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MEDICAL SURGICAL NURSING: STUDY DIABETIS MELLITUS
and ACUTE HEMORRHAGIC PANCREATITIS
NOTE: 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
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
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
T3T
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 , hypo thyroidism; if decreased , hyper thyroidism) 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
o PRIMARY - failure of the thyroid gland to secrete T3 & T 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 T & T 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 & T 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 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 glotti s → 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
surgery → post-op bc of stress or wound infection , the remaining thyroid gland is compensating → produces elevated T3 & T 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
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
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
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 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 L → 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 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
but among clients w/ subarachnoidal obstruction, there is no change in pressure
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
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
