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N3523 Adult and Older Adult Health Care II > Exam 1 - Study Material > Flashcards

Exam 1 - Study Material Flashcards

1
Q

What should the nurse consider before giving insulin to a patient?

A
  • Always check the blood sugar before giving insulin
  • Know onset and duration of insulins
  • Always have another nurse check what is drawn, the amount, etc.
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2
Q

How should insulin be administered?

A
  • Using thumb and forefinger, pinch skin at the injection site. Inject at 90 degree angle. DO NOT ASPIRATE FOR BLOOD RETURN
  • Place alcohol swab or cotton over site and withdraw needle
  • DO NOT MASSAGE area after injection
  • Dispose of needle in appropriate puncture resistant container
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3
Q

How should pre-filled syringes of insulin be stored and how long are they stable?

A
  • Pre-filled syringes store in vertical position in refrigerator.
  • Stable x1 week-max 2 wks
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4
Q

What types of insulin are there, and what is the onset and duration for each?

A
  1. —Rapid acting/Short duration (10-30min / 3-6.5hr)
  2. Slower acting/Short duration (30-60min / 6-10hr) regular & (15-30min / 6.5hr) exubera
  3. —Intermediate duration (60-120min / 16-24hr)
  4. —Long duration (70min / 24 hr)
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5
Q

What are some Rapid acting/Short duration insulins?

A
  • —lispro (Humalog)
  • aspart (NovoLog)
  • glulisine (Apidra)
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6
Q

What are some nursing implications of Rapid acting/Short duration insulins?

A
  • —Give with meals to control postprandial rise in glucose to control glucose between meals & HS
    • If no food is given within a short perioid of time pt. will get in a hypoglycemic state.
  • All of them are clear solutions— –> look out for cloudiness
  • All 3 require prescriptions (Insulin Lispro, Aspart & Glulisine)
  • —Do NOT give IV
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7
Q

What are some adverse effects of insulin?

A
  • —Hypoglycemia
  • edema
  • weight gain
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8
Q

What are some Slower acting/Short duration insulins?

A
  • Humulin R (regular human insulin)
  • Novolin R
  • Exubera
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9
Q

What are some nursing implications of Slower acting/Short duration insulins?

A
  • Humulin & Novolin R do not need an Rx to get, **except Exubera **
  • —SQ inj, SQ infusion, IM inj, oral inhalation & off label IV—
  • Only insulin given by IV
  • —Can be inhaled or injected AC to control postprandial hyperglycemia
  • —Infused SQ to provide basal glycemic control
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10
Q

What are some Intermediate duration insulins (NPH insulins)?

A
  • Humulin N
  • Novolin N
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11
Q

What are some nursing implications of Humulin N & Novolin N insulins?

A
  • —Cloudy suspension should be gently shaken b/4 administration—
  • Available without prescription—
  • The protamine component slows absorption & delays DOA—
  • Do not administer at mealtime but use bid between meals & at bedtime—
  • Is the only long acting insulin that can be mixed with a short acting insulin
    • ​—Draw short acting insulin into syringe first to avoid contamination of NPH vial.
    • —If have to give a short acting & long acting insulin mix the preparations rather than inject them separately.
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12
Q

What are some long duration insulins?

A

—Insulin Glargine (Lantus)

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13
Q

What are the nursing implications of —Insulin Glargine (Lantus)?

A
  • —Clear colorless solution, do NOT mix with other insulins and do NOT give IV—
  • Long DOA 24 h, qd dosing SQ injection
  • —Because of long DOA and a stable steady state there is less risk of hypo or hyperglycemia.
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14
Q

You should —Discard insulin that has any precipitate except for which type of insulin?

A

NPH insulins (Humulin N & Novolin N)

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15
Q

What is Insulin Release Stimulated By?

A
  • Glucose
  • Ketone Bodies
  • Proteins
  • Glucagon
  • Gastric Secretions
  • Salicylates- asprin – can lead to hypoglycemia
  • Hyperkalemia
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16
Q

What is Insulin Release Inhibited by?

A
  • Hypoglycemia
  • Hypokalemia
  • Catecholamines (NE and Epi
  • Beta-Blockers
  • Calcium Channel Blockers
  • Phenytoin
  • Alcohol (this will decrease glucose levels for a while)
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17
Q

What is glycogenolysis?

A

breakdown of hepatic and muscle glycogen to glucose.

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18
Q

What is gluconeogenesis?

A

conversion of fatty acids and protein to glucose. Ketone bodies are created during this process

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19
Q

What are the Signs & Symptoms of High glucose levels?

A
  • Increased urination (Polyuria)
  • Increased thirst (Polydipsia)
  • Increased hunger (Polyphagia)
  • Weight loss
  • Weakness and fatigue
  • Blurred vision
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20
Q

What are the SQ injection sights for insulin?

A
  • —upper arm, thigh (slowest) & abdomen (fastest)
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21
Q

What type(s) of insulin can be given IV and why is it given?

A
  • —ONLY Regular insulin can be given IV.
  • Usually given for ketoacidosis or hyperkalemia
  • —Insulin is given to ALL pts. that have type I
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22
Q

In what situations would you want to supplement additional doses of insulin?

A
  • —During infection
  • stress obesity
  • the adolescent growth spurt
  • pregnancy (after 1st trimester)
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23
Q

What are some Nursing Diagnoses for anemia?

A
  • —Activity intolerance
  • —Imbalanced nutrition: Less than body requirements —
  • Knowledge deficit —
  • Noncompliance with prescribed therapy —
  • Altered tissue perfusion —
  • Fatigue
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24
Q

What are the 2 types of diabetes mellitus?

A
  • Type 1 (Beta-cell destruction, usually leading to absolute insulin deficiency)
  • Type 2 (ranging from predominatly insulin resistance with relative insulin deficiency to predominattly an insulin secretory defect with insulin resistance)
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25
Q

What causes Type 1 Diabetes?

A
  • Peak age of diagnosis = 12 years
  • Autoimmune loss of β cells
    • Gene-environment trigger cell-mediated destruction of pancreatic cells
    • Slowly progressive, T-cell-mediated Lymphocyte & macrophage infiltration → inflammation → β cell death
    • Autoantibodies produced against islet cells, insulin, other cytoplasmic proteins
       T helper lymphocytes → IL-4 → B lymphocyte proliferation & antibody production, IL-2 → T cytotoxic (CD8) cells, and IFNγ → macrophage activation
  • Altered β & α cells → excess glucagon → hyperglycemia
  • Non-immune is a secondary result of other diseases (pancreatitis)
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26
Q

What are the clinical manefistations of Type 1 Diabetes?

A
  • Acute onset of “3Ps” (polydipsia, polyuria, polyphagia )
  • Weight loss
  • fatigue
  • glucosuria (excessive glucose in urine)
  • hyperglycemia
  • thirst
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27
Q

What are some complications of type 1 diabetes?

A
  • Dehydration
  • Diabetic ketoacidosis (DKA) (fruity odor to breath,
  • Failure to thrive in small children/infants
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28
Q

What is the treatment of Type 1 Diabetes?

A
  • Insulin
  • diet
  • exercise
  • Blood Gas monitoring,
  • Islet cell/pancreas transplant
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29
Q

What are some risk facotrs for Type 2 diabetes?

A
  • Genetic-environmental interaction
  • Metabolic syndrome: central obesity (strongest factor)
  • Dyslipidemia
  • High blood pressure
  • Inactivity
  • Gestational DM + insulin during pregnancy, baby > 9 lb birthweight, maternal postpartum obesity
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30
Q

What causes Type 2 diabetes?

A
  1. insulin resistance (relative insulin deficiency) → pancreatic β cell dysfunction → absolute insulin deficiency
  2. insulin secretory defect with insulin resistance
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31
Q

What are some lab tests for Diabetes and what do their values mean?

A
  • Fasting blood glucose 100 > 126 mg/dL = prediabetes
  • Oral Glucose Tolerence Test 140 > 200 mg/dL = prediabetes
  • Non-fasting blood glucose > 200 mg/dL + polyuria, polydipsia = You have diabetes
  • Glycosylated( glucose-bound) Hgb HBA1c
  • Normally between 4-6%, it is increased with hyperglycemia
    • Blood glucose control over 2 – 4 mo
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32
Q

What is Hemoglobin A1c?

A

A measure of the total hemoglobin over 3 months; this value reflects the average glucose level over those 3 months.

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33
Q

Describe the HBA1C lab results

A
  • 4-6% = Glucose level 60-120
  • 7% = Glucose of 150
  • 8% = Glucose 180, fair
  • 9% = Glucose > 210, poor results
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34
Q

What is the ideal level that Hemoglobin A1c should be kept at with patients with diabetes?

A

HbA1c < 7%

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35
Q

What is the recommended Hemoglobin A1c levels for the elderly?

A

7.0-7.9%

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36
Q

How is insulin released?

A
  • Beta cells of islets of Langenhans
    • ↑ blood glucose →↑ insulin release
    • 2-3 hr after meal, then basal rate occurs
  • Insulin levels low between meals
  • Insulin binding
    • Binds to insulin receptors to ↑ glucose transporter molecules; used for energy or stored as glycogen; negative feedback (↓ glucose & ↓ insulin release)
  • ANS effects
    • PNS ↑, SNS ↓
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37
Q

What are the clinical manefistations of Type 2 diabetes?

A
  • Asymptomatic or vague (e.g., fatigue)
  • Visual changes
  • Nephropathy
  • Coronary artery disease (CAD)
  • Peripheral vascular disease (PVD)
  • Recurrent infections
  • Neuropathy (paresthesias, weakness)
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38
Q

What is the treatment for Type 2 diabetes?

A

oral hypoglycemics, diet, exercise

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39
Q

What are type 2 diabetes medications used for?

A
  • Decreasing insulin resistance and increasing insulin sensitization (ie, metoformin)
  • Interfering with the digestion and absorption of dietary carbohydrates (ie, acarbose)
  • Augmenting insulin secretion and action (ie, sulfonylureas)

Diet, exercise, oral agents should be used first before resorting to insulin.

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40
Q

What are some acute complications with Diabetes Mellitus?

A
  • Hypoglycemia
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
  • Somogyi effect
    • Blood glucose fluctuations: hypoglycemia → rebound hyperglycemia
  • Common in children with DM Type 1
  • Dawn phenomenon
    • Early AM rise in blood glucose
    • Related to nocturnal elevations of GH?
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41
Q

What drugs lower blood glucose when combined with insulin?

A
  • —sulfonylureas
  • meglitinides
  • beta blockers
  • alcohol
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42
Q

What drugs counteract the actions of insulin & produce hyperglycemia?

A
  • thiazide diuretics
  • glucocorticoids
  • sympathomimetics
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43
Q

What drug(s) can mask the signs and symptoms of hypoglcemia?

A
  • Beta blockers
  • —(tachycardia, palpitations) & also cause further hypoglycemia by blocking glycogenolysis.
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44
Q

What causes hypoglycemia?

A
  • insulin overdose
  • reduced intake of food
  • vomiting/diarrhea
  • excess alcohol
  • unaccustomed exercise
  • childbirth
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45
Q

Hypoglycemia is defined by what blood glucose level?

A

< 60 mg/dl

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46
Q

What are the signs and symptoms of a rapidly falling blood glucose levels?

A
  • —activation of the sympathetic nervous system leading to –>
  • tachycardia, palpitations, sweating, nervousness
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47
Q

What are the signs and symptoms of a slowly falling blood glucose levels?

A

—HA, confusion, drowsiness & fatigue

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48
Q

What can be used to treat falling blood glucose levels (rapid or slow)?

A
  • —Take fast acting sugar
  • glucose tablets, OJ, sugar cubes, honey, corn syrup, non diet soda
  • —If pt has severe hypoglycemia IV glucose is preferred
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49
Q

What produces glucagon and what are it’s effects?

A
  • —Glucagon is produced by alpha cells in the pancreas.
  • ↑ plasma levels of glucose & relaxes smooth muscle in the GI tract.—
  • ↑ blood glucose levels following insulin overdose.
  • It promotes breakdown of glycogen, ↓ glycogen synthesis & stimulates biosynthesis of glucose.
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50
Q

How can glucagon be administered?

A

—IM, SQ & IV

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51
Q

What is the MOA for Sulfonylureas?

A

—Stimulates the release of insulin from pancreas depending on how much glucose there is (insulin sensitivity) –> can lead to hypoglycemia

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52
Q

What are some nursing considerations for sulfonulureas?

A
  • —Only works in type 2 diabetes—
  • Can be used alone or in combo—
  • Avoid during pregnancy/nursing mothers
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53
Q

What are some side effects of sulfonylureas?

A
  • —Hypoglycemia (fatigue, excessive hunger, profuse sweating, palpitations)—
  • Weight gain
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54
Q

What are the Drug interactions for sulfonylureas?

A
  • —Alcohol (disulfuram rxn)—
  • Drugs that intensify hypoglycemia: NSAIDS’s, sufonamide antibiotics, ranitidine & cimetidine—
  • Beta blockers – beta rec promote insulin release & mask S/Sx of hypoglycemia
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55
Q

What are some 1st generation Sulfonylureas?

A
  • Tolbutamide
  • Acetoheamide
  • Tolazamide
  • Chloropamide
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56
Q

What are some 2nd generation Sulfonylureas?

A

Glipizide

Glyburide

Glime

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57
Q

What are some Metglitinides/Short-Acting Secretagogues?

A
  • —Repaglinide (Prandin)
  • nateglinide (Starlix)
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58
Q

What is the MOA for Metgilitinides/Short-acting Secretagogues

A
  • —Stimulates the release of insulin from pancreas depending on how much glucose there is (insulin sensitivity) –> can lead to hypoglycemia
  • It is glucose dependant (if no glucose no insulin is produced) pt MUST eat no longer than 30 min after drug intake
  • Works exactly the same as Sulfonylureas
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59
Q

What are some nursing implications for Metglitinides/Short-Acting Secretagogues?

A
  • —Only approved for type 2
  • —If no response with sulfonylureas there will be no response with metglitinides—
  • Approved for monotx or combo with metformin or a glitazone
  • Use this drug if pt. has allergic reaction to sulfonlureas
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60
Q

What are the side effects and drug interactions of Metglitinides/Short-Acting Secretagogues?

A
  • Side effects:
    • —Hypoglycemia (Less than with sulfonylureas), weight gain
  • ​​​Drug interactions
    • ​—Gemfibrizol (causes hypoglycemia)
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61
Q

What are the different types of Biguanides?

A

—Metformin (Glucophage, Fortamet, Glumetza, Riomet)

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62
Q

What is the MOA for metformin?

A
  • —Dec glucose production in the liver & enhances glucose uptake & utilization by muscle.
  • Does NOT promote insulin release
  • Dec LDL and triglyceride levels.
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63
Q

What are the nursing implications for metformin?

A
  • —Because of MOA could possibly use it in pts with type 1 also—
  • Can be used alone or with sulfonylureas or Exenatide—
  • Absorbed slowly from small intestine and excreted unchanged in the kidneys (Check renal fxn, creatine cl)
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64
Q

What are the contraindications for metformin?

A
  • —Males with creatine clearance > 1.5—
  • Females with creatine clearance > 1.4—
  • Liver dz, alcohol excess or pt. with shock (cause hypoxemia), alcohol use—
  • Heart Failure
  • Severe infection (stop metformin, start temporary insulin)
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65
Q

What are the side effects of metformin?

A
  • —Weight loss, Dec appetite, nausea, diarrhea, dec absorption of vit B12 & folic acid—
  • can cause lactic acidosis (rare, but mortality rate of 50%) S/Sx are: hyperventilation, myalgia, malaise & unusual somnolence
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66
Q

What is the MOA for Thiazolidinediones (Glitizones)?

A
  • —Dec insulin resistance by inc insulin sensitivity of skeletal muscle, liver & adipose tissue (cellular response to insulin inc).
  • Insulin must be present for drug to work.
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67
Q

What are some nursing implications for Thiazolidinediones (Glitizones)?

A
  • —Only approved for type 2— DM
  • Approved for monotx & for combo with metformin, sulfonylurea or insulin (carefully b/c insulin & glitizones cz edema).
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68
Q

What are some adverse effects of Thiazolidinediones (Glitizones)?

A
  • —Fluid retention (edema & wt gain), inc HDL, LDL and triglycerides
  • —Contraindicated in Class III or IV heart failure or hepatoxicity
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69
Q

When should you cheeck blood glucose levels?

A
  • Before breakfast, lunch, & dinner, and before bedtime snack
  • 1-2 hours after a meal
  • Periods of stress, illness, or surgery
  • Pregnancy; changes in treatment plan
  • When suspect low blood sugar
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70
Q

When should a patient with diabetes not excercise?

A
  • Test blood sugar before & after exercise
  • Do not exercise if blood glucose 100 < or > 240 and there are ketones in urine
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71
Q

What is Diabetic ketoacidosis?

A

A problem that occurs in people when the body cannot use glucose as a fuel source because there is no insulin or not enough insulin; Fat is used for fuel instead producing ketones which build up in the body.

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72
Q

What causes Diabetic ketoacidosis?

A
  • Precipitated by intercurrent illness or inadequate insulin Rx
  • Insulin deficiency → ↓ glucose uptake, ↑ fat mobilization with release of fatty acids, ↑ gluconeogenesis, ↑ ketogenesis
  • Hepatic overproduction of acids → metabolic
    acidosis
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73
Q

What are the manifestations of Diabetic ketoacidosis?

A
  • polyuria & dehydration (osmotic diuresis from hyperglycemia)
  • ketonuria
  • hyperkalemia (shift of K+ out of cell in exchange for H+)
  • metabolic acidosis
  • Kussmaul respirations
  • postural dizziness,
  • ↓ LOC, nausea,
  • thirst
  • glycosuria
  • BG > 250 mg/dL
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74
Q

What is the treatment for Diabetic ketoacidosis?

A
  • insulin (↓ hyperglycemia & hyperkalemia by transport of glucose & K+ into cell),
  • fluids (correct dehydration) –> 0.9% NS at 500 ml/hr for 1st hr
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75
Q

What is Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)?

A

A serious condition most frequently seen in older persons in which blood sugar levels rise, and your body tries to get rid of the excess sugar by passing it into your urine

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76
Q

What causes Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)?

A
  • Precipitated by stress, noncompliance with meds
  • More common in type 2 DM
  • Relative insulin deficiency → hyperglycemia → solute diuresis → dehydration → hyperosmolality
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77
Q

What are the manifestations of Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)?

A
  • glycosuria
  • polyuria
  • thirst
  • polydipsia,
  • ↓ BP, ↑ HR,
  • weakness,
  • N & V,
  • stupor,
  • seizures,
  • coma,
  • Blood Glucose > 600 mg/dL, pH > 7.30
  • serum osmolarity > 320 mOsm/L,
  • ↓ K+
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78
Q

What is the treatment for Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)?

A
  • insulin
  • rapid fluid replacement
  • K+ replacement
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79
Q

What are some chronic complications with chronic Diabetis Mellitus?

A
  • Microvascular disease
  • Macrovascular disease
  • Infection
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80
Q

What are some characteristics associated with Microvascular disease with Diabetes Mellitus?

A
  • Hyperglycemia → capillary basement membrane thickening with endothelial cell hyperplasia → ↓ tissue
  • Pathology related to ↑ blood glucose level & duration of disease
  • Sequelae: retinopathy → blindness, nephropathy → ESRD, & neuropathies
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81
Q

What are some characteristics associated with Macrovascular disease with Diabetes Mellitus?

A
  • Fibrous plaques associated with proliferation of subendothelial smooth muscle in arterial wall
  • Contributions to premature atherosclerosis: hyperglycemia, ↑ triglycerides, ↑ LDL, ↓ HDL,
  • Sequelae: coronary artery disease (CAD), stroke, & peripheral vascular disease (PVD)
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82
Q

What are some nursing interventions for anemia?

A
  • —Monitor VS and pulse oximetry, provide supplemental oxygen as needed
  • Monitor for potential complications
  • Blood or blood product transfusions
  • Drug therapy
  • —Dietary and lifestyle changes —
  • Patient teaching —
    • Nutrition intake —
    • Compliance with drug therapy
    • —Balance physical activity, exercise & rest
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83
Q

What is anemia from chronic disease?

A

Anemia resulting from decreased erythropoiesis in individuals with conditions of chronic systemic disease or inflammation.

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84
Q

What causes anemia from chronic disease?

A

This type of anemia results from:

  1. ↓ erythrocyte life space
    1. from ↑ destruction of RBC’s
    2. ↑ lactoferrin binding → ↑ iron storage → ↓ avaliablity of iron for blood
  2. Suppressed production of erythropoietin
  3. Ineffective bone marrow eryhroid progenitor response to erythropoietin
  4. Altered iron metabolism and iron sequestration in macrophages
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85
Q

What are the clinical manifestations of anemia from chronic disease?

A
  • Tachycardia, murmurs, orthostatic hypotension, Dyspnea, tachypnea
  • Headache, fatigue, lightheadedness, pallor, intermittent claudication
  • Low levels of circulating iron (
  • Very high lvls of total body iron storage
  • Normal to high serum ferritin levels
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86
Q

How would you treat anemia from chronic disease?

A

Treat the underlying cause:

  1. Arthritis
  2. Malignancies
  3. AIDS
  4. Chronic kidney disease
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87
Q

What is aplastic anemia?

A

Anemia caused by pancytopenia (a reduction or absence of all 3 blood cell types) from failure or suppression of bone marrow to produce adequate amounts of blood cells.

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88
Q

What causes aplastic anemia?

A
  • Caused by a bone marrow dysfunction which is hereditary or acquired (autoimmune, cancer, vitamin deficiency, etc)
  • This results in T-cells attacking hemopoietic stem cells lead to their apoptosis which in turn causes pancytopenia (↓ RBCs, ↓ WBCs, ↓ platelets).
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89
Q

What are the clinical manifestations of aplastic anemia?

A
  • Hypoxemia (low blood oxygen)
  • Pallor (paleness)
  • Fatigue, fever, dyspnea (difficulty in breathing)
  • Hemorrhaging due to ↓ platelets
    • ↓ platelets also leads to easy bruising
  • GI bleeding
  • Prolonged bleeding
  • ↓ leukocyte production leads to more frequent and prolonged infections
  • Ulcerations in mouth
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90
Q

What is folate deficiency anemia?

A

A deficiency in folate causes this anemia, and leads to the RBC’s becoming Macrocytic (larger than normal) & normochromic (w/ normal hemoglobin)

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91
Q

What causes anemia with folate deficiency?

A
  • A diet deficient in folate (young women, malnutrition, alcoholics)
  • Diets low in vegtables
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92
Q

What are the clinical manifestations of folate deficiency anemia?

A
  • Tongue ulcerations
  • stomatitis (inflammation of the mouth)
  • **flatulence, **
  • watery diarrhea
  • ↓ Hgb
  • ↑ MCV > 98
  • MCHC WNL
  • **Serum folate < 5 ng/mL **
  • ↑ risk fetal malformations,
  • CVD in adults
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93
Q

What is the treatment for folate deficiency anemia?

A
  • folic acid supplements
  • blood transfusion if severe
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94
Q

What is Hemolytic anemia?

A

A premature accelearted destruction of erythrocytes either episodically or continually

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95
Q

What causes hemolytic anemias?

A
  • Genetic defect (in erythrocytes)
  • Idiopathic
  • Severe burn or infection, DIC, hemodialysis
  • Exposure to incompatible blood, drug, or toxin
  • Malaria
  • Newborn hemolytic disease
  • Transfusion reaction
  • Sickle cell anemia, thalassemia (defective Hgb)
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96
Q

What are the clinical manifestations of drug-induced hemolytic anemia?

A
  • Jaundice - Occurs when heme destruction exceeds liver ability to conjuagte an excrete bilirubin
  • Splenomegaly
  • thromboembolism formation – Especially pulmonary embolisms
  • Erythroid hyperplasia - Abnomrally increased numbers of erythrocyte stem cells in bone marrow
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97
Q

How do you treat drug induced hemolytic anemias?

A
  1. Hepten model - Cessation of administration of the antibiotic (penicillin, cephalosporins, hydrocortisone) results in rapid resolution of the anemia.
  2. Immune complex formation - Treated by removing the cause or treating the underlying disorder
  3. Autoimmune model - Treated by removing the cause or treating the underlying disorder

Corticosteroids and or Rituximab (an antibody that supresses B cells) can be used to help less the effects of autoimmune responses

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98
Q

What is a Transfusion Reaction Hemolytic anemia?

A

A life-threatening Immune-mediated destruction of ABO antigens on blood because of incompatible blood types.

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99
Q

What are the clinical manifestations of a Hemolytic anemia transfusion reaction?

A
  • Fever/chills
  • flank pain
  • hematuria
  • facial flushing
  • chest/low back/abdominal pain
  • N & V
  • renal failure
  • ↓ BP
  • ↑ HR
  • dyspnea
  • shock
  • death
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100
Q

How would you treat a Transfusion Reaction Hemolytic anemia?

A
  • Prevention!
    • Verify correct patient, correct blood
    • Patient assessment
  • Immediately stop transfusion
  • ↑ fluids to flush kidneys
  • Support ABC
  • Antihistamine & steroid for anaphylaxis
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101
Q

What are some nursing interventions for transfusion reactions?

A
  • —Stop transfusion If acute transfusion reaction occurs ( flushing, itching, difficulty breathing, hives or other rashes)
  • —Maintain a patent IV line with NS
  • —Notify blood bank and physician immediately —
  • Monitor VS and urine output
  • —Treat symptom as per physician’s order —
  • Save blood bag and tubings & send to blood bank —
  • Complete transfusion reaction reports —
  • Document on transfusion reaction form and chart
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102
Q

What is Iron Deficiency anemia?

A

Anemia as a result of inadequate dietary intake of iron or a result of excessive blood loss

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103
Q

What causes iron deficiency anemia?

A
  • deficient diet
  • chronic blood loss
  • malabsorption disorder
  • A ↓ in RBC’s causes the bone marrow to produce small Hgb-deficient RBC’s
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104
Q

What are some characteristics of iron deficiency anemia?

A
  • Slowly develops
  • Most common wordwide
  • RBC’s are Microcytic (smaller than normal), hypochromic (paler than normal)
  • ↑ risk: pregnant/menstruating women, toddlers, GI/renal/liver disease, chronic blood donation, vegetarian diet, ↓ SES
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105
Q

What are the clinical manifestations of iron deficiency anemia?

A
  • DOE
  • cold intolerance
  • HA
  • brittle/thin/concave nails
  • maybe mouth sores,
  • pica & leg cramps if severe
  • cognitive impairment
  • burning mouth/glossitis
  • dysphagia
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106
Q

What are some Nursing Interventions for Iron-Deficiency Anemia?

A
  • —Dietary teaching- Iron rich foods (beans,, organ meat-liver, red meat, leafy green veggies, raisins & molasses) and increase fiber —
  • Avoid dairy or antacids with iron intake —Supplemental iron (PO iron should be taken 1 hour before meals or 2 hours after). —
  • Vitamin C (ascorbic acid) enhances iron absorption —
  • Discuss diagnostic studies to identify cause
  • —Emphasize compliance with dietary & drug therapy —
  • Lifelong iron supplementation for some patients
  • —Stools may become black
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107
Q

What are some lab valves associated with iron deficiency anemia?

A
  • Hgb < 8 gm/dL – systemic signs; < 5 gm/dL – heart failure, death
  • ↓ Hgb, Hct, serum iron, ferritin (diagnostic), transferrin; ↑ TIBC
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108
Q

What is the treatment for iron deficiency anemia?

A
  • iron supplementation (ferrous better absorbed), take w/ vitamin C because it will enhance absorption
    • Take supplements on an empty stomach, use straw if liquid iron
  • ↑ Iron in diet
  • Fix underlying disease
  • It takes 6-12 months to see change
  • caution with IV iron dextran (anaphylaxis)
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109
Q

What is hemochromatosis?

A

An overload of iron in the body, can occur from too much iron supplementation.

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110
Q

What is pernicious anemia?

A

Anemia characterized lack of intrinsic factor that results in macrocytic (larger than normal) and normochromic (normal hemoglobin lvls) RBC’s.

111
Q

What causes Pernicious anemia?

A
  • Congenital or autoimmune deficiency of intrinsic factor that impairs absorption of Vitamin B12 → ↑ abnormal RBC production
  • Defective DNA synthesis caused by Vitamin B12 deficiency
    • Deficient gastric hormone needed for absorption
    • Deficient dietary intake
112
Q

What are the clinical manifestations of pernicious anemia?

A
  • Infections
  • weakness
  • fatigue
  • distal paresthesias/distal neuropathies (stocking-glove – irreversible nerve demyelination)
  • ataxia
  • sallow skin
  • memory loss
  • beefy/sore red tongue
  • loss of appetite, hepatomegaly
  • ↓ Hgb, ↓ Hct, ↓ retic, ↑ ferritin
  • serum B12 < 100 pg/mL, achlorhydria (gastric biopsy)
113
Q

What are the treatment options for pernicious anemia?

A
  • Rx: IM or s. q. Vitamin B12 (long-term)
  • Increase amount of animal produces eaten (they contain vitamin b12)
  • Follow up with reticulocyte count
114
Q

What is Leukocytosis?

A
  • ↑ WBCs
    • Occurs from as a normal inflammatory/infection response
      • A significant cause of persistent leukocytosis is hematologic maligancy – Leukemia
    • ↑ eosinophils with asthma, allergic response
    • ↑ blasts (acute leukemia)
  • Left shift
    • ↑ immature neutrophils (bands)
115
Q

What is Leukopenia?

A
  • ↓ WBCs (any or all) < 2000
    • Due to: Prolonged stress, viral infection, bone marrow disease, radiation, chemotherapy, SLE, thyroid disease, Cushing syndrome, drugs (e.g., NSAID, antibiotics, etc.)
    • This ↑ infection risk
  • Generally defined as “immunocompromised” when neutrophil count is < 500 / mm3
116
Q

What are the normal platelet count lab values?

A
  • WNL = 140,000 – 340,000/mm3
  • Thrombocytopenia = < 100,000/mm3
  • Spontaneous bleeding = < 20,000
  • ↑ thrombosis – thrombocytosis
117
Q

What is Thrombocytopenia?

A

↓ in # of circulating platelets

118
Q

What causes thrombocytopenia?

A

1. Decreased platelet production in bone marrow:

  • Bone marrow deficiency
  • Drugs (Aspirin, chemo, alcohol, sulfa, Methotrexate)
  • Toxins / Infectious agents
  • Malignancy (Leukemias)

2. Increased platelet consumption:

  • Disseminated intravascular coagulation (DIC)

3. Increased platelet destruction:

  • Due to antibodies
  • Immune (Idiopathic) thrombocytopenic purpura (ITP)- most common cause
  • Lupus Erythematosus
  • Malignant Lymphoma
  • Chronic Lymphocytic Leukemia –CLL
  • Medications- Heparin-induced –HIT

4. Due to infections:

  • Bacteremia
  • Post viral infection
  • Sequestration of platelet in an enlarged spleen
119
Q

What are some clinical manifestations of Thrombocytopenia?

A
  • ↑bleeding risk
  • Petechiae (small, sq bleeds)
  • Purpura (large, sq bleeds)
  • Ecchymosis (bruising)
120
Q

What is purpura?

A

The appearance of red or purple discolorations on the skin that do not blanch on applying pressure.

  • They are caused by bleeding underneath the skin usually secondary to vasculitis or dietary deficiency of vitamin C (scurvy).
  • Purpura measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.[2]
121
Q

How would you care for a patient with thrombocytopenia?

A
  • —Care is based on the etiology
  • If it is an immunologic cause, such as— Immune Thrombocytopenic Purpura (ITP), the patient will:
    • receive Corticosteroids
    • have a Splenectomy (surgery)
    • Intravenous Immunoglobulin -Immunosuppressives (Rituxan, Cyclosporine)
    • have a Platelet transfusion
  • If it is drug induced, such as with heparin-inducted thrombocytopenia, then:
    • Discontinue heparin, don’t give warfarin
    • Give Protamine sulfate to treat heparin overdose
  • If it is a physiologic cause then give platlet transfusions (but they generally are not that sucessful)
122
Q

What are some nursing diagnoses for patients with thrmbocytopenia?

A
  • —Risk for bleeding
  • —Risk for injury
  • Knowledge deficit —
  • Ineffective tissue perfusion
123
Q

What are some nursing interventions for a patient with thrombocytopenia?

A

—Health promotion

  • Avoidance of excessive use of OTC drugs (ASA)
  • Seek medical care for bleeding tendencies
  • Monitor pts receiving chemo

— Bleeding precautions

 - Avoid IM’s, indwelling catheters, enemas, suctioning, shaving razors.  **Use stool softeners, soft-bristled toothbrushes, no flossing**.  Apply pressure to puncture sites.  **Pad rails….prevent falls.**
124
Q

What is thrombocytosis?

A

An —Abnormal increase in number of circulating platelets (> 600,000)

125
Q

What are the clinical manifestations and complications of thrombocytosis?

A

Manifestations

  • Bruising or bleeding from various sites (nose, mouth, gums, stomach and intestinal tract)
  • Headache
  • TIA & diplopia

Complications

  • Stroke
  • Heart attack
  • clot in the blood vessels
126
Q

What are some treatments for thrombocytosis?

A
  • —Treat the underlying cause
  • —Low dose Aspirin
  • Hydroxyurea or Anagrelide - to suppress platelet production by the bone marrow
  • Interferon-alfa-2b –lower platelet counts
  • —Severe life-threatening thrombocytosis - platelet pheresis to lower the platelet count to safer levels
127
Q

What is Hemophilia?

A

Hereditary coagulation disorders (defective or deficient coagulation factor) that is sexually transmitted

128
Q

What is Leukemia?

A
  • Cancer of one WBC type in bone marrow due to ↑ proliferation at expense of other cell types
  • Malignant Leukemic cells predominate in bone marrow → ↓ circulating levels of non-leukemic cells → generalized clinical manifestations
129
Q

What causes Leukemia?

A
  • Genetic predisposition + mutating event
  • radiation exposure
  • chemotherapy
  • pesticide exposure
  • PMH of hematopoiesis disease (e.g., Hodgkin lymphoma, multiple myeloma, polycythemia vera, sideroblastic anemia)
  • Philadelphia chromosome
130
Q

What are the clinical manifestations of Leukemia?

A
  • Manifestations are Fewer with chronic leukemia until advanced
  • Pallor, fatigue (anemia), Pancytopenia
  • Frequent infections (↓ WBC)
  • Bleeding/bruising (thrombocytopenia)
  • Progressive bone pain (pressure of cell accumulation in bone marrow)
  • Weight loss
  • Lymphadenopathy, hepatomegaly, splenomegaly (leukemic cell infiltration of lymphoid organs)
131
Q

How would you care for a person with leukemia?

A

Management:

  • —Goal is to attain remission
  • —Prognosis is directly related to ability to maintain a remission
  • —Chemotherapeutic treatment —Radiation therapy
  • —Stem Cell transplantation

Precautions:

  • Strict hand washing
  • Single patient room & visitor restrictions to protect pt from others who may have conditions that may increase the probability of transmitting infections
132
Q

What are some nursing diagnoses for a patient with leukemia?

A
  • —Risk for infection
  • —Imbalanced nutrition
  • —Fatigue and activity intolerance
  • —Self-care deficit
  • —Deficient knowledge
  • —Ineffective Protection
  • —Impaired mucous membrane
  • —Anxiety —Disturbed body image —Potential for spiritual distress
133
Q

What are some nursing interventions for a patient with leukemia?

A
  • —Bleeding precautions if platelets are low
  • —Teachings (meds, disease process, complications)
  • —Mucositis —– Frequent, gentle oral hygiene —Soft toothbrush, or if counts are low, sponge-tipped applicators
  • Improving Nutrition:
    • —Oral care before and after meals —
    • Administer analgesics before meals
    • —Appropriate treatment of nausea (induced from chemo)
134
Q

What are the 2 classes of Leukemias?

A
  1. Lymphocytic – immature lymphocytes
  2. Myelocytic – pluripotent myeloid stem cells
135
Q

What are the 4 types of leukemias?

A
  1. Acute Lymphocytic Leukemia (ALL)
  2. Chronic Lymphocytic Leukemia (CLL)
  3. Acute Myelocytic Leukemia (AML)
  4. Chronic Myelocytic Leukemia (CML)
136
Q

What are some characteristics of Acute Lymphocytic Leukemia?

A
  • Progression = Rapid
  • Adult vs Child = Most common in children
  • Survival rate = 91%
  • Primary cell involved = Greater than 30% lymphoblasts and B cells
137
Q

What are some characteristics of Chronic Lymphocytic Leukemia?

A
  • Progression = slow
  • Adult vs Child = Most common in adults
  • Survival rate = 85%
  • Primary cell involved = Monoclonal B
138
Q

What are some characteristics of Acute Myelocytic Leukemia?

A
  • Progression = rapid
  • Adult vs Child = Most common adult form
  • Survival rate = 24%
  • Primary cell involved = Precursor myeloid cells
139
Q

What are some characteristics of Chronic Myelocytic Leukemia?

A
  • Progression = Slow
  • Adult vs Child = Found mostly in adults
  • Survival rate = NO CURE
  • Primary cell involved = Neutrophilic or eosinophilic or clonal; arise from a hematopoietic stem cell
140
Q

What is a Hodgkin Lymphoma?

A
  • Cancer of single group of lymphoid tissue (localized nodal involvement)
  • Clonal disorder of B cell, T cell, or monocyte
141
Q

What are some characteristics of Hodgkin Lymphomas?

A
  • Nodal involvement = Localized to single axial group of nodes (e.g., cervical, mediastinal, para-aortic)
  • Extranodal involvement = Rare
  • Spread = Orderly spread
  • Fever, night sweats, weight loss = common
  • Reed Sternberg cells = Present
  • Extent of disease = Often localized
  • Common in young adults & 60s
  • Reed-Sternberg cells – large, atypical cells (diagnosis is based on the presence of these cells
142
Q

What causes Hodgkin Lymphomas?

A
  • unknown – evidence of ↓ T-cell-mediated immunity during disease & remission
  • May be Genetic
  • May be due to the Herpes virus, Epstein-Barr virus
  • —Seen commonly in patients receiving immunosuppressive therapy (renal transplant)
143
Q

What are the clinical manifestations of Hodgkin Lymphomas?

A
  • Painless lymph node enlargement above level of diaphragm:
    • cervical, supraclavicular, mediastinal, axiliary, or inguinal lymph nodes
    • Nodes remain moveable and nontender
  • Cough, dyspnea, chest discomfort (mediastinal masses)
  • Night fever & sweats with pruritis (B symptoms)
  • Weight loss in advanced stages
144
Q

What is the treatment for Hodgkin Lymphomas?

A

—Treatment depends on the nature and extent of the disease:

  • Multidrug chemotherapy (ABVD—adria, bleo, vinblastine, dacarbazine)
  • Radiation therapy
  • Bone marrow transplant
  • Targeted biological (e.g., receptor-specific antibodies) therapy
145
Q

How would you care for a patient with Hodgkin’s lympoma?

A
  • Manage their pain
  • —Physical, psychosocial, spiritual needs must be addressed
  • —Long-term evaluation of patient —
    • Consequences may not be apparent for many years
    • —Decrease risk of 2nd cancers (smoking, alcohol, exposure to environmental carcinogens and excessive sunlight
146
Q

What is Non-Hodgkin Lymphoma?

A

Diffuse cancer of lymph tissue primarily B cell lymphocyte (involves multiple peripheral nodes).

It is a progressive clonal expansion of B cells, T cells, or NK cells

147
Q

What causes non-hodgikin lymphomas?

A
  • Cause unknown – viral?
  • There is damage to proto-oncogenes or tumor-suppressor genes resulting in cell immortalization which results in malignant cells.
  • Lymphomas most likely originate from mutations in cellular genes.
148
Q

What ares some characteristics of non-hodgikin lymphomas?

A
  • More common in elderly
  • Poorer prognosis than Hodgkin, but variable
149
Q

What are the clinical manifestations of Non-Hodgkin lymphomas?

A
  • Nodal involvement = Multiple peripheral nodes
  • Extranodal involvement = Common
  • Spread = Noncontiguous
  • Fever, night sweats, weight loss = Uncommon
  • Reed Sternberg cells = Not Present
  • Extent of disease = Rarely localized
  • Painless lymphadenopathy, splenomegaly
  • Back & neck pain
150
Q

How would you manage a patient with Non-hodgkin’s lymphoma?

A
  • —Treatment is determined by type & stage of the disease (Interferon, chemotherapy and/or radiation therapy)
  • —More aggressive lymphomas are more responsive to treatment
  • —Patients are Asymptomatic with advanced disease
151
Q

What is multiple myeloma?

A
  • Clonal plasma cell cancer disorder with slow proliferation of B lymphocyte & plasma cells
  • They disperse throughout circulation & deposit in bones usually resulting in destruction of the bone.
152
Q

What causes multiple myeloma?

A
  • Chromosomal translocations (breakpoints) in plasma cells is responsible for development of myeloma in most individuals.
  • A progression of further secondary genetic alterations causes development to an aggressive multiple myeloma
153
Q

What are some characteristics of multiple myeloma?

A
  • Plasma cells produce abnormally large amounts of one class of immunoglobulin, usually IgG (which is defective). (Bence-Jones proteins)
  • Myeloma cells in the bone marrow secrete hepatocyte growth factor and parathyroid homrone-related peptide that stimulate osteoclasts to reabsorb bone, resulting in bone lesions and hyper calcemia.
  • This is because the malignant plasma cells multiply and crowd out normal blood cells, and it is this that ultimately causes the breakdown of bone.
  • High mortality – No cure
154
Q

What are the clinical manifestations of multiple myelomas?

A
  • Bone pain & fractures (from the break down of bone)
  • Weight loss, fatigue
  • Neurologic impairment from hypercalcemia (bone breakdown)
  • Proteinuria (Bence-Jones proteins from excessive defective IgG’s being produced)
  • Infection from ↓ B-cell function
  • Hypercalcemia
155
Q

What is Disseminated Intravascular Coagulopathy (DIC)?

A
  • An aquired clinical syndrome that prevents a person’s blood from clotting normally.
  • It characterized by the widespread activation of coagulation, resulting in fibrin clots in medium and small vessels throughout the body.
  • This can result in consumption of platlets and clotting factors leading to severe bleeding
156
Q

What causes Disseminated Intravascular Coagulopathy (DIC)?

A
  • Platelet consumption → hemorrhage
  • Complication of shock, sepsis, major burn, cancer
  • Hypoxemia & acidemia → damaged vascular endothelial cells → extensive activation of platelets & intrinsic coagulation pathway → vascular microthrombi
  • Tissue damage → ↑ thromboplastin → activates extrinsic coagulation pathway → extensive clotting → ↑ fibrinolysis → release of anticoagulation enzymes into circulation → vicious cycle of simultaneous clotting & bleeding
157
Q

What are the clinical manifestations of Disseminated Intravascular Coagulation (DIC)?

A
  • Highly variable: acute vs. chronic (covert)
  • Hemorrhage, hypotension, shock, hematuria
  • ↓ LOC, neurologic deficits
  • Cyanosis, respiratory distress, ischemia, multiple organ failure
  • ↓ platelets, ↑ FDP, ↓ fibrinogen, prolonged clotting, ↓ levels of anticoagulant measures
  • High mortality with acute
158
Q

What are the treatment options for Disseminated Intravascular Coagulation (DIC)?

A
  • Treat underlying cause
  • Give heparin, if no CNS bleeding (prevent conversion of fibrinogen → fibrin)
    • Selected indications only
    • Controversial
  • Low-molecular-weight heparin (↓ new thrombi formation)
  • Volume replacement (to replace loss of blood)
  • Fresh frozen plasma (FFP), cryoprecipitate, & platelet transfusions
  • Antithrombin drugs (activated protein C)?
    • Inhibit adhesion of neutrophils to endothelium
    • Degrade activated clotting factors (e.g., APC)
159
Q

What is sickle cell disease?

A

An inherited incurable disease that leads causes abnormal an abnormal form of hemoglobin in the RBC which causes the RBC to stiffen and elongate

160
Q

What causes sickle cell disease?

A
  • —Blood loss
  • Hypoxia or deoxygenation caused by:
    • —Viral or bacterial infection (most common precipitating factor)
    • —High altitude
  • —Emotional/physical stress —
  • Surgery
161
Q

What are some clinical manifestations of sickle cell disease?

A
  • Typical patient is anemia, and is asymptomatic except during sickling episodes
  • —Symptoms result from chronic hemolysis or thrombosis & can be —
    • pain and swelling —
    • Pallor of mucous membranes (skin ashen/grayish) —
    • Hemolytic jaundice & prone to gall stones (cholelithiasis) —
    • Fatigue & ↓ exercise tolerance
    • Dehydration
    • Vasoocclusion - Hallmark symptom
162
Q

What is the primary symptom of sickle cell disease?

A

—Pain as a result of tissue ischemia (back, chest, abdomen & extremities), stroke, priapism (painful, prolonged erection)

163
Q

How would you manage patients with sickle cell disease?

A
  • —No specific treatment for SCD —
  • Alleviate symptoms of disease complications
  • —Minimize end-organ damage —
  • O2 for hypoxia and to control sickling
  • Manage pain with: ASA, NSAIDS, Morphine
164
Q

What would you teach a patient with sickle cell disease?

A

—Avoid high altitudes, maintain fluid intake, seek treatment for respiratory infections promptly, control pain

165
Q

What are some treatment options for sickle cell disease?

A
  • —Folic acid daily supplements —
  • Blood transfusions in crisis —
  • Hydroxyurea:Antisickling agent
  • —Arginine: Antisickling agent
  • —Peripheral Blood Stem Cell Transplant
166
Q

What are some nursing diagnosis for patients with sickel cell anemia?

A
  • Acute pain R/T tissue hypoxia
  • Knowledge deficit
  • Fluid volume deficit
  • Coping, ineffective/ Powerlessness
  • Risk for Infection
  • Activity intolerance
  • Tissue perfusion, altered
  • Gas exchange, impaired
167
Q

What must you do before administering blood?

A
  • —Review patient history
  • —Perform patient teaching and obtain informed consent
  • Equipment: IV (use at least a 20-gauge needle (18 or 16G for rapid transfusion) and appropriate tubing, normal saline
  • ALWAYS use special blood tubing (Y type for Normal Saline and the other arm for the blood product) with a special filter (microaggregate filter)
  • When Flushing - verify IV line patency before requesting blood product from blood bank
    *
168
Q

What must you do before transfusing blood?

A
  • take baseline VS before transfusion. If fever, notify MD
  • Pre-medication- (Tylenol & Benadryl)
  • Begin blood transfusion slowly (2cc/min) and stay in room for the 1st 15 minutes or 50 cc of blood transfusion (reactions may occur at this time). Blood Transfusion should not take > 4 hours. Platelets can be transfused over 15 to 30 minutes
  • Monitor vital signs –after 1st 15 minutes, retake VS and follow hospital policy
  • —Cross-check- Need 2 licensed nurses to check patient ID and blood product ID data including expiration date
169
Q

What is a cancer?

A

A malignant disease characterized by:

  • A series of cellular, genetic aberrations that cause abnormal cell proliferation.
  • Unchecked local growth and invasion of surrounding tissue.
170
Q

What are the different grades of cancers?

A
  • Grade 0 - normal tissue
  • Grade 1 - well-differentiated
  • Grade 2 - moderately differentiated
  • Grade 3 - poorly differentiated
  • Grade 4 - very anaplastic
171
Q

What are the different stages of cancer?

A
  1. Stage 0 - in situ
  2. Stage I - local
  3. Stage II - limited local spread
  4. Stage III - extensive local/regional spread
  5. Stage IV - metastasis
172
Q

Why would you want to start screening certain people for cancer early?

A
  • To find the cancer at an early stage when it is less likely to have spread and is easier to treat.
  • Early detection can:
    • identify cancers at a treatable stage
    • decrease treatment time
    • improve quality of life improve chances of survival
173
Q

What is screening and why do patients get screened?

A
  • The early detection of disease by use of tests, examinations, or other procedures prior to the development of symptoms
  • Assumptions:
    • early detection=favorable prognosis
    • cost effective
    • widely available
    • acceptable to population
    • adequate sensitivity, specificity
174
Q

What are 7 warning singnals for cancer?

A
  1. Change in bowel or bladder
  2. Unusual bleeding or discharge
  3. Sore that does not heal
  4. Obvious change in wart or mole
  5. Thickening or lump
  6. Nagging cough or hoarseness
  7. Indigestion or difficulty swallowing
175
Q

When should women get a clinical breast exam?

A
  • Women in 20s-30s, recommended that CBE be part of their periodic health exam at least every 3 years.
  • Asymptomatic women > 40 – receive CBE annually
176
Q

Who and when should people get a mammogram?

A
  • Who: Women aged > 40 years
  • Begin annual mammography at age 40 years
177
Q

Who and when should people get a Pap Smear?

A
  • Who: Women aged > 18 years
  • Begin approximately 3 years after a woman begins having vaginal intercourse, but no later than 21 years of age
178
Q

Who and when and how should people begin checking for colorectal cancer?

A

Who & when: Men and women aged 50

What:

  • A fecal occult blood test (FOBT) every year
  • A flexible sigmoidoscopy (FSIG) every five years
  • Annual fecal occult blood test and flexible sigmoidoscopy every five years
  • A double-contrast barium enema every five years
  • A colonoscopy every ten years
179
Q

When should men begin screening for prostate cancer?

A
  • Begin testing at age 45
  • African-American men are at high risk for this patient
180
Q

What are the 3 goals for cancer treatment?

A
  1. Cure - eradication of cancer cells in the body.
  2. Control - containment of the growth of cancer cells without complete eradication.
  3. Palliation - comfort and relief of symptoms when the possibility of cure is hopeless.
181
Q

What are some common nursing diagnoses for post-op cancer patients?

A
  • Anxiety
  • Fear
  • Denial
  • Knowledge deficit
  • Decisional conflict
  • Role strain
182
Q

Describe surgical intervention for cancer

A
  • Oldest method of cancer treatment
  • Best chance for cure
  • 55% of all cancer pts
  • Often the initial form of cancer treatment
  • Aims: removal of all tumor with negative margins (surgen will keep removing tissue until there isn’t anymore) – removal of surrounding tissues/organs
183
Q

What are some patient risk factors for infections postoperatively?

A
  • Increased age
  • Cancer
  • Obesity
  • Diabetes
  • Immune suppressed
  • Malnutrition
184
Q

What are some surgical risk factors with infections postoperatively?

A
  • Emergent surgery
  • Surgery lasting >2 hours
  • Multiple procedures
  • Abdominal pelvic surgery
185
Q

What are some Postoperative diagnoses (immediate period)?

A
  • Pain
  • Altered nutrition
  • Altered mobility
  • Altered fluid volume
  • Altered urinary/bowel elimination
  • Altered protection
  • High risk for infection
186
Q

What are some nursing diagnosis with Lymphedema and how can you treat this?

A
  • Risk for injury RT increased risk of infection & lymphedema 2nd axillary node dissection
  • Treat it with:
    • Exercise
    • Elevation
    • Compression
    • Prevention
    • S/S of infection
    • Wearing a compression sleeve
187
Q

Describe arm care after an Axillary Lymph Node Dissection

A
  • Avoid burns while cooking or smoking
  • Avoid sunburns
  • Have all injections, vaccinations, blood samples, & blood pressure tests done on the unaffected arm when possible
  • Use an electric razor with a narrow head for underarm shaving to reduce the risk of nicks or scratches
  • Carry heavy packages or handbags with the other arm
  • Wash cuts promptly, treat them with antibacterial medication, & cover with a sterile dressing; check often for redness, soreness or other signs of infection
188
Q

Describe Postmastectomy Exercise

A
  • Begins after postoperative period (Day 1 & 2)
  • Encourage patient to focus on the elbow, wrist, & hand of the affected side.
  • Have them:
    • active elbow flexion & extension
    • Gently squeezes a soft rubber ball
    • Does deep breathing to facilitate lymph flow
    • Shoulder shrugs & active ROM, including flexion & abduction – 2nd day postop
    • Use unaffected arm
  • Do not abduct the arm, raise the arm or elbow above the shoulder height until the drains are removed.
  • Exercises are important to prevent muscle shortening
189
Q

What is lymphedema?

A

Is the accumulation of excessive proteins, edema, chronic inflammation, & fibrosis secondary to the impairment of the lymph vessels.

190
Q

What are some goals in treating lymphedema?

A
  • Reduction in volume of the edema
  • Restoration of ROM
  • Assistance with restoring the normal external appearance
  • Reduce pain & coping skills
  • Improve QOL
  • Enhance person’s self-esteem
191
Q

How would you care for a laryngectomy preoperative care patient?

A
  • Assess oral cavity
  • Assess nutritional status
  • Assess ETOH use (CAGE)
  • May need to provide nutritional supplementation prior to surgery
  • May need dental work before surgery (to prevent infection)
  • WATCH FOR ASPIRATION – GIVE SUCTIONING & MANAGE SECRETIONS
  • Prevent infection by checking dressing and wound!
192
Q

What are some Swallowing Technique after a Partial Laryngectomy?

A
  • Begin with soft or semi soft foods.
  • Stay with a nurse or swallowing specialist during meals until you have mastered the technique of swallowing without choking.
  • Tell patient to:
    1. Take a deep breath
    2. Bear down to close the vocal cords
    3. Place food into your mouth
    4. Swallow
    5. Cough to rid the closed cord of accumulated food particles
    6. Swallow
    7. Cough Breath
193
Q

How would you care for a patient with a total laryngectomy posoperatively?

A

Alteration in airway

  • Laryngectomy tube
  • Humidity
  • HOB 45 degrees, DO NOT LIE FLAT !
  • Suction

Alterations in nutrition

  • Enteral feeding for 7-10 days

Impaired Communication

  • Writing
  • Artificial larynx
  • Esophageal speech

–Day 5 – will begin to cork the tracheostomy tube to begin the weaning process

194
Q

What would you teach a patient with a total laryngectomy involving home care?

A
  • not to lift objects heavier than 10 lbs for 4 months after surgery.
  • Avoid water sports –can’t protect airway
  • Take special precautions when gardening, etc not to get dust, dirt into stoma
  • Management of drain
  • Stoma bib
  • Takes up to 3 months to fully recover from surgery
195
Q

What is the purpose of chemotherapy?

A

To Administer the largest dose possible,
to kill the largest number of cancer cells, while inducing reversible and tolerable “therapeutic index”

196
Q

What are the side effects of chemotherapy?

A
  • Kills all cells which are dividing rapidly
  • Mucous membranes, bone marrow, and hair follicles most acutely affected
  • Stomatitis, esophagitis, enteritis
  • Neutropenia
  • Alopecia – hair loss
  • Nausea & vomiting (also chemically-mediated)
  • Skin changes , sperm
  • Increased potential for infection
197
Q

What does the absolute neutrophil count reflect?

A
  • It reflects the patients risk for infection
  • Chemotherapy is frequently held if the WBC’s are between 1000-3000/mm3 or if the ANC is below 1500 cells/mm3.
  • Not significant ANC 1500-2000
  • Minimal ANC 1000-1500
  • Moderate ANC 500-1000
  • Severe ANC < 500
198
Q

What is neutropenia and how can this affect a patient?

A

Low levels of neutrophils, < 500 -1000.

A neutropenic patient can not mount an adequate inflammatory response to an infecting organism.

199
Q

What are the signs of infection for an immunocompromised patient?

A
  • NO signs of heat, swelling, redness, exudate formation
  • Fever is the only indicator of an infection
  • Progression from localized infection to life-threatening sepsis is so rapid
    • fatality rate is 18% to 40% in the first 48 hours.
200
Q

What are the most frequent sites of infection for an immunocompromised patient?

A
  • Mucous membranes
  • Lungs
  • Skin
  • Venipuncture sites
  • Catheter sites
  • Perineal area
  • Perirectal area
201
Q

What would you assess in a patient who has a potential for a systemic infection in general?

A
  • Check pt. history
  • ANC
  • Vital signs
  • Comprehensive physical exam
  • Skin integrity
  • Assess for redness, pain, discoloration, swelling. Examine skin folds, wound sites , suspicious lesions
202
Q

What are measures the nurse can take to detect an early infection of the pulmonary system?

A
  • Check if Pt has Hx. of Dysphagia, diminished gag reflex, tobacco use, exposures.
  • RR, effort, pattern, and depth of respiration, use of accessory muscles
  • Auscultate chest
  • Check for any recent changes in pylmonary status
203
Q

What are measures the nurse can take to detect an early infection of the oral mucosa?

A
  • Check pt. hx for Chemotherapy, radiation to head/neck, tobacco, ETOH use, periodontal disease, hydration, nutritional status.
  • Assess Oral cavity - color, moisture, lesions, ulcerations, amount and character of saliva
  • Patients routine for oral hygiene
204
Q

What are measures the nurse can take to detect an early infection of the rectal mucosa?

A
  • Check pt. hx for diet, sexual practices, medications, chemotherapy, HIV status, change in bowel habits
  • Assess for erythema, ulceration, hemorrhoids, bleeding
  • Assess character, frequency of bowel movements
205
Q

What are measures the nurse can take to detect an early infection of the genitourinary system?

A
  • Check pt hx for Benign prostatic hypertrophy, HIV status, bladder -toxic chemotherapy, symptom of GU infection (dysurina, urinary frequency, urgency, hematuria, pruritis, vaginal/penile discharge)
  • Examine: genitilia - lesions, ulcerations, discharge
  • Assess Characteristics of urine - color, turbidity, odor
206
Q

What are measures the nurse can take to detect an early infection of the central nervous system?

A
  • Assess for Subtle changes in neurologic function can signify either the onset of an infection or progression of a malignancy.
  • Assess for Headache, fever, meningismus, personality changes, focal neurological signs, nuchal rigidity, altered mental status, seizures
207
Q

What are some nursing interventions to prevent or minimize infections?

A
  • –Vital signs including temperature for fever.
  • –Prophylactic pulmonary hygiene measures especially for B cell deficiencies
  • –Monitor CBC with differential
  • –Meticulously clean sources where bacteria live
  • –No fresh cut flowers or live plants in room
  • –Encourage regular personal hygiene (include oral care) –Protect from other persons with infections
  • –Assign only healthy HCP to care for patient
  • –Avoid injections
208
Q

When are patients at risk for bleeding and what would you teach them?

A
  • Platelet count < 100,000/mm3
  • Risk for bleeding high if < 25,000/mm3
  • Patient teaching
    • avoid aspirin, NSAIDs nprevent constipation nD/C use of razors nsoft tooth brushes abstain from sexual
  • assess their fall risk
209
Q

What can cause oral toxicity?

A
  • 2-3 X more often in hematologic malignancies; 75% BMT patients
  • Direct effect (cytotoxic) or indirect (related to myelosuppression)
  • Dose-related, common with antimetabolites & some antibiotics
  • Risk factors: elderly, pre-existing oral disease, local irritants, poor oral hygiene, myelosuppression
210
Q

How often should oral hygiene be given to chemotherapy patients?

A
  • After each meal and at HS at least
  • Lubrication of lips; saliva substitutes
  • Soft toothbrush & unwaxed floss if platelet ct ok and no lesions
  • Daily flouride if xerostomia
211
Q

Describe the impact of chemotherapy induced Nausea and Vomiting

A
  • Experienced by over 50% of all patients receiving chemotherapy
  • Decreased Quality Of Life
    • lmost feared side effect
    • worsens throughout the treatment
    • can lead to non-compliance
  • Physiological
    • ldehydration
    • fluid and electrolyte imbalance
    • esophageal tears
212
Q

What factors influence the amount of N/V experienced while on chemotherapy?

A
  • Age
  • Previous emetic control
  • Sex
  • Course number
  • History of motion sickness
  • History heavy alcohol use - will cause less N/V
  • Anxiety - will cause more
213
Q

What is fatigue?

A
  • extreme tiredness or weariness resulting from physical or mental activity that is Not relieved by rest
  • Causative factors in absence of anemia unknown; most often with cytokines
  • DECREASES Quality of life
  • Interventions:
    • –energy conservation
    • –setting priorities
    • –nutrition,
    • physical activity within limits
214
Q

What does the HIV virus target?

A

the HIV virus targets cells with CD4 receptors, which are expressed on the surface of T lymphocytes, monocytes dendritic cells & brain microglia.

215
Q

What are some common ways HIV is transmitted?

A
  • Having sex (anal, vaginal, or oral) with someone who is HIV +
  • Sharing needles or injection equipment with a user who is HIV +
  • HIV+ women to their babies during pregnancy, during birth or through breastfeeding
  • Occupational exposure
  • (rare) Blood transfusion/organ transplant
  • NOT through casual contact, insect bites, toilet seats
216
Q

What body fluids contain high amounts of HIV and can infect you?

A
  • Blood
  • Semen
  • Pre-seminal fluid
  • Breast milk
  • Vaginal fluids
  • Rectal (anal) mucous
  • Amniotic fluid
  • Cerebrospinal fluid
  • Synovial fluid
217
Q

What are some body fluids that don’t contain enough HIV to infect you?

A
  • Nasal fluid
  • saliva
  • sweat
  • tears
  • feces
  • urine
  • vomit
218
Q

What are some Risk Factors for HIV Transmission?

A
  • Viral load
  • Lack of circumcision
  • Sexual risk
  • Presence of ulcerative sexually transmitted diseases
  • Nitrate inhalant use
  • Host factors
  • Genetic factors
219
Q

What are the Universal precautions for healthcare workers?

A
  • Routinely using barriers (such as gloves and/or goggles) when anticipating contact with blood or body fluids.
  • Immediately washing hands and other skin surfaces after contact with blood or body fluids.
  • Carefully handling and disposing of sharp instruments during and after use.
220
Q

What are some diagnostic tests for HIV?

A
  • EIA (Enzyme immunoassay)(aka ELISA, enzyme-linked immunosorbent assay)
  • Western blot
  • Orasure
  • Home Access HIV-1 Test System
  • Oraquick Rapid HIV-1 Antibody Test
221
Q

What are the stages of HIV infection?

A
  1. Viral transmission
  2. Primary infection (acute HIV infection or acute seroconversion syndrome)
  3. HIV asymptomatic (clinical latent period)
  4. HIV symptomatic (AIDS-related complex)
  5. AIDS (CD4 count less than 200)
  6. Advanced HIV infection (CD4 count less than 50)
222
Q

What are some characteristics of primary HIV infection and what are some symptoms experienced?

A

Characteristics:

  • lack of HIV antibodies
  • Period of rapid viral replication and dissemination through the body
  • Viral set point: balance between amount of HIV and the immune response- steady state infection

​Symptoms:

  • Acute retroviral syndrome: fever (38-40C), lymphadenopathy, sore throat, rash, myalgia/arthralgia, & headache plus mucocutaneous ulcers & prolonged duration suggestive of HIV
223
Q

What are some characteristics of Asymptomatic HIV infection?

A

Characteristics:

  • More than 500 CD4+ T lymphpocytes/mm3
  • Upon reaching the viral set point, chronic asymptomatic state begins
  • Body has sufficient immune response to defend against pathogens
  • **Usually 8-10 years before major complication **
224
Q

What are some characteristics of symptomatic HIV infection?

A

Characteristics:

  • 200–499 CD4+ lymphocytes/mm3
  • CD4 T cells gradually fall.
  • The patient develops symptoms or conditions related to the HIV infection, which are not classified as category C conditions
  • Patients who are once treated for a category B condition are considered category B
  • Category B conditions include: candidiasis (oropharyngeal or vulvovaginal), herpes zoster, oral hairy leukoplakia, ITP, PID, peripheral neuropathy
225
Q

What are CDC category B conditions?

A

conditions caused by the HIV infection or a defect in cellular immunity OR considered to have a clinical course or require management that is complicated by HIV infection

226
Q

What are some characteristics of AIDS?

A
  • CDC category C
  • Less than 200 CD4+ lymphocytes/mm3
  • As levels drop below 100 cell/mm3 the immune system is significantly impaired
  • Development of listed conditions
227
Q

What are the goals of HIV therapy

A
  • Maximal & durable suppression of viral load
  • Restoration and/or preservation of immunologic function
  • Improvement of QOL
  • Reduction of HIV-related morbidity and mortality
228
Q

How would you achieve the goals of HIV therapy?

A
  • Maximize adherence to the antiretroviral regimen
  • Rational sequencing of drugs
  • Preservation of future treatment options
  • Use of resistance testing in selected clinical settings.
229
Q

What are some common side effects for Nonnucleoside reverse transcriptase inhibitors (NNRTIs)?

A
  • Rash
  • Erythema multiforme
  • Liver toxicity
  • Headache
230
Q

What are some common side effects for Neucleoside Reverese Transcriptase Inhibitors (NRTIs)?

A
  • Lipodystrophy especially fat atrophy
  • Peripheral neuropathy with ddI, d4T,
  • Life threatening (rare) lactic acidosis with hepatic steatosis
231
Q

What are some common side effects for protease inhibitors?

A
  • Hyperglycemia
  • Hyperlipidemia
  • Lipodystrophy
  • GI- diarrhea, nausea, abdominal pain, dyspepsia
  • Serious liver problems possible
  • Skin rash
  • Fever
232
Q

What are some respiratory clinical manifestations of HIV / AIDS?

A
  • Pneumocystic carini pneumonia (PCP):
    • Most common infection
    • Initial symptoms may be nonspecific and may include nonproductive cough, fever chills, dyspnea, and chest pain
    • If untreated, progresses to pulmonary impairment and respiratory failure

Treatment: TMP-SMZ or pentamidine, prophylactic TMP-SMZ

  • Mycobacterium avium complex (MAC)
  • Tuberculosis
    • ​Without prophylactic treatment, 80% of all people infected with TB will develop PCP
233
Q

What are some GI clinical manifestations of HIV / AIDS?

A
  • Loss of appetite
  • Nausea & vomiting
  • Oral candidiasis
    • May progress to esophagus and stomach if untreated
    • Treatment with Mycelex troches or nystatin, ketoconazole
  • Diarrhea related to HIV infection or enteric pathogens
    • Octretide acetate for severe chronic diarrhea
  • ​Wasting syndrome
234
Q

What is wasting syndrome?

A
  • 10% weight loss and chronic diarrhea or chronic weakness and fever with absence of other cause
  • Protein energy malnutrition
  • Anorexia, diarrhea, GI malabsorption, and lack of nutrition may contribute
235
Q

What are some oncologic clinical manifestations of HIV/AIDS?

A
  • Kaposi’s sarcoma
    • Cutaneous lesions, but may involve multiple organ systems
    • Lesions cause discomfort, disfigurement, ulceration, and potential for infection
  • B-cell lymphomas
  • Invasive cervical cancer
236
Q

What are some neurologic manifestations of HIV/AIDS?

A
  • HIV encephalopathy
  • Progressive cognitive, behavioral, and motor decline
  • Probably directly related to the HIV infection
  • Cryptococcus neoformans
  • Peripheral neuropathy
  • Other neurologic disorders
  • Depression!!
237
Q

What would you assess in a patient with HIV/AIDS?

A
  • Assess physical and psychosocial status - ID potential risk factors, including hx risky sexual behavior or IV/injection drug use
  • Identify potential risk factors - IV drug abuse, risky sexual practices
  • Immune system function
  • Nutritional status - obtain diet hx, ID factors that may interfere with oral intake- anorexia, nausea, vomiting, oral pain, difficulty swallowing.
  • **Skin integrity - **membranes:daily inspect for breakdown, ulceration or infection. Oral cavity for redness, ulcerations, candidasis. Perianal area for excoriation or infection. Wound cultures to ID infectious organisms
  • **Respiratory status - **monitor pt for cough, sputum production (TB), SOB, orthopnea, tachypnea, chest pain. Assess breath sounds. Other modalities: CXR, ABG, pulse ox, PFTs
  • **Neurologic status - **LOC, orientation (person, place, time), memory lapses. Sensory deficits (visual changes, headache, numbness/tingling in extremities), motor involvement (gait, paresis or paralysis), seizures?
  • Fluid and electrolyte balance - examine skin & mucous membranes for turgor & dryness. Assess for decreased mental status, muscle twitching, muscle cramps, irregular pulse, N&V, shallow respirations.
  • Knowledge level - about the disease & modes of disease transmission, treatment, family & friends level as well. Support resources also ID’d
238
Q

What are some nursing diagnoses for HIV/AIDS?

A
  • Impaired skin integrity r/t immunological deficit, diarrhea
  • Grieving: individual r/t loss of physical & psychosocial well-being
  • Diarrhea r/t inflammatory bowel changes
  • Risk for infection r/t inadequate immune system
  • Fatigue r/t disease process, stress, decreased nutritional intake
  • Chronic pain r/t tissue inflammation & destruction
  • Imbalanced nutrition: less than body requirements
  • Social isolation r/t self-concept disturbance, therapeutic isolation
239
Q

What would be the nursing interventions for the nursing diagnosis: Diarrhea R/T infection, food intolerance & medications?

A
  • Assess for s/sx skin breakdown, dehydration
  • Labs: O&P x 3, chemistry, stool cultures
  • Assess bowel pattern and factors that may exacerbate diarrhea
  • Administer medications (antidiarrheals) as prescribed, may be ATC (kaopectate or Sandostatin)
  • Dietary counseling: Avoid foods that act as bowel irritants, such as raw fruits and vegetables, carbonated beverages, spicy foods, and foods of extreme temperatures
  • Small, frequent meals, calorie dense
  • Adequate fluid intake especially between meals
  • Food safety: discard expired food, wash hands, clean countertops
  • Perineal care daily & prn (see bowel incontinence car plan)
240
Q

What would be the nursing interventions for the nursing diagnosis: Imbalanced nutrition: less than body requirements R/T high metabolic needs, nausea, vomiting, diarrhea, difficulty chewing or swallowing, and anorexia

A
  • Nutritional assessment at each visit
  • Monitor food intake (I & O); calorie counts
  • Monitor weight at least weekly.

•Note labs: serum albumin, prealbumin, total protein, ferritin, transferrin, hemoglobin, hematocrit & elecgtrolytes

  • Serum albumin
  • Referral to dietician
  • Recognize that clients with chronic disease related malnutrition may need calories to maintain nutritional status
  • Provide small, frequent meals and snacks, high in protein & calories.
  • Consider offering 30ml of nutritional supplement q hour if anorexic
  • Use antiemetics if needed.
  • Provide meticulous mouth care before each meal
  • Medications that stimulate appetite

•

241
Q

What would be the nursing interventions for the nursing diagnosis: Pain R/T neuropathy, myelopathy, malignancy, or infection

A
  • Assess/perform comprehensive pain assessment (location, quality, onset/duration, temporal profile, intensity, aggravating & alleviating factors, effects on function & QOL)
  • Ask client to ID pain level that will allow performance of desired activities & achieve acceptable QOL
  • Assess for burning or tingling in the extremities, severe headaches, tenderness in lymph nodes, diagnosis of malignancies, presence of lesions.
  • Identify the source of pain.
  • Manage chronic pain using a multimodal approach; administer medications as ordered for pain relief such as anticonvulsant, local anesthetic and opioid.
  • Non-pharm measures:
  • Ensure proper body alignment/positioning.
  • Relaxation techniques
  • Back rubs
  • Distraction
  • Guided imagery
  • Watch for signs of depression
242
Q

What would be the nursing interventions for the nursing diagnosis: Altered nutrition: less than body requirements RT high metabolic needs, nausea, vomiting, diarrhea, difficulty chewing or swallowing, and anorexia

A
  • Nutritional assessment at each visit
  • Referral to dietician
  • Monitor I & O; calorie counts.
  • Provide meals & snacks with high protein and calories.
  • Provide small, frequent meals.
  • Monitor weight at least weekly.
  • Use antiemetics if needed.
  • Provide meticulous mouth care at least every 2 hr..
  • Treat OIs affecting eating.
  • Medications that stimulate appetite
  • Low fat diet, lactose free
243
Q

What is Rheumatoid arthritis and what are some nursing considerations of this disease?

A
  • Rheumatoid arthritis (RA) is a long-term disease that leads to inflammation of the synovial membranes
  • It involves symmetric joints (if one joint is inflammed, the other one will be too). Other musculoskeletal illnesses invovle isolated or unilateral joints.
  • RA pain is worse in the morning when arising.
  • RA stiffness occurs in the morning and after rest periods
  • Movement decreases pain
244
Q

What are the signs and symptoms of Rheumatoid arthritis?

A
  • Edema
  • fatiuge
  • weakness
  • anorexia,
  • Weight loss,
  • low grade fever,
  • lymphadenopathy
  • Joint problems over time:
    • Occur symmetrically
    • Alteration in the wrist
    • Ulnar drift
    • Boutonniere deformity
    • Swan-neck deformity
    • Rheumatoid nodules

Stiffness after prolonged periods of inactivity

245
Q

What is the diagnostic criteria for Rheumatoid arthritis?

A

Diagnostic criteria: (1 to 4 different symptoms for at least 6 weeks)

  1. Morning stiffness
  2. Swelling in at least 3 joints
  3. Hand joint swelling
  4. Symmetrical involvement
  5. Subcutaneous nodules
  6. Positive RF
  7. Radiographic changes (decalcification)
246
Q

What are the characteristics of Rheumatoid Arthritis?

A
  • Characteristic symmetric joint swelling with stiffness, warmth, tenderness, and pain
  • Stiffness prominent in the AM and subsides during the day
  • Duration of stiffness an indicator of disease activity; may develop permanent deformities.
247
Q

What are some medications used to treat rheumatoid arthritis?

A
  • NSAIDS + PPI
  • Methotrexate (MTX)
  • Glucocorticoids
  • Cyclooxygenase-2 (COX-2) inhibitor

​Goals: Relieve pain, increase mobility/function & maintain life as usual (family & work)

248
Q

What are some Possible Surgeries for RA?

A
  1. Arthroscopy (visualizing joint)
  2. Arthodesis (bone fusion)
  3. Arthroplasty (total joint replacement)

**Can correct deformities, improve function, ease pain & increase self-esteem **

249
Q

What is Osteoarthritis and what are some nursing implications for this disease?

A
  • Osteoarthritis (OA) is the most common joint disorder, which is due to aging and wear and tear on a joint.
  • asymetric pain is localized and is worse usually later in the day
  • Movement increases pain
    *
250
Q

What is Osteoporosis?

A

A decrease in skeletal bone mass occuring when rate of bone resorption is > than that of bone formation

251
Q

What are some risk factors w/ osteoarthritis?

A
  • age > 50
  • Family history ( eg Rheumatoid Arthritis)
  • Obesity
  • Joint abnormality
  • History of trauma
252
Q

What are some factors that can cause Osteoporosis?

A
  • age
  • Gender - Female
  • family history
  • estrogen deficiency
  • small stature
  • race – Northern European descent
  • Heavy cigarette and/or ETOH use
  • Poor diet with low Ca intake
  • Periods of immobilization
  • Use of steroids
  • Sedentary lifestyle
253
Q

What are some risks associated w/ osteoporosis?

A

The weakened bone state increases the risk for stress fractures: especially at the hip, wrist, and verebrae.

254
Q

What population is more prone to Systemic Lupus Erythematosus (SLE)?

A
  • More African-Americans- 3 times more than Caucasians
  • Usually younger women (18-45 years)
255
Q

What is Systemic Lupus Erythematosus (SLE)?

A

An autoimmune disorder in which Autoantibodies are created, ue to defect in T-suppressor cells (and NK cells are also suppressed), they circulate in blood, & deposit (usually) in kidneys, brain, or heart.

**This is both a type 2 and type 3 hypersensitvity **

256
Q

What are the manifestations of SLE?

A
  • Fever
  • Anorexia
  • Malaise
  • Weight loss
  • Butterfly rash (< 50%)
  • Discoid rash (40%)
  • Sensitivity to sunlight (photosensitivity) 40%
  • Splenomegaly
  • Fingertip lesions (raynad’s phenomena)
  • Periungal erythema
  • Splinter hemorrhages
  • Alopecia
257
Q

How would you manage a patient with SLE?

A
  • Mild symptoms: bedrest, midafternoon naps, avoidance of fatigue
  • Sun protection
  • Topical steroids for isolated skin lesions
  • NSAIDS for arthritis, arthralgias, fever
  • Hydroxycholoroquine for rashes or joint symptoms not responsive to NSAIDS
  • Glucocorticoids for life-threatening manifestations
258
Q

How would you diagnose SLE?

A

1. Serum ANA level (also elevated in RA, scleroderma, CA, TB, hepatitis) –>
ANA + 95% of patients

Antiphospholipid antibody + & arterial or venous clotting – patient will be on coumadin and INR needs to be > 3

  1. Serum C-reactive protein (CRP) & sedimentation rate (ESR) measures inflammation levels
  2. Serum complement tests measures amount of proteins in antigen-antibody reaction
  3. CXR, EKG, MRI- organ involvement
259
Q

What are the goals of care for a patient with SLE?

A
  • maintenance of skin integrity
  • promotion of healthy lifestyle
  • reduction of stress
  • maintenance of proper nutrition
  • promotion of comfort
  • increase in self-dependence
  • maintenance of well-being
260
Q

What are some medications used to treat SLE?

A

Medications:

a. Corticosteroids
b. Immunosuppressants
c. Antimalarials
d. NSAIDS
e. Meds for specific organ involvement

** proteinuria – ACE inhibitor**

** hypertension – antihypertensive agents**

261
Q

What is Scleroderma?

A

A autoimmune connective tissue disease that causes thickening & hardening of skin, blood vessels, & internal organs, and is more prominent in women (4:1 women to men)

262
Q

What are some characteristics of scleroderma?

A
  • excessive collagen deposition
  • Microvascular injury
  • changes in humoral & cellular immunity
263
Q

What are the manifestations of Scleroderma?

A

Calcium deposits beneath skin

Raynaud’s phenomenon

Esophageal motility decreased / GI problems

Sclerodactyly / swelling fingers & toes

Telangiectasia (dilation of vessels)

Sjogren’s Syndrome (salivary ducts)

Heart, kidney, lung involvement\

REMEMBER CREST

264
Q

What are some treatment options for scleroderma?

A

Primary medications:

a. Corticosteroids
b. Immunosuppressants

Nursing care:

  • skin care
  • pain management,
  • dietary changes
265
Q

What is multiple sclerosis?

A

A progressive degenerative disease that affects the myelin sheath & conduction pathway of the CNS, slowing down the .

266
Q

What does multiple sclerosis affect the most?

A

Especially affected: optic nerves, pyramidal tracts, posterior columns, brain stem nuclei, & the periventricular region of the brain?

267
Q

What are some motor assessment findings associated with multiple sclerosis?

A
  • intention tremor
  • Positive Babinski’s reflex
  • Inc. or hyperactive DTRs
  • May report tinnitus, vertigo, hearing loss
  • may have facial weakness, dysphagia
  • Lhermitte’s sign - an electrical sensation that runs down the back and into the limbs
268
Q

What are some sensory assessment findings associated with multiple sclerosis?

A
  • numbness, tingling, burning, crawling sensations.
  • Demyelination of spinal cord - may experience bowel & bladder dysfunction; dysfunction in sexuality
269
Q

What are some nursing diagnoses related to multiple sclerosis?

A
  • Impaired Physical mobility RT to muscle weakness, awkward movements, fatigue & incoordination.
  • Sensory/perceptual alterations RT visual, motor, & sensory changes
  • Body image disturbances & altered role performance RT changes caused by the disease process
  • Self care deficit RT motor deficits, weakness, spasticity or fatigue
  • Sleep pattern disturbances RT muscle spasms & pain
  • Altered nutrition: less than body requirement RT dysphagia, & inability to feed oneself
  • Pain RT sensory changes, muscles spasms
270
Q

What are some nursing interventions realted to sensory changes & safety with multiple sclerosis?

A

Sensory / perceptual:

  • Visual changes - help pt. In developing compensatory strategies
    • An eye patch that is alternated from eye to eye every few hours helps relieve diplopia
    • Peripheral vision deficits - scanning techniques by having pt. Move head from side to side.
    • Visual acuity - corrective lesions may help

Safety:

  • Avoid environmental clutter
  • avoid overexposure to heat & cold - use thermometer
  • shoes at all times.
271
Q

What are some treatment options for multiple sclerosis?

A

Acute exacerbations:

  • Steroid therapy - watch for S/E of therapy

​Long-term treatment:

  • Novantrone (chemotherapeutic agent)
  • Beta Interferon
    • Watch for depression
272
Q

What are some Drugs to reduce muscle spasticity in multiple sclerosis?

A
  • baclofen (Lioresal)
  • diazepam (Valium)
  • Dantrolene (Dantrium)
273
Q

How would you care for a multiple sclerosis patient with Impaired Urinary Elimination & Constipation?

A
  • Fluid intake at least 2000cc/hr
  • Void every three hours – may have to use intermittent catheterization
  • High-fiber, fluids - prevent constipation
274
Q

How would you care for a multiple sclerosis patient with a body image disturbance?

A
  • Maintain independence in all activities as coordination allows.
  • Encourage pt. To ventilate feelings of frustration & anger.
  • Work on strategies with family & pt. To minimize the impact of decreased mobility.

N3523 Adult and Older Adult Health Care II (9 decks)

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