Nurs 332 Midterm 2 Flashcards
(232 cards)
1
Q
Electrolytes
A
Electrically charged micro-solutes required for enzyme activities, muscle contraction, and metabolism
2
Q
Extracellular Electrolytes
A
Sodium (Na)
Chloride (Cl)
Calcium (Ca)
3
Q
Intracellular Electrolytes
A
Potassium (K)
Magnesium (Mg)
Phosphorus/Phosphate (PO4)
4
Q
Normal Sodium (Na) Levels
A
135-145mEq/L
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)
6
Q
What regulates Sodium (Na)
A
GFR and aldosterone
7
Q
What is the most abundant extracellular electrolyte
A
Sodium (Na)
8
Q
Causes of hyponatremia
A
Sweating, diuretics, lack of dietary intake, HF
9
Q
hyponatremia
A
low sodium
10
Q
Causes of hypernatremia
A
Na intake, dehydration, HF, SIADH (polyuria)
11
Q
Hypernatremia
A
high sodium
12
Q
S&S of hyponatremia
A
hypotension, confusion, headache, lethargy, seizures, decreased muscle tone, muscle twitching, tremors, vomiting, diarrhea
13
Q
S&S of hypernatremia
A
confusion, thirst, HTN, tachycardia, restlessness, seizure, coma, hyperreflexia, muscle twitching, N/V
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)
15
Q
Normal Chloride (Cl) Levels
A
95-105mEq/L
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
17
Q
Danger levels for chloride (Cl)
A
<80 and >115
18
Q
Causes of hyperchloridemia
A
Cl gain, decreased excretion, fluid shifts
19
Q
Causes of hypochloridemia
A
Cl loss, inadequate intake or absorption, fluid shifts
20
Q
hyperchloridemia
A
high chloride
21
Q
hypochloridemia
A
low chloride
22
Q
S&S of hyperchloridemia
A
BP changes, increased HR, edema, agitation, headache, changes in LOC, nausea, weakness
23
Q
S&S of hypochloridemia
A
BP changes, increased HR< hypotension, confusion, disorientation, muscle spasms/cramps/paralysis, bradypnea, shallow resps
24
Q
Treatment of chloride imbalances
A
Check other lyte levels (Cl is never alone), assess vitals (BP)
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Drugs that increase Cl
ammonium chloride, KCl, NaCl
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Drugs that decrease Cl
RL, sodium bicarb
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Normal Calcium (Ca) levels
2.3-2.8mmol/L
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Calcium (Ca) function
blood coagulation, neuromuscular contraction, enzymatic activities, bone integrity.
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Where is calcium stored
bone, small amounts in ECF and soft tissue
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What is calcium (Ca) regulated by
Parathyroid hormone, calcitonin, and calcitrol
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Calcium and phosphorus relationship
Inverse - if Ca is high, phos is low
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Causes of hypercalcemia
increased absorption, calcium release from bone, increased available Ca
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hypercalcemia
high calcium
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Hypocalcemia
Decrease intake/absorption, decrease available Ca, increased renal excretions, Ca loss
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hypocalcemia
low calcium
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S&S of hypocalcemia
Muscle cramps, N/T, tetany, irritability, reduced cognitive ability, seizures, ECG changes, decreased BP, bone fractures, abnormal clotting
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S&S of hypercalcemia
anorexia, cardiac dysrhythmias, constipation, PUD, lethargy, depression, fatigue, confusion, coma, pathologic bone fractures, renal stones
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Treatment of calcium imbalances
Assess chvosteks and trousseaus signs, treat the cause, IV calcium chloride (Low), monitor ECG and diet.
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Normal Potassium (K) Levels
3.5-5.1mEq/L
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Potassium (K) Functions
Cardiac and neuromuscular function, nerve impulse conduction, and carbohydrate metabolism, maintain homeostasis in blood
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Causes of hyperkalemia
increased K intake, supplements, decreased output, fluid shifts
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Hyperkalemia
High potassium (K)
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Causes of Hypokalemia
decreased K intake, GI loss, Urinary excretion, fluid shifts
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Hypokalemia
Low potassium (K)
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S&S of hypokalemia
resp arrest, N/V, diarrhea, ileus, muscle fatigue, cramps, confusion, depression, lethargy, dysrhythmias, irregular pulse, cardiac arrest
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S&S of hyperkalemia
Weakness, muscle cramps, N/V, diarrhea, ABD cramps, ECG changes, metabolic acidosis
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Danger zone of potassium (K)
<2.5 OR >6.5 - respiratory arrest and lethal arrhythmias
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Treatment of hypokalemia
IV KCl (high risk) - oral K or KCl elixer,, treat causes
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Treatment of hyperkalemia
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)
50
Normal Magnesium (Mg) Levels
1.3-2.5mEq/L
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Magnesium (Mg) Function
Ensures sodium and potassium transport across cell membranes, protein and carb metabolism, nerve cell conduction & CNS messaging, neuromuscular activity
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Causes of Hypermagnesemia
Excessive intake, increased absorption, renal retention
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Hypermagnesemia
High magnesium
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Causes of hypomegnesemia
Magnesium loss, inadequate intake, impaired absorption, fluid shifts
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Hypomagnesemia
Low magnesium
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S&S of hypomagnesemia
Life threatening cardiac arrythmias, hypotension, disorientation, anorexia, N/V, ABD distention, constipation, neuromuscular irritability and hyperactivity
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S&S of hypermagnesemia
Heart blocks, hypotension, wide QRS, lethargy, decreased LOC, N/V, muscle weakness, respiratory depression (d/t muscle weakness), absent DTR
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ECG changes for hypomagnesemia
Torsades, PVC, Vtach, Vfib, cardiac arrest
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ECG changes for hypermagnesemia
Complete heart block, bradycardia, cardiac arrest
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Normal Phosphorus/Phosphate (PO4) Levels
1.7-2.6mEq/L
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Phosphorus/Phosphate Functions
Teeth and bone development, normal neuromuscular function, production of ATP. Protein, fat and carb metabolism, maintains acid-base balance
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Causes of Hyperphosphatemia
PO4 gain, increased absorption or retention, fluid shifts
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Causes of Hypophosphatemia
PO4 loss, inadequate intake, impaired absorption, increased excretion, fluid shifts, refeeding syndrome
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S&S of hypophosphatemia
weakness, N/T, fractures, diminished myocardial function, disorientation, seizure, coma
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S&S of hyperphosphatemia
Muscle cramping, weakness, tachycardia, diarrhea, nausea, ABD cramping
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Treatment of Hypophosphatemia
IV NaPO4 or K2PO4, PO phosphate
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Treatment of Hyperphosphatemia
Diuretics, oral antacids, vitamin D
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Kidney Functions
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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Blood Urea Nitrogen normal levels
2.9-8.2mmol/L
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Blood Urea Nitrogen (BUN
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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Creatinine normal level
50-110mmol/L
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Creatinine
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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What is the most reliable measure of renal health
Creatinine
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Azotemia
Poison (waste products) in the blood
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Acute Kidney Injury (AKI)
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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Pre-renal injury
Decrease in renal blood flow (inadequate perfusion)
30-60%
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Intra-renal injury
Something that damages the structures of the kidney (infection, drug toxicity)
20-40%
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Post-renal injury
Obstruction to urine outflow (kidney stone, prostate cancer)
1-10%
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RIFLE AKI criteria
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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Acute tubular necrosis (ATN)
Destruction of renal tubular epithelial cells from ischemia or sepsis
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Nephrotoxic drugs
ACEs/ARBs, NSAIDs, Chemo, CT contrast, Antibiotics
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Rhabdomyolysis
Massive breakdown of skeletal muscle (trauma) - release of myglobin (plugs glomeruli and damages lining in tubules)
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Risk factors for kidney injury
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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S&S of kidney injury
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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Normal daily urine output
1500-2000mL/day
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Normal relationship of BUN and creatinine
Normal = 10-15:1 ratio BUN:creatinine
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Creatinine clearance
urine creatinine x urine volume/ serum creatinine
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Glomerular filtration rate (GFR) normal
125mL/min
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AKI treatment goals
Restore perfusion to kidneys, control fluids and electrolyte balance, treat acid-base imbalances, prevent and treat infection (sepsis)
90
Pre-renal diagnosis
Electrolytes, urea, creatinine, fluid status
91
Pre-renal management
IV fluids OR diuretics, stop nephrotoxins
92
Intra-renal Diagnosis
Urinalysis, renal ultrasound
93
Intra-renal Management
Infection - antibiotics
Remove renal stones
94
Post-renal diagnosis
Bladder scan, check catheter, CT KUB/renal ultrasound
95
Post-renal treatment
Check catheter
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Treating Fluid Overload
Diuretics, fluid restriction, HR/BP/lungs/heart/ECG, I&O, daily weights, watch electrolyte imbalances, monitor HF
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Chronic Kidney Disease (CKD)
Slow, progressive, irreversible loss of renal function, affecting nearly all organ systems
98
Causes of CKD
Primary renal condition (polycystic kidney disease, glomerulonephritis), other diseases that produce long-term renal insult (DM, HTN)
99
Risk factors for CKD
DM, HTN, proteinuria, family Hx, increasing age (fewer nephrons)
100
Osteodystrophy
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
Metastatic calcifications
deposits of crystals may lodge in organs and vessels
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Chronic Uremia CV manifestations
Anemia (from hemolysis, bone marrow suppression, decreased erythropoietin and iron, weakness and fatigue, decreased blood viscosity, decreased platelets (bleeding)
103
Goals of CKD treatment
Manage fluid volume, improve cardiac function, enhance nutrition, prevent injury, avoid acid-base imbalance, treat anemia, treat electrolyte imbalances
104
When is RRT required
When kidneys are functioning at < 10-15% of their normal rate
105
Types of RRT
1) Hemodialysis (AKI, CKD)
2) Peritoneal dialysis (CKD)
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Dialysate
Uses osmosis and oncotic pressure to transfer fluids/particles back and forth across the semi-permeable membrane
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Peritoneal Dialysis
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
Advantages of Peritoneal Dialysis
Can be done on a regular basis, can be done at home, relieves uremic symptoms, greater flexibility with treatment
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Disadvantages of Peritoneal Dialysis
Infection risk, permanent cath in abdomen, can’t get wet, dialysis daily, slow, abdominal discomfort
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Hemodialysis system - blood compartment
Contains electrolytes, wastes, toxins, and excess water.
Exerts oncotic and hydrostatic pressure
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Hemodialysis System - Dialysate compartment
Contains electrolytes similar to plasma, circulates on outside of tubing system, semi-permeable membrane, adjustable
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Advantages of Hemodialysis
Relieves uremic symptoms, quick and efficient, requires 3 treatments/wk, most people have suitable vessels
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Disadvantages of Hemodialysis
New medications, fluid restriction, vascular access and anticoags, need to plan around hemodialysis schedule, travel to the unit, restricts activity
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Continuous Renal Replacement Therapy (CRRT)
For patients who are hemodynamically unstable (AKI), allows for gradual removal of excess electrolytes/fluids - Critical Care ONLY
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Complications of kidney Transplant
Rejection, infection, CV disease, malignancies, recurrence of original renal disease, corticosteroid-related complications
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Kehr’s Sign
Pain in left should - sign of hemorrhage
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Cullen’s sign
Periumbilical ecchymosis - sign of hemorrhage
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Grey Turner’s sign
Bruising to flank - sign of hemorrhage
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Cancer
Abnormal cell growth where cellular regulation is lost
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Cellular Regulation
Genetic and physiologic processes that control cellular growth, replication, differentiation, and function
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Benign Tumor cells
Normal cells but are growing in wrong place or wrong time (ex. skin tags, mole)
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Cancer cells
Abnormal, no useful function, harmful to normal body tissues
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Carcinogenesis
Process of changing a normal cell into a cancer cell - loss of cellular regulation
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Initiation phase
“carcinogens” can change activity of cellular genes, so the cell becomes cancerous
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Promotion Phase
Enhanced growth by promoters (latency)
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Progression Phase
Continued change of the cancer cell, making it more malignant over time (can develop own blood supply, further mutations)
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Benign Tumor Characteristics
Well-differentiated (resembles host tissues), slow growing, enclosed in a capsule, localized/non-invasive, tightly adhere
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Malignant Tumor Characteristic
Some/no cellular differentiation, variable/fast growing/multiplying, invasive, loose adherence
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Steps of Metastasis
Malignant transformation
Tumor vascularization
Blood vessel penetration
Arrest and invasion
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Malignant Transformation
Some normal cubodial cells have undergone malignant transformation and have divided enough times to form a tumorous area within the cuboidal epithelium
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Tumor Vascularization
Cancer cells secrete vascular endothelial growth factor (VEGF), stimulated the blood vessels to bud and form new channels that grow into the tumor
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Blood vessel penetration
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
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Arrest and Invasion
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.
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4 Ways of Cancer Metastasis
Lymphatics spread
Arteriovenous spread
Serous cavity spread
CSF spread
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Lymphatic spread
Cells invade lymphatic vessels where they travel to lymph nodes
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Arteriorvenous spread
Enter blood vessels near primary tumor and travel to the next capillary network they encounter
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Serous cavity spread
Serous membranes (pleura, peritoneum) are invaded by tumors
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CSF spread
Cells spread through CSF
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Grading of Tumors
How similar cancer cells look to parent cells
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Staging of Tumors
Exact location of the cancer and whether metastasis has occurred.
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Grade 1 tumor
Well-differentiated
142
Grade 2 tumor
Moderately differeniated
143
Grade 3 tumor
Poorly diferentiated
144
Grade 4 tumor
Undifferentiated
145
Cancer Staging
Primary Tumor (T)
Regional Lymph Nodes (N)
Distant Metastasis (M)
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S&S of cancer - CAUTION
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
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Primary Cancer Prevention
Genetic screening, avoiding carcinogens, removing “at risk” tissues, vaccination
148
Secondary Prevention
Self-exams, FIT test/colonoscopy, PAP tests
149
Radiation Therapy
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
Chemotherapy
Systemic therapy: antineoplastic/cytotoxic drugs, single drug or combo
151
Neoadjuvant chemo
Shrink tumor before surgery or radiation
152
Adjuvant chemo
Kill remaining cancer following surgery or radiation
153
Antimetabolites MOA
Act as “counterfeit” metabolites that fool cancer cells into using the antimetabolites in cellular reactions
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Antitumor Antibiotics MOA
Damage the cell’s DNA and interrupt DNA or RNA synthesis
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Antimitotic MOA
Interfere with the formation and actions of microtubules so that cells cannot complete mitosis during cell division
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Alkylating Agents
Prevents proper DNA and RNA synthesis, which inhibits cell division
157
Topoisomerase Inhibitors MOA
When drugs disrupt the topoismerase enzyme, proper DNA maintenance is prevented, resulting in increased DNA breakage and eventual cell death
158
Chemo Side effects
Extravasation/Infltration, hematopoietic effects (anemia, neutropenia, thrombocytopenia), N/V, alopecia, mucositis, changes in cognitive function
159
Immunotherapy
Stimulates body’s natural defences (immune system) to attack the cancer
160
Sides effects of Immunotherapy
“Itis” of everything
161
Monoclonal Antibodies
Infusion of antibodies formed against targets known to be present on certain types of cancer cells
162
Targeted therapy
Block the growth and spread of cancer by interfering with the specific cellular growth pathways/molecules involved in cancer cells
163
Endocrine therapy
To treat tumors that are hormone-sensitive (breast and cancer cancer)
164
Acute survival
Time from diagnosis to completion of initial treatment
165
Extended survival
Beginning to return to normal life after treatment, “watchful waiting” fear of reccurence
166
Permanent survival
Long-term adaptation to life beyond canver
167
Leukemia
Blood Cancer, results from loss of normal cellular regulation (uncontrolled production of immature WBCs in bone marrow)
168
Hematopoietic
Stem cells arising from bone marrow
169
Acute Leukemia
Blood stem cells are prevented from maturing, resulting in blast cells overtaking bone marrow
170
Chronic Leukemia
Blood stem cells partially develop, however, the partially mature cells don’t function quite like normal WBCs that are fully mature
171
Lymphocytic/Lymphoblastic
Leukemic cells coming from the lymphoid pathway
172
Myelocytic/Myeloblastic
Leukemic cells coming from myeloid pathway
173
ALL (Lymphoblastic)
ACUTE
Progressive proliferation of immature blast cells, in CHILDREN, infiltrate spleen, lymph nodes, CNS
174
3 Phases of treatment for ALL
1) Remission induction
2) CNS prophylaxis
3) Post-remission
175
AML (Myelogenous)
ACUTE
Abnormal propagation of immature myeloid cells in the bone marrow, common in older adults, poor prognosis
176
2 Phases of treatment AML
Induction
Consolidation Therapy
177
CLL (lymphoblastic)
CHRONIC
Develops slowly, largely asymptomatic, most common leukemia in adults
178
Treatment for CLL
May not require treatment, therapy based on stage and symptoms
179
CML (myelogenous)
CHRONIC
Chromosome mutation, 3 phases:
1) chronic
2) accelerated
3) blast/blast crisis
180
Treatment for CML
PO tyrosine kinase inhibitors (TKIs)
181
Pancytopenia
Leukopenia (immunodeficient)
Thrombocytopenia (bleeding)
Erythrocytopenia (anemia)
182
S&S of Leukemia
Pancytopenia, malignant cell expansion (bone pain/tenderness, blood vessel/circulation problems), infiltration (liver and spleen enlargement), CNS symptoms
183
Hematopoietic Stem Cell Transplantation (HSCT)
Stem cells taken from bone marrow or blood stream (bone marrow transplant)
184
Lung Cancer
Due to impaired cellular regulation in the bronchial epithelium, typically grows slowly
185
Lung Cancer Metastasis
Direct extension, blood circulation, lymph glands
186
Types of Lung cancer
Small cell carcinoma (SCLC) - 15-20%
Non-small cell carcinoma (NSCLC) 75-85%
187
Lung Cancer Diagnosis
CXR, CT, pleural effusion presence, biopsy, MRI, PET, sputum sample
188
Oncological Emergencies
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
Hyperleukocytosis
WBC count >100x109/L in a pt with leukemia
190
Leukostasis
Symptomatic hyperleukocytosis, BF obstruction can cause organ damage
191
Treatment of Hyperleukocytosis
Hydration (IV fluids), Reduce uric acid (allopurinol/rasburicase), rapidly reduce number of circulating blast cells
192
Most common metabolic emergency
Hypercalcemia
193
Hypercalceima
Serum Ca >2.6, associated with bone destruction
194
S&S of hypercalcemia
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
Hypercalcemia Treatment
Fluid resuscitation (IV NS)
Biphosphonates (blocks resorption of calcium)
Calcitonin and corticosteroid (temporary)
196
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Inappropriate production and secretion of ADH, causes kidneys to excessively absorb water, dilutes blood sodium
197
SIADH management
Correct fluid overload, increase sodium (restrict fluids, hypertonic saline admin, monitor fluid and lytes)
Monitor LOC (cerebral edema causes increased ICP)
198
Superior Vena Cava Syndrome (SVC)
Compression/obstruction of superior vena cava, happens when tumors are in mediastinum or near chest wall, can happen from thrombus
199
Treat SVC
ABC’s, dexamethasone then surgery/radiation, stent, thrombolytic therapy
200
S&S of SVC
Face/neck/arm swelling/erythema, cough, dyspnea, orthopnea, engorged blood vessels, JVD, stridor, headache/confusion (increased ICP),
201
Disseminated Intravascular Coagulation (DIC)
Extensive, widespread abnormal clotting
202
Malignant Pleural Effusion
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
S&S of Malignant pleural effusion
Dyspnea, tachypnea, non-productive cough, chest pain, pleuritic rub
204
Treatment of Malignant pleural effusion
Thoracoscopy (VATS), throacentesis, chest tube, draine, pleurodesis (talcum powder)
205
Malignant Cardiac Tamponade
Accumulation of fluid in pericardial sac, applying pressure on the heart (effusion can lead to tamponade)
206
S&S of Malignant cardiac tamponade
Sudden SOB, tachycardia, tachypnea, shock (cardiogenic)
207
Neutropenia
Not enough neutrophils
208
Myelosuppression
Suppression of bone marrow
209
Neutrophils
A type of WBC produced in bone marrow then “pushed out” in blood stream, first line of defence against bacterial and fungal infections
210
Normal neutrophil range
1.50-7.50
211
Impact of neutropenia
IMMUNOSUPPRESSION
212
High risk ANC
Less than 0.1x10x9/L, this means they are at increased risk of infection
213
Equation of ANC
% segs + %bands/100)x total WBC counta
214
Vital Sign alterations in febrile neutropenia
Tachycardia, hypo or hyperthermia, HTN first then hypotnesion, SOB and increased RR, low SaO2
215
Common sites of infection during neutropenia
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
How to promote neutrophil recovery
Hematopoietic growth factors (filgrastim = daily injection, peg-filgrastim = long acting)
217
Side effect of granulocyte colony stimulating factors
Bony pains (bone marrow), splenic rupture, fever
218
Nursing Actions for Febrile neutropenia
VS Q4H, septic workup, ABX, accurate ins and outs (renal function), daily BW, S&S of sepsis
219
Tumor Lysis Syndrome (TLS)
Oncologic emergency related to high turnover (destruction) of cancer cells - can lead to organ impairment and damage
220
Patho of TLS
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
Electrolytes affected by TLS
Uric acid (high), Potassium (high), Phosphorus (high), calcium (low)
222
Hyperuricemia
DNA released is broken down into uric acid (insoluble) - urine crystals in renal tubules or collecting ducts accumulate - renal obstruction - intrarenal failure
223
Complications of Hyperuricemia
Reduced UO, renal failure, reduced renal blood flow, disrupted renal function, crystal deposits in joints (gout)
224
S&S of Hyperuricemia
DIC, decreased urine output, N/V, weakness, cardiac abnormalities, confusion
225
Prophylactic treatment of TLS
Hydration to maintain urine output, monitoring ins and outs
226
Treatment for Hyperuricemia in TLS
Rasburicase - degrades pre-existing uric acid
227
Spinal Cord Compression (SCC)
Tumor in epidural space encroaches on spinal cord or cauda equina, medical emergency (rarely fatal but can cause neuro defects)
228
S&S of SCC
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
Diagnosis of SCC
Neuro assessments, spinal cord XR, bone scan, MRI, CT
230
Treatment of SCC
High-dose steroids (buys time, pain relief), Radiation therapy (treatment of choice), surgery, chemotherapy
231
Prevention of SCC
Bisphosphonates - decrease skeletal complications of bony metastasis
232
