increased, pleocytosis)  gamma globulin = 3-9% (if increased, multiple sclerosis (specifically, IgG))  post op - right after the removal of spinal needle, prone position for 30 mins-1 hr then flat on bed for 6-8 hours to prevent spinal headache due to the leakage of CSF into subarachnoid spaces  queckenstedt / spinal manometry / spinal dynamic test - done to evaluate the CSF pressure when the jugular vein has been compressed for about 6-12 seconds; it is normal for the CSF pressure to rise but among clients w/ subarachnoidal obstruction, there is no change in pressure Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  pneumoencephalogram - x-ray of the brain ventricles after the introduction of air/oxygen (contrast medium) o prior to xray, prep the client for lumbar puncture wherein 20 ml of CSF is aspirated o right after aspiration, 20 ml of O2 is introduced and it flows along the brain ventricles then a series of x-ray of the brain ventricles is taken  cerebral angiogram / carotid/femoral arteriography - x-ray of the cerebral vascular system after the injection of a dye (conray or diodrast) into the carotid or femoral arteries o secure an informed consent and prepare a local anesthesia o place client on NPO to prevent the dilution of the dye o ask for a history for allergies to seafood o inform client that right after the injection of dye, they will experience flushing of the skin, warm sensation, metallic taste in the mouth o prevent bleeding  post op, place an ice collar or ice cap around the neck to prevent bleeding after a carotid arteriography  after a femoral arteriography, get a sand bag and place it over the inguinal area to apply pressure on the femoral artery  femoral arteriography → immobilize the affected leg and keep it in an extended position → DO NOT FLEX THE LEG, check the pulse distal to the puncture (popliteal and dorsalis pedis)  to assess for arterial insufficiency, check the color and temperature of the leg → pallor and coldness if there is arterial insufficiency  myelogram - x-ray of the subarachnoidal spaces after giving a dye (pantopaque, myodin) injected into subarachnoidal spaces o NOTE: when injecting any drug into the subarachnoidal space → intrathecal / intraspinous  EEG - measurement of the electrical activities of the brain o avoid stimulants 24 hours to EEG; prior eeg, no colas, no caffeinated beverages, no depressants (phenytoin/Dilantin, sodium luminal/Phenobarbital, carbamazepine/Tegretol, clonazepam/Clonopin)  if EEG is to be done to a client with a history of seizures, administer anticonvulsants (if withheld, the seizure will happen more frequently → status epilepticus o NO need for NPO → regular diet prior to EEG (state of hypoglycemia will alter brain wave activity / metabolic depression) o electrodes are placed on the head → ensure a clean scalp by rendering hair shampoo  EMG / Jolly's test / nerve conduction velocity - measurement of the electrical activities of the peripheral muscle done to diagnose muscle dystrophy and peripheral nerve injuries o several wires / needles will be attached to the peripheral muscles and the machines will evaluate the electrical activity  CT scan o if without contrast, no NPO o with contrast, NPO for at least 4 hours and prep for administration of thallium/technetium /neohydrin IV  MRI  skull x-ray PARKINSON'S DISEASE / PARALYSIS AGITANS  degeneration of the basal ganglia due to decreased supply of dopamine  risk factors o strongest risk factor → previous history of encephalitis o head trauma, smoking, atherosclerosis, carbon monoxide exposure, the use of contraceptive pills o high among male  pathophysiology o neuronal degeneration and the substantia nigra of the midbrain → decreased inhibitory neurotransmitter (dopamine) → decreased dopamine → impairment of the extrapyramidal tract (basal ganglia - center of coordination) → imbalance in voluntary movements → triad symptoms Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  impairment of the basal ganglia → weakness of the muscles of expression → mask like facies / blank facies  imbalance in voluntary movements → impairment of the muscles responsible for speech → drooling of the saliva & microphonia (slow monotonous voices with poor articulation)  triad symptoms →  → tremors initially felt in the upper extremities (experienced at rest), disappears with any purposeful movement, increases with walking, anxiety, etc  pill-rolling movement of the thumb against the finger → earliest manifestation of PD  → rigidity → micrographia (small, minute illegible handwriting) and cogwheel rigidity (with every passive movement of the extremities, there will be jerky motion)  → bradykinesia - slow physical response  can also be dyskinesia - difficulty in initiating movement  bc of rigidity and bradykinesia → freezing phenomenon (transient inability to perform active movement) and shuffling/propulsive/festination gait (walking on their toes in an accelerated pace)  management o dopamine cannot be given as it does not cross the blood brain barrier o L-dopa/levodopa (dopaminergic) → metabolic precursor to dopamine (it will be absorbed by substantia nigra and acted on by an enzyme called decarboxylase and converted into dopamine)  levedopa/Dopar, carbidopa/Sinemet, amantadine HCl/Symmetrel  nursing responsibilities  it can cause postural hypotension → remind to gradually change position  can cause dysrhythmias → monitor pulse rate before and after administration  inform client not to be alarmed bc drug can cause the darkening of the sweat and urine  advise not to take any drug/food contained vit. B6 bc it will reverse the effects of L-dopa (e.g. pyridoxine, green leafy vegetables, liver, cereals, fruits) o bromocriptine/Parlodel → stimulates the substantia nigra to release indogenous insulin o to relieve tremors & rigidity, anticholinergics are given (trihexyphenidyl/Artane, benztropin mesylate/Cogentin, biperidine HCl/Akineton) o highly controversial bc of the risk of hypertensive crisis → MAOIs → given to prevent the breakdown of dopamine (selegiline/Eldepryl/Carbex) o surgical procedures done to interrupt the nerve fibers pathway (stereotactic surgery - requires the use of an electrical stimulator)  thalamotomy - destruction of the thalamus using an electrical stimulator  pallidotomy - destruction of the globus pallidus (located deep inside the basal ganglia) using an electrical stimulator  nursing responsibilities o give priority to the triad symptoms  impaired physical mobility  to relieve them of tremors, give the client a stress ball  rigidity → comprehensive exercise program to improve muscle tone and muscle strength to prevent contracture deformity  tremors & rigidity → self-care deficit  bradykinesia → risk for constipation  risk for physical injury bc of triad symptoms o mask like facies → impaired body image o microphonia → impaired communication MYASTHENIA GRAVIS  an autoimmune disease causing failure of the transmission of impulses to the myomuscle neural nerve, myoneural junction due to a blockage or a destruction to the acetylcholine receptor  axon → excitatory neurotransmitter (acetylcholine) → normally attaches to the acetylcholine receptor of the muscle fiber → muscle contracts Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  autoimmune → antibodies which block/destroy the acetylcholine receptors → reduced uptake/concentration of acetylcholine and reduced number of functioning acetylcholine receptors → muscles will NOT contract → muscles become weak, paralyzed, atonic → progressive widespread weakness of several muscles  early onset in female (20-30 years old); late onset among male (after age 40)  diagnosis o tensillon test/edrophonium test  give tensilon 8-10 mg/IV → 30 seconds-1 min after → evaluate muscle tone & muscle strength (if positive, it should improve)  within next 3-5 minutes, symptoms will return  symptoms o early stage of MG →  → ocular muscle → diplopia, ptosis (weakening of the eyelid)  → lingual muscle & facial muscle → difficulty of swallowing, impairment in mastication, "snarling smile" (teeth are clenched and the jaw tends to hang open) o upper & lower extremity muscles o proximal & distal muscles o late stage of MG →  involvement of the diaphragm, intercostal muscle → respiratory paralysis → respiratory arrest → myasthenia crisis  MYASTHENIA CRISIS: establish an airway → prepare for intubation (endotracheal/tracheostomy tube) & administer an anticholinesterase or a cholinergic agent (Prostigmine/neostigmine, Mestinon/pyridostigmine)  anticholinesterase - increases the concentration of acetylcholine & increases the number of functioning acetylcholine receptors  observe the client for signs & symptoms of cholinergic crisis → parasympathetic symptoms (low BP, decreased BP, RR, diarrhea, etc) → give an anticholinergic (atropine sulfate or Hyoscine/scopolamine)  management o thymectomy → removal of the thymus gland  thymus gland is located below the suprasternal notch  from the thymus gland originates the T cells → responsible for production of antibodies → since MG is autoimmune, remove the source of antibodies  majority of the client with MG manifest a thymoma (a benign tumor); after adolescence, our thymus gland is inactivated → the thymoma causes the gland to become hyperactive (like all tumors do) o plasmapheresis (plasma exchange) - separates the antibodies from the blood to be replaced by a donor plasma MULTIPLE SCLEROSIS  demyelination (destroyed, damaged myelin sheath) of the nerve fibers of the brain and the spinal cord  nerve fibers (axons & dendrites) are lined with a fat-like substance which forms a sheath called the myelin sheath which will regulate and conduct the flow of electrical impulses (it becomes faster if myelinated) o white matter of the brain is myelinated as well as the spinal cord  destruction of myelin sheath may be autoimmune or it can be caused by pregnancy, stress, post-viral disease, toxic drugs like amphetamines  high among female  once destroyed, the myelin sheath may be replaced by sclerotic patches of necrotic tissues → triggers an inflammatory reaction → formation of an inflammatory exudate → o → inflammatory edema o → scarring/fibrosis → failure in transmission of the electrical impulses → CHARCOT'S TRIAD SYMPTOMS o CHARCOT'S TRIAD  tremors (usually felt in lower extremity) → ataxic (bc of the demyelination of cerebellum), spastic gait Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  nystagmus (movement of the eye from side to side) → bc of the demyelination CN III (oculomotor - pupil constriction, eye accommodation), IV (trochlear - superior oblique), VI (abducens - lateral rectus)  additional info - strabismus is the movement of the eye towards the midline; dysconjugate is the movement of the eye away from midline  scanning of speech → difficulty in pronouncing the first word/first syllable of a statement bc of the demyelination of the frontal lobe o there is loss of sensation of pain, touch sensation → demyelination of parietal lobe o Lhermittes sign - when the patient bends forward, there is an electrical stimulation down the back bc of the demyelination of the spinal cord o behavioral symptoms (euphoria, apathy) due to affectation of the white matter of the frontal lobe  diagnosis o lumbar puncture (elevated CSF protein, elevated gamma globulin) o MRI - evaluates the extent of demyelination  management - symptomatic, supportive o steroidal preparation → reduces the edema around the site of demyelination → symptoms are not manifested o give the drug in a combination of ABCR (in any autoimmune disease) → prevents the proliferation/activation of T cells  A - Avonex  B - Betaseron  C - Copaxone  R - Rebif GBS (GUILLAIN BARRE SYNDROME)  same symptoms as MS & same management; however, there is o polyradiculoneuritis → demyelination of several cranial nerves causing paralysis of the ocular, oropharyngeal, and facial muscles → ptosis, diplopia; difficulty of swallowing, chewing o peripheral neuritis → bc of demyelination of peripheral nerves → ASCENDING PARALYSIS o autonomic dysfunction → over excitation / under excitation of the sympathetic nerve & parasympathetic nerve fibers  affects both sexes (GBS = Girl Boy Sexes) ALS (amytrophic lateral sclerosis) / Lou Gehrig's disease  degenerative disease common among males  degeneration of the motor nerves of the anterior horn of spinal cord, cerebral cortex, upper motor and lower motor neurons  there is increased glutamate which is responsible for the relay of impulses between motor neurons  weakness, dysphagia, fasciculation (twitching of small muscle group)  upper and lower neurons affectation → loss of voluntary control o upper motor neuron → hypertonia → spasticity; no muscle atrophy; hyperactive reflexes o lower motor neuron → hypotonia → flaccidity; there is muscle atrophy; hypoactive/absent reflexes  management o spasticity → baclofen o administer an antiglutamate (Rilutek/riluzole) → prevent further destruction of motor neurons CEREBROVASCULAR ATTACK / CEREBROVASCULAR DISEASE / BRAIN ATTACK / APOPLEXY  cerebral ischemia (decreased blood supply) → cerebral infarct (death of tissue due to ischemia)  cerebral anoxia of more than 4 mins → irreversible cerebral damage which is cerebral infarct  pathophysiology o THROMBOSIS (occlusive)  likely results from DM, atherosclerosis, smoking, hypertension  gradual onset of symptoms  manifests pre-monitory symptoms of TIA (transient ischemic attack) Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  TIA (or mini stroke) - nuchal/nape pain, lightheadedness, paresthesia, syncope, transient loss of speech and memory → lasts for 24 hours o EMBOLISM (occlusive)  likely results from MI, endocarditis, dysrhythmias, fractures, cancer  sudden onset of symptoms o HEMORRHAGE (hemorrhagic)  likely results from longstanding hypertension, aneurysm (pouching, ballooning, distention of a weak wall of an artery)  if the bleeding is between the skull and dura → epidural bleeding → arterial in origin; poorer prognosis  between the dura and arachnoid → subdural bleeding → venous in origin  between arachnoid and pia mater → subarachnoid bleeding  sudden onset of symptoms, appearance of symptoms if aggravated by stress & physical activity o symptoms depend on the areas of necrosis o thrombus & embolus will also cause symptoms of INCREASED INTRACRANIAL PRESSURE  earliest sign - restlessness with hippus (alternate dilatation-constriction of the pupil)  projectile vomiting  papilledema / choked disc  headache (cephalgia) upon arising and worsened with position change  LATE SIGNS  Cushing's triad changes → increased systolic BP and normal or decreased diastolic, increased and widening pulse pressure, decreased PR, decreased RR  temperature will increase initially (as the ICP increases, the cerebral metabolism increases) but as the level of consciousness continues to deteriorate, the temperature will decrease  increased ICP maybe be caused by  increased volume of the CSF (e.g. hydrocephalus, brain tumor obstructing the flow of CSF)  increased brain tissue bulk or tissue size (e.g. meningitis, encephalitis, brain abscess)  increased cerebral blood flow (e.g. coughing, sneezing, straining when constipated)  when the level of pCO2 is increased → state of hypercarbia → hypercapnia  pCO2 has the characteristic of dilating cerebral blood vessels → increased cerebral blood flow → cerebral congestion → increased ICP  management o reduce ICP  administering cerebral decongestant (mannitol, dexamethasone)  mannitol → hyperosmolar → movement of fluid from interstitial to intravascular → increase renal perfusion → increased urinary output  dexamethasone/Decadron (the only steroidal preparation that can cross the blood-brain barrier) → reduces cerebral edema → brain tissue bulk is reduced  mechanical ventilation / ambu-bag  when pCO2 is increased → increased ICP  mechanical ventilation promotes hyperventilation → increased RR → excreted the retained CO2, reducing the level of pCO2 → decreased ICP o antithrombolytic / antiplatelet aggregate  aspirin  in ortho, used as NSAID  most common discomfort associated → GI upset  ascriptin  aspilet  dipyridamole/Persantin, Pexid (coronary vasodilator)  Ticlopidine/ticlid  clopidogrel/Plavix, Clovix o anticoagulant Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  coumadin / warfarin / dicoumarol → PO  heparin / lovenox / clexane → SQ, IV  danger - bleeding  heparin  lab test: aPTT (30-45 seconds) & PTT (60-70 seconds)  antidote: protamine sulfate  warfarin  lab test: PT (11-16 seconds)  antidote: vitamin K o plasminogen activator  converts plasminogen to plasmin (causes the lysis/dissolution of the blood clot)  streptokinase / urokinase / t-PA (tissue type plasminogen activator)  Abbokinase / Retavase/reteplase  danger - bleeding  antidote: aminocaproic acid/Amicar BRAIN TUMOR  according to origin o brain tissue - glioma o cranial nerve - neuroma o brain covering - meningioma  according to location o cerebrum, anterior 2/3 of the brain - supratentorial o cerebellum, brain stem, posterior 1/3 of the brain - infratentorial  manifests symptom of increased ICP o earliest sign of brain tumor → papilledema bc of the compression of the optic chiasm  management o craniotomy / craniectomy  coronal/butterfly incision → flap is lifted → surgeon drills into cranium → burr holes  after surgery,  DO NOT place the client on a shock (trendelenburg) position → increases ICP, the abdominal content can compress on diaphragm causing respiratory distress  ADDITIONAL INFO: back lying with pillow is called horizontal; flat on bed without pillow is called dorsal  POSITION depending on location  supratentorial surgery → goal is to promote venous return to heart → elevate the head up to 45 degrees  infratentorial surgery → goal is to prevent compression on brain stem → elevate the head up to 15 degrees; but client CANNOT BE PLACED ON HIS BACK (to prevent brain stem from getting compressed)  allowed to place a small pillow, with head turned to un-operated side (especially if bone flap has not been placed back [normally not placed back until 3-5 days post op to allow brain expansion bc tissue has been traumatized → inflamed → inflammatory edema])  however, if there is a need for the client to be turned to operated side, it should be done for not more than 20 minutes to prevent cerebral edema  DO NOT suction the client bc this increases ICP; the mere insertion of the catheter will trigger the coughing reflex → increased ICP  if there is a need for suctioning (e.g. drooling, etc), oropharyngeal suctioning → should not be done for more than 10 seconds  NO nasopharyngeal suctioning bc it can cause injury to the nasal mucosa causing CSF leakage  CSF leakage → look for halo ring (moisten the gauze with leaking fluid → halo ring on gauze) and presence of glucose  DO NOT restrain the client → client becomes agitated → increased ICP Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  DO NOT insert a rectal tube, rectal thermometer, no manual extraction of feces (→ valsalva maneuver → increased ICP) & (→ vagal stimulation/parasympathetic stimulation → decreased BP, bradycardia)  REMIND client to AVOID becoming constipated → straining at stool → increased cerebral blood flow → increased ICP o radiotherapy  external (cobalt 60 / teletherapy / external beam ray / linear accelerator)  done on outpatient basis; emits alpha & beta gamma rays  explain that it is a painless procedure  pencil or ink marking made in the skin indicated the area to be exposed to the chemicals  remind client not to remove any pencil markings  advise to avoid pressure over the site, not to expose the area to sunlight  avoid local hot/cold application over the site  advise to cleanse the area with water (no soap; hypoallergenic/oatmeal bar soap is allowed bc its non-irritating) and pat dry  remind the client not to use oils, creams, lotions  observe the client for signs & symptoms for radiation sickness / radiation reaction; can be manifested →  → locally (reaction similar to a first degree burn) - erythema, dryness of skin, loss of skin hair, blister formation, skin desquamation  → systemically - anemia, leukopenia, thrombocytopenia, sterility  our bone marrow and gonads are very sensitive to radiation → depression of the bone marrow & destruction of gonads  if client manifests anemia, leukopenia, thrombocytopenia → PANCYTOPENIA  internal  radiation coming from inside the body of the client  implant/insert of isotope into a cavity - intracavitary implantation of an isotope (radium seed/radar seed)  intratumor or intralesion - brachytherapy (cesium 137)  per orem - RAI131, RAI125 (liquid)  intra-arterial perfusion - RAgold 198, RAphosphorus 132 (liquid)  nursing responsibilities  isolate the client (bc the radiation is coming from the client) → there will be boredom → offer any form of diversional therapy  radiation sign must be posted at the door of the room (observe placarding)  anything that comes in contact w/ the client is considered contaminated → provide client with a separate set of articles (preferably, disposable like disposable utensils, etc); linens should be separate from the linens of other clients  in UNSEALED, all excreta/vomitus are considered contaminated with radiation → wear gloves when handling excreta/vomitus, throw the excreta directly into the toilet bowl and flush twice or thrice  time - stay for not more than 30 minutes per shift / not more than 5 minutes per exposure  distance - maintain a distance of 3-6 feet from the site of radiation (for example, if sealed radiation is @ vagina - stay @ head of bed, breast part - stay @ foot of bed, urinary bladder - @ head part of the bead)  shielding - use a lead apron  prevent accidental dislodgement of the radium  proper anchorage  place client in complete bed rest  do not allow the client to use a bed pan (insert an indwelling Foley catheter)  enema prior to insertion of isotope Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  avoid any food that stimulates defecation (avoid roughage, fiber in the diet)  if there is dislodgement → pick it up with long forceps, rinse with saline or water, immediately put it back in lead container  common problems  after removal of isotope, observe for dysuria and burning sensation upon urination → urethral atrophy;  observe for hematuria → radiation cystitis  shortening of vaginal canal  sealed (radium seed / radar seed, cesium 137) - can come in forms like a bead, wire, needle  unsealed (RAI131, RAI125, RAgold198, RAphosphorus132) - liquid form HEMAVASCULAR BLOOD DYSCRASIA  may result from o decreased production of the different blood cells (pancytopenia) o overproduction of both normal and defective cells o a disorder of the spleen (storage of different blood cells) o defect in the coagulation mechanism (hemophilia, DIC as a complication of abruptio placenta)  DIAGNOSTIC o CBC, Hgb, Hct o bleeding time, clotting time, prothrombin time o erythrocyte index  NCV (mean corpuscular volume) - evaluates the size of the red blood cell  80-94 cubic microns  below normal → microcytic cell  above normal → macrocytic cell  abnormality in cell size → anisocytosis  mean corpuscular hemoglobin - evaluates the hemoglobin content of a red blood cell  22-28 micromicrograms  below normal → hypochromic  above normal → hyperchromic  mean corpuscular hemoglobin concentration - evaluates the hemoglobin content in grams per 100 ml of packed RBCs  30-36 grams/100 ml of packed RBC o Coombs' test - evaluate for the presence of immune bodies that adhere to the RBC causing hemolysis & agglutination of the RBC o Schilling test - evaluate the rate of absorption of the cyanocobalamin (vit. B12) → diagnoses pernicious anemia  administer per orem radioactive vitamin B12 → 24-hour urine specimen → following day, find for the presence or absence of 12 in the urine  gastric mucosa secretes an intrinsic factor that is essential in the absorption of vit. B12 then about 8-12% is excreted and present in the urine  pernicious anemia → absence of B12 from the urine (there was no absorption in the first place)  lifetime parenteral B12 (not per orem → not absorbed) o bone marrow tap / puncture / aspiration / biopsy - evaluate the size (microcytic or macrocytic) shape, characteristic of the different blood cells  poikilocytosis → any abnormality in the shape of the cell  RBC is disc shaped  platelet is  metarubricyte cell → nucleated cell  erythroblast (has nucleus) → RBC (has no nucleus); if an RBC has a nucleus, it’s a metarubricyte cell  nursing responsibilities  secure a consent; prepare local anesthesia  position depends on the site to be punctured Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  anterior iliac crest → supine  posterior iliac crest → prone, lateral  sternum → supine  vertebral body  in children, the site is the long bones (most commonly the femur, humerus); cannot be used in adults bc the number of marrows in long bones decreases as we age  after bone marrow puncture, apply pressure dressing over the site to prevent bleeding o lymph node biopsy o blood typing ANEMIA  due to decreased erythropoiesis (formation, maturation process of the RBC) o elements essential for erythropoiesis → iron, folic acid, vit. B12, vit. C, protein  protein - for the cell wall to be formed (protein)  iron - for the pigment hemoglobin to be formed (iron)  vit. C needed for the absorption of iron  folic acid - essential for the maturation process of RBC o vit B12 - synthesis of nucleic acid  due to increased hemolysis o at times, more RBC is destroyed than formed; RBC destruction > RBC formation → hemolytic anemia  due to bone marrow repression  due to blood loss o cells are normocytic, normochromic  IRON DEFICIENCY ANEMIA / MICROCYTIC, HYPOCHROMIC ANEMIA o cells are microcytic, hypochromic o vinson-plummer syndrome →  → dysphagia  → atrophic glossitis (inflammation of the tongue)  → stomatitis/mucositis (inflammation of oral mucosa)  MEGALOBLASTIC ANEMIA o FOLATE DEFICIENCY ANEMIA  cells are macrocytic, hyperchromic o PERNICIOUS ANEMIA  cells are macrocytic, hyperchromic  beefy red tongue (the result of gastric atrophy and the malabsorption of vitamin B12)  paresthesia (without B12, there will be nerve degeneration manifested by paresthesia) → need vit. B1, B6, B12  HEMOLYTIC ANEMIA o RBC destruction is greater than RBC formation o exposure to ionizing radiation, post-viral disease, effect of toxic drugs and chemicals (prolonged use of penicillin, chloramphenicol), transfusion of an improperly cross matched blood o elevation of unconjugated bilirubin bc of the rapid hemolysis of RBC → hyperbilirubinemia → hemolytic jaundice  HYPOPLASTIC ANEMIA / APLASTIC ANEMIA o depressed bone marrow activity o undergoing chemotherapy, radiotherapy o bone marrow depression →  → unable to produce adequate number of WBC → leukopenia → prone to infection  → unable to produce adequate number of platelets → thrombocytopenia → prone to bleeding  NORMOCYTIC, NORMOCHROMIC ANEMIA o due to menstruation, trauma, surgery o hypovolemia (will only lead to shock if the blood loss is about 15-25% of the circulating blood volume)  normal circulating blood volume → 4-6 L Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  signs and symptoms o decreased hemoglobin (oxygen carrier) count → reduction in the O2 carrying capacity of blood → tissue hypoxia →  → brain (cerebral hypoxia) → restlessness, headache, syncope, irritability  → heart (myocardial hypoxia) → anginal pain, increased PR, weakness, easily fatigued (earliest indicator of anemia)  → respiratory (hypoxia) → increased RR, dyspnea  → GIT (gastric hypoxia) → anorexia, angular cheilosis (lesion at the angles/corners of the mouth)  → skin and mucous membrane → pallor, brittle hair, intolerance to cold, brittle nails (→ "spoon shaped" → koilonychia)  nursing responsibilities o decreased erythropoiesis → give the elements essential to erythropoiesis  high protein diet, high folic acid diet (green leafy vegetables, eggs, milk)  administer hematinic agents to increase the blood heme (iron) o provide an environment that is warm o reduce energy expenditure → provide moderation in physical activity with periods of rest o if bone marrow depression is the cause  practice reverse isolation (bc of leukopenia)  avoid any form of trauma/injury (bc of thrombocytopenia) → soft bristled toothbrush, electric razor, avoid forceful blowing of the nose (bc of epistaxis), avoid becoming constipated (straining → rectal bleeding), no parenteral injections (if needed, use the sharpest needle for injection) o blood transfusion  due to erythropoiesis & hemolysis → packed RBCs  due to bone marrow depression & blood loss → fresh, whole blood transfusion o surgical management  hemolytic anemia → splenectomy (will act as a reservoir/graveyard for blood cells → stores the abnormal RBCs that is easily hemolyzed)  hypoplastic anemia → bone marrow transplantation  donors  twin (syngeneic bone marrow transplantation)  any related/unrelated individual (allogeneic bone marrow transplantation) as long as there is a compatible human leukocyte antigen  patient himself (autologous bone marrow transplantation) → harvested during remission period when their symptoms are absent POLYCYTHEMIA VERA  primary polycythemia vera - hyperproliferative bone marrow of unknown cause  secondary polycythemia vera - result from tissue hypoxia (e.g. common among mountain climbers, COPD, prolonged use of diuretics)  tissue hypoxia → release of humoral substitute → erythropoietin → stimulates bone marrow activity → o → increased erythropoiesis →  → increased production of basophils → release of B histamines → pruritus  → capillary congestion  → reddish mucosa → plethora (excess volume of blood causing swelling and a reddish complexion)  → capillary engorgement → bleeding → anemia  → hemoconcentration  → HPN  → headache, dizziness, blurring of vision  → sluggish blood → thrombus forms  → compensatory hypertrophy → hepatosplenomegaly  organ whose main function is phagocytosis is the spleen → it will hypertrophy / compensate first before the liver o → increased cell activity → increased cell metabolism → increased temperature & weakness  management Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072 o increase fluid intake to dilute the blood (as it is rich in RBC) o hyperactive bone marrow activity → methotrexate, mexate o blood phlebotomy → open a vein to gradually withdraw the blood (which is rich in RBC) LEUKEMIA  neoplastic disease; cancer of the white blood cell  uncontrolled, abnormal proliferation/multiplication of the immature WBC (blast cells)  blast cells → prone to infection  proliferating cells → o → cellular activity increased → increased cellular metabolism → increased body temperature & body weakness o → cells can crowd/congest/accumulate inside the marrow →  → joint pain, joint swelling  → prevent/hinder the production of the different blood cells → decreased RBC (→ anemia), decreased platelets (→ thrombocytopenia → bleeding [bleeding gums, epistaxis, hematuria, melena, etc.])  in advanced stage → invade/infiltrate vital organs → spleen (splenomegaly), liver (hepatomegaly), brain (increased ICP), kidneys (renal insufficiency → renal failure)  types o acute lymphocytic leukemia (ALL) - most common in children bc of the lymphoid immaturity of the child o chronic myelocytic leukemia (CML) - most common in adults MULTIPLE MYELOMA  cancer of the plasma cells  plasma cells secrete immunoglobulin (a protein essential for antibody production) o in multiple myeloma, there is proliferation of abnormal plasma cells →  → abnormal immunoglobulin called M-protein  → hemoconcentration → increased peripheral resistance → hypertension, thrombus formation  → increased cellular activity → increased cellular metabolism → increased body temperature & body weakness  → secretes an autoclast (bone destruction cells) activating factor → increased bone destruction/increased bone resorption/demineralization of the bones → calcium losses from the bones →  → brittle bones → pathological fractures  → calcium goes to the blood → hypercalcemia → hypercalciuria → calcium crystallization → nucleus/nidus formation → stone develops → kidney stone  diagnosis o bone marrow puncture/bone marrow tap/bone marrow biopsy (most definitive/reliable diagnostic test)  NOTE: if the procedure is invasive, it is the most definitive/reliable test o Bence-Jones protein → diagnose the presence of protein/immunoglobulin in urine (most definitive laboratory test) o hematocrit → evaluate blood dilution o x-ray of bones o serum calcium o sulkowitch urine test → presence of calcium in the urine HODGKIN'S / MALIGNANT LYMPHOMA / LYMPHOSARCOMA  cancer of the lymphoid organs with proliferation of lymphocytes  risk factor - positive family history, exposure to environmental carcinogen, previous viral infection (Epstein-Barr virus), high among male before age 20 and after age 50  diagnostic - lymph node biopsy to detect the presence of Reed-Stenberg cells  A symptoms → local manifestations (earliest manifestations) o painless lymph adenopathy (enlarged lymph nodes) Downloaded by Pipit Lim ([email protected])  lOMoARcPSD|46770072  B symptoms → systemic manifestations o weight loss, fever, night sweats  management o localized lymph node enlargement → excision of the lymph node with radiation therapy o systemic lymph node enlargement → chemotherapy CHEMOTHERAPY (management of leukemia, multiple myeloma, hodgkin's)  hormonal o to reduce cellular metabolism by providing an environment that is non-favorable for the growth of cancer cells o estradiol, halotestin, DES (diethylstilbestrol)  polyfunctional alkylating o binds to DNA → preventing cell replication o Alkeran/melphalan, myleran/Busulfan, leukeran/Chlorambucil, cytoxan/Cyclophosphamide, Ifex/ifosfamide, platinol/Cisplatin  nitrosureas o binds to DNA → preventing cell replication o carmustine, lomustine  vinca alkaloids / mitotic spindle poison o considered mitonic inhibitors o vincristine/Oncovin, vinblastine/Velbee/Velban  antimetabolites o fosters cell death by interfering in the cellular metaboli