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
 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
  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
 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
  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
 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
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
 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
  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
 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
 normal response: flexion of the toes
  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
  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
  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
  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)
  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
  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
  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
  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
  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
  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
 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)
  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 metabolic processes
o 5-FU/5 Fluorouracil, Purinethol/6 Mercaptopurine, cytosar/ara c/Cytarabine
 antitumor / antibiotic
o inhibits cell division by interfering in the synthesis of nucleic acid
o doxorubicin/Adriamycin, Actinomycin/dactinomycin, plicamycin/Mithramycin, bleomycin
 nursing responsibilities
o since they are potent therapeutic agents which destroys both normal and abnormal cells →
protect skin from any splashes of the drug → wear mask, gown, gloves when preparing the drug
o nausea, vomiting → administer anti-emetic (ondansetron/Zofran, alprazolam/Xanax) 30 mins.
before chemotherapy
o stomatitis → render meticulous oral care, use an alkalinizer as mouth wash, avoid
irritants/spices/bulky, coarse foods (hard to digest)
o exposure to sunlight will destroy the potency of anti-cancer drugs → IV bottle and tubing
should be covered with carbon paper; dim the light inside the room
o drugs are nephrotoxic (esp. Platinol/cisplatin) → increase fluid intake to reduce the toxicity of
the drugs
o doxorubicin is toxic to myocardium → dysrhythmia → before administering, make sure client is
hooked/connect to a cardiac monitor
o bone marrow depression → anemia, leukopenia → complete bed rest, reverse isolation,
neutropenic diet (avoid raw food, raw vegetables)
o drugs are hepatoxic → liver enzyme tests

IMMUNOTHERAPY

 agent used is BRM - biologic response modifier

o interferon, interleukin
 modifies the response of the immune system to cancer cells

GASTROINTESTINAL
ESOPHAGEAL
ACHALASIA / APRESTALSIS / MEGAESOPHAGUS / CARDIOSPASM

 absence or degeneration of the myenteric plexus (or auerbach plexus) which innervates or stimulates
muscle activity → peristaltic activity that propels the food forward
 o food accumulates at the lower end of the esophagus → lower portion of esophagus distends,
dilates → megaesophagus
o failure of the cardiac sphincter to relax to allow the food to enter the spasm → cardiospasm
 symptoms
o food accumulates @ the lower end of the esophagus →
 → food compresses on sternum → chest pain, sternal pain
 → undergoes decomposition process → halitosis
 → decomposition yields a chemical → chemical esophagitis → difficulty of swallowing
(dysphagia), pain upon swallowing (odynophagia)
 → esophageal obstruction → regurgitation of a small amount of gastric content w/o
vomiting effort → heartburn (pyrosis)
 management - surgery
o esophagomyotomy - opening/division of the esophageal muscle fiber
o cardiomyotomy / heller’s surgery - opening/division of the esophageal and cardiac muscle fiber
o nissen fundoplication - the fundus of the stomach is taken and used to wrap the lower end of
esophagus (to increase the pressure @ LES)

(ESOPHAGEAL) DIVERTICULUM

 outpouching, ballooning of esophageal wall

o upper third of esophagus → zenker/pulsion diverticulum
o middle third of esophagus → traction diverticulum
o lower third of esophagus → epiphrenic diverticulum
 cause - congenital weakness of the esophageal wall, chronic esophagitis, upper abdominal trauma
 symptoms → SEE ACHALASIA
 management - surgery
o excision of the esophageal sac (the outpouching)
o pulsion diverticulum → removed via a cervical incision
o traction & epiphrenic diverticulum → removed via a transthoracic incision (client with a chest
tube)

GERD (GASTROESOPHAGEAL REFLUX DISEASE)

 inappropriate relaxation of the lower esophageal sphincter (LES) causing the back flow of the gastric
content into the esophagus
 risk factors - pregnancy, obesity, caffeine, smoking, alcohol, diet high in fat, high level of estrogen
 symptoms → see ACHALASIA
 management → increase the pressure @ the lower esophageal sphincter
 administer Urecholine/bethanecol, domperidone

MANAGEMENT OF ESOPHAGEAL DISORDERS

 conservative management / health teachings include

o remind to assume an upright position when eating
o avoiding eating/drinking 2 hours before sleeping
o assume an upright position when sleeping / elevate the head
o stop smoking, stop taking alcohol, avoid caffeine
o maintain ideal body weight
o avoid spices, irritants in diet
o render oral care (bc of halitosis)
o avoid very hot/cold drinks
o small frequent, feeding
 post op
o extra oral feedings via TPN (hyperalimentation)

STOMACH
PEPTIC ULCER DISEASE (PUD)

 erosion of a circumscribed area in the GI tract due to the digestive action of HCl and pepsin
 o pepsin (protein and living tissue digesting enzyme) → autodigestion
o however, we have protective mechanisms against pepsin
 our GI tract continuously secretes mucin which provides a protective coating/film for the
GIT
 our GI tract has continuous blood supply → prevents gastric anoxia
 duodenum contains bile & pancreatic enzymes which are alkaline → neutralizes the
acidity of GI tract
o basic physiopathological changes taking place in ulcer is the absence of the barriers → PEPTIC
ULCER DISEASE
o sites continuously bathed with pepsin & are prone to erosions:
 lower end of esophagus → esophagus ulcer
 lesser curvature of stomach → gastric ulcer (poor man's ulcer)
 upper end of the duodenum → duodenal ulcer (rich man's ulcer)
 predisposing factors
o poor dietary habits - omitting meals and eating hurriedly
 food serves as a buffer to HCl → when meals are missed, there is no buffer → gastric
ulcer
 when eating hurriedly, hypermotility of GI tract → rapid entry of food into duodenum →
increased acid load into duodenum → increased acid chyme into duodenum →
duodenal ulcer
 lower economic strata → no food → no buffer → gastric ulcer
o stress
 any prolonged, repeated exposure to a stressor → parasympathetic response
synonymous to vagal response → increase gastric secretions → increased gastric
motility → duodenal ulcer
 executive / high economic strata → duodenal ulcer
o ulcerogenic agents - NSAIDs, ASA, steroids
o gastric stimulants - alcohol, caffeine, colas
o personality
 type A personalities are more prone to developing ulcers - highly competitive,
perfectionist
o age and sex
 gastric ulcer - both sexes, above age 40
 duodenal ulcer - male, ages 30-40
o smoking
 nicotine will cause vasoconstriction → gastric anoxia and destroys the alkalinity of bile &
pancreatic enzymes
o H. pylori / Helicobacter pylori
 presence of this microorganism → releases an enzyme that destroys the gastric mucosa
→ loss of mucin (loss of protection against pepsin)
 can be acquired from eating raw meat
o blood type
 Olcer → peptic ulcer
 if O blood type → high level of pepsinogen which is acted upon by HCl to
produce pepsin
 cAncer → cancer of the stomach

GASTRIC ULCER DUODENAL ULCER

mid epigastric gnawing pain that radiates to the left mid epigastric gnawing pain that radiates to the right

30 mins - 2 hours after meals 2-4 hours after meals

food aggravates the pain food relieves the pain

vomiting relieves the pain no vomiting

weight loss weight gain

decreased HCl → hypochlorhydria increased HCl → hyperchlorhydria

hematemesis (vomiting blood/coffee ground vomitus) melena

 management
o avoid predisposing factors
o administer buffers to HCl (food and antacids)
 advice regularity in eating
 low protein (bc protein stimulates the release of HCl), increased carbohydrate with
inclusion of polyunsaturated fats (fat stimulates the intestinal mucosa to secrete a
hormone called enterogastrone → decreases gastric secretion & gastric motility)
 antacids
 can cause constipation or diarrhea (depending on the content)
 constipation → Al OH, cal carbonate
 diarrhea → mg oxide, mg hydroxide → both contained in milk of
magnesia
 follow with water bc w/o water the antacid will simply coat the mucosa
 if liquid, should be 1 tbsp; if solid, should be 2-3 tabs (find out if there's a need
for it to be chewed)
 best time to take an antacid → an hour after meal (food is about to leave the
stomach), in between meals, at night (when the level of HCl is at its peak)
o H2 receptor antagonist
 blocks the release of histamine (a gastric stimulant) by parietal cells
 best taken → before meals
 if ordered with an antacid, there should be an interval of 30 mins to 1 hr → H2 blocker
should be given first (before an antacid) to prevent a delay in the absorption of the H2
blocker (bc the antacid has a local coating effect)
o proton pump inhibitor
 prevents the secretion of HCl
 best taken → if single dose, before dinner or at bedtime; if taken twice a day, before
breakfast & before dinner
o observe the client for signs and symptoms of peptic ulcer complications
 perforation w/ peritonitis
 if the ulcer has invaded the serosa, the submucosa, the muscularis of the
stomach then it has perforated
 bc of perforation → leakage of gastric & intestinal content into peritoneal cavity
→ peritonitis
 abdominal distention, board-like rigid upon percussion, hypoactive/absent
bowel sounds, sudden onset of a severe abdominal pain
 management - billroth I, billroth II, gastrorrhaphy
 bleeding
 if the ulcer has eroded the surrounding blood vessel → bleeding
 melena or hematemesis
 pyloric obstruction
 narrowing/stenosis of the pyloris secondary to scarring/fibrosis of the tissue
 vomiting of undigested food, signs of fluid & electrolyte imbalances, epigastric
fullness
 management - pyloroplasty
 intractable ulcer
 management - antrectomy, vagotomy (palliative surgeries)
 management of complications - GASTRIC SURGERY
 incisions - upper midline incision (xiphoid down to umbilicus), left upper
paramedian incision
 billroth I - subtotal gastrectomy with gastroduodenostomy
 removal of the distal third of the stomach and the remaining portion is
anastomosed to the duodenum
 billroth II - subtotal gastrectomy with gastrojejunostomy
  removal of the distal third of the stomach and the remaining portion is
anastomosed to the jejunum
 billroth III - total gastrectomy with esophagojejunostomy → indicated for cancer
of the stomach
 removal of the entire stomach and the esophagus is anastomosed to the
jejunum
 gastrorrhaphy - suturing a perforated stomach
 antrectomy - antrum is removed (bc antral mucosa produces gastrin which
stimulates HCl production)
 vagotomy - part of the vagus nerve is removed (bc vagal stimulation/PN
stimulation → increased gastric secretions → increased gastric motility)
 pyloroplasty - reconstructive surgery done to enlarge the pyloric opening
 nursing responsibilities after gastric surgery
 true for ALL surgeries
 bladder atony
 paralytic ileus
 dehiscence, evisceration
 hypostatic pneumonia → atelectasis
 DVT, thrombophlebitis
 DUMPING SYNDROME
 rapid passage of hyperosmolar solution into jejunum →
 → local effect → jejunum distends → increased intestinal motility
 → systemic → fluid moves from intravascular to jejunum → shock-like
symptoms (hypovolemic shock)
 prevention
 lie down after eating
 eat in a recumbent or semi recumbent position
 take fluids in between meals but not with meals
 take dry meals
 no sweets, no food rich in carbohydrates → emptying time of
carbohydrates is 1-2 hrs after eating (while protein is 2-4 hours)
 if not prevented, administer an anticholinergic that delays gastric emptying
 propantheline bromide/Probanthine, dicycloverine/Bentyl
 marginal ulcer
 HCl is come in contact with the site of anastomoses
 pernicious anemia (stomach size is reduced → reduced gastric mucosa → reduced
intrinsic factor → malabsorption of vit. B12)
 malnutrition (malabsorption of diffferent nutrients, reduction in gastric capacity)

COLON
CHRONIC INFLAMMATORY BOWEL DISORDER
CROHN'S ULCERATIVE COLITIS

transmural inflammation (all layers) of the small and inflammation of the entire length of the colon (initially
large intestine (a segment/region is inflamed; most affected is the descending colon, specifically the recto-
commonly affected is the terminal ileum) sigmoid)

hereditary disease, autoimmune bacterial in origin, stress, allergen, autoimmune

pathologic lesion - enlarged submucosal lymph node,

pathologic lesion - diffuse, mucosal ulceration, appearance
Peyer's patches of intestine → cobble-stone like
of an inflammatory infiltrate → appearance of a crypt
mucosa, inflamed segment will appear as a constricted
abscess (full of pus)
segment of the colon → string sign

symptoms - pain @ RLQ, diarrhea (3-5 times/day with a symptoms - generalized crampy abdominal pain @ LLQ,
stool containing pus & mucus), semi-soft to soft stool, diarrhea (15-20 times/day with a stool containing mucus,
rarely bleeds, pus, & blood), liquid or watery stool, rectal bleeding

 management - rest the GI tract

 o client placed in NPO and placed on TPN
o diarrhea → restore fluid & electrolyte losses, antidiarrheal
o pain → antispasmodic
o NSAIDs to lessen inflammation
o ulcerative colitis → intestinal microbial (cotrimoxazole, metronidazole)
o after acute phase, client can eat but avoid irritants

INTESTINAL OBSTRUCTION

 mechanical
o occlusion in the colon intraluminally or extraluminally that can be due to a tumor, volvolus
(twisting), intussusception (telescoping), adhesion of the loop of the intestine, diverticulosis
 tumor sites commonly affected include the recto-sigmoid, descending colon
 predisposing factors → hx of Crohn's (small intestinal cancer), ulcerative colitis (colon
cancer), chronic constipation, polyposis (a precancerous lesion that is benign that can
lead to cancer), diet (high in saturated fats, high in protein, low in fiber),
 a polyp will take 2-3 years to become malignant
 colon cancer → diet high in beef
 change in bowel movement (alternate between constipation and
diarrhea), pencil like stool/ribbon life
 if right sided tumor, melena
 if left sided tumor, hematochezia
 rectal tumor → rectal bleeding
o DIVERTICULOSIS
 chronic constipation → increase intraluminal pressure in intestine (most common site:
recto-sigmoid) → colon outpouches (diverticulosis) → trapping of fecal matter → favors
growth of microorganism → diverticulitis → increased intestinal motility → diarrhea
 diet to prevent diverticulitis → high roughage
 diet to treat diverticulitis → low in fiber
 neurogenic/functional - no actual blockage but there is absence of peristalsis (paralytic ileus/adynamic
colon, hirschsprung disease)
o paralytic ileus can be caused by the effect of anesthesia, peritonitis, hypokalemia (which
influences intestinal tone)
 vascular - mesenteric thrombosis
 manifestations → signs of peritonitis
 management depends on the cause
o peritonitis → give intestinal antimicrobial, prepare for intestinal decompression (evacuate
intestinal content)
 tubes used for gastric decompression
 levin, salem, sump tubes, moss tubes, ewald tubes
 tubes used for intestinal decompression
 miller-abbott, cantor, harris, baker
o hypokalemia → administer K supplement
 NEVER give K by IV PUSH
 given only by DRIP or by INFUSION
o mechanical/vascular obstruction → colon surgery
 hemicolectomy (laparoscopic or open)
o APR / miles
o abdominal-perineal resection → surgical removal of the descending colon, sigmoid, rectum, and
anal sphincter with a creation of a permanent colostomy
o COLOSTOMY
 know the type of colostomy
 purpose (temporary, permanent)
 construction
 single barreled = one stoma, permanent,
 double barreled = two stomas, temporary
 proximal stoma - right side of abdomen that drains semi-formed
stool; it is the functioning stoma as it is closer to the functioning
small intestines
  distal stoma - left side of abdomen that drains mucus
 location
 RLQ - ascending colostomy
 below umbilicus - transverse colostomy
 LLQ - descending colostomy or sigmoid colostomy
 fluid/fecal matter
 liquid, watery stool - ascending colostomy
 soft, mushy stool - transverse colostomy
 semi formed to formed stool - descending colostomy
 establish a normal pattern of elimination via transverse and descending colostomy
(ascending cannot be regulated as it is liquid, watery stool)
 give a well-balanced diet
 regularity in doing colostomy irrigation
 best time to irrigate is closer to the usual pattern of elimination pre-
operation
 if there's no regular time, best time to irrigate is after breakfast
 rectal tube inserted into the stoma for 2-3 inches
 position - instruct patient to sit on toilet, feet apart and drain the
colostomy onto the bowl; if in bed, turn the patient to the left
 prior to irrigation, check the temperature of the solution (should be at
body temperature; if it is too cold → abdominal cramps, if too hot →
injure and traumatize the intestinal mucosa)
 if there are abdominal cramps, lower the irrigator can
 if 3-5 mins after lowering the can and telling the client to do
relaxation techniques, abdominal cramps do not stop → clamp
and stop doing temporarily the colostomy irrigation
 prevent offensive odor
 advise to avoid foods that will cause an offensive odor (boiled eggs, cabbage,
radish, celery)
 advise them to eat foods that will prevent the offensive odor like yogurt and
parsley
 use a deodorizer → karaya gel or charcoal filter disc
 change of the pouch when it is 1/3 - 2/3 full of fecal matter
 in the absence of a coloplast, use plastic as pouch
 prevent skin excoriation as fecal matter could leak out from the stoma → skin irritation
 the opening of the pouch should only be 1/8-1/4 inch bigger than the stoma
opening
 use a skin barrier (e.g. karaya powder or any ordinary talcum powder like starch
or cornstarch)
 remind client to avoid strenuous physical activity that can cause the prolapse of the
stoma
 activities allowed → swimming (bc lumen only opens if there is peristalsis),
sexual activity is not contraindicated

LIVER CIRRHOSIS

 laennec's / portal / atrophic / micronodular cirrhosis → alcoholism

 post necrotic cirrhosis → infection, intake of hepatotoxic drugs
 biliary cirrhosis → cholestasis
 cardiac → congestive heart failure (right sided heart failure)
 high among males after the age of 40
 number one cause of liver cirrhosis in the Philippines → malnutrition
 20% of cardiac output is delivered to the liver (making it a very vascular organ)
 SIGNS and corresponding DIAGNOSTICS
o liver cannot metabolize nutrients → weakness, weight loss
 galactose tolerance test → evaluates carbohydrate metabolism
 place client on NPO for 6-8 hours; following morning, place per IV 100 ml of 25%
galactose → 2-4 hrs later, extract venous blood → evaluate for the presence/absence of
galactose in blood
  (+) of galactose → liver damage (it should have been converted into glycogen)
o failure of liver to store iron and vit. B12 → anemia
o failure of liver to store vitamin K essential for the formation of prothrombin which is essential
for clot formation → vit. K deficiency → hypoprothrombinemia → bleeding
 PT time determination
 normal = 11-20 seconds; prolonged in liver cirrhosis
o liver cannot synthesize albumin and globulin → hypoalbuminemia → decreased colloidal
osmotic pressure → fluid shifts from intravascular to interstitial → edema, anasarca, ascites
 serum albumin
 ascites can compress on diaphragm → respiratory distress
 paracentesis / peritoneal tap to withdraw/aspirate the ascitic fluid
 informed consent; prepare local anesthetic agent
 take note of PT (any prolongation should promptly be reported to the doctor →
contraindication and paracentesis will be cancelled)
 position the client (supine or upright - more comfortable) and cleanse the site of
puncture (midway between the umbilicus and symphysis pubis)
 gradual removal of ascitic fluid is a must to prevent cardiovascular collapse
 monitor vital signs to assess for cardiovascular collapse
 empty the bladder because the site of puncture is very close to the bladder
 after paracentesis, replace the lost protein and potassium from the ascitic fluid
 high protein
 high potassium diet (carrot w/ skin, squash w/ skin, potato w/ skin,
tomato w/ skin, peas, beans)
 after paracentesis, observe the site of puncture for bleeding and signs of
peritonitis
o the functional unit of the liver is the hepatic lobules which contain the Kupffer cells (phagocytic
cells) → liver damage destroys Kupffer cells → phagocytosis not performed → prone to
infection
 CBC with differential count
o liver does not synthesize bilirubin → elevation of both conjugated and unconjugated bilirubin
→ hyperbilirubinemia →
 → jaundice (hepatocellular jaundice)
 → pruritus
 → tea colored urine (dark colored)
 to evaluate hyperbilirubinemia, bilirubin studies (w/o NPO)
 normal (direct) conjugated = 0 to 0.3 mg/dL
 normal (indirect) unconjugated = 0.1 to 1 mg/dL
 normal total bilirubin = lower than 1.5 mg/dL
o liver is a detoxifying organ → makes substances less toxic/less poisonous → will normally
detoxify aldosterone, barbiturates, poisonous substances, sex hormones, ammonia → failure to
detoxify →
 → aldosterone → hyperaldosteronemia → edema, anasarca, ascites
 serum aldosterone
 → sex hormones → increased level of sex hormones (causes vasodilation) in the blood
→ palmar erythema, gynecomastia, acne, hirsutism, spider
meli/angioma/telangiaectasis (→ vasodilation of minute venules, arterioles seen on
chest, face, abdomen)
 → ammonia is not converted into urea → increased ammonia → ammonia intoxication
→ irritates the meninges of the brain → hepatic encephalopathy (hepatic coma)
 impending hepatic coma → slowness in response, inappropriate response,
mental confusion, sleep reversal (asleep in the morning, awake at night)
 blood test w/ NPO → serum ammonia determination
 → ammonia intoxication → mental deterioration, flapping tremors → (+) asterixis
 → ammonia breakdown → methylmercaptan → fetor hepaticus
 earliest symptom of hepatic coma → sleep reversal
 earliest sign of hepatic coma → (+) asterixis
 o earliest manifestation → hepatomegaly bc decreased glycogenolysis and decreased
gluconeogenesis → oxidation of fatty acids, decreased release of triglycerides → deposition of
fatty acids within the hepatic lobules → fatty liver (hepatomegaly)
o late manifestation → micronodular atrophic liver (small contracted atrophic liver) / shrinkage
of liver
 OTHER DIAGNOSTIC SCANS
o ultrasound of the liver
o liver scan
 NPO for at least 4 hours, prep for IV administration of contrast medium
 contrast medium (radioactive rose bengal, radioactive iodinated serum albumin)
o liver biopsy
 nursing responsibilities - see paracentesis
 puncture site @ right subcostal
o peritoneoscopy
 direct visualization of the anterior portion of the liver
 small stab wound/incision is made below the umbilicus → peritoneoscope will be
introduced at the site
 prepare client like you would for a minor surgery
o enzymatic test
 SGOT - serum glutamic oxaloacetic transaminase / AST - serum aspartate
aminotransferase
 SGPT - serum glutamic pyruvic transaminase / ALT - serum alanine aminotransferase
 SLDH - serum lactate dehydrogenase
 isoenzyme 1 & 2 - elevates when there is myocardial insult/damage
 isoenzyme 3 - elevates when there is lung parenchymal damage (e.g.
bronchogenic cancer)
 isoenzyme 4 & 5 - elevates liver disease, skeletal muscle
o most definitive diagnostic - peritoneoscopy with liver biopsy
 management
o regeneration of liver cells
 protein + multivitamin supplement (essentiale forte / phospholipid)
o avoid hepatotoxic agents
 stop taking alcohol, sedatives, barbiturates
o vitamin k deficiency → administer vit. k
o limit fluid & sodium intake
o monitor daily weights, I&O
o get abdominal circumference once a day
o avoid any trauma or injury (bc of easy bruising due to vit. K deficiency and leg edema)
o correct electrolyte problems (hypernatremia, hypokalemia brought about by
hyperaldosteronemia)
o prevent the onset of hepatic coma
 exogenous source of ammonia → food containing protein, drugs containing amine
radicals like cough syrup
 endogenous source of ammonia → urease splitting microorganism which add on protein
to convert protein into ammonia
 if with end stage hepatic disease → low protein diet
 control GI bleeding as our blood contains protein (and therefore, ammonia)
 any form of GI bleeding precipitates hepatic coma
 anti-coma regimen
 enema - cleanses the colon of the urease splitting microorganism
 neomycin by enema or NGT - non-absorbable antibiotic which prevents the
growth of urease splitting microorganisms
 lactulose / Duphalac per orem - a laxative which increases the excretion of
ammonia in stool, reduces the pH of the colon making it non-favorable for the
growth of urease splitting microorganisms
 complications
o essentially, liver cirrhosis is chronic inflammation process accompanied by scarring/fibrosis
which replaces the normal liver cells → scarred fibrotic issue obstructs the flow of portal venous
 blood → backflow into the portal system → portal congestion → portal hypertension →
collateral circulation established / rerouting of portal venous blood due to the drowning of the
portal system (via the esophagogastric vein [upper gi tract], superior rectal vein [lower gi tract])
→ pressure in the veins will decrease → dilatation of the veins → esophageal varices and
hemorrhoids
o it is possible to have portal congestion without esophageal varices but it is not possible to have
varices without congestion → ESOPHAGEAL VARICES results from portal hypertension
o portal hypertension / congestion → ascites, hydrothorax
 reduce the portal pressure
 medically - propanolol, sandostatin
 surgically
 portocaval shunting - anastomose portal vein w/ inferior vena cava
 mesocaval shunting - anastomose superior mesenteric vein w/ inferior
vena cava
 splenorenal shunting - anastomose splenic vein to left renal vein
 hassab - splenectomy w/ gastric devascularization → gastric blood vessel
is removed

o esophageal varices
 if non bleeding, sclerotherapy with sodium morrhuate or sotradecol sodium which will
cause the hardening/thickening of the wall → wall is inelastic → any increase of
pressure will not prompt the vein to dilate → it cannot rupture
 avoid activities that will decrease intrathoracic or intracavinal pressure
 control bleeding varices
 chemically - pitressin, vasopressin tannate, epinephrine (as they are all potent
vasoconstrictors)
 mechanically - esophageal tamponade
 Singetaken-Blakemore tube
 inflated with 25 ml of water (cardiac balloon) and 175 ml of water (esophageal
balloon) which compress a bleeding esophageal varices
 with 4 lumens
 with balloon rupture, rises up to oropharynx to obstruct the airway → have
scissors on hand to cut the 4 lumens
o hemorrhoids

GALL BLADDER and BILE DUCT

 liver produces the bile

 the gall bladder stores the bile
 liver → right hepatic duct + left hepatic duct = common hepatic duct + cystic duct (from gall bladder) =
common bile duct + pancreatic duct = ampulla of vater → duodenum (sphincter of oddi)
o conjugated bilirubin is converted into urobilinogen (which gives the color of stool and urine) by
the normal flora in the duodenum
 bile salts emulsify the fat and absorb vitamins A, D, E, K
 CHOLECYSTITIS - inflammation of the gall bladder

 CHOLANGITIS - inflammation of the common bile duct

 CHOLELITHIASIS - stone in the gall bladder
o diagnosis → cholecystography/gall bladder series (x-ray of the gall bladder) which involves
administration of dye per orem (telepaque, bilopten, oragrafin)
o dissolve gall stone → chenodeoxycholic acid, ursodeoxycholic acid as well a mixture of honey
and olive oil
 CHOLIDOCHOLITHIASIS - stone in the gall bladder and bile ducts
o biliary colic - severe right upper quadrant pain radiating to the right shoulder occurring after a
fatty meal
 analgesics to relieve
o elevation in conjugated bilirubin → hyperbilirubinemia → jaundice (obstructive jaundice),
pruritus, tea colored urine
 o stone in the cystic duct → will not reach the duodenum → not converted into urobilinogen →
decreased urobilinogen → acholic stool (clay colored stool)
o bile did not reach duodenum → decreased or no bile salts in duodenum →
 → fat indigestion → nausea, vomiting, dyspepsia, steatorrhea (bulky, greasy, foul
smelling stool with fat globules)
 limit fat in diet
 → vitamin K deficiency → hypoprothrombinemia → bleeding
 administration of vitamin K
o diagnosis
 level of conjugated bilirubin, urobilinogen in stool, fat in stool, PT
 choliangiogram → x-ray of the bile duct after giving a dye (hypaque/diatrozate,
cholografin/adipiodone)
 ERCP (endoscopic retrograde cholangio pancreatography)
o dye is instilled a dye via an endoscope down to the duodenum → flows along the ducts (from
the duodenum) → x-ray is taken as the dye flows
 SURGERIES - incision @ right subcosta, r. kocher
o CHOLECYSTECTOMY
 laparoscopic surgery
 open surgery
o CHOLIDOCHOLITHOTOMY - stone removal from the bile ducts
o CHOLIDOCHOTOMY - opening of the ducts
o CHOLEDOCHOSTOMY - opening for drainage
o CHOLEDOCHO-JEJUNOSTOMY - anastomose the bile duct to jejunum
o T-TUBE → diverts the flow of the bile until the post-operative edema subsides, prevents bile
peritonitis
 output bottle is placed in line with the abdomen or the incision → bile will drain only if
the pressure increases in the duct
 bile can leak out from the site of tube insertion → can cause skin excoriation → use a
skin barrier
 output of bile is increasing in amount (more than 500-800 ml/24 hours) → obstructed
bile duct → bc it's not entering the duodenum but entering the output bottle

SUMMARY OF JAUNDICE
 increased unconjugated bilirubin → hemolytic jaundice (in hemolytic anemia)
 increased conjugated bilirubin → obstructive jaundice
 increased conjugated and unconjugated bilirubin → hepatocellular jaundice
PANCREATITIS / AHP (ACUTE HEMORRHAGIC PANCREATITIS)

 male - alcoholism
 female - cholelithiasis
 other factors - penetrating duodenal ulcer, drug induced (use of immunosuppressants,
antihypertensives, diuretics), abdominal trauma
 trypsinogen → converted into trypsin by enterokinase → digests pancreatic cell and surrounding cell
membranes → pancreatic cell destruction → release of histamine and bradykinin → vasodilation &
increased capillary permeability →
o → edematous pancreatic capsule → left flank pain radiating to the back relieved by bending or
sitting up / epigastric pain → vomiting
o → pancreatic cell necrosis → leukocytosis (causes sepsis), hyperglycemia (causes coma),
hyperbilirubinemia (increased conjugated bilirubin → obstructive jaundice), hypocalcemia (bc
trapping of calcium in feces), increased serum amylase and lipase (bc of pancreatic destruction)
o → interstitial bleeding → accumulation of bloody fluid inside peritoneal cavity → peritonitis (+)
Blumberg (rebound tenderness), (+) Cullen sign (ecchymosis, bluish dislocation at periumbilical
area), (+) Turner (ecchymosis @ left flank)
 best confirms AHP → lipase (bc it is solely pancreatic in origin while amylase is released by the salivary
gland and it remains elevated in blood in about 3-4 days while lipase remains in the blood for 2 weeks)
 management
o relieve flank pain
o restore fluid & electrolyte losses
o leukocytosis → third gen antimicrobial
 o hyperglycemia → insulin (rapid acting)
o hypocalcemia → calcium prep
o interstitial bleeding → plasma expander (dextran, valuven, plasmanate)
o rest GI tract and prevent pancreatic enzyme stimulation
 place on NPO immediately
 prep for gastric decompression immediately → insert NGT
 drug which prevents the production pancreatic enzyme → sandostatin/ocreotide

EYES
GLAUCOMA

 ciliary body secretes aqueous humor → posterior chamber → space between iris & cornea → anterior
chamber → trabecular meshwork → canal of schlemm → venous system
 amount of aqueous humor secreted by ciliary body = amount of aqueous humor absorbed in the
anterior chamber → if there is a discrepancy bet. production and absorption → increased ICP
 risk factors - old age, heredity, presence of an eye tumor, trauma, myopia (nearsightedness)
 open angle glaucoma / chronic → obstruction of the flow of aqueous humor @ trabecular meshwork
(bc of hardening of meshwork)
 closed angle glaucoma / acute → obstruction @ the angle of the iris & cornea (the space has been
blocked by dilation)
 diagnosis
o tonometry to measure intraocular pressure (normal - 10-21) - diagnoses glaucoma
 Schiot’s tonometer
 goldmann applanation tonometer
o gonioscopy to visualize the juncture/angle between the iris and cornea - diagnoses the type of
glaucoma
 manifestations
o increased IOP → headache and vomiting
o closed angle / acute glaucoma → sudden onset of pain
o open angle / chronic glaucoma → asymptomatic
o loss of peripheral vision → tunnel vision
o halos / rainbow around light
o client will mention bumping objects on sides (bc of loss of peripheral vision)
 management
o open angle glaucoma → trabeculotomy (opening of hardened meshwork), trabeculoplasty
(repair of the hardened thickened meshwork) → aqueous humor will be free flowing
o closed angle glaucoma → iridectomy, iridotomy
o medications
 miotic → pupillary constrictor → pilocarpine, carbachol
 carbonic anhydrase inhibitor → prevents the production of aqueous humor
(acetazolamide/Diamox, methazolamide, dorzolamide)
 beta blocker (instilled topically) → prevents the production of aqueous humor (timolol
maleate/Timoptic, betaxolol/Betoptic)
 prostaglandin analog → promotes the outflow of aqueous humor (travoprost,
latanoprost)
 hyperosmolar solution → reduces IOP (mannitol per IV, glycerol/glycerin per orem)

CATARACT

 part of the aging and degenerative process → senile cataract

 baby born from a mother with german measles → congenital cataract
 DM, prolonged use of steroid, severe malnutrition and dehydration → metabolic cataract
 prolonged exposure to UV light → traumatic cataract
 diagnose
o ophthalmoscopy using slit-lamp microscope or biomicroscope
 earliest manifestation → gradual, painless loss of vision
 health teachings
o use of antioxidant (betacarotene, vit. A, zinc) → to prevent progression of opacity
 o use of bifocals /magnifying lens → to improve clients vision
 management
o ICCF (intracapsular cataract extraction) - remove the opacified lens including the posterior
capsule
o ECCF (extracapsular cataract extraction) - an opening is made into the capsule to remove the
opacified lens (+ an implantation of intraoperative lens can be done)
 POST OP ICCF & ECCF → bleeding from tension on the suture line (limbus incision) →
manifested by severe headache → avoid activities that will increase IOP
o phacoemulsification - ultrasonic probe is used to break the lens into pieces or fragments and
the fragments will be suctioned out → an intraoperative lens can be done

PANOPTHALMITIS

 any break in sepsis can be the cause

 manifested by chemosis (edema of the conjunctiva), erythema, photophobia, hypopyon (accumulation
of inflammatory exudate inside the anterior chamber), eye discharges
 prepare the client for
o enucleation - removal of eyeball including the sclera, cornea, and optic nerve
o evisceration - removal of eyeball, leaving the sclera, cornea, and optic nerve
o exenteration - removal of the eyeball, including the surrounding structure leaving only the
bony orbit

RETINAL DETACHMENT

 two primitive retinal layers → inner sensory layer, outer pigmented epithelium
 between three could be serous fluid accumulation → the layers could separate → exudate retinal
detachment
 right after the retina is the choroid → if client is diabetic there could be the formation of a fibrous band
between the retina and choroid → presence of fibrous band or scar →layers will separate > traction
retinal detachment (in diabetic patients, most common type of RD)
 between retina and choroid there could be seepage of vitreous fluid > rhegmatogenous retinal
detachment
 client may complain of floaters/flashes of light or a curtain pull
 rest the eye & cover it with an eye pad → immediately prep for emergency surgery
 SURGERY
o PHOTOCOAGULATION → delivers an intense beam of light → heat from the light will cause a
coagulant which will seal the retinal hole between retina and choroid 
o SCLERAL BUCKLING / SILICONE BAND → will use a silicone implant to cause the retina and
choroid to attach again→ done for 8-12 hrs guided by a microscope 

POSITIONING IN EYE DISORDERS

 post cataract & glaucoma → prevent increased IOP → unaffected side
 retinal detachment w/o surgery → affected side to allow gravitational flow
 retinal detachment post-op → unoperated side  

Hope this helped somehow. Never doubt yourself, I know you can and you will pass the board exam this June.
So chin up, future RN! Don’t give up now! We’re almost there! Kayang kaya natin to.
Keep fighting and keep praying for that license (and for others too).
God bless, Salutaris Manibus. 
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