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YEAR 3 > Nurs 332 Midterm 2 > Flashcards

Nurs 332 Midterm 2 Flashcards

1
Q

Electrolytes

A

Electrically charged micro-solutes required for enzyme activities, muscle contraction, and metabolism

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2
Q

Extracellular Electrolytes

A

Sodium (Na)
Chloride (Cl)
Calcium (Ca)

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3
Q

Intracellular Electrolytes

A

Potassium (K)
Magnesium (Mg)
Phosphorus/Phosphate (PO4)

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4
Q

Normal Sodium (Na) Levels

A

135-145mEq/L

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5
Q

Sodium (Na) Function

A

a) Responsible for amount of water retained or excreted
b) required for transmission of impulses across muscles/nerves (sodium pump)
c) important in acid-base balance (increase/decrease pH with bicarb)

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6
Q

What regulates Sodium (Na)

A

GFR and aldosterone

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7
Q

What is the most abundant extracellular electrolyte

A

Sodium (Na)

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8
Q

Causes of hyponatremia

A

Sweating, diuretics, lack of dietary intake, HF

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9
Q

hyponatremia

A

low sodium

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10
Q

Causes of hypernatremia

A

Na intake, dehydration, HF, SIADH (polyuria)

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11
Q

Hypernatremia

A

high sodium

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12
Q

S&S of hyponatremia

A

hypotension, confusion, headache, lethargy, seizures, decreased muscle tone, muscle twitching, tremors, vomiting, diarrhea

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13
Q

S&S of hypernatremia

A

confusion, thirst, HTN, tachycardia, restlessness, seizure, coma, hyperreflexia, muscle twitching, N/V

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14
Q

Treatment of sodium imbalance

A

Find and treat cause, monitor cerebral changes, resp status (if muscle weakness), do not increase Na levels too fast (can cause CNS irritation and pulmonary edema)

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15
Q

Normal Chloride (Cl) Levels

A

95-105mEq/L

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16
Q

Chloride (Cl) Functions

A

a) Works with sodium to regulate body fluids (osmosis)
b) follows sodium (where sodium goes, chloride goes)
c) works with Mg and Ca to maintain nerve transmission and muscle contraction and relaxation

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17
Q

Danger levels for chloride (Cl)

A

<80 and >115

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18
Q

Causes of hyperchloridemia

A

Cl gain, decreased excretion, fluid shifts

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19
Q

Causes of hypochloridemia

A

Cl loss, inadequate intake or absorption, fluid shifts

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20
Q

hyperchloridemia

A

high chloride

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21
Q

hypochloridemia

A

low chloride

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22
Q

S&S of hyperchloridemia

A

BP changes, increased HR, edema, agitation, headache, changes in LOC, nausea, weakness

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23
Q

S&S of hypochloridemia

A

BP changes, increased HR< hypotension, confusion, disorientation, muscle spasms/cramps/paralysis, bradypnea, shallow resps

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24
Q

Treatment of chloride imbalances

A

Check other lyte levels (Cl is never alone), assess vitals (BP)

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25
Q

Drugs that increase Cl

A

ammonium chloride, KCl, NaCl

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26
Q

Drugs that decrease Cl

A

RL, sodium bicarb

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27
Q

Normal Calcium (Ca) levels

A

2.3-2.8mmol/L

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28
Q

Calcium (Ca) function

A

blood coagulation, neuromuscular contraction, enzymatic activities, bone integrity.

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29
Q

Where is calcium stored

A

bone, small amounts in ECF and soft tissue

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30
Q

What is calcium (Ca) regulated by

A

Parathyroid hormone, calcitonin, and calcitrol

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31
Q

Calcium and phosphorus relationship

A

Inverse - if Ca is high, phos is low

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32
Q

Causes of hypercalcemia

A

increased absorption, calcium release from bone, increased available Ca

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33
Q

hypercalcemia

A

high calcium

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34
Q

Hypocalcemia

A

Decrease intake/absorption, decrease available Ca, increased renal excretions, Ca loss

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35
Q

hypocalcemia

A

low calcium

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36
Q

S&S of hypocalcemia

A

Muscle cramps, N/T, tetany, irritability, reduced cognitive ability, seizures, ECG changes, decreased BP, bone fractures, abnormal clotting

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37
Q

S&S of hypercalcemia

A

anorexia, cardiac dysrhythmias, constipation, PUD, lethargy, depression, fatigue, confusion, coma, pathologic bone fractures, renal stones

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38
Q

Treatment of calcium imbalances

A

Assess chvosteks and trousseaus signs, treat the cause, IV calcium chloride (Low), monitor ECG and diet.

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39
Q

Normal Potassium (K) Levels

A

3.5-5.1mEq/L

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40
Q

Potassium (K) Functions

A

Cardiac and neuromuscular function, nerve impulse conduction, and carbohydrate metabolism, maintain homeostasis in blood

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41
Q

Causes of hyperkalemia

A

increased K intake, supplements, decreased output, fluid shifts

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42
Q

Hyperkalemia

A

High potassium (K)

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43
Q

Causes of Hypokalemia

A

decreased K intake, GI loss, Urinary excretion, fluid shifts

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44
Q

Hypokalemia

A

Low potassium (K)

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45
Q

S&S of hypokalemia

A

resp arrest, N/V, diarrhea, ileus, muscle fatigue, cramps, confusion, depression, lethargy, dysrhythmias, irregular pulse, cardiac arrest

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46
Q

S&S of hyperkalemia

A

Weakness, muscle cramps, N/V, diarrhea, ABD cramps, ECG changes, metabolic acidosis

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47
Q

Danger zone of potassium (K)

A

<2.5 OR >6.5 - respiratory arrest and lethal arrhythmias

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48
Q

Treatment of hypokalemia

A

IV KCl (high risk) - oral K or KCl elixer,, treat causes

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49
Q

Treatment of hyperkalemia

A

Kayexalate (promote uptake of K into bowels and excretes in stool) , insulin (forces K into cells), furosemide, IV sodium bicarb (binds to K), Ventolin neb (Force K back into cells)

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50
Q

Normal Magnesium (Mg) Levels

A

1.3-2.5mEq/L

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51
Q

Magnesium (Mg) Function

A

Ensures sodium and potassium transport across cell membranes, protein and carb metabolism, nerve cell conduction & CNS messaging, neuromuscular activity

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52
Q

Causes of Hypermagnesemia

A

Excessive intake, increased absorption, renal retention

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53
Q

Hypermagnesemia

A

High magnesium

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54
Q

Causes of hypomegnesemia

A

Magnesium loss, inadequate intake, impaired absorption, fluid shifts

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55
Q

Hypomagnesemia

A

Low magnesium

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56
Q

S&S of hypomagnesemia

A

Life threatening cardiac arrythmias, hypotension, disorientation, anorexia, N/V, ABD distention, constipation, neuromuscular irritability and hyperactivity

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57
Q

S&S of hypermagnesemia

A

Heart blocks, hypotension, wide QRS, lethargy, decreased LOC, N/V, muscle weakness, respiratory depression (d/t muscle weakness), absent DTR

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58
Q

ECG changes for hypomagnesemia

A

Torsades, PVC, Vtach, Vfib, cardiac arrest

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59
Q

ECG changes for hypermagnesemia

A

Complete heart block, bradycardia, cardiac arrest

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60
Q

Normal Phosphorus/Phosphate (PO4) Levels

A

1.7-2.6mEq/L

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61
Q

Phosphorus/Phosphate Functions

A

Teeth and bone development, normal neuromuscular function, production of ATP. Protein, fat and carb metabolism, maintains acid-base balance

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62
Q

Causes of Hyperphosphatemia

A

PO4 gain, increased absorption or retention, fluid shifts

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63
Q

Causes of Hypophosphatemia

A

PO4 loss, inadequate intake, impaired absorption, increased excretion, fluid shifts, refeeding syndrome

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64
Q

S&S of hypophosphatemia

A

weakness, N/T, fractures, diminished myocardial function, disorientation, seizure, coma

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65
Q

S&S of hyperphosphatemia

A

Muscle cramping, weakness, tachycardia, diarrhea, nausea, ABD cramping

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66
Q

Treatment of Hypophosphatemia

A

IV NaPO4 or K2PO4, PO phosphate

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67
Q

Treatment of Hyperphosphatemia

A

Diuretics, oral antacids, vitamin D

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68
Q

Kidney Functions

A

Filtration, reabsorption, secretion and excretion, acid-base balance, maintain fluid & electrolyte balance, remove metabolic waste and toxins from body, immunity, regulates BP and release renin, produces active form of vitamin D

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69
Q

Blood Urea Nitrogen normal levels

A

2.9-8.2mmol/L

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70
Q

Blood Urea Nitrogen (BUN

A

Reflects GFR and urine concentrating capactiy, increases as GFR decreases (hydration status, level of catabolism, protein intake, and GI bleed), BUN is reabsorbed back into blood

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71
Q

Creatinine normal level

A

50-110mmol/L

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72
Q

Creatinine

A

End-product of muscle metabolism, released into blood at constant rate, eliminated at a rate r/t renal function, NOT reabsorbed back into blood

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73
Q

What is the most reliable measure of renal health

A

Creatinine

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74
Q

Azotemia

A

Poison (waste products) in the blood

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75
Q

Acute Kidney Injury (AKI)

A

Abrupt decrease in kidney function (can’t regulate fluid & electrolytes, rapid decrease in urine output, elevated BUN and/or creatinine = decreased GFR)

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76
Q

Pre-renal injury

A

Decrease in renal blood flow (inadequate perfusion)
30-60%

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77
Q

Intra-renal injury

A

Something that damages the structures of the kidney (infection, drug toxicity)
20-40%

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78
Q

Post-renal injury

A

Obstruction to urine outflow (kidney stone, prostate cancer)
1-10%

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79
Q

RIFLE AKI criteria

A

RISK (50% increase sCr)
Injury (100% increase sCr)
Failure (150% increase sCr) or anuria for > 24 hours
Loss (>4wks)
End-stage (permanent loss)

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80
Q

Acute tubular necrosis (ATN)

A

Destruction of renal tubular epithelial cells from ischemia or sepsis

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81
Q

Nephrotoxic drugs

A

ACEs/ARBs, NSAIDs, Chemo, CT contrast, Antibiotics

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82
Q

Rhabdomyolysis

A

Massive breakdown of skeletal muscle (trauma) - release of myglobin (plugs glomeruli and damages lining in tubules)

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83
Q

Risk factors for kidney injury

A

HTN, trauma, DM, nephrotoxic agents, exposure to heavy metals or organic solvents, recent hypotensive episode, tumor or vascular obstruction, infection/sepsis, age

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84
Q

S&S of kidney injury

A

Urine output change, pulmonary edema, metabolic acidosis, K excess, Na imbalance, Ca deficit, PO4 excess, anemia, increased creatinine and urea, headache, confusion, irritability, seizure, asterixis, fluid overload, HTN, MI, uremic frost, dry itchy skin, N/V, malnutrition, ulcers

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85
Q

Normal daily urine output

A

1500-2000mL/day

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86
Q

Normal relationship of BUN and creatinine

A

Normal = 10-15:1 ratio BUN:creatinine

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87
Q

Creatinine clearance

A

urine creatinine x urine volume/ serum creatinine

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88
Q

Glomerular filtration rate (GFR) normal

A

125mL/min

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89
Q

AKI treatment goals

A

Restore perfusion to kidneys, control fluids and electrolyte balance, treat acid-base imbalances, prevent and treat infection (sepsis)

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90
Q

Pre-renal diagnosis

A

Electrolytes, urea, creatinine, fluid status

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91
Q

Pre-renal management

A

IV fluids OR diuretics, stop nephrotoxins

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92
Q

Intra-renal Diagnosis

A

Urinalysis, renal ultrasound

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93
Q

Intra-renal Management

A

Infection - antibiotics
Remove renal stones

94
Q

Post-renal diagnosis

A

Bladder scan, check catheter, CT KUB/renal ultrasound

95
Q

Post-renal treatment

A

Check catheter

96
Q

Treating Fluid Overload

A

Diuretics, fluid restriction, HR/BP/lungs/heart/ECG, I&O, daily weights, watch electrolyte imbalances, monitor HF

97
Q

Chronic Kidney Disease (CKD)

A

Slow, progressive, irreversible loss of renal function, affecting nearly all organ systems

98
Q

Causes of CKD

A

Primary renal condition (polycystic kidney disease, glomerulonephritis), other diseases that produce long-term renal insult (DM, HTN)

99
Q

Risk factors for CKD

A

DM, HTN, proteinuria, family Hx, increasing age (fewer nephrons)

100
Q

Osteodystrophy

A

Mineral metabolism disorders - metastatic calcifications and bone disease.
Hyperphosphatemia causes hypocalcemia - increases PTH- calcium resorption from bone = bone loss
Decreased vitamin D activation - increased PTH = impaired osteoblast function

101
Q

Metastatic calcifications

A

deposits of crystals may lodge in organs and vessels

102
Q

Chronic Uremia CV manifestations

A

Anemia (from hemolysis, bone marrow suppression, decreased erythropoietin and iron, weakness and fatigue, decreased blood viscosity, decreased platelets (bleeding)

103
Q

Goals of CKD treatment

A

Manage fluid volume, improve cardiac function, enhance nutrition, prevent injury, avoid acid-base imbalance, treat anemia, treat electrolyte imbalances

104
Q

When is RRT required

A

When kidneys are functioning at < 10-15% of their normal rate

105
Q

Types of RRT

A

1) Hemodialysis (AKI, CKD)
2) Peritoneal dialysis (CKD)

106
Q

Dialysate

A

Uses osmosis and oncotic pressure to transfer fluids/particles back and forth across the semi-permeable membrane

107
Q

Peritoneal Dialysis

A

Peritoneal cavity is the semipermeable membrane - sterile cath is inserted and dialysate is instilled through it. Fluid stays in cavity (instill period) and then is drained

108
Q

Advantages of Peritoneal Dialysis

A

Can be done on a regular basis, can be done at home, relieves uremic symptoms, greater flexibility with treatment

109
Q

Disadvantages of Peritoneal Dialysis

A

Infection risk, permanent cath in abdomen, can’t get wet, dialysis daily, slow, abdominal discomfort

110
Q

Hemodialysis system - blood compartment

A

Contains electrolytes, wastes, toxins, and excess water.
Exerts oncotic and hydrostatic pressure

111
Q

Hemodialysis System - Dialysate compartment

A

Contains electrolytes similar to plasma, circulates on outside of tubing system, semi-permeable membrane, adjustable

112
Q

Advantages of Hemodialysis

A

Relieves uremic symptoms, quick and efficient, requires 3 treatments/wk, most people have suitable vessels

113
Q

Disadvantages of Hemodialysis

A

New medications, fluid restriction, vascular access and anticoags, need to plan around hemodialysis schedule, travel to the unit, restricts activity

114
Q

Continuous Renal Replacement Therapy (CRRT)

A

For patients who are hemodynamically unstable (AKI), allows for gradual removal of excess electrolytes/fluids - Critical Care ONLY

115
Q

Complications of kidney Transplant

A

Rejection, infection, CV disease, malignancies, recurrence of original renal disease, corticosteroid-related complications

116
Q

Kehr’s Sign

A

Pain in left should - sign of hemorrhage

117
Q

Cullen’s sign

A

Periumbilical ecchymosis - sign of hemorrhage

118
Q

Grey Turner’s sign

A

Bruising to flank - sign of hemorrhage

119
Q

Cancer

A

Abnormal cell growth where cellular regulation is lost

120
Q

Cellular Regulation

A

Genetic and physiologic processes that control cellular growth, replication, differentiation, and function

121
Q

Benign Tumor cells

A

Normal cells but are growing in wrong place or wrong time (ex. skin tags, mole)

122
Q

Cancer cells

A

Abnormal, no useful function, harmful to normal body tissues

123
Q

Carcinogenesis

A

Process of changing a normal cell into a cancer cell - loss of cellular regulation

124
Q

Initiation phase

A

“carcinogens” can change activity of cellular genes, so the cell becomes cancerous

125
Q

Promotion Phase

A

Enhanced growth by promoters (latency)

126
Q

Progression Phase

A

Continued change of the cancer cell, making it more malignant over time (can develop own blood supply, further mutations)

127
Q

Benign Tumor Characteristics

A

Well-differentiated (resembles host tissues), slow growing, enclosed in a capsule, localized/non-invasive, tightly adhere

128
Q

Malignant Tumor Characteristic

A

Some/no cellular differentiation, variable/fast growing/multiplying, invasive, loose adherence

129
Q

Steps of Metastasis

A

Malignant transformation
Tumor vascularization
Blood vessel penetration
Arrest and invasion

130
Q

Malignant Transformation

A

Some normal cubodial cells have undergone malignant transformation and have divided enough times to form a tumorous area within the cuboidal epithelium

131
Q

Tumor Vascularization

A

Cancer cells secrete vascular endothelial growth factor (VEGF), stimulated the blood vessels to bud and form new channels that grow into the tumor

132
Q

Blood vessel penetration

A

Cancer cells have broken off from the main tumor. Enzymes on the surface of the tumor cells to enter the blood vessels and travel around the body

133
Q

Arrest and Invasion

A

Cancer cells clump in blood vessel walls and invade new tissue areas. If new tissue areas have the right conditions to support the continued growth of cancer cells, new tumors (metastatic tumors) will form at this site.

134
Q

4 Ways of Cancer Metastasis

A

Lymphatics spread
Arteriovenous spread
Serous cavity spread
CSF spread

135
Q

Lymphatic spread

A

Cells invade lymphatic vessels where they travel to lymph nodes

136
Q

Arteriorvenous spread

A

Enter blood vessels near primary tumor and travel to the next capillary network they encounter

137
Q

Serous cavity spread

A

Serous membranes (pleura, peritoneum) are invaded by tumors

138
Q

CSF spread

A

Cells spread through CSF

139
Q

Grading of Tumors

A

How similar cancer cells look to parent cells

140
Q

Staging of Tumors

A

Exact location of the cancer and whether metastasis has occurred.

141
Q

Grade 1 tumor

A

Well-differentiated

142
Q

Grade 2 tumor

A

Moderately differeniated

143
Q

Grade 3 tumor

A

Poorly diferentiated

144
Q

Grade 4 tumor

A

Undifferentiated

145
Q

Cancer Staging

A

Primary Tumor (T)
Regional Lymph Nodes (N)
Distant Metastasis (M)

146
Q

S&S of cancer - CAUTION

A

C: change in bowel or bladder habits
A: A sore throat that doesn’t heal
U: Unusual bleeding or discharge
T: Thickening of a lump in breast or elsewhere
I: Indigestion or difficulty swallowing
O: Obvious change in a wart or mole
N: Nagging cough or hoarseness

147
Q

Primary Cancer Prevention

A

Genetic screening, avoiding carcinogens, removing “at risk” tissues, vaccination

148
Q

Secondary Prevention

A

Self-exams, FIT test/colonoscopy, PAP tests

149
Q

Radiation Therapy

A

HIgh-energy radiation to kill cancer cells while having minimally damaging effects on surrounding normal tissue (direct damage to DNA, can’t reproduce, cell dies)

150
Q

Chemotherapy

A

Systemic therapy: antineoplastic/cytotoxic drugs, single drug or combo

151
Q

Neoadjuvant chemo

A

Shrink tumor before surgery or radiation

152
Q

Adjuvant chemo

A

Kill remaining cancer following surgery or radiation

153
Q

Antimetabolites MOA

A

Act as “counterfeit” metabolites that fool cancer cells into using the antimetabolites in cellular reactions

154
Q

Antitumor Antibiotics MOA

A

Damage the cell’s DNA and interrupt DNA or RNA synthesis

155
Q

Antimitotic MOA

A

Interfere with the formation and actions of microtubules so that cells cannot complete mitosis during cell division

156
Q

Alkylating Agents

A

Prevents proper DNA and RNA synthesis, which inhibits cell division

157
Q

Topoisomerase Inhibitors MOA

A

When drugs disrupt the topoismerase enzyme, proper DNA maintenance is prevented, resulting in increased DNA breakage and eventual cell death

158
Q

Chemo Side effects

A

Extravasation/Infltration, hematopoietic effects (anemia, neutropenia, thrombocytopenia), N/V, alopecia, mucositis, changes in cognitive function

159
Q

Immunotherapy

A

Stimulates body’s natural defences (immune system) to attack the cancer

160
Q

Sides effects of Immunotherapy

A

“Itis” of everything

161
Q

Monoclonal Antibodies

A

Infusion of antibodies formed against targets known to be present on certain types of cancer cells

162
Q

Targeted therapy

A

Block the growth and spread of cancer by interfering with the specific cellular growth pathways/molecules involved in cancer cells

163
Q

Endocrine therapy

A

To treat tumors that are hormone-sensitive (breast and cancer cancer)

164
Q

Acute survival

A

Time from diagnosis to completion of initial treatment

165
Q

Extended survival

A

Beginning to return to normal life after treatment, “watchful waiting” fear of reccurence

166
Q

Permanent survival

A

Long-term adaptation to life beyond canver

167
Q

Leukemia

A

Blood Cancer, results from loss of normal cellular regulation (uncontrolled production of immature WBCs in bone marrow)

168
Q

Hematopoietic

A

Stem cells arising from bone marrow

169
Q

Acute Leukemia

A

Blood stem cells are prevented from maturing, resulting in blast cells overtaking bone marrow

170
Q

Chronic Leukemia

A

Blood stem cells partially develop, however, the partially mature cells don’t function quite like normal WBCs that are fully mature

171
Q

Lymphocytic/Lymphoblastic

A

Leukemic cells coming from the lymphoid pathway

172
Q

Myelocytic/Myeloblastic

A

Leukemic cells coming from myeloid pathway

173
Q

ALL (Lymphoblastic)

A

ACUTE
Progressive proliferation of immature blast cells, in CHILDREN, infiltrate spleen, lymph nodes, CNS

174
Q

3 Phases of treatment for ALL

A

1) Remission induction
2) CNS prophylaxis
3) Post-remission

175
Q

AML (Myelogenous)

A

ACUTE
Abnormal propagation of immature myeloid cells in the bone marrow, common in older adults, poor prognosis

176
Q

2 Phases of treatment AML

A

Induction
Consolidation Therapy

177
Q

CLL (lymphoblastic)

A

CHRONIC
Develops slowly, largely asymptomatic, most common leukemia in adults

178
Q

Treatment for CLL

A

May not require treatment, therapy based on stage and symptoms

179
Q

CML (myelogenous)

A

CHRONIC
Chromosome mutation, 3 phases:
1) chronic
2) accelerated
3) blast/blast crisis

180
Q

Treatment for CML

A

PO tyrosine kinase inhibitors (TKIs)

181
Q

Pancytopenia

A

Leukopenia (immunodeficient)
Thrombocytopenia (bleeding)
Erythrocytopenia (anemia)

182
Q

S&S of Leukemia

A

Pancytopenia, malignant cell expansion (bone pain/tenderness, blood vessel/circulation problems), infiltration (liver and spleen enlargement), CNS symptoms

183
Q

Hematopoietic Stem Cell Transplantation (HSCT)

A

Stem cells taken from bone marrow or blood stream (bone marrow transplant)

184
Q

Lung Cancer

A

Due to impaired cellular regulation in the bronchial epithelium, typically grows slowly

185
Q

Lung Cancer Metastasis

A

Direct extension, blood circulation, lymph glands

186
Q

Types of Lung cancer

A

Small cell carcinoma (SCLC) - 15-20%
Non-small cell carcinoma (NSCLC) 75-85%

187
Q

Lung Cancer Diagnosis

A

CXR, CT, pleural effusion presence, biopsy, MRI, PET, sputum sample

188
Q

Oncological Emergencies

A

Febrile neutropenia, Acute tumor lysis syndrome (TLS), Leukostasis, Hypercalcemia, SIADH, Superior Vena Cava Syndrome, Malignant pleural effusion, DIC, spinal cord compression (SCC), cardiac tamponade

189
Q

Hyperleukocytosis

A

WBC count >100x109/L in a pt with leukemia

190
Q

Leukostasis

A

Symptomatic hyperleukocytosis, BF obstruction can cause organ damage

191
Q

Treatment of Hyperleukocytosis

A

Hydration (IV fluids), Reduce uric acid (allopurinol/rasburicase), rapidly reduce number of circulating blast cells

192
Q

Most common metabolic emergency

A

Hypercalcemia

193
Q

Hypercalceima

A

Serum Ca >2.6, associated with bone destruction

194
Q

S&S of hypercalcemia

A

Polydipsia and polyuria, constipation, drowsiness, confusion, hyporeflexia, dry mouth, N/V, decreased appetite, skeletal pain, kidney stones, abd pain, altered cognition, severe muscles weakness

195
Q

Hypercalcemia Treatment

A

Fluid resuscitation (IV NS)
Biphosphonates (blocks resorption of calcium)
Calcitonin and corticosteroid (temporary)

196
Q

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

A

Inappropriate production and secretion of ADH, causes kidneys to excessively absorb water, dilutes blood sodium

197
Q

SIADH management

A

Correct fluid overload, increase sodium (restrict fluids, hypertonic saline admin, monitor fluid and lytes)
Monitor LOC (cerebral edema causes increased ICP)

198
Q

Superior Vena Cava Syndrome (SVC)

A

Compression/obstruction of superior vena cava, happens when tumors are in mediastinum or near chest wall, can happen from thrombus

199
Q

Treat SVC

A

ABC’s, dexamethasone then surgery/radiation, stent, thrombolytic therapy

200
Q

S&S of SVC

A

Face/neck/arm swelling/erythema, cough, dyspnea, orthopnea, engorged blood vessels, JVD, stridor, headache/confusion (increased ICP),

201
Q

Disseminated Intravascular Coagulation (DIC)

A

Extensive, widespread abnormal clotting

202
Q

Malignant Pleural Effusion

A

Caused by cancer cells spreading to pleural space - increased production of pleural fluid and decreased absorption of fluid - restrict lung expansion and lung volume, decreased gas exchange

203
Q

S&S of Malignant pleural effusion

A

Dyspnea, tachypnea, non-productive cough, chest pain, pleuritic rub

204
Q

Treatment of Malignant pleural effusion

A

Thoracoscopy (VATS), throacentesis, chest tube, draine, pleurodesis (talcum powder)

205
Q

Malignant Cardiac Tamponade

A

Accumulation of fluid in pericardial sac, applying pressure on the heart (effusion can lead to tamponade)

206
Q

S&S of Malignant cardiac tamponade

A

Sudden SOB, tachycardia, tachypnea, shock (cardiogenic)

207
Q

Neutropenia

A

Not enough neutrophils

208
Q

Myelosuppression

A

Suppression of bone marrow

209
Q

Neutrophils

A

A type of WBC produced in bone marrow then “pushed out” in blood stream, first line of defence against bacterial and fungal infections

210
Q

Normal neutrophil range

A

1.50-7.50

211
Q

Impact of neutropenia

A

IMMUNOSUPPRESSION

212
Q

High risk ANC

A

Less than 0.1x10x9/L, this means they are at increased risk of infection

213
Q

Equation of ANC

A

% segs + %bands/100)x total WBC counta

214
Q

Vital Sign alterations in febrile neutropenia

A

Tachycardia, hypo or hyperthermia, HTN first then hypotnesion, SOB and increased RR, low SaO2

215
Q

Common sites of infection during neutropenia

A

Anus (no suppositories, proactive bowel care)
Perineum (cleanse daily)
Skin and mucous membranes (daily showers, dressing changes, oral care)
Resp tract
GI tract (prolonged = risk of typhilitis = inflammation of small intestine or colon)
GU tract (UTI)

216
Q

How to promote neutrophil recovery

A

Hematopoietic growth factors (filgrastim = daily injection, peg-filgrastim = long acting)

217
Q

Side effect of granulocyte colony stimulating factors

A

Bony pains (bone marrow), splenic rupture, fever

218
Q

Nursing Actions for Febrile neutropenia

A

VS Q4H, septic workup, ABX, accurate ins and outs (renal function), daily BW, S&S of sepsis

219
Q

Tumor Lysis Syndrome (TLS)

A

Oncologic emergency related to high turnover (destruction) of cancer cells - can lead to organ impairment and damage

220
Q

Patho of TLS

A

Chemo causees malignant cells to die and burst - they release their contents into blood stream. This rapid release can cause rapid electrolyte shifts and lead to lyte values outside of normal ranges

221
Q

Electrolytes affected by TLS

A

Uric acid (high), Potassium (high), Phosphorus (high), calcium (low)

222
Q

Hyperuricemia

A

DNA released is broken down into uric acid (insoluble) - urine crystals in renal tubules or collecting ducts accumulate - renal obstruction - intrarenal failure

223
Q

Complications of Hyperuricemia

A

Reduced UO, renal failure, reduced renal blood flow, disrupted renal function, crystal deposits in joints (gout)

224
Q

S&S of Hyperuricemia

A

DIC, decreased urine output, N/V, weakness, cardiac abnormalities, confusion

225
Q

Prophylactic treatment of TLS

A

Hydration to maintain urine output, monitoring ins and outs

226
Q

Treatment for Hyperuricemia in TLS

A

Rasburicase - degrades pre-existing uric acid

227
Q

Spinal Cord Compression (SCC)

A

Tumor in epidural space encroaches on spinal cord or cauda equina, medical emergency (rarely fatal but can cause neuro defects)

228
Q

S&S of SCC

A

Thoracic presentation - lung or breast
Lumbosacral presentation - colorectal or prostate
Muscle weakness (unsteadiness, footdrop, paralysis), sensory impairment (paralysis, loss of bowel and bladder control, paraplegia)

229
Q

Diagnosis of SCC

A

Neuro assessments, spinal cord XR, bone scan, MRI, CT

230
Q

Treatment of SCC

A

High-dose steroids (buys time, pain relief), Radiation therapy (treatment of choice), surgery, chemotherapy

231
Q

Prevention of SCC

A

Bisphosphonates - decrease skeletal complications of bony metastasis

232
Q
A

YEAR 3 (14 decks)

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