exams 1-4 cont. Flashcards

1
Q

the nurse is admitting a client diagnosed with primary adrenal cortex insufficiency (addison’s) which clinical manifestations should the nurse expect to assess?

A

bronze pigmentation hypotension and anorexia

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2
Q

The nurse is developing a plan of care for the client diagnosed with acquired immunodeficiency syndrome (aids) who has developed an infection in the adrenal gland. Which client problem is highest priority ?altered body imageactivity intoleranceimpaired copingfluid volume deficit

A

fluid volume deficit

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3
Q

the nurse is planning the care of a client diagnosed with Addison’s . which intervention should be included ?

A

administer steroid medications

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4
Q

The client is admitted to rule out cushing’s syndrome. Which laboratory tests should the nurse anticipate being ordered?

A

plasma levels of ACTH and cortisol

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5
Q

The client has developed iatrogenic cushing’s disease. Which statement is the scientific rationale for the development of this diagnosis.the client has an autoimmune problem causing the destruction of the adrenal cortexthe client has been taking steroid medications for an extended period for another disease processthe client has a pituitary gland tumor causing the adrenal glands to produce to much cortisolthe client has developed an adrenal gland problem for which the healthy care provider does not have an explanation

A

The client has been taking steroid medications for an extended period for another disease process

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6
Q

The nurse is performing discharge teaching for a client diagnosed with cushing’s disease. which statement by the client demonstrates an understanding of the instructionsI will be sure to notify my health care provider if i start to run a feverbefore I stop taking the prednisone, I will be taught how to taper it offIf i get weak and shaky, I need to eat some hard candy or drink some juiceIt is fine if I continue to participate in weekend games of tackle football

A

I will be sure to notify my health care provider if i start to run a fever

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7
Q

The charge nurse of an intensive care unit is making assignments for the night shift. Which client should be assigned to the most experienced intensive care nurse ?The client diagnosed with respiratory failure who is on a ventilator and requires frequent sedationThe client diagnosed with lung cancer and iatrogenic cushing’s disease with ABGs of PH 7.35 PaO2 88, Paco2 44, and HCo322The client diagnosed with Addison’s disease who is lethargic and has a BP of 80/45, P 124 and R28The client diagnosed with hyperthyroidism who has undergone a thyroidectomy two days ago and has a negative trousseau’s sign

A

The client diagnosed with Addison’s disease who is lethargic and has a BP of 80/45, P 124 and R28

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8
Q

The nurse writes a problem of “altered body image” for a 34 year old client diagnosed with Cushing’s disease. Which intervention should be implemented

A

Use therapeutic communication to allow the client to discuss feelings

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9
Q

The client diagnosed with Addison’s disease is admitted to the ER after a day at the lake. The client is lethargic, forgetful, and weak. Which intervention should the nurse implement.

A

Start an IV with an 18 gauge needle and infuse NS rapidly

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10
Q

The nurse manager of a medical surgical unit is asked to determine if the unit should adopt a new care delivery system. Which behavior is an example of an autocratic style of leadership?call a meeting and educate the staff on the new delivery system being used. organize a committee to investigate the various types of delivery systemswait until another unit has implemented the new system and see if it works outdiscuss with the nursing staff if a new delivery system should be adopted

A

call a meeting and educate the staff on the new delivery system being used.

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11
Q

The client diagnosed with cushing’s disease has undergone a unilateral adrenalectomy. Which discharge instructions should the nurse discuss with the client?Call a meeting and educate the staff on the new delivery system being usedorganize a committee to investigate the various types of delivery systemswait until another unit has implemented the new system and see if it works outdiscuss with the nursing staff if a new delivery system should be adopted.

A

wait until another unit has implemented the new system and see if it works out

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12
Q

The client diagnosed with a pituitary timor developed syndrome of inappropriate antidiuretic hormone (SIADH). Which interventions should the nurse implement?

A

assess for N/V and weigh daily

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13
Q

The nurse is admitting a client to the neurological intensive care unit who is postoperative transsphenoidal hypophysectomy. which data warrant immediate intervention?The client is alert to name but is unable to tell the nurse the locationthe client has an output of 2500 ml since surgery and an intake of 1,000 mlthe clients vital signs are 97.6,88,20,130/80The client has a 3 cm amount of dark red drainage on the turban dressing

A

the client has an output of 2500 ml since surgery and an intake of 1,000 ml

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14
Q

which laboratory value should be monitored by the nurse for the client diagnosed with diabetes insipidus

A

serum sodium

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15
Q

the nurse i discharging a client diagnosed with diabetes insipid us. which statement made by the client warrants further interventioni will keep a list of my medications in my wallet and wear a medic alert braceleti should take my medication in the morning and leave it refrigerated at homei should weigh myself every morning and record any weight gainIf I develop a tightness in my chest, I will call my health care provider

A

i should take my medication in the morning and leave it refrigerated at home

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16
Q

the client is admitted to the medical unit with a diagnosis of rule out diabetes insipidus. Which instructions should the nurse teach regarding a fluid deprivation test?

A

The client will be NPO and vital signs and weights will be done hourly until the end of the test

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17
Q

The nurse is caring for clients on a medical floor . Which client should be assessed first.the client diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH) who has a weight gain of 1.5 pounds since yesterdaythe client diagnosed with a pituitary timor who has developed diabetes insipid us and has an intake of 1500 and an output of 1600 in the last 8 hrs.The client diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH) who is having muscle twitchingthe client diagnosed with diabetes insipid us who is complaining of feeling tired after having to get up at night

A

The client diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH) who is having muscle twitching

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18
Q

The nurse is planning the care of a client diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH). Which interventions should be implemented? Select all that applyRestrict fluids per health care provider orderassess level of consciousness every 2 hoursprovide an atmosphere of stimulationmonitor urine and serum osmolalityweigh the client every 3 days

A

Restrict fluids per health care provider orderassess level of consciousness every 2 hoursmonitor urine and serum osmolality

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19
Q

The nurse is caring for a client diagnosed with Diabetes insipid us. Which intervention should be implemented

A

assess tissue turgor every four hours

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20
Q

The UAP complains to the nurse she has filled the water pitcher four times during the shift for a client diagnosed with a closed head injury and the client has asked for the pitcher to be filled again. Which intervention should the nurse implement first

A

assess the client for polyuria and polydipsia

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21
Q

The nurse is admitting a client diagnosed with syndrome of inappropriate antidiurectic hormone (SIADH). Which clinical manifestations should be reported to the health care provider Serum sodium of 112 and a headacheserum potassium of 5.0 and a heightened awarenessserum calcium of 10 and tented tissue turgorserum magnesium of 1.2 and large urinary output

A

Serum sodium of 112 and a headache

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22
Q

The male client diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH) secondary to cancer of the lung tells the nurse he wants to discontinue the fluid restriction and does not care if he dies. Which action by the nurse is an example of the ethical principle of autonomy

A

notify the health care provider of the clients wishes and give the client fluids as desired

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23
Q

The client is diagnosed with hypothyroidism. Which signs/symptoms should the nurse expect the client to exhibit?

A

complaints of extreme fatigue and hair loss

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24
Q

The nurse identifies the client problem risk for imbalanced body temperature for the client diagnosed with hypothyroidism. Which intervention should be included in the plan of care

A

discourage the use of an electric blanket

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25
Q

the client diagnosed with hypothyroidism is prescribed the thyroid hormone levothyroxine (synthroid) which assessment data indicate the medication has been effective

A

the clients temperature is WNL

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26
Q

Which nursing intervention should be included in the plan of care for the client diagnosed with hyperthyroidism

A

provide 6 small well balanced meals a day

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27
Q

The client is admitted to the ICU diagnosed with myxedema coma. Which assessment data warrant immediate intervention by the nurse serum glucose of 74pulse ox reading of 90%telemetry reading showing sinus bradycardiathe client is lethargic and sleeps all the time

A

pulse ox reading of 90%

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28
Q

Which medication order should the nurse question in the client diagnosed with untreated hypothyroidism

A

sedatives

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29
Q

which statement made by the client makes the nurse suspect the client is experiencing hyperthyroidismi just don’t seem to have any appetite anymorei have a bowel movement about every 3-4 daysmy skin is really becoming dry and coursei have noticed all my collars are getting tighter

A

i have noticed all my collars are getting tighter

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30
Q

The 68 year old client diagnosed with hyperthyroidism is being treated with radioactive iodine therapy. Which interventions should the nurse discuss with the client

A

explain it will take up to a month for symptoms of hyperthyroidism to subside

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31
Q

The nurse is teaching the client diagnosed with hyperthyroidism. Which information should be taught to the client? Select all that applyNotify the HCP if a 3 lb weight loss occurs in 2 daysdiscuss ways to cope with the emotional labilitynotify the HCP if taking over the counter medscarry a medical identification card or braceletteach how to take thyroid medications correctly

A

Notify the HCP if a 3 lb weight loss occurs in 2 daysdiscuss ways to cope with the emotional labilitynotify the HCP if taking over the counter medscarry a medical identification card or bracelet

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32
Q

The nurse is providing an in service on thyroid disorders. Once of the attendees asks the nurse why don’t the people in the united states get goiters as often? Which statement by the nurse is the best responseit is because of the screening techniques used in the USit is a genetic predisposition rare in the North AmericansThe medications available in the US decrease goitersIodized salt helps prevent the development of goiters in the US

A

Iodized salt helps prevent the development of goiters in the US

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33
Q

The nurse is preparing to administer the following medications. Which med should the nurse question administering

A

the loop diuretic to the client with a potassium level of 3.3

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34
Q

Which signs/symptoms should make the nurse suspect the client is experiencing a thyroid storm

A

hyperpyrexia and extreme tachycardia

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35
Q

Problems in the hypothalamus that change the function of the anterior pituitary land result in which condition

A

secondary pituitary dysfunction

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36
Q

Which are hormones produced and secreted by the anterior pituitary gland (select all that apply)Growth Hormone ProlactinThyrotropin (TSH)serotoninGonadotropins (FSH and LH)epinephrine

A

Growth Hormone ProlactinThyrotropin (TSH)Gonadotropins (FSH and LH)

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37
Q

a malfunctioning posterior pituitary gland can result in which disorders (select all that apply)hypothyroidismaltered sexual functionDiabetes insipidusgrowth retardationsyndrome of inappropriate antidiuretic hormone (SIADH)

A

Diabetes insipidussyndrome of inappropriate antidiuretic hormone (SIADH)

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38
Q

a malfunctioning anterior pituitary gland can result in which disorders (select all that apply)pituitary hypo functionpituitary hyper functiondiabetes insipidushypothyroidismosteoporosis

A

pituitary hypo functionpituitary hyper functionhypothyroidismosteoporosis

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39
Q

The assessment findings of a male patient with anterior pituitary tumor include reports of changes in secondary sex characteristics such as episodes of impotence and decreased libido. The nurse explains to the patient that these findings are a result of overproduction of which hormone

A

PRL inhibiting secretion of gonadotropins

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40
Q

a patient with PRL secreting tumor is likely to be treated with which medication

A

dopamine agonists

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41
Q

a patient is prescribed bromocriptine mesylate (parlodel). which information does the nurse teach the patient (select all that apply) get up slowly from a lying positiontake medication on an empty stomachtake daily for purposes of raising GH levels to reduce symptom of acromegalybegin therapy with a maintenance level dosereport watery nasal discharge to the health care provider immediately

A

get up slowly from a lying positionreport watery nasal discharge to the health care provider immediately

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42
Q

Patients diagnosed with an anterior pituitary tumor can have symptoms of acromegaly or gigantism. These symptoms are a result of overproduction of which hormone

A

GH

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43
Q

The nurse is performing an assessment of an adult patient with new onset acromegaly. What does the nurse expect to find

A

thickened lips

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44
Q

When analyzing laboratory values, the nurse expects to find which value as a direct result of overproduction of GH

A

hyperglycemia

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45
Q

In caring for a patient with hyperpituitarism, which symptoms does the nurse expect the patient to report (select all that apply) joint painvisual disturbanceschanges in menstruationdecreased libidoheadache

A

joint painvisual disturbanceschanges in menstruationdecreased libidoheadache

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46
Q

a deficiency of which anterior pituitary hormones is considered life threatening (select all that apply)GHmelanocyte stimulating hormone (MSH)PRLTSHACTH

A

TSHACTH

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47
Q

Which statements about the etiology of hypopituitarism are correct? (select all that apply)dysfunction can result from radiation treatment to the head or braindysfunction can result from infection or a brain tumorinfarction following systemic shock can result in hypopituitarismsevere malnutrition and body fat depletion can depress pituitary gland functionThere is always an underlying cause of hypopituitarism

A

dysfunction can result from radiation treatment to the head or braindysfunction can result from infection or a brain tumorinfarction following systemic shock can result in hypopituitarismsevere malnutrition and body fat depletion can depress pituitary gland function

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48
Q

which statement about hormone replacement therapy for hypopituitarism is correct.

A

testosterone replacement therapy is contraindicated in men with prostate cancer

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49
Q

a femal patient has been prescribed hormone replacement therapy. What does the nurse instruct the patient to do regarding this therapy

A

take measures to reduce risk for hypertension and thrombosis

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50
Q

A patient requires 100 g. of oral glucose for suppression testing and GH levels are measured serially for 120 minutes. The results of the suppression testing are abnormal. The nurse assesses for the signs and symptoms of which endocrine disorder

A

hyperpituitarism

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51
Q

a patioent is recovering from a transsphenoidal hypophysectomy. What postoperative nursing interventions apply to this patient (select all that apply)vigorous coughing and deep breathing exercisesinstruction on the use of a soft bristled toothbrush for brushing the teethstrict monitoring of fluid balancehourly neurologic checks for first 24 hoursinstructing the patient to alert the nurse regarding postnasal drip

A

strict monitoring of fluid balancehourly neurologic checks for first 24 hoursinstructing the patient to alert the nurse regarding postnasal drip

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52
Q

Following a hupophysectomy the patient requires instruction on hormone replacement for which hormones (select all that apply)cortisolthyroidgonadalvasopressinPRL

A

cortisolthyroidgonadalvasopressin

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53
Q

After a hypophysectomy, home care monitoring by the nurse includes assessing which factors (select all that apply)hypoglycemiabowel habitspossible leakage of csf24 hour intake of fluids and urine output24 hour diet recallactivity level

A

bowel habitspossible leakage of csf24 hour intake of fluids and urine output24 hour diet recallactivity level

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54
Q

Postoperative care for a patient who has had a transsphenoidal hypophysectomy includes which intervention

A

testing nasal drainage for glucose to determine whether it contains CSF

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55
Q

While caring for a post op patient following a transphenoidal hypophysectomy, the nurse observes nasal drainage that is clear with yellow color at the edge. This halo sign is indicative of which condition

A

drainage of CSF from the patients nose

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56
Q

A patient with hpophysectomy can post op experience transient diabetes insipidus Which manifestation alerts the nurse to this problem

A

output much greater than intake

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57
Q

The action of ADH influences normal kidney function by stimulating which mechanism

A

distal nephron tubules ad collecting ducts to reabsorb water

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58
Q

What is the disorder that results from a deficiency of vasopressin (ADH) from the posterior pituitary gland called

A

diabetes insipidus

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59
Q

Which statements about diabetes insipid us are accurate (select all that apply)it is caused by ADH deficiencyIt is characterized by a decrease in urinationUrine output of greater that 4 L/24 hours is the first diagnostic indication the water loss increases plasma osmolaritynephrogenic DI can be caused by lithium (eskalith)

A

It is caused by ADH deficiencyUrine output of greater that 4 L/24 hours is the first diagnostic indication the water loss increases plasma osmolarity

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60
Q

What does the nurse instruct patients with permanent DI to do (select all that apply)continue vasopressin therapy until symptoms disappearmonitor for recurrence of polydipsia and polyuriamonitor and record weight dailycheck urine specific gravity three times a weekwear a medical alert bracelet

A

monitor for recurrence of polydipsia and polyuriamonitor and record weight dailywear a medical alert bracelet

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61
Q

A patient uses desmopressin acetate metered dose spray as a replacement hormone for ADH. Which is an indication for another dose ( select all that apply) excessive urinationspecific gravity of 1.003dark concentrated urineedema in the legsdecreased urination

A

excessive urinationspecific gravity of 1.003

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62
Q

The nurse is caring for a patient with DI. What is the priority goal of collaborative care

A

correct the water metabolism problem

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63
Q

Which medications are used to treat DI (select all that apply)chlorpropamide (diabinese)desmopressin acetate (DDAVP) lithium (Eskalith)Vasopressin (Pitressin)Demeclocycline (declomycin)

A

chlorpropamide (diabinese)desmopressin acetate (DDAVP) Vasopressin (Pitressin)

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64
Q

Which patients history puts him or her at risk for developing SIADH?

A

58 year old with metastatic lung or breast cancer

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65
Q

which statement about the pathophysiology of SIADH is correct

A

water retention results in dilution hyponatremia and expanded extracellular fluid (ECF) volume

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66
Q

Which statement about the etiology and incidence of SIADH is correct

A

demeclocycline may be used to treat SIADH

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67
Q

The effect of increased ADH in the blood results in which effect on the kidney

A

tubular reabsorption of water increases

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68
Q

In SIADH as a result of water retention from excess ADH which laboratory value does the nurse expect to find (select all that apply)increased urine osmolality (increased sodium in urine)elevated serum sodium levelincreased specific gravity ( concentrated urine)decreased serum osmolaritydecreased urine specific gravity

A

increased urine osmolality (increased sodium in urine)increased specific gravity ( concentrated urine)decreased serum osmolarity

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69
Q

Which nursing intervention is the priority for a patient with SIADH

A

restrict fluid intake

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70
Q

Which type of IV fluid does the nurse use to treat a patient with SIADH when the serum sodium level is very low

A

3% normal saline

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71
Q

In addition to IV fluids a patient with SIADH is on a fluid restriction as low as 500 to 600 /24 hours. Indicate the serum and urine results that demonstrate effectiveness of this treatment by writing increases or decreases for each item belowurine specific gravity resultsserum sodium resultsurine output

A

urine specific gravity results (dec)serum sodium results (inc.)urine output (inc.)

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72
Q

which medications are used in SIADH to promote water excretion without causing sodium loss (select all that apply)Tolvaptan (samsca)demeclocycline (declomycin)furosemide (lasix)conivaptan (vaprisol)spironolactone (aldactone)

A

Tolvaptan (samsca)conivaptan (vaprisol)

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73
Q

Which statement about pheochromocytoma is correct

A

it is a catecholamine producing tumor

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74
Q

A patient in the emergency department is diagnosed with possible pheochromocytoma. What is the priority nursing intervention for this patient

A

monitor blood pressure for severe hypertension

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75
Q

the nurse expects to perform which diagnostic test for pheochromocytoma

A

24 hour urine collection for vanillylmandelic acid (VMA)

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76
Q

Which intervention applies to a patine with pheochromocytoma

A

instruct not to smoke or drink coffee

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77
Q

which intervention is contraindicated for a patient with pheochromocytoma

A

palpating the abdomen

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78
Q

which diuretic is ordered by the health care provider to treat hyperaldosteronism

A

spironolactone ( aldactone)

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79
Q

which statement about hyperaldosteronism is correct

A

hypokalemia and hypertension are the main issues

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80
Q

when diagnosed with cushing syndrome the manifestations are most likely related to an excess production of which hormone

A

cortisol from the adrenal cortex

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81
Q

what is the most common cause of endogenous hypercortisolism or cushing syndrome

A

hyperplasia of the adrenal cortex

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82
Q

Which are the physical findings of cushing’s syndrome? (select all that apply)moon faced appearancedecreased amount of body hairbarrel chesttruncal obesitycoarse facial featuresthin easily damaged skinexcessive sweatingextremity muscle wasting

A

moon faced appearancetruncal obesitythin easily damaged skinextremity muscle wasting

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83
Q

When assessing a patient with cushing’s syndrome, what does the nurse expect to find

A

hypertension

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84
Q

which lab findings does the nurse expect to find with cushing’s syndrome (select all that apply)decreased serum sodiumincreased serum glucoseincreased serum sodiumincreased serum potassiumdecreased serum potassium

A

increased serum glucoseincreased serum sodiumdecreased serum potassium

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85
Q

the nurse determines a priority patient problem of altered self concept in a female patient with cushion’s syndrome who expresses concern about the changes in her general appearance. What is the expected outcome for this patient

A

to verbalize an understanding that treatment will reverse many of the problems

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86
Q

Mitotane (lysodren)

A

adrenal vytotoxic agent used for inoperable adrenal tumors

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87
Q

aminoglutethimide (cytadren)

A

adrenal enzyme inhibitor that decreases cortisol production

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88
Q

cyproheptadine (periactin)

A

interferes with ACTH production

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89
Q

a patient is scheduled for bilateral adrenalectomy. Before surgery, steroids are to be given. Which is the reasoning behind the administration of this drug

A

to compensate for sudden lack of adrenal hormones following surgery

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90
Q

The nurse is teaching a patient being discharged after bilateral adrenalectomy. What medication information does the nurse emphasize in the teaching plan

A

the patient should learn how to give himself an intramuscular injection of hydrocortisone

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91
Q

which statement about a patient with hyperaldosteronism after a successful unilateral adrenalectomy is correct

A

glucocorticoid replacement therapy is temporary

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92
Q

which are causes for decreased production of adrenocortical steroids (select all that apply) inadequate secretion of ACTHDysfunction of hypothalamic pituitary control mechanismadrenal gland dysfuctioncancerAIDS

A

inadequate secretion of ACTHDysfunction of hypothalamic pituitary control mechanismadrenal gland dysfuctioncancerAIDS

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93
Q

which patient is at risk for developing secondary adrenal insufficiency

A

patient who suddenly stops taking high dose steroid therapy

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94
Q

An ACTH stimulation test is the most definitive test for which disorder

A

adrenal insufficiency

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95
Q

which interventions are necessary for a patient with acute adrenal insufficiency ( addisonian crisis) (select all that apply)IV infusion of normal salineIV infusion of 3% salinehourly glucose monitoringinsulin administrationIV potassium therapy

A

IV infusion of normal salinehourly glucose monitoringinsulin administration

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96
Q

a patient in the ER who reports lethargy, muscle weakness, nausea, vomiting , and weight loss over the past weeks is diagnosed with addisonian crisis (acute adrenal insufficiency) which drugs does the nurse expect to administer to this patient

A

solu-coref IV along with IM injections of hydrocortisone

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97
Q

The nurse determines that the administration of hydrocortisone for Addisonian crisis is effective when which assessment is made

A

lethargy improving; patient alert and oriented

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98
Q

which nursing intervention is a preventive measure for adrenocortical insufficiency

A

reducing high dose glucocorticoid doses gradually

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99
Q

The nurse should instruct a patient who is taking hydrocortisone to report which symptoms to the health care provider for possible dose adjustment (select all that apply)rapid weight gainround facefluid retentionGI irritationUrinary incontinence

A

rapid weight gainround facefluid retention

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100
Q

The nurse determines that the patient in acute adrenal insufficiency is responding favorably to treatment when

A

the patient appears alert and oriented

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101
Q

when assessing a patient who is returned to the surgical unit following a thyroidectomy. the nurse would be most concerned if the patient

A

makes harsh, vibratory sounds when she breathes

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102
Q

an IV hydrocortisone treatment is started for a patient being taken to surgery for a bilateral adrenalectomy. The nurse explains to the patient that this is done to

A

provide substances to respond to stress after removal of the adrenal glands

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103
Q

a priority nursing intervention for a patient with primary adrenal cortex dysfunction would be to

A

monitor vital signs and the patients physiologic response to stress

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104
Q

signs and symptoms of hyperthyroidism

A

weight loss with increased appetiteincreased HR, palpitationsphotophobiamanic behaviordyspnea with or without exertioninsomniaincreased stoolscorneal ulcersirritabilityfine, soft, silky, body hairincreased libidoheat intolerance, warm skindiaphoresistremors

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105
Q

signs and symptoms of hypothyroidism

A

constipationdecreased libidocold intolerancefatigue, increased sleepingimpaired memoryfacial puffinessweight gaindry, coarse, brittle hair

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106
Q

which assessment finding should trigger a more detailed assessment of the patients endocrine system

A

changes in hair texture and distribution

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107
Q

which is a possible outcome for a patient experiencing an age related decrease in antidiurectic hormone

A

diluted urine and dehydration

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108
Q

a patient diagnosed with small cell lung cancer might present with endocrine symptoms consistent with

A

syndrome of inappropriate antidiurectic hormone (SIADH)

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109
Q

what is a priority question to ask a patient with a hypopituitary tumor

A

have you noticed a change in your libidohave you experienced a change in growth with your facial hair have you had an unexpected weight loss

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110
Q

which patient with cushing’s disease is at greatest risk for developing heart failure

A

42 year old with a serum creatinine level of 3.7 mg/dl

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111
Q

which factor is a hallmark assessment finding that signifies hyperthyroidism

A

heat intolerance

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112
Q

which factor is a main assessment finding that signifies hypothyroidism

A

cold intolerance

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113
Q

which sign/symptom is one of the first indicators of hyperthyroidism that is often noticed by the patient

A

vision changes or tiring of the eyes

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114
Q

which laboratory result is consistent with a diagnosis of hyperthyroidism

A

increased serum T3 and T4

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115
Q

the lab results for a 53 year old patient indicate a low T3 level and elevated TSH. What do these results indicate

A

hypothyroidism

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116
Q

the clinical manifestations of hyperthyroidism are known as which condition

A

thyrotoxiocosis

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117
Q

what is the most common cause of hyperthyroidism

A

grave’s disease

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118
Q

the nurse assessing a patient palpates enlargement of the thyroid gland, along with noticeable swelling of the neck. How does the nurse interpret the finding

A

Goiter

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119
Q

The nurse is assessing a patient diagnosed with hyperthyroidism and observes dry, waxy swelling of the front surfaces of the lower legs. How does the nurse interpret this finding

A

pretibial myxedema

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120
Q

which statement best describes globe lag in a patient with hyperthyroidism

A

upper eyelid pulls back faster than the eyeball when the patient gazes upward

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121
Q

the nurse is assessing a patient with graves disease and observes an abnormal protrusion of both eyeballs. how does the nurse document this assessment finding

A

exophthalmos

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122
Q

which statements about hyperthyroidism are accurate (select all that apply)it is most commonly caused by Grave’s diseaseit can be caused by overuse of thyroid replacement medicationit occurs more often in men between the ages of 20-40weight gain is a common manifestationserum T3 and T4 results will be elevated

A

it is most commonly caused by Grave’s diseaseit can be caused by overuse of thyroid replacement medicationserum T3 and T4 results will be elevated

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123
Q

the nurse is providing instructions to a patient taking levothyroixine (synthroid). When does the nurse tell the patient to take this medication

A

on an empty stomach

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124
Q

the nurse is providing instructions to a patient who is taking the antithyroid med propylthiouracil (PTU). The nurse instructs the patient to notify the health care provider immediately if which s/s occurs

A

dark colored urine

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125
Q

a patent who has been diagnosed with Graves disease is going to receive radioactive iodine (RAI) in the oral for of 131I. What does the nurse teach the patient about how this drug works

A

it destroys the tissue that produces thyroid hormones

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126
Q

A patient who has been diagnosed with Graves disease is to receive radioactive iodine (RAI) in the oral form of 131 I as treatment. What instructions does the nurse include in the teaching plan about preventing radiation exposure to others (select all that apply)do not share a toilet with others for 2 week after treatmentflush the toilet threw times after each usewash clothing separately from others in the householdlimit contact with pregnant women infants and childrendo not use a laxative within 2 weeks of having the treatment

A

do not share a toilet with others for 2 week after treatmentflush the toilet threw times after each usewash clothing separately from others in the householdlimit contact with pregnant women infants and children

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127
Q

which statements about hyperthyroidism are accurate (select all that apply)it occurs more often in womenit can be caused by iodine deficiencyweight loss is a common manifestationit can be caused by autoimmune thyroid destructionmyxedema coma is a rare but serious complication

A

it occurs more often in womenit can be caused by iodine deficiencyit can be caused by autoimmune thyroid destructionmyxedema coma is a rare but serious complication

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128
Q

the nurse is assessing a patient with a diagnosis of hashimoto’s disease. what are the primary manifestations of this disease (select all that apply)dysphagiapainless enlargement of the thyroid glandpainful enlargement of the thyroid glandweight lossintolerance to heat

A

dysphagiapainless enlargement of the thyroid gland

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129
Q

lab findings of elevated T3 and T4 decrease TSH and high thyrotropin receptor antibody titer indicate which condition

A

graves disease

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130
Q

uncommon; usually occurs with large follicular carcinomas

A

thyroid carcinoma

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131
Q

T3 and T4 secretion increased before destruction of gland. hyperthyroid state usually transient

A

thyroiditis (radiation induced)

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132
Q

autoimmune disease antibodies bind to TSH receptors and rep them activated increasing the size of the gland and increasing the production of thyroid hormones

A

graves disease

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133
Q

multiple thyroid nodules resulting in thryoid hyperfunction

A

toxic multinodular goiter

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134
Q

pituitary adenoma resulting in excessive TSH secretion

A

pituitary hyperthyroidism

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135
Q

after a visit to the heath care providers office a patient is diagnosed with general thyroid enlargement and elevated thyroid hormone level. This is an indication of which condition

A

hyperthyroidism and goiter

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136
Q

which condition is a life threatening emergency and serious complication of untreated or poorly treated hypothyroidism

A

myxedema com

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137
Q

a patient with exophthalmose from hyperthyroidism reports dry eyes especially in the morning. The nurse teaches the patient to perform which intervention to help correct this problem

A

tape the eyes closed with nonallergenic tape

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138
Q

which factors are considered to be triggers for thyroid storm (select all that apply)infectioncold tempsvigorous palpation of a goiterpregnancyextremely warm temps

A

infectionvigorous palpation of a goiterpregnancy

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139
Q

a patient has the following assessment findings; elevated TSH level , low T3 and T4 level difficulty with memory, lethargy, and muscle stiffness. These are clinical manifestations of which disorder

A

hypothyroidism

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140
Q

a patient has been prescribed thyroid hormone for treatment of hypothyroidism . Within what time frame does the patient expect improvement in mental awareness with this treatment

A

2 weeks

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141
Q

which signs and symptoms are assessment findings indicative of thyroid storm (select all that apply)abdominal pain and nauseahypothermiafevertachycardiaelevated systolic blood pressure bradycardia

A

abdominal pain and nauseafevertachycardiaelevated systolic blood pressure

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142
Q

management of the patient with hyperthyroidism focuses on which goals (select all that apply)blocking the effects of excessive thyroid secretiontreating the s/s the patient experiencesestablishing euthyroid functionpreventing spread of the diseasemaintaining an environment of reduced stimulation

A

blocking the effects of excessive thyroid secretiontreating the s/s the patient experiencesestablishing euthyroid functionmaintaining an environment of reduced stimulation

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143
Q

which are preoperative instructions for a patient having thyroid surgery (select all that apply)teach postop restrictions such as no coughing and deep breathing exercises to prevent strain on the suture lineteach the moving and turning technique of manually supporting the head and avoiding neck extension to minimize strain on the suture lineinform the patient that hoarseness for a few days after surgery is usually the result of a breathing tube used during surgeryhumidification of air may be helpful to promote expectoration of secretions. suctioning may also be usedclarify any questions regarding placement of incision complications and post op carea supine position and lying flat will be maintained post op to avoid strain on the suture lineteach the patient to report immediately any respiratory difficulty tingling around the lips or fingers, or muscular twitchinga drain may be present in the incision. all drainage and dressings will be monitored closely for 24 hours

A

teach the moving and turning technique of manually supporting the head and avoiding neck extension to minimize strain on the suture lineinform the patient that hoarseness for a few days after surgery is usually the result of a breathing tube used during surgeryhumidification of air may be helpful to promote expectoration of secretions. suctioning may also be usedclarify any questions regarding placement of incision complications and post op careteach the patient to report immediately any respiratory difficulty tingling around the lips or fingers, or muscular twitchinga drain may be present in the incision. all drainage and dressings will be monitored closely for 24 hours

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144
Q

the nurse is preparing for a patient to return from thyroid surgery. What priority equipment does the nurse ensure immediately available? (select all that apply)tracheostomy equipmentcalcium gluconate or calcium chloride for IV administrationhumidified oxygensuction equipmentsandbags

A

tracheostomy equipmentcalcium gluconate or calcium chloride for IV administrationhumidified oxygensuction equipmentsandbags

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145
Q

after a thyroidectomy, a patient reports tingling around the mouth and muscle twitching. Which complication do these assessment findings indicate to the nurse

A

hypocalcemia

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146
Q

the nurse assesses a patient post thyroidectomy for laryngeal nerve damage. which findings indicate this complication (select all that apply)dyspneasore throathoarsenessweak voicedry cough

A

hoarsenessweak voice

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147
Q

after hospitalization for myxedema a patient is prescribed thyroid replacement medication. which statement by the patient demonstrates a caret understanding of this therapy?

A

Ill be taking thyroid medication for the rest of my life

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148
Q

which statements about thyroiditis are accurate (select all that apply)it is an inflammation of the thyroid glandHashimoto’s disease is the most common typeit always resolves with antibiotic therapythere are three types: acute, subacute, and chronicthe patient must take thyroid hormones

A

it is an inflammation of the thyroid glandHashimoto’s disease is the most common typethere are three types: acute, subacute, and chronicthe patient must take thyroid hormones

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149
Q

which statements about acute thyroiditis are accurate (select all that apply)it is caused by a bacterial infection of the thyroid glandit is treated with antibiotic therapyit results from a viral infection of the thyroid glandsubtotal thyroidectomy is a form of treatment manifestations include neck tenderness fever and dysphagia

A

it is caused by a bacterial infection of the thyroid glandit is treated with antibiotic therapymanifestations include neck tenderness fever and dysphagia

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150
Q

serum calcium levels are maintained by which hormone

A

parathryroid hormone (PTH)

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151
Q

PTH production

A

raises calcium levels

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152
Q

calcitonin production

A

lowers calcium levels

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153
Q

Bone changes in the older adult are often seen with endocrine dysfunction and increased secretion of which substance

A

PTH

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154
Q

In addition to regulation of calcium levels PTH and calcitonin regulate the circulating blood levels of which substance

A

phosphate

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155
Q

a patient has a positive Trousseau’s or Chvosteks sign resulting from Hypoparathyroidism. What condition does this assessment finding indicate

A

hypophosphatemia

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156
Q

which food does the nurse instruct a patient with hypoparathyroidism to avoid

A

fresh fruit

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157
Q

a patient with continuous spasms of the muscles is diagnosed with hypoparathyroidism . The muscle spasms are a clinical manifestation of which condition

A

tetany

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158
Q

causes of hypoparathyroidism

A

removal of the thyroid gland parathyroidectomy

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159
Q

causes of hyperparathyroidism

A

chronic kidney diseasevitamin D deficiencyneck traumacarcinoma of the lung kidney or GI tract producing PTH like substance

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160
Q

a patient has hyperparathyroidism and high levels of serum calcium. Which initial treatment does the nurse prepare to administer to the patient

A

force fluids (intravenous or oral) and administer lasix

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161
Q

which are assessment findings of hypocalcemia (select all that apply)numbness and tingling around the mouthmuscle crampingmental status changes including irritability fever tachycardia

A

numbness and tingling around the mouthmuscle crampingmental status changes including irritability

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162
Q

which medication therapies does the nurse expect patient with hypoparathyroidism to receive (select all that apply)calcium chloridecalcium gluconatecalcitrolmagnesium sulfateergocalciferol

A

calcium chloridecalcium gluconatecalcitrolmagnesium sulfateergocalciferol

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163
Q

discharge planning for a patient with chronic hypoparathyroidism include which instructions (select all that apply)prescribed medications must be taken for the patient’s entire lifeeat foods low in vitamin D and high inphophoruseat foods high in calcium but low in phosphorusafter several weeks, medications can be discontinuedkidney stones are no longer a risk to the patient

A

prescribed medications must be taken for the patient’s entire lifeeat foods high in calcium but low in phosphorus

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164
Q

in older adults assessment findings of fatigue altered thought processes, dry skin and constipation are often mistaken for signs of aging rather than assessment findings for which endocrine disorder

A

hypothyroidism

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165
Q

which conditions may precipitate myexedema coma (select all that apply)rapid withdrawal of thyroid medicationvitamin D deficiencyuntreated hypothyroidismsurgeryexcessive exosure to iodine

A

rapid withdrawal of thyroid medicationuntreated hypothyroidismsurgery

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166
Q

interpersonal or domestic violence

A

a pattern of coercive behavior in which one person attempts to control another through threats or actual use of physical violence, sexual assault and/or verbal and psychological abuse.

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167
Q

what is one of the most common causes of injury to women

A

battering

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168
Q

what has changed over the years as far as domestic violence

A

Increased awareness, ability to obtain help, and more readily available information have helped in raising the rate of reporting.Increasing incidence of men reporting victimization at the hands of women.

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169
Q

effects of family violence

A

•It isolates the person being abused and robs inner strength, self-worth and the ability to make personal choices. Often people experiencing abuse begin to feel responsible for the abuse.••It traumatizes children, destroying their ability to feel safe in the world and causing them to feel responsible for the abuse.

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170
Q

effect on children with domestic violence

A

–Development adversely affectedEnergy needed to accomplish developmental tasks successfully goesto coping with family violence

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171
Q

effect on adolescents domestic violence

A

–Poorer coping and social skills–Higher incidence of dissociativeidentity disorder–Poorer impulse control

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172
Q

secondary effects of violence

A

•Anxiety•Depression•Suicidal ideation

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173
Q

Types of maltreatment

A

•Physical violence: infliction of physical pain or bodily harm•Sexual violence: any form of sexual contact or exposure without consent•Emotional violence: infliction of mental anguish; threatening, humiliating, intimidating, isolating behavior•Physical neglect: failure to provide medical, dental, or psychiatric care as needed•Developmental neglect: failure to provide nurturing and stimulation needed to ensure meeting developmental milestones•Educational neglect: depriving a child of an education•Economic maltreatment: illegal or improper exploitation of funds or other resources for own person gain or withholding of support

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174
Q

actual occurence of violence requires

A

1.Perpetrator2.Vulnerable person3.Crisis situation

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175
Q

characteristic of perpetrator

A

•Their needs are more important than the needs of others•Extreme pathological jealousy•May control family finances•Likely to abuse alcohol or drugs•Poor social skills, relationship with partner enmeshed and codependent

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176
Q

characteristics of vunerable person (partner)

A

•Legal marriage or pregnancy may initiate or increase violence•Greatest risk for violence when partner attempts to leave relationship

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177
Q

characteristics of a vunerable person (child)

A

•Younger than 3 years•Perceived as different•Product of an unwanted pregnancy•Premature•Prolonged illness

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178
Q

characteristics of a vulnerable person (elderly)

A

•Poor mental or physical health•Dependent on perpetrator•Female, older than 75 years, white, living with a relative•Daughter is caring for elderly father who abused her when she was a child•Elderly woman cared for by husband who has abused her in the past

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179
Q

what is a crisis situation

A

•Situation that puts stress on a family with a violent member

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180
Q

cycle of violence

A

•Process of escalation/de-escalationTension-building stageAttempts to reduce tension by both partnersAcute battering stageHoneymoon stageTension builds and cycle continues

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181
Q

phase I (tension building phase)

A

•Abuser:–Demonstrates increased tension by lashing out at victim/minor battering–Has increased fear of abandonment, jealousy, possessiveness–Interprets victim’s withdrawal as rejection -> more angerVictim: Becomes nurturing & compliant to prevent escalation Often accepts abuse as legitimate Denies own anger/rationalizes abuser’s behavior Increased battering -> decreased ability to cope -> withdrawal

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182
Q

phase II (acute battering incident)

A

•Abuser:–Justifies behavior to self – wants to “just teach a lesson” -> severe battering–Cannot understand what happened, doesn’t know how control was lost–Often minimizes severity of batteringVictim: May intentionally provoke abuser’s behavior because tension of Phase I has become unbearable Knows from experience that once acute phase is over things will be better Beating is severe & victim can often describe violence in detail, dissociating self from own body Help is sought if severe injury, victim fears for own life or severe injury/death to children

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183
Q

PHASE III: Calm, Loving, Respite (Honeymoon)

A

•Abuser:–Loving, kind, contrite–Promises to never repeat behavior–Begs forgiveness, fears losing victim so attempts to charm–Believes can control behavior & now that “lesson has been taught”, victim will not “act up” again–Plays on victim’s feelings of guilt for having “provoked” the incidentVictim: Desperately wants to believe abuse won’t happen again Relives dream of “ideal” love & chooses to believe that the “ideal” is really what is shared with abuser This loving phase becomes victim’s perception of relationship Victim bases staying in the relationship on this “magical” ideal phase.

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184
Q

Which rationale best explains why a nurse needs to be aware of feelings while working with a family experiencing family violence?a.Self-awareness protects one’s own mental health.b.Strong negative feelings interfere with assessment and judgment.c.Strong positive feelings lead to underinvolvement with the victim.d.Positive feelings promote the development of sympathy for patients.

A

b.Strong negative feelings interfere with assessment and judgment.

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185
Q

A person at the emergency department reports severe headaches. The individual isaccompanied by a spouse who insists on staying in the room during the examination and answering all questions. The patient avoids eye contact, has a sad affect, and has slumped shoulders. A concussion is diagnosed. Assessment of which additional problem haspriority?a.Risk of domestic abuseb.Phobia of crowded placesc.Major depressiond.Migraine headaches

A

a.Risk of domestic abuse

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186
Q

A married individual has recently been absent from work for 3-day periods on several occasions. Each time, the individual returned to work wearing dark glasses. Facial and body bruises were apparent. The assessment priority when the occupational health nurse interviews the patient is:a.interpersonal relationships.b.work responsibilities.c.socialization skills.d.physical injuries.

A

d.physical injuries.

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187
Q

A patient has a history of physical violence against family when frustrated and then periods of remorse after each outburst. The plan of care would be considered successful when the patient:a.expresses frustration verbally instead of physically.b.agrees to seek counseling.c.explains the rationale for behaviors to the victim.d.identifies three personal strengths.

A

a.expresses frustration verbally instead of physically.

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188
Q

A woman was grabbed by a man as she walked home from work. The attacker put a gun to her head, taped her mouth, tied her hands, took her to a remote location, and raped her. When she was found she was taken to the emergency department, where she received care. Which aspect of this crisis produced the greatest amount of psychological trauma?a.The threat to her lifeb.The memory of the eventc.The physical pain experiencedd.The collection of evidence

A

a.The threat to her life

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189
Q

A patient was abducted and raped at gunpoint by an unknown assailant. Which assessment finding best indicates the patient is in the acute phase of the Rape-trauma syndrome?a.Confusion and disbeliefb.Flashbacks and dreamsc.Decreased motor activityd.Fears and phobias

A

a.Confusion and disbelief

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190
Q

When an emergency department nurse teaches a victim of Rape-trauma syndrome about reactions that may be experienced during the long-term phase, which symptoms should be included? (More than one answer is correct.)a.Flashbacks, dreamsb.Decreased motor activityc.Development of fears and phobiasd.Feelings of numbnesse.Syncopal episodes

A

a.Flashbacks, dreamsc.Development of fears and phobiasd.Feelings of numbness

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191
Q

The nervous system consists of

A

Central nervous system Peripheral nervous system Autonomic nervous system

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192
Q

The neuron is

A

the structural and functional unit of the nervous system. Neurons initiate and transmit impulses to other neurons.

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193
Q

The neuron’s function

A

Composed of an axon and one or more dendrites. Axon transmits impulses away from the cell body to dendrites of other neurons or directly to the cell bodies of other neurons. Dendrites receive impulses and conduct them toward the nerve cell body.

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194
Q

Neuron’s have both a

A

sensory and motor components

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195
Q

synapse

A

is the junction between neurons where an impulse is transmitted.

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196
Q

axon

A

long branch, transmits impulses

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197
Q

dendrites

A

receive impulses from other neurons

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198
Q

synapse

A

bridge between the axon and dendrites

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199
Q

neurotransmitters

A

are chemical agents involved in transmission of the impulse across the synapse.you need these in order for the impulses to go over the bridge.

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200
Q

Myelin Sheath

A

sheath is a wrapping of a fatty material that protects and insulates the nerve fibers and enhances the speed of impulse conduction.

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201
Q

Afferent Neuron

A

sensory neuron that transmits impulses from the peripheral receptors to the Central Nervous System (CNS).

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202
Q

Efferent Neuron

A

is a motor neuron that conducts impulses from the CNS to the muscles and glands.

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203
Q

Myelin Sheath

A

acts like a wire. has the copper on the inside and a rubber coating that protects it. When that plastic coating breakdown, the wire doesn’t work. Same things happen to a myelin sheath. Sometimes if its not a lot of damage, it can repair itself, but if there is too much damage, then it will bot be able to be repaired.

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204
Q

internuncial neurons

A

( interneurons) are connecting links between afferent and efferent neurons.

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205
Q

central nervous system is composed of

A

brain and spinal cord

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206
Q

the brain is composed of

A

cerebrum, corpus callosum, basal ganglia, Diencephalon, brainstem, cerebellum

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207
Q

how do neurons work

A

the afferent neuron reports to the brain that there is something wrong. The brain then reports to the efferent neuron to physically change the situation. i.e. if your hand is on a hot stove, the afferent neuron reports this to the brain and then the brain tells the efferent neuron to remove your hand.

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208
Q

internuncial neurons

A

the links between the afferent and efferent neurons

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209
Q

cerebrum

A

outermost area is the cortex Has two hemispheres Each hemisphere is divided into four lobes ( frontal, Parietal, Temporal and Occipital )

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210
Q

corpus callosum

A

large fiber tract that connects the two hemispheres

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211
Q

basal ganglia

A

islands of gray matter within white matter of cerebrum that regulate and integrate motor activity originating in the cerebal cortex. Part of the extrapyramidal system.

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212
Q

diencephalon

A

the connecting part of the brain between the cerebrum and the brain stem. It contains the: a. Thalamus b. Hypothalamus

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213
Q

brainstem

A

contains midbrain, pons and medulla oblongatarespiratory, vasomotor, and cardiac type functions

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214
Q

cerebellum

A

coordinates muscle tone and movements and maintains equilibriumissues in cerebellum causes ataxia, unsteady gait, surroundings.

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215
Q

frontal lobe

A

motor function, intellectual function, personality, injury to this lobe changes a person’s personality . Broca’s area is located in the frontal lobe. This is the motorized speech area. Allows us to speak and say what we want to say, be able to communicate. If there is a lesion on the frontal lobe, it causes aphasia and issues with expression through speech.

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216
Q

parietal lobe

A

sensory stimulation, sensation, touch, pressure, takes info coming in and makes sense of it .

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217
Q

temporal lobe

A

sensory stimulation, hearing, auditory, receptive, it contains wernicke’s area. This is the sensory speech area. Helps us to understand what someone is saying to us and what is written. If someone has a lesion on wernicke’s area, it causes issues with reception of what we say to them. It’s like we are speaking gibberish.

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218
Q

Occipital Lobe

A

everything associated with vision. this is where basal ganglia is located. These regulate motor activity that originates in the cerebral cortex. Parkinson’s is caused from this area

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219
Q

spinal cord

A

Serves as a connecting link between the brain and the peripheryExtends from foramen magnum to the second lumbar vertebra.Ascending tracts are sensory pathwaysDescending tracts are motor pathways

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220
Q

cerebrospinal fluid

A

Surrounds brain and spinal cordOffers protection by functioning as a shock absorberAllows fluid shifts from the cranial cavity to the spinal cavityCarries nutrients to and from the nerve cellstoo much CSF causes ICP, hydrocephaluscertain things cause CSF leakage. Its very clear color. It is very high in glucose when tested.

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221
Q

what is distinct of CSF

A

The center is clear and the rest is like a yellow halo coming out around it. you can see this if you catch it on a gauze pad

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222
Q

vascular supply of the CNS

A

Two internal carotid arteries anteriorlyTwo vertebral arteries leading to basilar artery posteriorlyThese arteries communicate at the base of the brain through the Circle of WillisAnterior, Middle and Posterior cerebral arteries are the main arteries for distributing blood to each hemisphere of the brainBrainstem and Cerebellum are supplied by branches of the vertebral and basilar arteriesVenous blood drains into dural sinuses then into internal jugular veins

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223
Q

peripheral nervous system

A

Spinal Nerves- 31 pairs carry impulses to and from the spinal cord. Each nerve is attached to spinal cord by two roots:

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224
Q

two roots of the peripheral nervous system are

A

dorsal posterior root, and the ventral anterior root

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225
Q

Dorsal posterior root

A

contains afferent sensory nerves

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226
Q

ventral anterior root

A

contains efferent motor nerve fibers

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227
Q

cranial nerves

A

12 pairs that carry impulses to and from the brain. Have sensory, motor or mixed functions.

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228
Q

The 12 cranial nerves

A

I Olfactory: Sensory-carries impulses for sense of smellII Optic: Sensory-carries impulses for visionIII Oculomotor: Motor-muscles for pupillary constriction, elevation of upper eyelid; 4 out of 6 extraocular movementsIV Trochlear: Motor-muscles for downward, inward movement of the eyeV Trigeminal: Mixed-impulses from face, surface of eyes (corneal reflex); muscles controlling masticationVI Abducens: Motor- muscles for lateral deviation of eyeVII Facial: Mixed- impulses for taste from anterior tongue; muscles for facial movementVIII Acoustic: Sensory-impulses for hearing (cochlear division) and balance (vestibular division)IX Glossopharyngeal: Mixed-impulse for sensation to posterior tongue and pharynx ; muscles for movement of soft pharynx (elevation) and swallowing X Vagus: Mixed- impulses for sensation to lower pharynx and larynx; muscles for movement of soft palate, pharynx, and larynx XI Spinal accessory: Motor-movement of sternomastoid muscles and upper trapezius muscles XII Hypoglossal: Motor-movement of tongue

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229
Q

autonomic nervous system

A

Part of peripheral nervous systemIncludes those peripheral nerves (both cranial and spinal) that regulate functions occurring automatically in the bodyRegulates smooth muscle, cardiac muscle, and glands.Components: Sympathetic and Parasympathetic

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230
Q

neurological exam

A

Mental Status Exam (Cerebral Function) Appearance and behavior Level of Consciousness Intellectual Function Emotional Status Thought Content Language and SpeechCranial NervesCerebellar FunctionMotor FunctionsSensory FunctionsReflexes

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231
Q

five point level of consciousness scale

A

1 Alert: Normal mental activity, aware, mentally functional2 Obtunded/Drowsy: Sleepy, very short attention span, can respond appropriately if aroused3 Stupor: Apathetic, slow moving, blank expression, staring, aroused only by vigorous stimuli4 Light coma: Not oriented to time, place or person. Aroused only by painful stimuli- response is only a grunt or grimace or withdrawal from pain5 Deep Coma: No response except decerebrate or decorticate posture

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232
Q

decerebrate posturing

A

Decerebrate posture is an abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backwards. The muscles are tightened and held rigidly. This type of posturing usually means there has been severe damage to the brain.

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233
Q

decorticate posturing

A

Decorticate posture is an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight. The arms are bent in toward the body and the wrists and fingers are bent and held on the chest.This type of posturing is a sign of severe damage in the brain. People who have this condition should get medical attention right away.

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234
Q

pupil reaction and eye movement

A

Observe size, shape and equality of pupils (note size in millimeters)Test reaction to light—pupillary constrictionCorneal ReflexOculocephalic Reflex

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235
Q

motor function

A

Test movement of extremitiesTest muscle strength MOTOR SCALE5/5 moves against gravity and resistance4/5 moves against moderate resistance3/5 moves against gravity only2/5 moves but not against gravity1/5 muscle contracts-no movement0/5 no visible or palpable movement

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236
Q

parasympathetic nervous system

A

acetocholine

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237
Q

sympathetic nervous system

A

norepinephrine

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238
Q

abnormal respiratory movements

A

Cheyne-StokesCentral Neurogenic HyperventilationApneustic BreathingCluster BreathingAtaxic BreathingGasping BreathingDepressed Breathing

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239
Q

first assessment in neuro

A

patient answering questions appropriately, or are they way off

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240
Q

Second assessment in neuro

A

does there body language and facial expressions congruent with what they are saying

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241
Q

third assessment neuro

A

hows there speech clear slurred, normal rate and rhythm

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242
Q

fourth assessment neuro

A

do they answer you completely

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243
Q

fifth assessment neuro

A

how is there appearance, are they neat and dressed appropriately for the weather, for their age

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244
Q

sixth assessment neuro

A

how do they interact, are they angry, hostile, euphoric, do they answer you and treat you appropriately

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245
Q

neuro health history, presenting problem

A

Behavior changes, memory loss, mood changes, nervousness or anxiety, Headache, seizures, syncope, vertigo, Loss of consciousness, speech problems Vision, smell or motor problems, sensory problems

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246
Q

diagnostic procedures for neuro

A

Xrays Computed Tomographic Scan (CT scan) Positron Emission Tomographic Scan (Pet scan) Magnetic Resonance Imaging (MRI) Carotid Doppler Studies Cerebral Angiography Myelogram Lumbar Puncture

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247
Q

Increased Intracranial Pressure Pathophysiology

A

Increase in brain tissue, vascular tissue, and cerebral spinal fluid volume can cause an increase in pressure within the cranial cavityIncrease ICP can be caused by tumors, abscesses, hemorrage, edema, hydrocephalus, inflammationUntreated can lead to displacement of brain tissue (herniation)

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248
Q

sixth assessment of neuro

A

is the patient hallucinating, or seeing things

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249
Q

Compensatory Mechanisms with Increased ICP

A

Cerebral blood flow decreases causing inadequate tissue perfusion.Leads to increased PCO2 and decreased PO2Triggers vasodilation and more cerebral edemaCan lead to herniation and death

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250
Q

assessment findings of ICP

A

Change in level of consciousnessChanges in vital signs - widening pulse pressure - pulse bounding and slows - abnormal respiratory patterns - Elevated temperaturePupillary changesMotor/Sensory abnormalitiesHeadache, projectile vomiting, hiccuping, papilledema

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251
Q

medical management of ICP

A

Goals: Treat cause, control seizures and other complicationsMaintain fluid and electrolyte balanceSurgical intervention if neededCorticosteroidsOsmotic diuretics, systemic diureticsFluid restrictionBarbituates, analgesicsAirway management

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252
Q

nursing care for ICP

A

Maintain patent airway and adequate ventilationMonitor vital signs and neuro checksMaintain fluid balanceProper positioningPrevent further increases in ICPMonitor I&O carefullyPrevent complications of immobilityGive medications as orderedAssist with ICP monitoringCare of patient with hyperthermia

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253
Q

if your unable to solve a neurological assessment question its called

A

discalcula

254
Q

expressive aphasia or nonfluent aphasia

A

inability to speak and write (broca’s)

255
Q

receptive aphasia or fluent aphasia

A

cannot understand what you are saying to them. Like you’re speaking gibberish to them (wernicke’s)

256
Q

global aphasia

A

they have both receptive and expressive aphasia (fluent and confluent) effects both broca’s & wernicke’s areas

257
Q

What causes ICP

A

anything that takes up home in the skull and takes up space essentially is ICPI.E. :fluid that comes into the brain tissues/cellsbloodtumorblockage of fluid

258
Q

what fluid do you NOT use with a brain injury

A

dextrose 5% in water NEVER EVER use this. Causes ICP

259
Q

ICP left untreated

A

causes herniation of the brain. Brain goes down into the brain stem and patient dies

260
Q

another problem with ICP

A

the body tries to compensate but compensatory mechanism doesn’t help .

261
Q

when you have ICP what happens

A

impairs circulation to the brain. your not going to have adequate perfusion of oxygen . This causes increased PCO2 levels in the blood. this triggers a reaction in the brain. The brain responds by causing vasodilatation. This causes even more cerebral edema. The compensatory mechanism can complicate things.

262
Q

why do we do ABG’s on brain injury patients

A

we are looking to see if they an elevated PCO2 and low PO2. this will trigger the compensatory mechanism. Which we DONT WANT

263
Q

First signs and symptoms of ICP

A

First thing you notice, change in LOC of your patient. There is some change (become nervous, agitated, hyper, apathetic, problems concentrating, stupor)

264
Q

Classic signs and symptoms of ICP

A

widening pulse pressure (systolic elevates, diastolic stays the same. no wider than 40mmg)Bradycardia (but a bounding pulse)elevated temp (late symptom)sometimes low temp (paradoxical effect)changes in Respirations

265
Q

associated symptoms of ICP

A

headachesprojectile vomitinghiccupsoptic nerve can be swollen

266
Q

how do you treat ICP

A

treat the cause of the ICP.also treat seizures

267
Q

fluids and electrolytes

A

maintain fluid and electrolytes, but you need to monitor closely to prevent too much fluid and increasing their ICP.could be on a fluid restriction

268
Q

corticosteroids

A

often used for ICPdexamethasone (decadron) decreases inflammatory response at brain, and decreases ICP

269
Q

osmotic diurectics

A

mannitol works at cellular level to draw fluid out of the brain.given IV. (must have a Foley in, if they are on mannitol)

270
Q

systemic diurectic

A

lasixbumex must be loop given IV

271
Q

barbituates

A

they put them on these to to lower their metabolic rate, an increased metabolic rate increases their ICP

272
Q

analgesics

A

used for pain, but we don’t want to decrease their respirations

273
Q

monitor ABG’s in ICP for

A

we don’t want CO2 to increasewe don’t want O2 to decrease

274
Q

suctioning with ICP

A

suctioning pulls oxygen out. pre-oxygenate them before suctioning and then oxygenate them again after you suction.hold your breath when you do it don’t put suction on when you’re going in, only on outuse sterile gloves and sterile catheter

275
Q

how often do you do I & O’s with ICP

A

hourly

276
Q

positioning ICP

A

semi- fowlers(not so high that the head tilts forward, you want the neck in neutral type position)

277
Q

which way do you want to turn someone with ICP

A

left. You do not want to turn right. Bad draining with Right side in brain.you do not want hip flexion. you want LOG rolling. good free flowing motion

278
Q

epidural sensor

A

placed in epidural space.indirect measurement of ICP

279
Q

normal ICP rating

A

0-10anything sustained above 15 is NOT good

280
Q

intracranial pressure monitoring

A

catheter directly into ventricles in the brain. Measures the pressure directly in the brain. very invasive

281
Q

someone with an Intracranial pressure monitor

A

check tubing for bubbles and kinkschange dressingsmake sure any procedure that you do is sterile

282
Q

how to treat hyperthermia with ICP

A

tepid soaksif everything else fails then use a hyperthermia blanketmake sure they have a rectal probe in constantly check skin for frostbitethey will start shivering, so you need to put them on medication ( i.e. thorazine) to prevent shivering

283
Q

romberg test

A

stand with feet together with eyes openthen you have them close there eyes. if they have a cerebellar problem they start to drift. can’t maintain their position sense.

284
Q

if there is a cerebellar dysfunction

A

ataxia - hard time coordinating walk. (can’t go toe to heel)they adapt and use a wide stance because their center of balance is better

285
Q

what is different about a parkinson’s gait

A

no arm swing and they lean their head down and forward causing their back to hunch. huge safety issue

286
Q

motor function neuro

A

muscle sizetonestrengthany abnormal movements

287
Q

hyperkinesia

A

abnormal movements

288
Q

tremors

A

rhythmic (to and fro) movement

289
Q

Corea

A

uncooderinated movements

290
Q

deep pain stimuli

A

never use on a patient who is with it

291
Q

levels of reflexes

A

0- no reflex at all 1-hyporeflexia2- normal 3- slightly hyperactive4- hyperactive

292
Q

what is the ideal on the glascow coma scale

A

15

293
Q

what can make pupils look funny

A

cataract surgery can throw off a neuro assessment

294
Q

occular cephalic reflex

A

see if there is normal eye movementthey stand behind the individualthey will hold open there eyelidsthey move there head to one sideif the eyes are normal, they will go to the opposite side if they stay on the same side its abnormal

295
Q

dolls reflex/ conjugal movement

A

the normal movement of the eyes

296
Q

cheyne stokes

A

periods of hyperventilation, regular and rhythmicperiods of apneacerebral dysfunction and metabolic disorders cause this

297
Q

central neurogenic hyperventilation

A

rapid sustained respirations (higher 20s)but blood levels are normalusually brain stem dysfunction

298
Q

apneustic breathing

A

prolonged inspiratory phasehold it for a few secondsthen they will exhale caused by a problem in the pons

299
Q

what to look for with Cheyne stokes breathing

A

how long is the apnea lasting for.watch for a whole minute

300
Q

cluster breathing

A

a lot like cheyne-stokeswhen they are breathing its regular breathing, then periods of apneacaused by upper medulla or pons

301
Q

ataxic breathing

A

irregular breathingdamage to the medullamedications can cause it

302
Q

gasping breathing

A

also called kaussmal’sgasping breathingusually seen in dying patients

303
Q

depressed breathing

A

too much medicationlower respirations (8-10)

304
Q

neurological questions you can ask significant others

A

has there been behavior changesmemory lossmood changesheadaches seizuressyncopevertigoloss of consciousnessspeech problemsare they still able to do the ADL’s

305
Q

how is MS caused

A

interferes with the myelin sheath. Characterized by randomly scattered patches of demyelination in the brain stem, cerebrum, cerebellum and spinal cord.Periods of remission and exacerbation.When myelin sheath is first damaged symptoms may be mild or barely noticeable. Myelin can regenerate in very early stages.As disease progresses, loss of myelin permanently damages neurons.

306
Q

is MS one type of disease

A

no there are many different forms of MS. some more severe than others

307
Q

symptoms of MS

A

there are many different type of symptoms depending on where the myelin sheath is effected.

308
Q

progression of MS

A

Recovery following each exacerbation is increasingly less complete over time and permanent loss of function eventually occurs.Degree of disability varies. Some patients can maintain independence or assisted living throughout a normal life span. Others may be severely limited in activities or become bedridden in a few years.

309
Q

how do you know if your MS is going to be good or bad

A

In most cases the onset of MS at a young age indicates a more severe form of the disease with increased disability.

310
Q

statistics of MS

A

MS considered to affect young to middle-age adults. Onset 15 to 50 years of age.Women affected more than men.Higher rates in northern Europe, northern United States, southern Canada and southern Australia and New Zealand.Low rates in southern Europe, Japan, China and South America.Five times more prevalent in temperate climates ( between 45 and 65 degrees latitude ).African Americans have prevalence rate that is 40% that of European Americans. Suggests genetic susceptibility related to ethnicity.250,000 t0 350,000 people in US have MS

311
Q

causes of MS

A

Many experts believe MS is caused by an inflammatory response caused by an individual’s immune system, perhaps triggered by a virus in a genetically susceptible individual.Possible precipitating factors may include infection, emotional stress, excessive fatigue, pregnancy, and a poorer state of health.Role of precipitating factors is controversial.

312
Q

types of MS

A

Relapsing- remittingPrimary- ProgressiveSecondary-ProgressiveProgressive-Relapsing

313
Q

relapsing - remitting MS

A

Clearly acute attacks with full recovery or with sequelae and residual deficit upon recovery. Periods between disease relapses are characterized by lack of disease progression.

314
Q

primary-progressive MS

A

Disease progresses from onset with occasional plateaus and temporary minor improvements.Characterized with no remissions.

315
Q

secondary-progressive MS

A

Begins with an initial relapsing-remitting course, followed by progression at a variable rate, which may also include occasional relapses and minor remissions.May have plateaus.

316
Q

progressive-relapsing

A

Progressive disease from onset, with clear acute relapses, with or without full recovery.Periods between relapses are characterized by continuing progression.

317
Q

things that can cause an exacerbation of MS

A

include infection, emotional stress, excessive fatigue, pregnancy, and a poorer state of health.

318
Q

prognosis of MS

A

Has improved with new immune modulating drugs that slow the progression of the disease and decrease the number of episodes of active disease.Now life span is only slightly shorter than those without the disease.

319
Q

clinical symptoms of MS

A

Often insidious and gradual, with vague symptoms occurring intermittently over months or years.The disease may not be diagnosed until long after the onset of the first symptom.The disease has a varied distribution in the CNS so signs and symptoms vary over time.

320
Q

most common symptom of MS

A

eye problemvision issuesthey go to the eye doctor and find out there is problems with the optic nerveBlurred vision, scotomas (blind spots), diplopia, optic neuritisoften resolved in later stages

321
Q

how is MS diagnosed

A

spinal tap - through spinal fluidMRI can sometimes see the myelin sheath deterioration

322
Q

other common symptoms of MS

A

vague numbnessweird parasthesia’s, go around the trunk, or all the way around a limb. weird sensation altered sensations of pain, temperature, touchaltered position sensevertigoringing in earsloss of hearingneuropathic painLhermitte’s sign spasticity

323
Q

Lhermitte’ssign

A

electrical shock all the way down your spine to your lower limbs

324
Q

impaired motor function in MS

A

Weakness, paralysis, spasticity, tremors.Scanning speech. Cerebellar SymptomsNystagmus, ataxia, dysarthria, dysphagia, problems with balance, intention tremor.

325
Q

MS impaired bowel and bladder function

A

Constipation.Generally, there is urinary retention, but urgency and frequency may also occur. May have either a Uninhibited, spastic bladder or a flaccid bladder.

326
Q

sexual dysfunction in MS

A

Erectile dysfunction from spinal involvement.Women may experience decreased libido, difficulty with orgasmic response, painful intercourse, and decreased vaginal lubrication.MS has no apparent effect on pregnancy, labor & delivery and lactation. Some experience remission when pregnant.

327
Q

emotional effects of MS

A

Euphoria, mood swings.May be some problems with cognition, changes in mental status, attention deficits.Many people experience anger and/or depression.

328
Q

diagnostics for MS

A

History and physical evaluationCSF Analysis-increased protein, leukocytes and Ig immunoglobulinMRICT ScanVision testingEvoked response testing

329
Q

Medical management

A

CorticosteroidsImmunomodulatorsImmunosuppressantsMuscle RelaxantsCholinergicsAnticholinergics

330
Q

immunomodulators for MS

A

reduce the relapse by 30% decreased the appearance of new lesions by 80% causes flu like symptoms these drugs have to be given parentally A. INTERFERON 1A ( AVONEX) ** only drug that is not sub-Q - can cause CHF and Tachycardia B. INTERFERON 1B ( BETASERON ) -can cause CHF and Tachycardia C. GLATIRAMER ACETATE ( COPAXONE ) - can cause a lot of injection site reactions, also can cause palpitations and chest pain. D. REBIF - do not give to a patient with a history of depression.**Do not give certain drugs every day. They need to have at least 48 hrs between them . all these drugs can effect blood cells and the liver enzymes

331
Q

immunosuppressants for MS

A

II. ANTINEOPLASTIC AGENT—MITOXANTRONE ( NOVANTRONE ) decreases your immune response and periods of exacerbation.side effect is cardiotonic. can develop cardiomyopathy, can cause liver toxicity. Can effect your bone marrow. monitor CBC and liver function tests.

332
Q

corticosteroids for MS

A

reduce severity of exacerbation when you have them.treated for 1-5 days

333
Q

muscle relaxants for MS

A

baclovincan be a pump or POdantriun is another oneused for spastic episodesside effects : drowsy, dizzy, muscle weakness, tired, nauseadantriun can cause an erratic blood pressure Examples: Baclofen ( Lioresal ) , Dantrium ( Dantrolene ) & Valium ( Benzodiazepine )Common side effects of Dantrium & Baclofen are dizziness, drowsiness, fatigue, nausea.Baclofen is treatment of choice for spasticity. Will improve mobility. Can be given po, intrathecal injection and by a surgically implanted baclofen pump which is put in the abdomen and delivers the med directly into CSF.

334
Q

cholinergics for MS

A

urecholine increases tone of bladderSide effects are hypotension, heart block, cardiac arrest, faintness, bronchospasm, headache, nausea, diarrhea, vomiting, urgency, flushing,sweating.

335
Q

anticholinergics for MS

A

used for too much tone

336
Q

Corticosteroids for MS

A

(acth, solumedrol, predisone)IV corticosteroids have been effective in reducing severity of exacerbations in may patients.Reduces inflammation and edema at site of demyelination in neuron.IV steroids have less side effects than po steroids.Patient teaching—restrict salt intake, do not abruptly stop, know drug interactions.

337
Q

medications to treat Ataxia

A

Beta-blockers like InderalAntiseizure agents like Neurontin & Klonopin.Amantadine ( Symmetrel), Ritalin, Prozac and SSRIs are used to treat aspects of fatigue, depression and apathy.

338
Q

nursing interventions for MS

A

Assess for specific deficits r/t location of demyelinationPromote optimum mobilityTeach patient not to get overtired—can lead to exacerbation.Administer medicationsMaintain bowel & bladder eliminationPrevent complications of immobilityPrevent injury r/t sensory problemsProvide psychological support to patient, family members and significant others.For sexual dysfunctionFor pain controlExperimental Treatments

339
Q

discharge teaching for MS

A

Balance between rest & activityRegular exercise ie. Walking, swimming, biking in mild casesUse energy conservation techniquesWell-balanced diet—High protein with supplements, vitaminsFresh air and sunshineUse of medications and side effectsAlternate methods of sexual gratificationAvoid fatigue, stress, overheating, chilling, infection

340
Q

patients with MS

A

should not become overtired and overworked it promotes an exacerbation.

341
Q

what to watch with MS

A

watch laxatives, you do not want to create bulk because it will cause an obstruction

342
Q

what keeps dopamine in balance in Parkinson’s

A

acetocholine

343
Q

Parkinson’s

A

Progressive disorder with degeneration of nerve cells in the basal ganglia with generalized decline in muscular function.There is depigmentation of the substania nigra of the basal ganglia.Is a disorder of the extrapyramidal system. This includes all descending fibers in the cortical and subcortical motor centers that reach the medulla and spinal cord by pathways other than corticospinal tracts. Important in maintenance of equilibrium & muscle tone.

344
Q

effects of Parkinson’s

A

Selective depletion of dopamine producing neurons in the substania nigra in midbrain.Dopamine influences purposeful movement. Without it there is a loss of the inhibitory influence of the excitatory mechanisms of acetycholine which goes unopposed.Depletion of dopamine results in degeneration of the basal ganglia

345
Q

Statistics of Parkinson’s

A

Affects men more than women.Cause is unknown. Predominately idiopathic but research suggests several causative factors: genetics, atherosclerosis, excessive accumulation of oxygen free radicals, viral infections, head trauma, chronic antipsychotic medication and some environmental exposures.100 to150 persons/ 100,000 or about 50,000 new cases per year.Symptoms usually appear in fifth decade but some have been diagnosed by age 30.

346
Q

Four classic symptoms of of Parkinson’s

A

TremorsRigidityAkinesiaPostural Instability

347
Q

Tremors in parkinson

A

a slow, unilateral, resting tremor present in about 70% at the time of diagnosis. Disappears with purposeful movement. Starts on one side and progresses to the other.usually have resting tremors that will go away with purposeful movement

348
Q

rigidity in parkinsons

A

have stiffness of neck, trunk and shoulders commonly. Cogwheel rigidity common.

349
Q

Akinesia

A

(bradykinesia)slowness of movement. May exhibit “freezing phenomenon”. As dexterity declines, micrographia develops.tiny tiny writing is common in parkinsons

350
Q

Postural Instability

A

loss of postural reflexes. Stands with head bent forward. Shuffling, propulsive gait.

351
Q

autonomic symptoms of parkinsons

A

sweating, paroxyzsmal flushing, lacrimation, orthostatic hypotension, gastric and urinary retention, constipation, drooling, sensitivity to heat and sexual disturbances.

352
Q

psychiatric changes in parkinsons

A

depression, dementia, sleep disturbances, and hallucinations. May have cognitive, perceptual, & memory deficits though intellect is usually not affected. May see personality changes, psychosis, dementia and acute confusion in the elderly.

353
Q

what is a parkinsons patient at risk for as the disease progresses

A

respiratory & urinary infection, skin breakdown, and injury from falls.

354
Q

stage 1 of parkinson’s

A

mild tremors. unilateral . patient doesn’t even realize there is something going. inconsistent. Little problem with locomotion

355
Q

stage 2 of parkinson’s

A

symptoms are bilateral. slightly more tremors. Friends and family start to see something is wrong.

356
Q

stage 3 of parkinson’s

A

starting to slow with body motion . moderately severe disability. More issues with gait and stability.

357
Q

stage 4 parkinson’s

A

at this point they can’t live alone. very rigid. full blown tremors.

358
Q

stage 5 parkinson’s

A

they can’t stand or walk. Require nursing care

359
Q

what is usually the final demise of Parkinson’s patients

A

urinary tract or respiratory infection. They go septic

360
Q

diagnostic findings in parkinsons

A

Laboratory and imaging studies are not helpful in diagnosing condition. PET scanning is used to evaluate levodopa ( precursor to dopamine ) uptake.Disease is diagnosed by history and presence of 2 or more of the cardinal manisfestations.

361
Q

medical management of parkinson’s

A

control the symptomsDirected at controlling symptoms and maintaining functional independence because there is no medical or surgical treatment to prevent or cure the disease.We now have better symptom control measures.

362
Q

pharmacological therapy in parkinsons acts by

A

Increasing striatal dopaminergic activity b. Reducing excessive influence of excitatory cholinergic neurons. c. Acting on neurotransmitter pathways other than dopaminergic pathways.

363
Q

surgical management of parkinson’s

A

Thalamotomy and pallidotomy are effective in relieving many symptoms. Interrupts nerve pathways and alleviates tremor and rigidity. b. During thalamotomy stereotactic electrical stimulator destroys a portion of the thalmus to decrease tremors. Complications can be ataxia and hemiparesis. c. Pallidotomy destroys part of globus pallidum. Helps to decrease rigidity, bradykinesia & dyskinesia. Improves motor function and ADLs. Complications: stroke, visual changes, hemiparesisUse MRIs, CT scans and angiography to localize appropriate site. Have a stereotactic frame and make a burr hole to pass the electrode through it to target the area. Stereotactic procedures are completed on one side of the brain at a time. If there are bilateral symptoms, 6 months interval is suggested.

364
Q

neural transplantation in parkinson’s

A

Implantation of adrenal medulla tissue into corpus striatum to reestablish normal dopamine release. Research to transplant human fetal brain cells or genetically engineered cells . Recently (2000) fetal pig neuronal cells survived transplantation so may be alternate to human cell transplants.

365
Q

deep brain stimulation in parkinson’s

A

Recently approved by the FDA, pacemaker like brain implants show promising results in relieving tremors. Stimulation can be bilateral or unilateral. Electrode is placed in thalmus and connected to a pulse generator implanted in a subcutaneous subclavicular or abdominal pouch. Generator sends high frequency impulses through a wire placed under the skin to a lead anchored in the skull. The electrode blocks nerve pathways in the brain that cause tremor. Complication: lead leakage.

366
Q

nursing interventions in parkinson’s

A

Provide a safe environment. Measures to increase mobility. Activities to limit postural deformities. Improve communication. Maintain adequate nutrition. Enhance swallowingImprove urinary and bowel elimination. Support coping abilities. Promote home and community based care.

367
Q

drugs used for parkinson’s

A

Dopaminergic Agents a. Replacement ( Levodopa, Sinemet ) b. Dopaminergic Agonists: Bromocriptine Cabergoline ( Cabaser ) Pramipexole ( Mirapex ) Ropinirole ( Requip ) COMT Inhibitors —Entacapone ( Comtress ) Monomine Oxidase B Inhibitor—Selegiline Anticholinergics

368
Q

dopaminergic agents for parkinsons

A

A. Dopaminergic agents help replace lost dopamine or enhance function of the few neurons that are left to produce their own. B. Categories: 1. Replacement—replace dopamine to increase levels in the brain. Examples: Levodopa and Sinemet ( levodopa and carbidopa). 2. Dopaminergic Agonists—direct acting. Bind to receptor and stimulate receptor function. Mimic body’s own regulatory function. Examples: a. Bromocriptine b. Cabergoline ( Cabaser) c. Pramipexole (Mirapex) d. Ropinirole (Requip) 3. Indirect acting—Those that release dopamine. Example: Amantadine. C. Goal: Increase levels of dopamine in the brain to create a balance with acetycholine.

369
Q

COMT inhibitors

A

Entacapone (Comtress) for parkinsonsAction: Increases availability of levodopa by inhibiting COMT activity. COMT ( Catechol-O-Methyltransferase ) is an enzyme which is important in the central and peripheral metabolism of catecholamines ( dopamine, adrenalin, noradrenalin ) and levodopa. COMT activity in periphery reduces the amount of levodopa available for central conversion to dopamine. COMT inhibitors increase availability of levodopa in the brain and prolong its availability in plasma. Results in reduced requirement for levodopa. B. Example: Entacapone ( Comtress, Comtan) (4) C. Side effects / Adverse reactions: 1. Orthostatic hypotension, Hepatic Failure, nausea, vomiting, diarrhea, electrolyte imbalances. 2. Tolcapone was suspended because of concerns over severe hepatic reactions.

370
Q

Monomine Oxidase B inhibitor for parkinsons

A

SELEGILINE (ELDEPRY) A. Most non selective MAO Inhibitors have tyramine effect if taken with foods like cheese, red wins, beer, and yogurt that results in a severe hypertension. Selegiline does not elicit classic cheese effect at doses of 10mg or less per day. Is able to slow the progression of P.D. because it is neuro-protective and blocks the metabolism of dopamine. B. Theory is that substantia nigra’s destruction of cells is caused by MPP, the enzymatically active toxin of MPTP. Conversion is accomplished by MAO-B. By blocking enzyme, substantia nigra is spared. C. Selegiline has less side effects than most MAO Inhibitors so it is approved for use with levodopa and sinemet. It allows those doses to be decreased. Helps to delay levodopa’s loss of control of P.D. in 5 to 10 years. May delay it for 9 to 18 years. Dose is usually 5m BID. D. Side effects / Adverse reactions—usually mild 1. Nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion, dry mouth, hypotension. 2. If dose is increased more than 10mg per day, hypertensive crisis is possible.

371
Q

anticholinergics for parkinsons

A

used more for drug induced parkinson’s A. Action is to inhibit action of acetycholine resulting in a decrease in sweating, salivation, muscle tremors, and rigidity. Does little for bradykinesia. It reduces excessive cholinergic activity in the brain. B. Example: 1. Cogentin 2. Artane C. Side effects / Adverse reactions: 1. CNS—drowsiness, memory confusion, disorientation,hallucinations. 2. Constipation, nausea, vomiting, dry mouth 3. Urinary retention, pain on urination. 4. Blurred vision, dilated pupils, sensitivity to sun, tachycardia.

372
Q

replacement Dopaminergic agents for parkinsons

A
  1. Replacement—replace dopamine to increase levels in the brain. Examples: Levodopa and Sinemet ( levodopa and carbidopa).Levodopa a. Initially 250mg every 6 to 12 hours PO. Increase daily dose by 100 to 750mg every 3 to 7 days until desired response. Max dose-8 grams/day. Usual dose-3 to 6 grams /day. Requires 3 to 6 months to achieve optimal therapy. b. Increases levels of dopamine in the brain and relieves tremors, bradykinesia, and rigidity. Crosses blood-brain barrier. Metabolized in the liver and GI tract. Excreted by the kidneys. c. Interactions: 1. Haldol and phenothiazines block dopamine receptors in the brain so decrease levodopa effect. 2. B6 reverses effect of levodopa by promoting levodopa breakdown. 3. MAO I increase the risk of hypertensive crisis when used with levodopa. Must discontinue 2-4 weeks prior to starting levodopa. d. Contraindications: 1. Acute glaucoma, Melanoma, history of MI with residual arrhythmias, psychotic state. e. Side effects/ adverse reactions: 1. Orthostatic hypotension, cardiac arrhythmias, hemolytic anemias 2. May aggravate peptic ulcer and bronchial asthma. 3. Diplopia ,blurred vision, anorexia, nausea, vomiting, false positive urine glucose. Drowsiness. 4. Confusion, agitation, hallucinations, psychotic episodes, seizures, 5. Hepatoxicity. May cause urinary retention with renal disease. 6. May cause urine and sweat to turn dark. Incontinence. 7. Skin rash, increased sweating. (2) f. Benefits of levodopa do not persist indefinitely. Within 5 to 10 years many patients develop drug related symptoms like drug induced involuntary movements, end-of-dose deterioration, on-off motor fluctuations, psychiatric effects. g. Nursing Implications: 1. Proper history ie. hypotension, seizures, melanoma, glaucoma, meds patient is on. 2. Assess LFTs, RFTs, CBC 3. Assess for toxicity ( involuntary muscle twitching, facial grimacing, spasmotic winking, exaggerated protrusion of the tongue or behavioral changes. 4. Do not take with meals, however MD may order them taken 15 minutes after a meal to decrease gastric irritation. Taking with a meal may retard drug effect. 5. Move slowly for position changes. No driving if drowsy or visual problems. Routine follow-up. Therapeutic effect takes 2 to 3 weeks to achieve. Wait 8 hours before switching to sinemet—can cause toxicity. 2. Sinemet ( Carbidopa / Levodopa) a. Action—Carbidopa given with levodopa inhibits enzymatic conversion of levodopa to dopamine in the peripheral nervous system. Carbidopa does not cross the blood-brain barrier so levodopa is converted to active dopamine primarily in the brain. This decreases many unwanted effects caused by peripherally broken down levodopa. Carbidopa reduces the dose of levodopa needed.. Carbidopa is not effective alone. b. Dosages: 1. 10/100 mg 3 to8 times a day 2. 25/100 mg 3 to 6 times a day 3. 25/250 mg 3 to 4 times a day 4. Sinemet CR—1 tab BID * Maximum dose 200mg Carbidopa and 2 grams levodopa /day c. Side effects /adverse reactions 1. Same as with levodopa but less since lower doses of levodopa are used. 2. Mental depression, mood and mental changes. 3. Hypotension, hypertension, arrhythmias, dizziness. 4. Blurred vision, diplopia, dark urine and sweat, blood dyscrasias 5. Nausea, vomiting, diarrhea, constipation, anorexia. d. May need drug holiday after several years. With long term use, patients experience periods when they have good control (on-time) and periods when they have bad control (off-time). Sinemet CR increases on-time and decreases off-time.
373
Q

dopaminergic agonists for parkinsons

A

Dopaminergic Agonists 1. Action: Stimulate dopamine 2 receptors and antagonizes or blocks dopamine 1 receptors so they stimulate the release of dopamine in the substantia nigra. Can be given with sinemet so lower doses of levodopa needed to prolong “0n” time. (3) 2. Examples: Cabaser, Mirapex, Requip, Bromocriptine 3. Side effects / adverse reactions a. Hypotension, leg cramps, shock b. Drowsiness, confusion, dizziness, nightmares ,hallucinations, visual disturbances, uncontrolled movement of body, face, tongue, arms, hands, and feet. c. Nausea, vomiting, constipation, diarrhea, metallic taste. 4. Contraindications: Hypersensitivity to ergot alkaloids. Patients with severe ischemic PVD. Don’t give to kids under 15 years.F. Indirect Acting 1. Amantadine ( Symmetral) a. Is an antiviral that blocks the reuptake and storage of catecholamines, allowing for the accumulation of dopamine. Elicits release of dopamine from the nerve endings causing higher concentrations of dopamine in the CNS. b. Is more effective in early stages of P.D. when there is still a significant number of nerves to act on dopamine to be released. Usually only effective for 6 to 12 months. c. Dose: 100 to 400 mg / day d. Caution with patients with seizures, liver disease, psych problems, cardiac and renal disease. e. Side effects / adverse reactions: 1. Impaired concentration, mood changes, confusion, hallucinations, visual impairment, headache, irritability, nervousness. 2. Hypotension, nausea, vomiting, constipation ,anorexia 3. Purple re skin spots, dry mouth, nose, and throat. increased weakness f. Nursing Implications: 1. Monitor blood pressure. position changes slowly. 2. Don’t give last dose HS because it will cause insomnia. 3. Better to give in divided doses since it decreases the CNS side effects. 4. Can mix content of capsules with food and fluids. 5. Assess for purple mottling—usually disappears with continued treatment. 6. Therapeutic effects usually seen by end of first week.

374
Q

what vitamin should parkinson’s be careful with

A

B6. it diminishes levodopa in the body. So stay away from foods that have B6

375
Q

alcohol in parkinson’s

A

at later stages its good for them to have small amounts of alcohol to help with relaxation

376
Q

bowel habits for parkinson’s

A

try to keep them on their schedule. If they used to go to the bathroom after breakfast every morning, then place them on the commode every morning after breakfast.

377
Q

biggest side effects of parkinson’s drugs (across the board)

A

orthostatic hypertension

378
Q

parkinson’s drugs build up

A

you build up a tolerance. So you’ll have intermittent symptoms. They will usually take them off the drug for awhile and then re add it.

379
Q

what do you not want with parkinson’s drugs

A

we do not want peripheral metabolism in the brain

380
Q

major side effects of parkinson’s drugs (across the board)

A

Hypotension

381
Q

major issue with myasthenia gravis

A

not enough acetocholine

382
Q

myasthenia gravis definition

A

Definition: a. Disease of the neuromuscular junction characterized by fluctuating weakness of certain skeletal muscle groups especially the face & throat. b. Affects neuromuscular transmission of voluntary muscles of the body especially those innervated by the cranial nerves.

383
Q

issues with myasthenia gravis

A

c. Is purely a motor disorder with no effect on sensation or coordination. d. Results in inability for muscles to contract. e. There are periods of remission & exacerbations and a milder form does exist. f. Considered an autoimmune disease where antibodies destroy or block neuromuscular acetylcholine receptor sites.

384
Q

severity of myasthenia gravis

A

there are many different levels of this disease from mild symptoms to debilitating

385
Q

thymus gland and myasthenia gravis

A

. Thymus gland, which is usually inactive after puberty, continues to produce antibodies. It is believed that the thymus is the source of autoantigen that triggers the autoimmune response inMG. H. Prevents acetycholine from attaching to receptor site and from stimulating muscle contraction.

386
Q

viral infections and myasthenia gravis

A

Viral infections are suspected of precipitating an attack.

387
Q

statistics on myasthenia gravis

A

43 to 84 persons/ million affected.Peak age of onset in women is 20 to 40 yrs. Majority of men are over 50 yrs.Women are affected 3X more than men

388
Q

manifestations of myasthenia gravis

A

Fatigue and weakness of skeletal muscles generally worse with effort and relieved by rest. Patients can tire from combing hair or chewing.

389
Q

bulbar symptoms of myasthenia gravis

A

Bulbar symptoms: a. Weakness of face & throat b. Diplopia ( eye droop) , Ptosis, facial weakness, dysarthria, dysphagia, dysphonia.Complications: Difficulty closing eyes, aspiration, impaired communication & nutrition

390
Q

musculoskeletal and respiratory problems in myasthenia gravis

A

decreased function of hands, arms, legs and neck muscles. b. Weakening of intercostal muscles , decreased diaphragm movement, dyspnea, and poor gas exchange.Complications: a. Decreased ability to perform ADLs b. Immobility complications c. Inability to walk or eat d. Respiratory infections.There is no sensory loss. Reflexes are normal and muscle atrophy is rare.

391
Q

the course of myasthenia gravis

A

The course of the disease varies. Some have short-term remissions, others stabilize and others have severe progressive involvement.

392
Q

exacerbations of myasthenia gravis

A

Exacerbations can be precipitated by emotional stress, pregnancy, menses, illness, trauma, temperature extremes, hypokalemia, surgery & drugs

393
Q

diagnosis of myasthenia gravis

A

Patient history and physical examHave person look upward for 2 to 3 minutes. If MG there will be an increased droop of the eyelids so the person can barely keep eyes open.IV tensilon (anticholinesterase) test Electromyography ( EMG ) to measure electrical potential of muscle cellsAnti-ACH receptor antibodies in serum. Seen in 70 to 80 % of patients.

394
Q

IV tensilon (anticholinesterase) test

A

a. Drug facilitates transmission of impulses at myoneural junction. b. Within 30 seconds of injection most patients with MG improve substantially but is only temporary.

395
Q

prognosis of myasthenia gravis

A

No known cure but drug therapy helps

396
Q

medical management of myasthenia gravis

A

Drug Therapy: Maintenance of stable blood levels of medications is imperative to stabilize muscle strength. Meds must be given on time. a. Anticholinesterase Inhibitors: 1. Mestinon ( Pyridostigmine Bromide ) 2. Prostigmin ( Neostigmin Bromide b. Corticosteroids c. Immunosuppressive TherapyPlasmapheresisSurgical Management: Thymectomy a. Results in symptom remission in about 40%. Best if within 2 years of diagnosis

397
Q

what to remember about myasthenia gravis

A

drugs need to be on time. Do not want to be late. need to maintain a constant blood level

398
Q

anticholinesterase inhibitors for Myasthenia gravis

A

. Drugs increase available acetycholine at the junction. Given to increase the response of the muscles to nerve impulses to improve strength. Gives symptomatic relief. The maintenance dose is determined by testing.B. Maintenance of stable blood levels of these meds is imperative to stabilize muscle strength. Meds must be given on time since a delay can exacerbate muscle weakness and make it impossible for the patient to take meds by mouth.C. Common side effects of these drugs: CNS—irritability, anxiety, insomnia, headache, dysarthria, syncope, seizures, coma, diaphoresis RESP—increased bronchial secretions, bronchial spasm CARDIO—hypotension, tachycardia GI—abdominal cramps, nausea, vomiting, diarrhea, anorexia, increase salivation SKELETAL—spasms, fine twitching, weakness of muscles INTEG—rash, flushing, increased lacrimationD. Examples: 1. PYRIDOSTIGMINE BROMIDE (MESTINON) a. Most commonly used. Peaks in2hours. Duration is 3-6 hours 2. PROSTIGMIN (NEOSTIGMINE BROMIDE) a. Has less side effects than Mestinon. Dosage is increased gradually until maximum benefits. b. Give with milk, crackers, and buffering substances for GI distress. Small doses of Atropine may be given to decrease above side effects.

399
Q

corticosteroids and immunosuppresive therapy for myasthenia gravis

A

II. CORTICOSTEROIDS:A. Suppress immune response and decrease amount of antibody production.B. May use alternate day therapy.III. IMMUNOSUPPRESSIVE THERAPY:A. Reduces production of antireceptor antibodies. Are cytotoxic meds. B. Use drugs like Imuran, Cytoxan.

400
Q

common side effects of anti cholinesterase drugs

A

CNS: Irritability, fine twitching, anxiety, insomnia, headache, dysarthria, syncope, seizures, coma, spasms, weaknessRESP: Bronchial spasm, increased bronchial secretionsCardio: Hypotension, bradycardiaGI: Abdominal cramps, nausea, vomiting, diarrhea, heartburn, anorexia, increased salivationSkin: rash, flushing, sweating, tearing

401
Q

***Myasthenia Crisis

A

Usually caused by under medication. Can be triggered by infection, surgery, emotional stressors, and drugs. Many drugs are contraindicated or must be used with caution. These include anesthetics, antidysrhythmics, antibiotics, quinine, hypnotics, cathartics, diuretics, antipsychotics, barbituates, muscle relaxants, thyroid medications, sedatives, tranquilizers

402
Q

how is a myasthenia crisis manifested

A

Manifested by acute exacerbation of muscular weakness with acute respiratory distress, and inability to swallow or speak.Weakness of respiratory muscles causes respiratory depression and airway obstruction.Can have periods of apnea, extreme fatigue, fever, anxiety, restlessness, irritability, unable to move jaw and raise one or both eyelids.

403
Q

how can you determine its a myasthenia crisis

A

Need to confirm with Tensilon TestMay need plasmaphresis. Given meds parenterally until able to swallowWill be in ICU. Considered medical emergency.

404
Q

cholinergic crisis

A

Over medication is usually the cause.In addition to muscle weakness and respiratory depression, patients will have a variety of GI symptoms.Is a medical emergency. Will be in ICU. Confirm with Tensilon Test.

405
Q

Nursing care for a patient with myasthenia crisis

A

Improve respiratory function: a. Respiratory assessment, PFTs, ABGs, O2 sats. b. TCDB q 1-2 hrs, Spirometry, Chest PT, postural drainage, suctioning to remove secretions. c. Semi-fowlers position. Give emotional support. Maintain hydration to liquify secretions. Avoid drugs that aggravate the disease.

406
Q

Nursing care for a patient with myasthenia crisis

A

Impaired swallowing: a. Assess ability to manage various consistencies of foods. Get Speech Therapy consult. b. Assess for drooling, regurgitation through mouth & nose, and choking when swallowing. Standby suction.

407
Q

Nursing care for a patient with myasthenia crisis

A

c. Plan to promote medication effectiveness. Give drug 30 minutes prior to feeding. d. Rest prior to meals to decrease muscle fatigue. Have patient eat slowly, small bites of foods. Give cues. Upright position with head slightly flexed to facilitate swallowing. Know Heimlick manuever. e. Muscles of mastication are stronger in the morning so calories should be greatest at breakfast.Increases physical mobility: a. Plan rest periods with a realistic daily schedule. Use appropriate clothing b. Avoid activities that lead to crisis. c. Cervical collar for those with weak neck muscles. Adaptive self-care devices. d. ROJM, physical therapy, occupational therapy

408
Q

Nursing care for a patient with myasthenia crisis

A

Improve communication: a. Listen! Repeat what they say to clarify b. Set up some signalsImpaired vision: a. Tape eyes open for short periods. b. Artificial tears if lids don’t close completely. Sunglasses. Eye patch for double vision.

409
Q

how do you determine if its a myasthenia crisis or cholinergic crisis

A

tensilon test

410
Q

patient teaching for myasthenia gravis

A

Take medications at scheduled time.Report toxic effects of drugs and symptoms of disease.Take meds with milk or food to decrease GI effectsWear medi-alert. Check with MD regarding use of other medications.Maintain adequate diet, rest & activity.Avoid infections, extremes in temperature, alcohol, tobacco, and tonic water (quinine)

411
Q

ALS

A

Deteriorating disease of the motor system characterized by muscle weakness progressing to muscle atrophy and eventually paralysis and death.Does not involve autonomic changes, sensory alterations or cognitive changes. Affects motor neurons in the brainstem and spinal cord. Dead neurons can’t activate muscles

412
Q

possible causes of ALS

A

Exposure to heavy metals, viral infection.Is associated with HIV infection10% of ALS patients inherit it on an autosomal dominant gene that can result in the disease,Autoimmune destruction and neurotransmitter depletion

413
Q

statistics of ALS

A

RareOnset usually 40-70 yrs. Peak 55.Twice as common in men as womenProgresses rapidly. No cure. 50% patients die within 2-5 years of diagnosis due to respiratory failure..

414
Q

clinical symptoms of ALS

A

Weakness in extremities. Twitching in arms, trunk or legs. Uncoordinated movements.Loss of fine motor control of hands. Spasticity is usually present and stretch reflexes are brisk and overactive.Eventually, paresis, paralysis, loss moa ADL ability, total immobility.Difficulty speaking, chewing, swallowingVoice has nasal sound. Eventually can’t speak.Regurgitation of liquids through nose.Dyspnea, difficulty clearing airway with complications of pneumonia and respiratory failure.Emotional effects: Patient is cognitively intact while wasting away.

415
Q

diagnostic evaluation of ALS

A

First r/o other disordersEMG to differentiate between neuropathy or myopathyCK increasedMuscle biopsy shows atrophySerial muscle testingPulmonary function tests

416
Q

medical management of ALS

A

Basically supportive a. Quinine for muscle cramps b. Cervical esophogotomy to bypass larynxMay use drugs like Baclofen to decrease spasticity.Riluzole ( Rilutek ) a. Only drug approved for treatment ALS b. Has neuroprotective effect. Extends life for several months.Referral to VNS services

417
Q

Nursing Care for ALS

A

Improve respiratory function and maintain patent airway: a. Assess respiratory function and swallowing ability. Position change 1-2hrs. Suctioning, CPT, spirometry, oxygen as needed, elevate HOB, breathing exercises. b. Treat respiratory infections promptly c. Portable ventilatory support.

418
Q

higher incidence of ALS in

A

HIV positive patients

419
Q

nursing care for ALS

A

Maximize independence: a. AROJM to PROJM q 2hrs. Contractures can develop within a week. b. Utilize energy conservation measures. c. Stretching exercises, splints, assistive devices. d. Wheelchair when too weak

420
Q

nursing care for ALS

A

Nutritional support: a. Maintain nitrogen balance and hydration. Monitor albumin, hgb & hct, total protein levels. b. Calorie count, I&O, daily weight, and Dietary consult. c. Standby suction. Keep upright for 15-20 minutes after eating. Keep head slightly flexed. Don’t wash down foods with liquids. d. Will eventually need enteral feedings.

421
Q

nursing care for ALS

A

Communication: a. Work out plan for this before patient can’t talk. b. Eye movements and muscles remain intact so signals can be prearranged.Skin integrity: a. Assess, lubricate, keep clean & dry. b. Special beds, turn & position q 1-2 hrs. c. Treat skin breakdown immediately. d. Good catheter care. Monitor for infection.

422
Q

nursing care for ALS

A

Individual / Family coping: a. Requires realistic planning. b. Consider hospice referral, VNS, Physical & occupational & speech therapy, and dietary consult. c. Teaching of suctioning and home car e if family wants patient at home. d. Address patient’s interest in an Advance Directive/ Living Will. e. Refer to a support group, psychologist, social worker.

423
Q

the three things that cause someone to have a CVA

A

thrombus, embolism, hemorrhage

424
Q

when is it called an ischemic stroke

A

when its caused by a thrombus or embolism

425
Q

CVA

A

Is a sudden circulatory impairment of one or more blood vessels that supply the brain.Can result in destruction of brain cells (Infarction).Caused by sudden or gradual interruption of blood supply to the brain following a thrombus, embolism, or hemorrhage.

426
Q

risk factors for CVA

A

Hypertension, atherosclerosis, arteriosclerosis, DiabetesCardiac disease like valvular disease, chronic atrial fibrillation, myocardial infarction.Obesity, smoking, inactivity, stress and taking oral contraceptives.

427
Q

statistics for COPD

A

Third most common cause of death in US.Most common cause of permanent neurological disability in adults.Affects men more than women. Incidence increases with age.Stroke rate 50% higher in African American men and 130% higher in African American women than Caucasian.Death rate has decreased since the 1970s because of improved health habits.

428
Q

classification of an ischemic stroke

A

Ischemic Stroke: a. Thrombus caused by atherosclerosis, arteritis, or hypercoaguability of the blood. b. Embolism caused by atrial fibrillation, valvular disease, and endocarditis.

429
Q

classification of an hemorrhagic stroke

A

Hemorrhagic Stroke: a. Hypertensive intracerebral hemorrhage into brain tissue from rupture of small blood vessel. b. Ruptured aneurysm or arteriovenous malformation. c. Hypocoaguability of blood from blood dyscrasias.

430
Q

pathophysiology of CVA’s

A

Any condition that alters brain perfusion can lead to cerebral hypoxia.Prolonged hypoxia leads to infarction and permanent damage.Cerebral edema accompanies hypoxia and worsens initial deficits.Symptoms vary based on location and extent of injury.

431
Q

stages of thrombotic CVA

A

transient ischemic attack (TIAS)Stroke in evolutionCompleted Stroke

432
Q

Transient ischemic attack (TIAS)

A

Transient ischemic attack (TIAs) a. Warning sign of impending CVA. b. Brief period of neurological deficit lasting to no more than 24 hours. c. Complete recovery of symptoms.

433
Q

stroke in evolution

A

a. Progressive development of stroke symptoms over a period of hours to days.

434
Q

completed stroke

A

Neurological deficit remains unchanged for 2 to 3 day period.

435
Q

common side effects of a CVA involving the right side of the brain

A

Hemiplegia or hemiparesis on left side of body.Spatial-perceptual deficits.May not recognize hemiplegic part and has neglect or ignores it.Quick, impulsive behavior so safety risk.Performance memory deficits. Left visual field deficits.Indifference to disability.

436
Q

CVA involving the left side of the brain

A

Paralysis or hemiparesis of right side of body.Speech-language deficits if left brain dominant. Wernicke’s and Broca’s area on left hemisphere so can have aphasia.Behavior style- slow, cautiousMemory deficits with language.Right visual field deficits.Distress and depression r/t disability.

437
Q

other problems from CVA’s

A

DysphagiaAgnosiaApraxiaDysarthiaHemianopsia

438
Q

agnosia

A

—Inability to recognize sensory input.

439
Q

apraxia

A

—Inability to carry out previously learned motor skills with no weakness or sensory, cognitive, or coordination impairment.

440
Q

dysarthia

A

—Slurred speech because of motor impairment.Bowel and bladder incontinence.

441
Q

Hemianopsia

A

—Loss of vision toward hemiplegic side.

442
Q

stroke in the brainstem

A

Coordination problems.Problems with swallowing, eye movement, and sometimes paralysis.Some changes in levels of consciousness.

443
Q

stroke in the cerebellum

A

Problems with coordination, balance and eye movement.

444
Q

diagnostics tests for CVA

A

CT Scan which is highly sensitive to blood. Need to do it quickly to r/o hemorrhagic CVA.MRI to look at extent of ischemic stroke.Carotid ultrasound.Cerebral angiography.Transcranial doppler imagingEEGCardiovascular workup like ECG, Echocardiogram and telemetry

445
Q

medical management of CVA

A

Goal—maintain cerebral circulation to prevent ischemia of cerebral tissue.B/P in an acute stroke is lowered slowly since thought to be a protective mechanism in an ischemic stroke.Initially may be patient on bed rest with head of bed down for adequate circulation. HOB is elevated if the patient has a large ischemic stroke or hemorrhagic infarct to decrease ICP from edema.

446
Q

medical management of CVA continued

A

IV fluids to maintain circulatory volume and adequate B/P. May be restricted if large amount of cerebral edema is present.Patients with ischemic strokes may be given anticoagulants, vasodilators, and thrombolytics to prevent further damage. Antihypertensives are used if indicated. Remaining care consists of support of vital functions and prompt rehabilitation.Patients with hemorrhagic strokes are on complete bedrest with meticulous monitoring. May need surgery to stop bleed.New Solitaire procedure to evacuate thrombus

447
Q

new therapies used for patients with strokes

A

Constraint-induced movement therapy (CIMT)- emphasizes use of disabled limb by constraining unaffected limb. Force patient to try to use disabled limb. Encourages Brain Plasticity which makes it possible for another part of the brain to take up the functions of the injured p[art of the brain.Neuroprotection by preventing secondary brain injury by decreasing inflammation and blocking toxic chemicals created by dying brain cells.Implantation of neural stem cells to see if they can replace cells that have died.

448
Q

nursing care for a patient with CVA

A

Assessment of history of symptoms, co-existing health problems, subjective symptoms, focal deficits, generalized objective symptoms, communication deficits, perceptual deficits, mental status changes, sensory & motor deficits, potential nutritional problems, bowel & bladder alterations, symptoms of ICP.

449
Q

how long should someone be positioned on their effected side after a CVA

A

20-30 minutes . NO MORE

450
Q

seizures definition

A

Unpredictable event involving abnormal activity of the brain cells that often times disturbs consciousness and motor and sensory function.Uncontrolled electrical discharge of neurons in the brain that interrupts normal function.Often is a symptom of an underlying condition. May occur spontaneously without a cause or idiopathically as in epilepsy.

451
Q

idiopathic seizures

A

¾ can’t find the cause. May have something to do with heredity, environment, and acquired influences. Generally diagnosed before age of 20 yrs.

452
Q

causes of seizures

A

idopathicWithdrawal or overdose of certain drugs.Hypoxia, poisoning, metabolic disease.Over 50 yrs old usually cerebrovascular lesion or brain tumor.Birth injury, congenital defects, trauma.Noncompliance with anticonvulsant drugs.

453
Q

pathophysiology of seizures

A

Seizures are associated with hyperactive neurons. May remain localized as in partial seizures or spread throughout the entire cerebral cortex causing generalized seizures.Oxygen and nutritive stores are used up at an incredible rate. Body attempts to compensate with an increase in cerebral blood flow.With serial seizures as in status epilepticus, low glucose levels and low oxygen levels can occur. This can lead to permanent damage to brain cells.

454
Q

generalized seizures

A

initial onset is in both hemispheres of the brain. Usually involves a loss of consciousness and bilateral motor activity.

455
Q

simple partial seizure

A

begins in focal area of the brain. Symptoms are appropriate to a dysfunction of that area. No loss of consciousness. May be sensory, motor, or automatic type symptoms.

456
Q

complex partial seizure

A

Begins in a focal area of the brain but spreads to both hemispheres of the brain. Impairs consciousness.

457
Q

phases of major tonic-clonic seizure “grand mall”

A

preictal/aura phasetonic phase clonic phasepostictal phase

458
Q

preictal/ aura phase of tonic clonic seizure

A

time of uneasiness. Visual or auditory sensations may be felt by the patient. May occur several hours before actual seizure.

459
Q

tonic phase of tonic clonic seizure

A

period of loss of consciousness, excessive muscle contraction with initial crying out as air is forced out of lungs via vocal cords. Jaws clamp shut with possible damage to tongue. Apnea for approximately 15 seconds to 1 minute causes cyanosis. Pupils dilate and do not react. Heart rate decreases and there is incontinence of bowel and bladder.

460
Q

clonic phase of tonic clonic seizure

A

period of more violent, jerking movement accompanied by forceful rapid and deep respirations. See powerful rhythmic muscle contractions with facial grimacing. There is profuse sweating and salivation. Eyes roll back and heart rate increases. Respirations are loud and irregular. May last up to 5 minutes with movement slowing until all activity stops.

461
Q

postictal phase of tonic clonic seizure

A

period of recovery in which muscles are flaccid . Consciousness and normal pupil size returns. Patient is exhausted and may be confused, lethargic and complain of a headache. May sleep for hours. Pupil reaction normal.

462
Q

absence seizure “petit mall”

A

May be non-organic brain damage present.Must be differentiated from day dreaming. May go blank while speaking then continue where they left off.Sudden onset. May see twitching or rolling of the eyes with brief loss of consciousness.Can be precipitated by hyperventilation and flashing lights.

463
Q

atypical absence spell

A

staring spell

464
Q

myoclonic seizure

A

Sudden brief jerking of a muscle group that lasts a few seconds.Most common in children & elderly. Can be triggered by fatigue.

465
Q

atonic seizure

A

Drop attack seizure that involves either a tonic episode or a paroxysmal loss of muscle tone. Consciousness usually returns by the time the person hits the ground.

466
Q

simple partial seizures

A

Symptoms correspond to brain lobe involved and action it controls. There is no loss of consciousness.Temporal- emotional changes seen. Person has intense feelings like fear or bliss.Frontal- movement of an extremity or changes in speech. May repeat words continually.Parietal- tingling and feeling of warmth down one side of the body. Arm & leg movement may occur. May report numbness & tingling for a few minutes that goes away.Occipital- see flashing lights, fireballs, bright colors shooting across half the visual field.

467
Q

complex partial seizures

A

Begins in focal area but spreads to both hemispheres of brain. Impairs consciousness and there may be an aura.Person can’t respond appropriately to commands and won’t remember event.May see automatisms as in automatic involuntary behaviors such as chewing, lip smacking, undressing in public, eating dog food, laughing uncontrollably.May progress to generalized seizure with residual neurological deficit postictally. Called Todd’s paralysis with a focal weakness that resolves over time.

468
Q

complications of seizures

A

Status EpilepticusState of continuous seizure activity or a condition where seizures recur in rapid succession without return to consciousness between seizures.Brain uses more energy and oxygen than can be supplied. Neurons become exhausted and cease to function. Permanent damage may result.Can also have ventilatory insufficiency, hypoxia, cardiac arrhthymias, hyperthermia and systemic acidosis which may be fatal.Psychosocial- may have problem coping with stigma and legal sanctions like driving restrictions.

469
Q

diagnostic studies

A

Comprehensive description of seizure and patient’s health history.EEG may or may not show abnormality. Best done within 24 hours of seizure.CT/MRI done in new onset seizure to r/o lesion.Cerebral angiography & PET scans sometimes. Extensive blood work to r/o metabolic disorders.

470
Q

medical treatment

A

AnticonvulsantsSurgery to remove epileptic focusVagal Nerve StimulatorBiofeedback

471
Q

Dilantin ( Phenytoin sodium), Fosphenytoin (Cerebux)

A

For all types of seizures except absence, myoclonic & atonic. Used for status epilepticus. Can be given po and IVMonitor for gastric distress, gingival hyperplasia, anemia, ataxia, drowsiness, and nystagmus.Check CBC, calcium levels and therapeutic levels ( 10-20mcg/ml).

472
Q

Phenobarbital (Luminal)

A

For generalized tonic-clonic seizures and partial seizures. Less desirable because of sedation effects. Overdose can be fatal.Monitor for drowsiness, sleep disturbances, cognitive impairment, ataxia and depression.

473
Q

Carbamazepine (Tegretol)

A

For partial and generalized tonic-clonic seizures.Monitor for headache, dizziness, diplopia, blurred vision, nausea, vomiting & leukopenia.Monitor CBC

474
Q

gabapentin (neurontin)

A

For partial seizuresMonitor for ataxia, irritability, dizziness, fatigue, weight gain and increased appetite

475
Q

Clonazepam (Klonopin)

A

For absence, myoclonic and akinetic seizures.Monitor for drowsiness, ataxia, hypotension, respiratory depression and liver function tests.

476
Q

Valporic acid (Depakene)

A

Monitor for hair loss, tremor, increased LFTs, bruising, nausea, vomiting, indigestion, sedation, emotional disturbances, weakness & altered blood coagulation. Monitor CBC, PT, INR, PTT, & LFTs

477
Q

Lamotrigine (Lamictal)

A

For partial seizuresMonitor for diplopia, headaches, dizziness, drowsiness, ataxia, nausea, vomiting, and life-threatening rash when given with valporic acid

478
Q

more drugs used for status elepticus

A

Lorazepam (Ativan)Diazapam (Valium) Phenytoin (Dilantin)Monitor ABCs

479
Q

nursing assessment for seizures

A

History of seizure disorder and specific manifestations. Patient’s knowledge regarding seizure, prescribed meds & side effects, and degree of compliance.Description of aura and postictal feelings. Patient’s social adjustment.Laboratory and diagnostic results.

480
Q

nursing interventions for seizures

A

Institute seizure precautions per hospital policy.During seizure: a. Protect from injury b. Keep airway open c. Don’t leave patient alone. Observe & later report and record details of seizure in detail. d. Administer medications as ordered.At end of seizure: a. Take vital signs. Monitor neurological signs. b. Keep patient on his/her side. Allow patient to rest. c. Document the seizure

481
Q

patient teaching for seizures

A

Wear a medi-alertTake medication as ordered. Do not stop medications unless under physician supervision.Plan for periods of rest and activity.Avoid alcohol. Is contraindicated with anticonvulsantsEat a nutritious diet. Avoid stress. Practice good oral hygiene if on Dilantin.Job counseling if needed

482
Q

patient with a brain tumor

A

General Information: a. Broad term encompassing tumors found within the brain inside the skull compressing the brain. b. Some are malignant, some benign and all are life-threatening requiring aggressive treatment. c. Primary tumors originate in intracranial tissue or the meninges. d. Secondary tumors metastasize from malignant sites to the brain.

483
Q

statistics for brain tumors

A

8 out of every 100,000 adults and children are effected in the US.People of any age can have a brain tumor but it is most common in children under 15 and in older adults.Primary tumors are more common in males ( 1.5 to 1 ratio with females)

484
Q

causes of brain tumors

A

Primary brain tumors form when genetic structure of normal brain cells ( neurons & glial cells) change.Trigger can be genetic predisposition, environmental trigger or both. Exposure to radiation especially to head to treat other cancers or exposure to cancer-causing chemicals (vinyl chloride) can trigger them.

485
Q

signs and symptoms of brain tumors

A

Headache is early symptom seen in 50% of patients. Usually intermittent, moderate to severe, worse in morning and associated with nausea and/or vomiting. Patient may have diplopia, weakness and paresthesia with it.New onset seizure may be initial sign of brain tumor.Cognitive changes in memory, speech, communication and concentration. May notice changes in behavior, intellectual function, personality, planning and decision making abilityFatigue is common. May see metabolic abnormalities and poor functional state.Mass Effect: ICP, cranial nerve deficits, visual changes, deep comaFocal Deficits: motor, sensory, visual-spatial disorders, speech deficits, trouble with balance-coordination, projectile vomiting,

486
Q

frontal lobe brain tumor

A

Personality disturbances, inappropriate affect, motor dysfunction, seizures, aphasia (expressive).

487
Q

occipital lobe brain tumor

A

Visual disturbances, headache, seizures.

488
Q

parietal lobe brain tumor

A

Inability to replicate pictures, loss of right and left discrimination, seizures, paresthesias, sensory-perceptual deficits.

489
Q

temporal lobe brain tumor

A

Olfactory, visual,, or gustatory hallucinations, complex partial seizures or automatic behavior, aphasia (receptive)

490
Q

diagnosis of brain tumors

A

Careful history and neurological examEEG if seizuresMRI with contrast or CT to reveal tumorPET scan to measure cellular metabolismLumbar puncture: See increased protein. Do cytology.Biopsy if possible. Sometimes angiogram.

491
Q

glioma

A

Make up 50% primary tumors. Is a broad term. 77% are malignant-some benign) peak incidence is 75 to 84 yrs old. Classification is based on glial cell type: a. Astrocytoma- are glial cells that support and nourish neurons. Can be low, intermediate and high grade tumors. Low highest survival rate. Seen in children & young adults. Intermediate & high grade seen in adults. High grade glioblastoma is a very aggressive type. Most common malignant brain tumor. Survival less than a year.

492
Q

. Oliogodentroglioma

A

in glial cells that produce myelin to surround & insulate axons of the brain & spinal tumors. Usually can’t be removed by surgery totally.

493
Q

Ependymomas

A

glioma close ependyma (membrane lining ventricles) Common in kids. Benign in 85% of cases

494
Q

meningioma

A

25% of brain tumors. Most common in adults especially older adults. Affects women 2Xs more than men. Usually benign but expand and press on brain and spinal cord.

495
Q

other brain tumors

A

a. Ganglioma- rare. Usually benign. High cure rate. b. Medulloblastoma- fast growing malignant tumors common in kids. May be cured with radiation. c. Schwannoma-in bone in posterior skull. Form in cranial nerve 8 so hearing & balance affected. d. Lymphoma- usually seen in people with HIV/AIDS. Less common now with advances in AIDS’ treatment

496
Q

treatment goals for tumors

A

Identify tumor type and locationRemove or decrease size of tumorPrevent and manage ICP

497
Q

treatment approaches for brain tumors

A

Surgery- can be diagnostic and therapeutic. Some deep seated tumors can’t be removed but are accessible for biopsy. Most malignant tumors need additional treatment.Radiation- commonly given post-op for treatment of malignant tumors. May be used instead of surgery if tumor is inoperable or very responsive to radiation.Chemotherapy- can be used as additional therapy to treat a brain tumor or to treat recurrence, but blood-brain barrier is a problem. May be given mannitol to help drug to cross barrier.

498
Q

chemotherapy options for brain tumors

A

Combination chemotherapy- used to control multiple tumor types. More effective & better tolerated than monotherapy.Lower toxicity drugs- new generation of drugs being explored for brain tumorsHigh-dose chemotherapy- massive doses of a drug followed by giving an antidote. Growth factor inhibitor therapy- can help shrink tumor.Intracavity/interstitial therapy- giving chemo via implantable wafer directly into tumor.Microspheres- implanted in the brain to dissolve slowly and release drug contents over a particular time period. Can place several drugs in one capsule.Receptor-mediated permeabilizers (RMPs) are synthetic substances that help chemo to cross blood-brain barrier like mannitol.Reservoirs are surgically implanted under scalp with a tube leading into brain ventricle by which chemo can be delivered into CSF. Medication is injected into reservoir via syringe.

499
Q

nursing assessment for brain tumors

A

History data/ Objective data: Headaches, vomiting, papilledema, seizures, changes in mental status, focal neurological deficits, bowel& bladder function, balance & proprioception, coping abilities of patient & family, ability to perform ADLs, conversation ability.Diagnostic tests

500
Q

nursing diagnosis for brain tumors

A

Altered cerebral tissue perfusion r/t cerebral edemaPain (headache) r/t cerebral edema and increased intracranial pressure.Self-care deficit r/t altered neuromuscular function 2nd to tumor growth and cerebral edema.Anxiety r/t diagnosis and treatment regime.

501
Q

nursing interventions for brain tumors

A

Check vital signs, neuro. signs. Observe for ICPGive medications as ordered: Decadron, anticonvulsants, analgesics etc.Supportive CVA type care for focal neurological deficits.Prepare patient for surgery and other therapies.Provide care for effects of radiation and chemotherapy.Provide psychological support to patient & family.Provide patient teaching and discharge planning.

502
Q

nursing care pre-op for brain tumors

A

Routine pre-op careEmotional support. Explain what will happen post-opEvaluate and record baseline assessmentsAvoid measures that will increase ICPGive pre-op steroids as ordered. Patient will need IV and foley

503
Q

nursing care post-op for brain tumors

A

Care od unconscious patientMaintain patent airway and adequate ventilation.Monitor closely vital signs, neuro. Signs, changes in LOC, increased ICP, possible seizures, hyperthermia.Supratentorial Incision: above tentorium a. Keep HOB elevated 15 to 45% as ordered to promote venous outflow. b. Critical- must not lower head in acute for any procedure without written doctor’s order. c. Turn & position q 2hrs.Infratentorial incision- below the tentorium a. Keep HOB flat or elevated only to 20-30 degrees as ordered to prevent pressure on brain stem. b. Critical-must not elevate Hob in acute phase. Do not flex head on chest. c. Turn side to side q 2hrs using turning sheet. Keep in alignment. d. Check respirations closely and report any changes. Avoid measures that will increase ICP. e. May be NPO longer- possible impaired gag reflexMonitor fluid and electrolytes. Accurate I&O. May have to restrict fluids to decrease ICP. Observe for signs of Diabetes Insipidus and Inappropriate ADH secretion.Assess dressings frequently and report any abnormalities.Administer medications as ordered.Ice sometimes applied to decrease swelling of eyelids. Lubricate lids & areas around eyesRefer patient for rehabilitation

504
Q

statistics/risks for SCI

A

a. Catastrophic crisis but fairly stable incidence. 10,000new injuries per year. b. 80% affected are male. 60% of SCIs in persons 16-30 years old. c. 55% from motor vehicle accidents, 23% from falls, 16% from penetration injuries. Also, can result from occupational & sports injuries. d. Commonly affects motorcyclists, sky divers, football players, police, divers and military personnel. e. Alcohol and/or drugs may be present with the injuries. f. Falls are more common in the elderly. g. Slightly more than 50% of new SCIs involve the cervical spine.

505
Q

etiology of SCI

A

Injuries result most commonly from excessive flexion, hyperextension, compression & rotation on the spinal cord. a. Events that cause abrupt, forceful acceleration & deceleration are common initiating factors.Persons with chronic arthritis, stenosis, or osteoporosis are at high risk for injury.

506
Q

classification of SCI

A

Level as in the cervical, thoracic, or lumbar spine.Extent of injury: a. Can affect vertebrae, spinal column. Can be a fracture or a dislocation. b. Can affect anterior or posterior ligament causing compression on the spinal cord. c. May be concussion, contusion, compression or laceration or a penetrating missile to the spinal cord.

507
Q

mechanism of injury SCI

A

Mechanism of injury: a. Hyperflexion b. Hyperextension c. Compression injuries d. Rotational injuries e. Penetrating wounds

508
Q

hyperflexion SCI

A

Usually result of sudden deceleration like a head-on collision or from severe blow to the back of the head.Head and neck are forcibly hyperflexed and then snapped backward into forced hyperextension.Typically involves C5 & C6. May cause fracture of the vertebra, dislocation and/or tearing of the posterior ligaments.

509
Q

Hyperextension SCI

A

Usually result from acceleration as seen in rear-end collisions or as a result of falls where the chin is forcefully struck.Tends to cause significant damage because of the head’s downward & back arc being so great.C4 & C5 area of the spine is most often affected.

510
Q

compression injuries SCI

A

Cause the vertebra to squash or burst. Usually involves high velocity and can affect any part of the vertebra.Blows to the top of the head and forcible landing on the feet or buttocks can result in a compression injury.Can result from an axial loading force exerted straight up or down the spinal column as in a diving accident.

511
Q

rotational injuries SCI

A

Caused by extreme lateral flexion or twisting of the head or neck. The tearing of ligaments can easily result in dislocation as well as fracture.Soft tissue damage frequently complicates the primary injury.Can result in a highly unstable spinal injury involving more than one directional force.Penetrating Injuries can result from knives, bullets that penetrate the spinal column.

512
Q

cord concussion SCI

A

. Cord is severely jarred or squeezed as in sports injuries. No pathological changes are detectable in the cord but there is a temporary loss of motor and/or sensory function. Usually resolves in 24 to 48 hours.

513
Q

cord contusion SCI

A

a. Frequently caused by compression. Causes bleeding into the cord resulting in bruising and edema. b. Extent of damage reflects adequacy of overall perfusion to the cord and the severity of the inflammatory response.

514
Q

cord laceration SCI

A

a. Is an actual tear in the cord. Results in permanent damage since the neurons do not regenerate. b. Contusion, edema, and compression may also be present complicating the injury.

515
Q

Cord transection SCI

A

Complete transection is rare because of the strong, protective layers of the cord. b. When complete, there is a total loss of motor & sensory function below the level of injury. c. Is more common in the thoracic area because the cord is more narrow in this region.

516
Q

pathology of a cord transection

A

Spinal Shock: a. Entire cord below the level of the lesion fails to function resulting in spinal shock. b. Symptoms seen are: 1. Hypotension, bradycardia 2. Flaccid paralysis below the level of the injury 3. Lack of temperature control in affected parts 4. Absence of reflexes below the level of injury 5. Retention of urine and feces 6. Loss of sympathetic innervation causes peripheral vasodilation, venous pooling and a decrease in cardiac output.Effects generally seen with cervical and high thoracic injuries.Generally lasts 7 to 10 days after injury but can last longer.Indications that it has ended include spasticity, reflex emptying of the bladder and hyper-reflexia.Active rehabilitation may begin in the presence of spinal shock.

517
Q

clinical manifestations of SCI

A

Vary. A person with an incomplete lesion may have a mixture of symptoms. The higher the injury, the more serious the symptoms because of the nearness of the cervical spine to the medulla & brainstem.Quadriplegia occurs with injuries to C1 to C8. All four extremities are paralyzed. Respiratory paralysis occurs in lesions above C4 due to the lack of innervation to the diaphragm.Paraplegia occurs with injuries from T1 to L4 causing paralysis of the lower half of the body involving both legs.Trauma can also result in many other injuries like a head injury.

518
Q

Respiratory complications of SCI

A

Injuries above C4 may need mechanical ventilation. Below C4 may result in diaphragmatic breathing if the phrenic nerve is functioning but edema & hemorrhage can affect its functioning.Hypoventilation usually occurs with diaphragmatic breathing because there is a decrease in vital capacity & tidal volume.Cervical injuries can cause paralysis of the abdominal musculature and frequently the intercostal musculature. The patient cannot cough effectively to remove secretions. Can lead to atelectasis and pneumonia. Need good pulmonary toileting.

519
Q

cardiovascular complications of SCI

A

Any cord transection above T5 greatly decreases the influences of the sympathetic nervous system.Bradycardia results because of the influence of the parasympathetic system on the heart and vasodilation results in hypotension.May need to treat with meds to increase heart rate to prevent hypoxemia. May need to treat hypotension with IV fluids and vasopressor drugs. Need close cardiac monitoring

520
Q

urinary complications of SCI

A

Retention is common when patient is in spinal shock. The bladder is atonic and will become over distended.In the hyperirritable phase the bladder has a loss of inhibition of reflex from the brain so the patient voids small amounts frequently. The bladder still becomes distended because of inadequate emptying. Urinary retention increases chance of infection & urinary calculi. Catheterization is necessary. Indwelling foley should be removed as soon as possible and intermittent caths should begin after spinal shock resolves.

521
Q

gastrointestinal complications of SCI

A

If cord transection is above T5, the primary problems are related to hypomotility. Will contribute to a paralytic ileus and gastric distention.Patient may need a nasogastric tube to low suction for gastric decompression.Stress ulcers are common because excessive HCL acid is released in the stomach. May need proton pump inhibitor.May also have gall bladder stone formation, constipation and fecal impaction.

522
Q

integumentary complications of SCI

A

Lack of movement can cause tissue breakdown especially in areas of denervation. Muscles can atrophy in flaccid paralysis state and contractures can form in spastic state.Poikilothermism (adjustment of body temperature to room temperature) occurs in injuries where sympathetic innervation is interrupted.There is a reduction of heat generation because of minimal movement. There is a decreased ability to sweat, which also affects the ability to regulate body temperature.

523
Q

metabolic complications of SCI

A

Nasogastric suctioning can cause metabolic alkalosis and decreased tissue perfusion can lead to acidosis.A positive nitrogen balance and a high protein diet will help prevent skin breakdown , infections and will decrease the rate of muscle atrophy. Peripheral Vascular Complications:DVTs are common. Pulmonary embolisms can be a leading cause of death.

524
Q

emergency management of SCI

A

Monitor airway. Anticipate need for intubation if gag reflex is absent.Maintain cervical spine precautions Immobilize.Oxygen via cannula or non-rebreather mask. Monitor for respiratory distress.If not breathing, ventilate with ambu bag and oxygen.Need to establish IV access with large bore cath. May need IV fluids.Assess for other injuries. Control bleeding. Keep warm. Obtain good historyTransport to hospital

525
Q

medical care at hospital for SCI

A

Complete exam with neuro exam. ABGs, electrolytes, CBC, UA and Xray studies. CT scan, MRI.Skeletal traction to immobilize spine. May use Crutchfield or Vinke tongs which are attached to traction with weights. Need to maintain traction at all times. Aseptic technique must be used for pin care.If injury is stable, halo traction may be applied.IV fluids with moderate restriction during first 72 hours. I&O. Foley. NG tube to low suctionSurgical intervention may be needed.Medications like steroids, proton pump inhibitors.Physical and Occupational therapyExperimental treatments like regeneration therapy and hyperbaric chambers.

526
Q

nursing care for SCI

A

Manage spinal shock a. Vital signs, neuro signs, cardiac monitoring, maintain airway, cardiopulmonary functioning. b. Manage IV fluids to prevent hypotension. c. Support venous return with TEDs and SCDs. d. Maintain immobility. Turn & position maintaining alignment. Slowly change position. May need tilt table. e. Give good skin care. Maintain urinary and bowel elimination. f. Monitor temperature control. Observe for complications. Give medications as ordered. g. Give emotional support.

527
Q

nursing care (CHRONIC) for SCI

A

Continue to monitor cardiopulmonary function. Maintain urinary elimination with neurogenic bladder by intermittent catheterizations.Spasticity will need to be managed with medications like Baclofen, physical therapy, stretching exercises, and whirlpool baths.Maintain skin integrity.Psychological support to facilitate grieving. Initiate rehab program.

528
Q

autonomic dysreflexia SCI

A

There is an uncontrolled sudden increase in sympathic activity. Occurs in injuries above T6.Symptoms: a. Rise in BP to possible fatal levels b. Patient c/o severe headache. Will have sweating, bradycardia, goose-bumps, nasal congestion c. Blurred vision, convulsionsStimulus may be over-distended bladder or bowel, decubitus ulcer, chilling , pressure from bedclothes.Interventions: a. Raise patient to sitting level to decrease BP. Check for source of stimulus and treat. Give antihypertensives as ordered and monitor BP

529
Q

meningitis

A

Meningitis is an acute inflammation of the three membranes surrounding the brain and spinal cord ( pia mater, arachnoid, dura mater ).Also can affect the optic nerves.Is caused by bacteria, viruses and other organisms that can reach the CNS by : 1. blood, cerebral spinal fluid (CSF), lymph 2. direct extension from adjacent cranial structures from penetrating wounds, ICP monitoring, nasal, sinus, ear and mastoid bone infections , and skull fractures ( basilar).Bacterial meningitis is considered a medical emergency. Untreated mortality rate can be 100%

530
Q

pathophysiology of meningitis

A

Organism must overcome host defense mechanisms to invade and replicate in the CSF.Infection of the CSF and meninges causes an inflammatory response in the membranes and CSF.The infection spreads rapidly throughout the meninges and eventually invades the ventricles.Pathological alterations include hyperemia of meningeal vessels, edema of brain tissue, increased ICP, and a generalized inflammatory reaction with exudation of WBCs into the subarachnoid space.Hydrocephalus may be caused by exudate blocking small passageways between the ventricles.Infection usually occurs in fall, winter, and early spring and can be secondary to a viral respiratory infection.

531
Q

pneumococcal meningitis

A

by streptococcus pneumoniae. Most common type in adults, especially if history of pneumonia, sinus infection and trauma.

532
Q

haemophilius influenzae meningitis

A

caused by haemophilus influenzae. Most common in children especially if history of upper respiratory infection or ear infection.

533
Q

meningococcal meningitis

A

neisseria meningitidis. Highest incidence in children and young adults. Common outbreaks in college dorms and in military barracks. May have a petechial rash. About 10% develop overwhelming septicemia. Is highly contagious and has a high mortality rate if not treated immediately.

534
Q

risk factors for meningitis

A

Head trauma like the basilar fractureOtitis mediaSinusitisSystemic sepsisNeurosurgeryImmunocompromised individuals

535
Q

manifestations of bacterial meningitis

A

Onset usually sudden with fever, severe headache, chills. Older adult may not have fever but exhibit confusion.Restless, agitation, irritability, tachycardia.Signs of meningeal irritation such as nuchal rigidity, Kernig’s sign and Brudzinski’s sign.Altered LOC, confusion, photophobia, diplopia, vomiting, nausea, seizures in 1/3 of cases.Petechial rash in meningococcal meningitis.Coma is associated with a poor prognosis and occurs in 5-10% of cases.

536
Q

complications of meningitis

A

Increased ICP, altered mental status, residual neurological dysfunction.Cranial nerve dysfunction especially #8 with deafness.Hemiparesis, dysphagia, hemianopsia may occur. May resolve over time. If not, cerebral abscess, subdural empyema, subdural effusion or persistent meningitis suspected.Acute cerebral edema can cause seizures, occulomotor 3 palsy, bradycardia, hypertensive coma and death.HydrocephalusFriderichsen syndrome (meningococcal) with petechiae, DIC, hemorrhage and circulatory collapse.Arthritis, thrombophlebitis may develop in cerebral vessels with infarction.

537
Q

diagnostics for meningitis

A

History and physicalLumbar puncture for CSFCBC, coagulation studies, electrolytes, blood cultureCounterimmunoelectrophoresis to determine presence of viruses/protozoa\MRI, CT scan, PET scan

538
Q

collaborative care and treatment for meningitis

A

Immediate IV administration of antibiotics that cross the blood-brain barrierCorticosteroids prior to first dose of antibiotic. New research shows that killing bacteria may release toxic by-products that accelerate the inflammatory reaction and possible death.Strict respiratory isolation especially for meningococcal which is highly contagious. Recommended that patient remain on isolation for 24 hours after start of antibiotic.Medications for headache, fever. Anticonvulsants if seizure activity.Clear liquids as desired or tolerated. May need IV fluidsMannitol to decrease ICP.

539
Q

nursing care for meningitis

A

Continual assessment of vs, neuro signs, ICP, neurological deficits, complicationsCare of delirious patient, Give prn meds for anxiety, agitation to decrease fear and anxiety. Administer antibiotics and other meds as ordered.Low stimulation environment for disoriented patient. Dark room for photophobia. Maintain bedrest at first. Approach patient slowly and from the front to avoid stimulating and frightening the patient.

540
Q

ambulatory and home care for meningitis

A

Patient requires several weeks of convalescence before normal activities can be resumed.Adequate nutrition—high protein, high calorie diet in small more frequent feedings.Muscle rigidity may persist in neck and back of legs. Will need progressive ROJM. Warm baths may help. May need rehab for residual neurological deficits.Activity is gradually increased as tolerated. Will need a good balance between rest and activity.

541
Q

factors associated with burn injury/death

A

Careless smoking, alcohol/drug intoxicationOlder adults- ignition of clothing when cooking or smoking.National Institute of Burn Medicine notes that 75% of burns are caused by our own action.Toddlers/older adults from scalds.Match play in school age childElectrical injury in adolescent male.Cigarette smoking in adultsIndustrial settings- largest number of burn injuries are among electricians and chemical workers.

542
Q

goals r/t human burns

A

Prevention- advocate for legislation for work place safety.Life-saving measures for severely burned.Prevention of disability and disfigurement.Rehabilitation of patient through reconstructive surgery and rehabilitation programs.

543
Q

patient’s with burn injuries

A

Statistics: a. Incidence in US has decreased in last 20 yrs. Now 4.2/10,000. 45,000 hospitalized/year. b. 4,500 fire and burn deaths per year. Is decreased by 60%. c. Is 6th leading cause of accidental death. d. Highest risk for older adult. Most common burn is caused by scalds.

544
Q

etiology of burn injury

A

Caused by: Dry heat flame Moist heat flame (scald) Contact with a hot surface Chemicals Electricity Ionizing radiation

545
Q

dry heat (flame)

A

Caused by open flame as in house fire and explosion.Ignited clothing accounts for most injuries.Explosions result in flash burn injuries because there is a brief exposure to a high temperature.

546
Q

moist heat (scalds)

A

Caused by contact with a hot liquid or hot steam.Scald most common burn injury in toddlers and older adults.Hot liquid spills usually burn upper frontal surfaces of the body.Immersion scalds involve lower part of body.

547
Q

dry and moist heat burns

A

Dry heat and moist heat burns are considered to be thermal burns.Direct exposure to source of heat causes cellular destruction that can result in injury to vascular, boney, muscular and nervous tissue.Priority treatment: a. Extinguish flame- stop, drop & roll. b. Steam / Hot Liquid- consult with fire department. Remove smoldering clothing and metal objects.

548
Q

contact burns

A

Hot metal, tar, and grease can cause full-thickness burns when they contact the skin.A body part touching an iron or space heater is an example of a hot metal injury. Also, in industry exposure to molten metals.Tar and asphalt temperatures can be over 400 degrees so they can cause serious deep injuries within seconds when in contact with skin.Hot grease injuries are associated with cooking and are usually deep.

549
Q

chemical burn injury

A

Occur in the home, in industry, and as a result of deliberate assault.Tissue injury occurs when chemicals come in direct contact with the skin. Epithelial tissue is ingested by the chemical.Severity depends on the duration of contact, the concentration of the chemical, the amount of tissue exposed, and the action of the chemical.

550
Q

chemical burn (continued)

A

Alkalis found in oven cleansers, fertilizers, drain cleaners and heavy industrial cleaners damage tissue by causing it to liquefy (liquefication necrosis) and proteins are denatured. Allows for deeper spread of chemical and more severe burns.Acids found in bathroom cleansers, rust removers, chemicals for swimming pools and industrial drain cleaners damage tissue by coagulating cells and proteins ( coagulation necrosis). Tends to limit depth of damage.

551
Q

chemical burns (continued)

A

Organic compounds found in many chemical disinfectants and in gasoline cause damage by fat solvent action. Also, once absorbed can produce toxic effects on the kidneys and liver.Priority treatment: a. Brush off any dry chemicals present on skin clothing. Remove clothing. b. Ascertain chemical causing burn and consult Poison Control Center. Do not attempt to neutralize chemical unless it is positively identified and the appropriate neutralizing agent is available.

552
Q

electrical burn injury

A

An electrical injury happens when electrical current enters body. Called “Grand Masquerader” because small surface injury may be associated with severe internal injuries.Divided into high and low voltage with high being over 1000 volts.Tissue injury results from electrical energy being converted into heat energy.Extent of injury depends on type of current, pathway of flow, local tissue resistance, and duration of contact.Skin is most resistant organ. If skin resistance is overcome, the body acts as a conductor and current flows throughout the involved body part.Bone has high resistance because of its density. Current flows along surface of the bone and the heat generated damages adjacent muscle. Deep muscle injury may be present even when superficial tissue seem ok.

553
Q

electrical burns (continued)

A

The longer the electricity is in contact, the greater the damage. Duration is increased by tetanic contractions of flexor muscles preventing person from dropping source.Generally there is entry and exit wounds. Entrance site usually well defined and round, whereas exit site is explosive and surrounded by charred tissue.External burn injuries can occur when the current jumps or arcs between two surfaces. Injury is severe and deep.True electrical injury occurs when there is direct contact with the electrical source. Internal damage results as electricity travelson the inside to the outside. Organs in the path of the current may become ischemic or necrotic. More than 90% of injuries to extremities result in gangrene development and amputation.

554
Q

electrical burns continued

A

Alternating current as in homes, produces tetanic muscle contraction. This can inhibit respiratory effort and cause arrest.Direct current as in a lightening bolt exposes the body to very high voltage for an instant. Usually there is entry and exit wounds.Flash-over effect (unique to lightening) may save a person’s life since the current travels over the moist surface of the skin rather than internally.

555
Q

priority treatment of electrical burn injury

A

Disconnect electrical source.Smother any flames that are present.Initiate CPR. Get ECG if possible.Consult electrical specialist

556
Q

thermal burns

A

dry heat flame & moist heat flame (scald)

557
Q

radiation burns

A

Occurs with exposure to large doses of radioactive material.Most common injury is from therapeutic radiation. Injury is usually minor and there is rarely extensive skin damage.Injuries are more serious in industry when person is exposed to radioactive isotopes. The extent of the injury depends on the amount & type of energy deposited over time.Severity is determined by type of radiation, distance from the source, absorbed dose, and depth of penetration into body.

558
Q

radiation burn treatment

A

Shield skin appropriately for solar uv rays.Limit exposure time to radioactive agents like Xrays.If exposed to radioactive agent: a. Remove patient from the source. b. If exposed to radiation from an unsealed source, remove clothing with tongs or lead protected gloves. c. If radioactive particles are on the skin, send to nearest decontamination center for bathing or showering.

559
Q

old classification of burn death

A

First Degree- Damage limited to epidermis. Erythema appears and patient has pain.Second Degree- Damage to epidermis and dermis. Blisters and mild to moderate edema develops. Patient has pain.Third Degree- All dermal elements are effected. There will be white, brown, red, or black leathery tissue with thrombosed vessels, although no blisters appear. No pain.Fourth Degree- Damage extends to subcutaneous tissue, to the muscle and bone.

560
Q

superficial burn

A

Damage only to top layer of skin. See peeling of dead skin.Color is pink to red with mild edema. There is pain.No blisters. Healing time 3 to 5 days. No graft is needed.Examples would be a sunburn or flash burn.

561
Q

superficial partial thickness burn

A

Entire epidermis and variable portions of the dermis are destroyed.Color is pink to red with mild to moderate edema. Blisters are present and there is pain. Nerve endings may be exposed.Healing time is about 2 weeks.Examples are scalds, flames, brief contact with hot surface.

562
Q

deep partial thickness burn

A

Extends into deeper layers of the dermis. There are fewer healthy cells that remain. Blood vessels are patent. If blood supply degreases, ischemia can result and burn can convert to full thickness.Color is red to dry white with moderate edema. Blisters are rare and some eschar may be present. There is pain. Healing time is 2 to 6 weeks and if prolonged may need graft. There may be scars.Will blanche with pressure. Examples are scalds, flames, prolonged contact with hot surface, grease or chemicals.

563
Q

full thickness burn

A

Reaches through entire dermis and sometimes into subcutaneous fat. There is no residual epidermal cells to repopulate. Cannot heal on it’s own. Will need grafting. No blisters.Color black, waxy white, brown, yellow, or red with severe edema. Eschar and thrombosed vessels are present. Nerves may be totally destroyed so may not have pain. Tissue is leathery and does not blanche under pressure.Healing time weeks to months. Need grafts.Examples are scalds, flames and prolonged contact with hot objects, tar, grease, chemicals and electricity.

564
Q

deep full thickness burn

A

Extends further than subcutaneous Tissue like to fascia and tissues. Color is black with edema and pain is absent. There are no blisters. Healing time is weeks to months.Can be damage to muscles, bone and tendons. Need early excision and grafting. Amputation may be needed if an extremity is involved.

565
Q

burn zones

A

Burns have characteristic skin surface appearance that resembles a bull’s eye with most severe burn located in the center and lesser located along the periphery.May be 1-2-3 concentric 3 dimensional zones corresponding to depth of burn.

566
Q

minor burns

A

Deep partial thickness less than 15% TBSA.Full thickness less than 2% TBSA.No burns of eyes, ears, face, hands, feet or perineum.No electrical or inhalation injuries. No other complicated injuries.No patient over 60yrs and no chronic cardiopulmonary and endocrine disorders.Patient receives care at ER. Burn Center not needed.

567
Q

moderate burN

A

Deep partial thickness not more than 25%.Full thickness not More than 10%.No burns to eyes, ears, face, hands, feet, and perineum.No electrical or inhalation injuries.No chronic cardiopulmonary and endocrine disorder.Patient under 60yrs.Patient receives care at specialized center or Burn Center

568
Q

major burns

A

Partial thickness greater than 25% TBSA.Full thickness greater than 10% TBSA.Any burn involving eyes, ears, face, hands, feet, and perineum.Electrical and inhalation and complicated injuries. Patients 60 and older with chronic conditions.Patients receive care at nearest ER and are transferred to Burn Center.

569
Q

older adult considerations for burns

A

At risk for all degrees and severity for injury. Sensory awareness may be decreased with aging. May have cognitive impairment and start a fire by leaving cooking unattended. May delay treatment so increases risk for infection.Have thinner skin, decreased mobility and reaction time. Burn will be more extensive.Immune response is decreased so healing time is slower and there is increased risk of infection and sepsis. May have pre-existing conditions.

570
Q

cultural considerations for burns

A

For African Americans a sickle cell preparation may be appropriate if sickle cell status is unknown.Trauma can trigger a sickle cell crisis in those with the disease or the trait

571
Q

pathophysiology of burns

A

Tissue destruction results from coagulation & protein denaturation or from ionization of cellular contents when in contact with heat source.Early tissue damage may occur at temp. of 104 degrees F. (40 degrees C.). Irreversible damage to dermis occurs at temp. of 158 degrees F.Skin & mucosa of upper airways are most common sites of tissue destruction.Deep tissues including viscera can be damaged by electrical burns or through prolonged contact with burning agent.

572
Q

first effect of a burn

A

First effect a burn has is to produce a dilatation of the capillaries and small vessels in the area of the burn.This increases capillary permeability.There is a fluid shift from intravascular space to the interstitial area in burns over 20 to 30%. Period is known as third spacing or capillary leaking syndrome.In burns over 30%, capillary leaking is not confined to burn area alone. There is edema throughout the body.

573
Q

fluid leak of a burn

A

Generally, fluid leak occurs over first 24 to 48 hours post burn, peaking by 12 hours.Patient will need fluid resuscitation during this period.Plasma, proteins, and electrolytes are lost from vascular space but RBCs usually remain in vascular compartment which results in increased blood viscosity, hematocrit, and hemoglobin in early hours post burn.

574
Q

fluid loss of a burn

A

Fluid loss results in decreased fluid volume in vascular system and there is a fall in blood pressure and cardiac output. Causes burn shock.Response of sympathetic nervous system is an increase in peripheral resistance and an increased heart rate.

575
Q

when capillaries regain integrity with burns

A

As capillaries begin to regain their integrity (48 to 72 hours post burn) fluid returns to vascular space and patient moves into Acute Stage of burn care.Vascular compartment volume increases. Extra strain is placed on the heart and kidneys. If heart and renal system are adequate, urinary output is greatly increased.Diuresis continues for several days to two weeks with a loss in body weight.During this period patient is at risk for fluid overload and may require cardiotonic drugs and diuretics to support circulatory function and prevent CHF.Monitor B/P, pulse, central venous pressure, pulmonary artery wedge pressure and hourly urinary output.

576
Q

fluid electrolyte and blood needs of burns

A

In the Emergent Phase there is hyperkalemia, hyponatremia and metabolic acidosis.Aldosterone is released causing reabsorption of sodium and water in the renal tubules.Retained sodium accumulates in the interstitial tissue with fluid. Sodium pump fails (normally pumps NA out of cell and K into cells. Potassium is released into intravascular space.Also have evaporative fluid loss through the burn wound. May reach 3 to 5 liters per 24 hours.

577
Q

acute phase of burns

A

During Acute Phase (Fluid Remobilization) blood volume increases as fluid shifts from interstitial space to intravascular space. Leads to increased blood flow to kidneys and increased urinary output.Hyponatremia continues because of increased renal sodium excretion and loss of NA from wounds.Hypokalemia results from potassium moving back into cells and being excreted in urine output.

578
Q

emergent phase of burns

A

Metabolic acidosis remains a possibility because of loss of sodium bicarbonate in the urine .Hemoconcentration is seen in the Emergent Phase due to vascular dehydration. This increases blood viscosity, decreases flow through smaller vessels and can cause tissue hypoxia.

579
Q

acute phase of burns (cont)

A

During Acute Phase anemia often develops as a result of hemodilution but usually is not severe enough to warrant a blood transfusion.Abnormalities in coagulation may include decreased platelets ( thrombocytopenia) and prolonged clotting and prothrombin times.

580
Q

cardiac changes of burns

A

During Acute Phase anemia often develops as a result of hemodilution but usually is not severe enough to warrant a blood transfusion.Abnormalities in coagulation may include decreased platelets ( thrombocytopenia) and prolonged clotting and prothrombin times.

581
Q

pulmonary changes with burns

A

Direct injury to the lungs from contact with flames rarely occurs. Problems are caused by inhalation of superheated air, steam, toxic fumes or smoke.Direct Airway Injury: a. Causes inflammatory reaction with edema and airway obstruction. Possible at any time during first 48 hours. b. Patient becomes hoarse, has a brassy cough, has difficulty swallowing and may have stridor and wheezing.

582
Q

carbon monoxide poisoning with burns

A

a. One of leading causes of death associated with fire. b. Is rapidly transported across the alveolar membrane & binds with HGB in place of oxygen. Reduces oxygen delivery to tissues. c. Vasodilating effect causes “cherry red “ color. d. Effects: Headache, decreased cerebral function, nausea, drowsiness, dysrhythmias, coma, convulsions and possible death

583
Q

thermal heat injury

A

a. Usually limited to upper airway. Most damage occurs above the true vocal cords. b. Can produce airway obstruction anytime during resuscitation. Need early intubation. c. Inhaled steam can injure lower respiratory tract since H2O holds heat better than dry air. d. Ulcerations, redness, & edema of the mouth and epiglottis are first signs of upper airway obstruction. Stridor, hoarseness, and shortness of breath can also be seen.

584
Q

smoke poisoning

A

a. Caused by inhalation of toxic by-products produced when plastics and home furnishings are burned like hydrogen cyanide. b. Causes loss of ciliary action and severe mucosal edema. Surfactant activity is decreased causing atelectasis. c. In a few hours, sloughing of the tracheobronchial mucosa may occur and patient expectorates mucopurulent material with carbon particals.

585
Q

restrictive defects burns

A

. Full thickness burns encircling neck & thorax may result in great edema that can compress trachea and occlude airway. b. Chest excursion may be greatly restricted resulting in decreased tidal volume. c. May be decreased lung compliance, non- cardiogenic pulmonary edema, and ARDS d. May need to do escharotomy or fasciotomy to relieve the restriction.

586
Q

factors determining inhalation injury

A

Those injured in a confined space.Those with extensive burns or burns to face.Intra-oral charcoal, especially on teeth & gums.Those unconscious at time of injury.Those with singed hair, nasal hairs, eyelids & eyelashes.Those coughing up carbonaceous ( sooty) sputum.Changes in voice like hoarseness or brassy cough or stridor. Use of accessory muscles to breathe.Poor oxygenation and ventilation. Wheezing, bronchospasm & labored respiration.Edema, erythema & ulceration of airway mucosa.

587
Q

immunological effects of burns

A

Is a loss of skin integrity and there are abnormal inflammatory factors.Altered levels of immunoglobulins and a reduction in lymphocytes.Loss of skin surface also results in inability to regulate body temperature in early post burn. May manifest a low body temperature.As hypermetabolism resets core temperature, burn patients may become hyperthermic for much of post burn period, even in absence of infection.

588
Q

metabolic effects of burns

A

Serious burns increase metabolic needs by 100%.The patient’s oxygen and caloric needs are high. The increased production and loss of heat breaks down protein and fat (catabolism) so body uses glucose & calories causing a nitrogen loss.Patient’s caloric needs double or triple normal caloric needs. Needs peak 4 to 12 days post burn and can remain elevated for months until all wounds are closed.

589
Q

gastrointestinal effects of burns

A

Decreased peristalsis & bowel sounds can result in paralytic ileus. Gastric distention & nausea may lead to vomiting unless gastric decompression is initiated.Gastric bleeding may be seen in vomitus and in stools. Can develop stress ulcers. Need to be on proton inhibitor.

590
Q

renal effects of burns

A

Changes r/t decreased renal blood flow in emergent phase causes urine to be concentrated with a high specific gravity.Other substances may be present in blood that flows through kidneys. Destroyed RBCs release HgB and potassium. When muscle damage occurs a large oxygen carrying protein called myoglobin is released from damaged muscle and circulates to kidneys.Damaged cells release proteins that form uric acid. These large molecules may precipitate in kidney tubular system. May block blood & urine flow and may cause renal failure.Burgandy colored urine may indicate deep muscle burns.

591
Q

survival predictions of burns

A

Best in children and young adults (5 to 40 yrs)Burns of about 60% have 50% mortalityBurns more than 20% endanger lifePrognosis depends on depth & extent of burn and condition & age of patient.

592
Q

care of emergent phase of burns

A

Priorities:First AidPrevention of shockPrevention of respiratory distressWound assessment and initial careTreatment of concomitant injuries

593
Q

emergency room care burns

A

Maintain airway, breathing and circulation. May need endotrach or trach to maintain airway. May need humidified oxygen. May need suctioning.Determine fluid resuscitation. Needs central line.Put in foley for hourly outputs.Put in nasogastric tube for gastric decompression. Patient NPOManage pain with IV narcotics.Assess circulation distal to circumferential burns.Get height & weight. Give tetanus injectionDo initial wound assessment. Determine wound care.If inhalation injury suspected may need emergency bronchoscopyNeeds to be in a Burn Center

594
Q

fluid resuscitation for a burn patient

A

Parkland (Baxter) formula:4ml lactated ringers X kg body weight X % TBSA burned= total 24 hour fluid requirements. Give ½ of amount over first 8 hours and the rest of the amount over 16 hours.Brooke (Modified) formula:2ml lactated ringers X kg body weight X % TBSA burned = total fluid requirements. Give ½ amount of fluid over 8 hours and the rest over 16 hours.Winski formula:2ml lactated ringers X kg wgt X % TBSA burn with maintenance fluidIn addition to these fluids sometimes they need to give albumin and other IV fluids. Is a guideline.

595
Q

what makes a burn severe

A

if its of eyes, ears, face, hands, feet or perineum

596
Q

how to calculate fluids for burns

A

multiply weight (kg), by 4 ml, % of body burned. Then you divide that in 1/2. give 1/2 over first 8 hrs. give 2nd 1/2 over second 8 hrs.

597
Q

parameters for fluid of burns

A

alert and oriented 30-50 ml an hour of outputbelow 100 bpmsystolic BP at least 100 and abovecentral venous 5-10 m of mercurycentral wedge pressure 5-15 m of mercury

598
Q

what should you not have in a burn patients room

A

plants!! They carry pseudonomas.

599
Q

what kind of procedure is it when dealing with a burn patient

A

sterile technique. sterile gloves. sterile everything.

600
Q

burn care: intermediate/acute phase

A

Begins 48 to 72 hours after burn injury. Mobilization of fluid from interstitial space to intravascular space. Phase is concluded when burn area is completely covered by skin grafts or when wounds are healed. May take weeks to months.There is continued attention directed toward assessment and maintenance of: a. Cardiopulmonary function b. Fluid and electrolyte balance c. Gastrointestinal functionBurn wound care becomes another major focus of this stage. Goals are to: a. Cleanse and debride area of necrotic tissue that could promote bacterial growth. b. Promote wound re-epithelialization and/or successful skin grafting.

601
Q

which phase does hypokalemia take place in burns

A

intermediate acute phase

602
Q

pathophysiology of acute phase of burns

A

Is state of diuresis with fluid shifting back to intravascular space. May see: a. Hemodilution causing decreased Hematocrit. Blood cell concentration is diluted as fluid enters vascular compartment. Also there is a loss of RBCs destroyed at the burn site. b. Increased urinary output because there is increased blood flow to the kidneys which causes increased urine to form. c. A sodium deficit continues because with diuresis sodium is lost with water and the existing serum sodium is diluted by fluid coming into the vascular space. d. May see a potassium deficit because potassium shifts back into the cells. e. Metabolic acidosis can still be seen because the loss of sodium depletes bicarbonate.

603
Q

which phase is more on wound care (burns)

A

acute phase

604
Q

burns cardiopulmonary effects

A

As capillaries regain their integrity, fluid moves from the interstitial space to the vascular compartment. Diuresis occurs. Happens 48 hours or more post burn..If cardiac and renal functio0n are not adequate, fluid overload occurs with CHF.Patient may need fluids titrated. Cardiotonic drugs and diuretics may be necessary. If blood transfusions are necessary to treat blood loss & anemia, the patient must be carefully monitored. May need Swan-Ganz cath to monitor for fluid overload.Airway obstruction as a result of upper airway edema can take as long as 48 hours post burn to develop.

605
Q

neurological effects of burns

A

Patients can exhibit certain behaviors that aren’t totally understood.May be very disoriented. May be withdrawn, combative. May hallucinate and have frequent nightmares. Delirium is more acute at night. Behaviors eventually disappear.May be due to hypoxia, cerebral edema, sepsis, ICU psychosis and medications being given

606
Q

gastrointestinal effects of burns

A

Bowel sounds do return during this stage but the patient is still able to get a paralytic ileus.May also have diarrhea from enteral feedings and antibiotics. May have constipation from opioids.May also have Curling’s ulcer and need proton pump inhibitors.Will have transient elevated glucose levels needing glucoscans and insulin coverage.

607
Q

musculoskeletal effects on burns

A

As burn begins to heal & scar tissue forms, the skin becomes less supple and pliant. ROJM may be limited and contractures can form. Because of pain patient tends to be in a flexed position also leading to the formation of contractures.Splinting, proper positioning, and ROJM can help to prevent contractures.

608
Q

risk for infection burns

A

Infection can be a major cause of death for patients who survive the first few days post burn. Begins at burn site but can be carried into the blood stream causing sepsis.The most invasive wound infections are caused by pseudomonas, enterobacter, klebsiella, staph. aureus, candida and e. coli.Cultures of the burn wound should be done on admission and then twice a week.Symptoms of sepsis include hypo or hyperthermia, increased heart rate & respirations, decreased BP & decreased urinary output. May also have chills, malaise, and loss of appetite. WBCs usually 10,000 to 20,000 since patient is immunosuppressed.If infection is suspected, need to get cultures wound, blood, urine, IV site, pharynx, and sputum

609
Q

symptoms to look for infection in burns

A

any of these factors could mean sepsis. slight temp, Hypo or hyperthermia pulse starts to elevaterespirations start to elevateb/p decreasesurinary output starts to decrease

610
Q

nutritional needs for burns

A

A total assessment of nutritional needs is crucial to decrease catabolic states.The nurse and nutritionist collaborate to evaluate the patient’s energy needs.Enteral feedings may be needed to reverse negative nitrogen balance and to offset the hypermetabolism. Enteral feedings are contraindicated in with Curling’s ulcers, pancreatitis, and septic ileus. May need parenteral nutrition.As the patient begins to tolerate po feedings the enteral feedings can be titrated off.The patient will need high protein, vitamins A, C, E and a multivitamin with minerals such as zinc and iron to promote healing and hemoglobin formation.Encourage family to bring in favorite foods. Calorie counts & weekly weights.Offer burn frappes and snacks between meals. Avoid activities around meal time.

611
Q

skin debrediment burns

A

Need to remove necrotic tissue because it retards healing and prolongs inflammmation. Is the process of removing dead tissue from the wound.Types of Debridement: a. Natural debridement allows dead tissue to spontaneously separate from wound. b. Mechanical debridement uses a surgical scissors & forceps to separate and remove eschar. Done to the point of pain & bleeding. c. Enzymatic debridement uses an agent topically to dissolve and remove necrotic tissue. d. Surgical debridement excises the wound sequentially to the level of the fascia. Since this sacrifices viable fat & lymphatic tissue, it’s use is reserved for patients with extensive or full-thickness burns

612
Q

skin grafting burns

A

Priority areas are face, hands, feet, and areas involving joints. Permits earlier functional ability and reduces development of contractures.When burns are extensive on the chest and abdomen, grafting may be done to reduce extent of burn surface.Should have bacterial count of fewer than 100,000/gram of tissue to optimize graft take. A pre-op culture to r/o streptococcus is mandatory because the enzymes of this bacteria can dissolve the graft.Types of Grafts: a. Autograft is the patient’s own skin. Taken from donor sites. Can also grown via culture if larger pieces are needed. b. Homograft or Allograft is human skin harvested from cadavers. Rejected in 14 to 21 days. c. Heterograft or Xenograft is skin from an animal like a pig. Only temporary. Rejects early and more of a risk for infection. d. Synthetic materials like Biobrane

613
Q

complications of burns

A

Scars more likely if burn is below the level of the dermis. Wound is in a dynamic state for 1 to 2 years post burn. If appropriate measures are employed scar tissue will lose its redness and will soften. Jobs elastic garments help.Keloids are large heaped up masses of scar tissue that may extend beyond the wound surface. Seen more in dark pigmented persons.Failure to heal r/t inadequate nutrition. A serum albumin level below 2gm/dl is frequently a factor.Contractures because the burn wound will shorten and the flexor muscles are stronger, Splints, traction, purposeful movement and positioning in functional alignment help to prevent these.Morphine, MS contin, dilaudid, fentanyl and methadone may be used for analgesia. NSAIDS and neurontin may also be usedMay use ativan and versed to decrease anxiety and give short acting amnesia

614
Q

wound care burns

A

Need daily observation, assessment, cleansing, debridement and dressing application.May have to perform non-surgical debridement, dressing changes, topical antibiotic treatment, graft care and donor site care twice a day.May use hydrotherapy like a showering cart to cleanse wounds.During wound care pain management is needed. Narcotics, distraction, guided imagery and relaxation techniques can be used.Allow the patient to participate if possible to lower the patient’s anxiety. Multiple layers of gauze may be applied over topical agents on the wound depending on the depth of the injury, amount of drainage expected, area injured, and patient’s mobility. May be held in place by roller gauze or netting fabrics.

615
Q

nursing assessment burns

A

Vital signs, peripheral pulses, weights, pain level burn wound.Cardiopulmonary assessmentNeurological , gastrointestinal assessmentLaboratory findings

616
Q

nursing interventions burns

A

Prevent cardiopulmonary complications and infectionMaintain skin integrityManage painMaintain nutritionEmotional support/help with body imagePrevent hazards of immobilityPatient teaching

617
Q

topical wound agents for burns

A

BACITRACIN Antimicrobial agent. Used for partial thickness burns. Is painless and easy to apply. Wound should be cleansed thoroughly between dressings. Reapplication 2 to 4 times a day.GENTAMYCIN 0.1% Broad spectrum antibiotic for partial thickness burns. Is painless and easy to apply. Reapplication 3 to 4 times a day.XEROFORM (COVIDIEN) Petrolatum based fine mesh gauze impregnated with 3% bismuth tribromophenate. Mild antimicrobial abilities. Provides a protective barrier dressing that allows for epithelial tissue development. Does not manage high volumes of exudate. Apply to clean wound. Dressing becomes rigid as it dries onto wound.

618
Q

topical wound agents burns

A

SILVER-SULFADIAZINE (SILVADENE) Broad spectrum cream against gram negative & gram positive bacteria and Candida organisms. Used for deep partial and full thickness burns. Penetrates eschar to inhibit bacterial growth at dermis-eschar interface. Inhibits epithelial tissue development. May cause skin rash and transient decrease WBCs for 24 to 48 hours after application. Contraindicated for sulfa allergies. Change dressing every 12 to 24 hours. Apply ¾ inch layer directly to wound or impregnated gauze. Is painless and somewhat soothing. May cause slimy, grayish appearance. Discontinue when eschar is gone.

619
Q

topical wound agents burns

A

AQUACEL AG Composed of 1.2 % ionic silver. Creates a gel that absorbs wound drainage. Used for partial thickness and full thickness burns. May be covered by another dressing. Trim edges as it lifts. May leave yellow film-do not remove completely. Apply new dressings to cleansed wound. Can stay on up to 14 to 21 days. Has antimicrobial properties. Dressing becomes rigid when it dries out, decreasing range of motion. May cause pain as dressing dries out. May cause pain as dressing dries out.

620
Q

topical wound agents burns

A

MAFENIDE ACETATE (SULFAMYLON) Used for deep partial and full thickness burns especially ear burns. Effective against broad range of micro-organisms including pseudomonas and clostridium. Available as a water soluble cream or 5% topical solution. Penetrates thick eschar and cartilage. Inhibits epithelial tissue development. Plan for pain management on application. Apply cream in ¼ inch layer directly to wound or impregnate into gauze dressing BID orTID. Monitor for metabolic acidosis (inhibits carbronic anhydrase activity). Monitor for allergic rash. Use with caution in renal patients. Cleanse and debride burn areas before reapplying. Discontinue when eschar gone.

621
Q

topical wound agents burns

A

HYDROCOLLOIDS Contains gelatin, pectin, carboxy-methylcellulose together with polymers and adhesive. Used for small partial or full thickness burns. Absorbs exudate, forms viscous gel and is impermeable to bacteria. Reduces pain. Change dressing q 3-5 days. Helps with autolytic debridement. Good for minimal to moderate drainage. May macerate skin if drainage exceeds dressing’s ability to absorb it. Example: Duoderm

622
Q

topical wound agents burns

A

BIOBRANE Is a biosynthetic dressing made of silicone film bonded to a nylon membrane with collagen. Acts as a temporary dermal substitute for partial thickness and donor sites. Pores in membrane allow for dissipation of exudates. Closes wound and stays on until wound is healed. Reduces pain. Needs to be applied within 24-36 hours. No antimicrobial action.

623
Q

dermal replacements / synthetic substitutes

A

INTEGRA (ARTIFICIAL SKIN) Two layer man-made membrane used to replace dermis. Is covered with an autograft forming a functional dermis and epidermis.ALLODERM Man-made collagen matrix used to provide a dermal layer. Is covered with an autograft.

624
Q

rehabilition phase burns

A

Begins when patient’s burn wounds have healed and the patient is able to resume a level of self care activity.The goals are to assist the patient to resume a functional role in society & to accomplish functional and cosmetic reconstructive surgery.Still may have some electrolyte problems like: a. Calcium Deficit b. Potassium Deficit c. Negative nitrogen balance

625
Q

pathology changes and manifestations of burns

A

Burn wounds heal by either primary intention or by grafting, New skin appears flat and pink. In 4-6 weeks area becomes raised and hyperemic. If ROJM is not done, new tissue will shorten causing contractures.Mature healing takes 6 months to 2 years when suppleness returns and pink or red color has faded to a slightly lighter hue than unburned tissue.Takes longer for heavily pigmented skin to regain it’s color because many of the melanocytes are destroyed. Often skin never regains the original color.Scarring has two parts: discoloration and contour. Discoloration will fade with time but scar tissue tends to develop an altered contour. It no longer is flat but becomes elevated and enlarged above the original burn area. Pressure can help keep the scar flat. Gentle pressure can be maintained with Job’s custom fitted garments. These are worn up to 23 hours for as long as 12 to 18 months post burn. Are removed only for a short time for bathing.

626
Q

pathology changes and manifestations of burns

A

Patient frequently experiences itching when healing is occurring. “Corrective Concepts” a water-based moisturizer and benadryl can help decrease the itching. Old epithelium is replaced by new cells so flaking happens.Newly formed skin is extremely sensitive to trauma. Blisters and skin tears are likely to develop from slight pressure or friction. Skin is hypersensitive to cold, heat, and touch. Grafted areas are more likely to be hyposensitive until nerve regeneration occurs. Healed burn areas must be protected from direct sunlight for 6 to 9 months to prevent hyperpigmentation and sunburn injury.

627
Q

collaborative care burns

A

Both patient and family are encouraged to actively participate in care. The patient may go home with small unhealed wounds so education and hands-0n instruction for dressing changes and wound care are needed.Emollient water-based creams should be applied to skin that penetrate the dermis to keep the skin supple and to decrease itching.Continued Physical and Occupational Therapy is needed. Constant encouragement and reassurance is needed to maintain a patient’s morale, especially when the patient realizes recovery can be slow and rehabilitation will need to be the major focus for the next 6 to 12 months.There is a tremendous psychological impact on the patient so we need to be sensitive and attuned to the patient’s emotions and concerns. Patients need to be encouraged to discuss their fears regarding loss of their lives as they knew it, loss of function (temporary or permanent ), deformity & disfigurement, retun to home-life & work, and financial burdens.

628
Q

collaborative care burns cont.

A

Need to address spiritual & cultural needs. Early on bring family up to speed about situation, hospital chaplains, and community help groups.A person’s self-esteem is usually adversely affected by burns. Patient may have an overwhelming fear of the loss of a relationship. Encourage appropriate independence, and eventual return to pre-burn levels of activity. Interactions with burn survivors may bring comfort and help to restore self-esteem.Counseling services should be made available after the patient returns home.Patients need reassurance that their feelings during this time of readjustment are normal and that frustration is to be expected.Stress from the burn injury can sometimes precipitate a psychiatric/psychological crisis. Experience may be beyond the patient’s ability to cope. Short term counseling is helpful.

629
Q

Common emotional responses of burn patients

A

FEAR: Will I die? What will happen next? Will I be disfigured? Will my family and friends still love me?ANXIETY: I feel out of control. What’s happening to me? When will it end?ANGER: Why did it happen to me? Those nurses enjoy hurting me.GUILT: If only I’d been more careful. I’m being punished because of something I did.DEPRESSION: It’s no use going on. I don’t care what happens to me. I wish people would leave me alone.

630
Q

rehab phase burns

A

try to get them to return to societydo cosmetic surgery herenew skin looks flat and pink, if you don’t do something it raises and do hyperemicneed to do ROM to prevent contractionstakes 6 months to 2 years to healpink or red color fadesmake sure to use Jobes (compression)if your heavily pigmented it takes longer for color to returncan still be anemic in this phaseneed nutritional stuff, vitamins, still have electrolyte problemsstill need to have blood work doneitching is the worst as they are healingneed to prevent scratching

631
Q

what to know for test

A

different phases of burnsfluid shiftshow to calculate fluid for burnsknow the dressings for burnsalignment and functional position is very important to prevent contractorsappreciate the emotional toll it takeswhat we are monitoring for in burnsknow full thickness medsknow parkinson’s and dopamineknow parkinson’s stagesknow to keep patient functional as long as possible with parkinson’s tremors, rigidity, akinesea, posture, monitor orthostatic hypotension parkinson’ssinimet with parkinson’s (major drug)some parkinson’s drugs sometimes peter out, need a drug holiday. know MS and immune modulator drugsknow how immune modulator drugs are given and who has to learn to do itwhat might you get when starting immune drugs (flu like symptoms)immune drugs cause blood disgratiors and liver issuesno side effects of revib, copazone (MS)most important about MG (give drugs on time,) drugs can kick it off. take this into account. plasmaphoresis before surgeryknow difference between MG crisis and colinergic crisiswhens the best time to get calories into MG (morning)rest before you feed them (MG) what should you focus on with LG disease (communication before they lose it, advanced directives)LG can have a heredity factor (children should be tested)Huntinton’s you need to test its inheritedCVA’s know difference between right and left strokedifferent conditions of CVA’s (whats aphasia, ataxia….)know about care for CVA’sknow broca’s and weirnekiesknow ICPseizures (generalized vs. partials)crucial to document everything you see with a seizure. very detailed length, aura, what was jerking, how long did postdictal phase lastairway and safety with a seizurevery important for them to stay on meds (seizures)ativan is drug of choice for seizuresgingaval hyperplasia with dilantinbrain tumors - positioning with incisions and approach for after surgery (flat, log rolled, semi fowlers?)how to assess spinal cord injury, know difference between different kinds of spinal injurieshas to be moved in alignment,certain care has to be given depending on place of injuryknow spinal shock know differences in hematomas with head injuries, what do we do across the board, concussions, contusions, lacerations.CT with any head injury.