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NURS 320 > Exam 2 Study Guide > Flashcards

Exam 2 Study Guide Flashcards

1
Q

What are the general Principles of Virology?

A

a. A virus cannot replicate on its own. It must attach to and enter a host cell.
b. A virus then uses the host cell’s energy to synthesize protein, DNA and RNA.
c. Viruses are difficult to kill because they live inside cells. (Any drug that kills a virus also kills healthy cells)

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2
Q

What is the purpose and use of antiviral drugs?

A

Kill or suppresses the virus by destroying virions or inhibiting the ability of viruses to replicate; controlled by current antiviral therapy.

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3
Q

What drugs are used to treat influenza?

A

Amantadine and Rimantadine

Oseltamivir

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4
Q

Amantadine and Rimantadine

A

Only active against influenza A viruses

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5
Q

Oseltamivir

A
  • Active against influenza A and B.
  • Will reduce duration of illness.
  • Treatment should begin within two days of influenza onset.
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6
Q

Oseltamivir: Adverse Effects

A

Nausea and Vomiting

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7
Q

Herpes Zoster (Shingles)

A

Painful (opioids for pain control)
Follow nerve tracts (dermatitis): usually unilateral
Postherpetic neuralgias

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8
Q

What is used to treat Herpes Zoster (Shingles)?

A

Acyclovir

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9
Q

Acyclovir

A

Drug that speeds the recovery of shingles.

Used to suppress replication of HSV-1, HSV-2, and HSV-3.

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10
Q

Best results of acyclovir are seen when?

A

When the antiviral drug is started within 72 hours of symptom onset.

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11
Q

What are the adverse effects of acyclovir?

A

Nausea
Diarrhea
Headache
Burning when topically applied

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12
Q

HIV

A

Retrovirus (uses RNA as its genetic material)

Transmitted by sexual activity, intravenous drug use, perinatally from mother to child

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13
Q

What drugs are used to treat HIV?

A

Zidovudine
Nevirapine
Both are well tolerated.

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14
Q

What are the adverse effects of zidovudine?

A

BONE MARROW DEPRESSION
Nephrotoxicity
Hepatotoxicity
Decreased WBC

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15
Q

What are the adverse effects of nevirapine?

A 
Well tolerated.
Rash
Fever
Nausea
Headache
Abnormal liver function test results
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16
Q

What is the purpose and use of immunosuppressants?

A

a. Drugs that decrease or prevent immune response, thus suppressing the immune system.
b. Used to prevent or treat rejection of implanted organs or autoimmune disorders.

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17
Q

What are the nursing implications for immunosuppressants?

A
  • Patients taking immunosuppressants should be encouraged to take measures to reduce the risk of infection (i.e Avoid crowds and avoid people with colds or other infections)
  • Inform patients to immediately report fever, sore throat, chills, joint pain, fatigue, or other signs of a severe infection.
  • Interacts with grapefruit/grapefruit juice
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18
Q

What is an organ transplant?

A

Transplanted organs have antigens that trigger an immune response -> rejection.

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19
Q

What is azathioprine used for?

A

Prevents rejection of kidney transplants.

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20
Q

What are the adverse effects of azathioprine?

A

a. BONE MARROW SUPPRESSION
b. Development of lymphoma and other malignancies
c. Hepatosplenic T-cell lymphoma

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21
Q

What is SLE?

A

Multisystem autoimmune inflammatory disease.

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22
Q

What is the Pathophysiology of SLE?

A

Antibodies react with circulating antigen (nucleic acids, erythrocytes, phospholipids, lymphocytes, platelets, etc.) Reaction forms circulating immune complexes.

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23
Q

What are the clinical manifestations of SLE?

A

a. Photosensitivity, scaly erythmatous: Butterfly skin rash
b. Plaques with follicular plugging
c. Scarring
d. Nonerosive arthritis
e. Pancreatitis
f. Vasculitis
g. Anemia
h. GN
i. Pleural effusion
j. Endocarditis
k. Thrombosis of intracranial vessels

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24
Q

What are the treatment options for SLE?

A

a. Hydroxychloroquine
b. Glucocorticoids
c. NSAIDs
d. Immunosuppressive Agents
e. Chronic Support – education, counseling, eat well, exercise

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25
Q

What is RA?

A

a. Autoimmune disorder that causes inflammation and tissue damage in joints.
b. Can also cause anemia, inflammation in lungs, eyes, pericardium, and SQ nodules under the skin.

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26
Q

What are the clinical manifestations of RA?

A

a. Pain and Stiffness in joints (particularly in the wrist, hands, elbows, shoulders, knees and ankles)
b. Reduced ROM
c. Affects both sides equally

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27
Q

What drugs are used to treat RA?

A

a. Methotrexate (DMARDs)

b. Entaracept (DMARDs)

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28
Q

What are the adverse effects of methotrexate?

A

BONE MARROW SUPPRESSION

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29
Q

What are the adverse effects of etanercept?

A

Headache
Injection Site Reaction
URT Infection
Weakness and Dizziness.

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30
Q

What is MS?

A

Autoimmune response which causes:

i. Degeneration of CNS myelin
ii. Scarring in brain
iii. Loss of axons

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31
Q

What is the Pathophysiology of MS?

A

Autoreactive T and B cells cross the blood-brain barrier and recognize myelin and oligodendrocyte autoantigens

Triggers inflammation and loss of oligodendrocytes (myelin producing cells)

Activation of brain macrophages contribute to inflammation and injury with plaque formation and axonal degeneration

Loss of myelin disrupts nerve conduction and death of neurons and brain

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32
Q

What are the clinical manifestations of MS?

A

a. Paresthesia of the face, trunk or limbs
b. Weakness (all four limbs)
c. Impaired gait
d. Visual disturbances
e. Urinary incontinence

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33
Q

What are the treatment options for MS?

A

a. Corticosteroids
b. Immunosuppressants
c. Immune system modulators
d. Plasma exchange, Stem cell therapy
e. Regular Exercise, smoking cessation, decreased stress and extreme fatigue
f. Decrease heat exposure

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34
Q

What is hepatitis B?

A

Milder than Hep C, but can lead to hepatitis or liver failure and death.

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35
Q

How is one exposed to hepatitis B?

A

Transmitted through blood and body fluid exposure; maternal-baby exchange.

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36
Q

What are the clinical manifestations of hepatitis B?

A

..

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37
Q

What are the phases of hepatitis?

A

a. Prodromal
b. Icteric
c. Recovery Phase

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38
Q

What happens during the prodromal phase?

A

a. Lasts 1-21 days; Begins 2 weeks post exposure.

b. Ends with appearance of jaundice; fatigue, anorexia, malaise, N/V, cough, HA, and low-grade fever.

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39
Q

What happens during the icteric phase?

A

a. 1-2 weeks after prodromal phase; lasts 2-6 weeks
b. The movement of jaundice occurs.
c. Hepatosplenomegaly, dark urine and clay colored stools.

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40
Q

What happens during the recovery phase?

A

a. 2-4 months
b. Begins with resolution of jaundice (average 6-8 weeks after exposure)
c. Symptoms diminish but hepatomegaly remains.

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41
Q

What drug is used to treat Hepatitis B?

A

Telbivudine

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42
Q

What is Telbivudine?

A

a. Nucleoside analogue reverse transcriptase inhibitor

b. Treats Hep B

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43
Q

What are the adverse effects of telbivudine?

A

a. Fatigue
b. Headache
c. Diarrhea
d. Nausea
e. Pain in joints and muscles

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44
Q

What is hepatitis C?

A

a. Responsible for most cases of post-transfusion hepatitis.
b. Also implicated in infections related to IV drug use.
c. No vaccine yet.

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45
Q

How is one exposed to Hepatitis C?

A

a. 50-80% of hepatitis C cases result in chronic hepatitis.

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46
Q

What are the clinical manifestations of Hepatitis C?

A

..

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47
Q

What drugs are used to treat Hepatitis C?

A

a. Interferon
b. Ribavirin
c. Sofosbuvir

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48
Q

What are the adverse effects of interferon?

A

Fatigue, muscle aches, fever/chills, loss of appetite, SUPPRESSION OF BONE MARROW AND PRODUCTION OF RBCs

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49
Q

Interferon

A

Stimulates the body’s immune system to clear the virus. Good for acute

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50
Q

What are the adverse effects of ribavirin?

A

a. Rash
b. Conjunctivitis
c. Anemia
d. Mild Bronchospasm

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51
Q

What are the adverse effects of sofosbuvir?

A

a. Few side effects: fatigue, headache, nausea and difficulty sleeping.

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52
Q

When sofosbuvir is given with amiodarone, what can happen?

A

May cause slow HR which can lead to death.

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53
Q

What are the functions of the liver?

A
  1. Stores large amounts of blood
  2. Synthesis of all clotting factors
  3. vitamin K storage
  4. Kupffer cells
  5. Fat synthesization
  6. Synthesizes phospholipids and cholesterol
  7. Synthesizes plasma proteins
  8. Synthesizes serum enzymes
  9. Gluconeogenesis
  10. Detoxification
  11. Storage of minerals and vitamins
  12. Bile production
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54
Q

What are the clinical manifestations of liver disorders?

A

a. Portal Hypertension
b. Ascites
c. Hepatic Encephalopathy
d. Jaundice
e. Hepatorenal Syndrome

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55
Q

What are the causes of acute liver failure?

A

a. Acetaminophen OD
b. Viruses: Hepatitis A, B and C
c. Reaction to prescription/herbal medication
d. Ingestion of wild mushroom

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56
Q

What are the causes of chronic liver failure?

A

a. Viruses: Especial Hepatitis B and C
b. Hemochromatosis (too much iron storage)
c. Severe malnutrition
d. Long term alcohol consumption
e. Cirrhosis

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57
Q

What is cirrhosis?

A

a. Irreversible inflammatory disease that disrupts liver function and structure.
b. Normal liver cells are replaced with scar tissue -> fibrosis.

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58
Q

What is the Pathophysiology of cirrhosis?

A
  1. Inflammation
  2. Fibrosis and scarring -> portal HTN, splenomegaly, varices, decreased bilirubin matabloism -> increased unconsummated bilirubin (remains fat soluble) -> jaundice
  3. Decreased bile in the GI -> light/clay colored stool
  4. Decreased fat digestion -> decreased Vitamin K -> decreases clotting factors -> increases bleeding tendencies.
  5. Increased urobilinogen -> concentrated dark urine.
  6. Decreased protein hormones like angiotensinogen -> activates compensatory
  7. Increased ammonia and presence of toxic substances -> encephalopathy
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59
Q

What are the treatment options for cirrhosis?

A

a. Beta Blockers
b. Nitrate
c. Diuretics
d. Lactulose
e. FFP
f. Neomycin/Metronidazole

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60
Q

What are adverse effects of diuretics?

A

Drop in Ca, take calcium supplements

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61
Q

What are the adverse effects of vitamin K?

A

a. Pain, swelling, soreness @ injection site
b. Flushing, taste changes, dizziness, rapid heart beat
c. Sweating and SOB
d. Treats and prevents unusual bleeding by increasing body’s production of clotting factors.

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62
Q

What are the adverse effects of lactulose?

A

a. Gas, bloating, burping, stomach pain, cramps and nausea.
b. Serious side effects: excessive diarrhea, vomiting and muscle cramps/weakness.
c. Is a laxative -> traps toxic compounds in the colon; loosens or increases frequency in stools

63
Q

What causes a UTI?

A

Most common pathogen: E. Coli

64
Q

What are kidney stones?

A

a. Masses of crystals, protein or other substances form within and may obstruct the urinary tract.

65
Q

What are the risk factors for kidney stones?

A

a. Family history
b. Dehydration
c. Diet (high in protein, sodium and sugar)
d. Overweight and obesity
e. Digestive Diseases and surgery (IBS, Chronic diarrhea, gastric bypass surgery)
f. Other medical conditions (Polycystic kidney disease, hyperparathyroidism)
g. Medications (diuretics and calcium based antacids)

66
Q

What are the types of kidney stones?

A
  1. Calcium or Phosphate
  2. Struvite
  3. Uric Acid
67
Q

Calcium or Phosphate Renal Calculi

A

caused by idiopathic calcium absorption (hypercalciuria, hyperparathyroidism, plus prolonged immobilization)

68
Q

Struvite Renal Calculi

A

Includes Mg, Ammonium and Phosphate; Forms into alkaline urine during infection.

69
Q

Uric Acid Renal Calculi

A

Excessive amount from endogenous purines and food; Consistent acidic urine increases risk.

70
Q

What is a UTI?

A

Inflammation of the urinary epithelium caused by bacteria.

Most common - bladder (cystitis)

71
Q

What are the clinical manifestations of a UTI?

A

a. Often asymptomatic
b. Frequency, Urgency
c. Dysuria
d. Suprapubic/low back pain
e. Severe Symptoms: Hematuria, Cloudy Urine and Flank Pain

72
Q

What is the Pathophysiology of a UTI?

A

..

73
Q

What are drugs used to treat UTIs?

A

Bactrim (Sulfonamides)

Macrobid (Nitrofurantoin)

74
Q

What is sulfonamide?

A

Antibiotic
Bacteriostatic - Inhibits bacterial growth by inhibiting folic acid synthesis
Patient use drink lots of fluid to avoid crystallization which would add more problems (masses of protein in urine -> obstruction)

75
Q

What are fluoroquinolones?

A

First line antibiotic
Bactericidal
Inhibits DNA gyrase

76
Q

Levofloxacin

A

Fluoroquinolone

77
Q

Ciprofloxacin

A

Fluoroquinolone

78
Q

What are adverse effects of sulfonamide?

A

Rashes: **Stevens Johnson Syndrome, Severe reaction to medication
Component of crystallization: may cause calculi -> obstruction

79
Q

What are adverse effects of fluorquinolones?

A

CNS: Headache, dizziness, insomnia, depression, restlessness, convulsions, neuropathy
GI: Nausea, constipation, increased AST and ALT levels, flatulence, heartburn, vomiting, diarrhea, oral candidiasis, dysphagia
Integumentary: Rash, pruritus, urticaria, flushing
Other: RUPTURE OF TENDONS AND TENDONITIS**, fever, chills, blurred vision, tinnitus

Prolonged QT interval

80
Q

What is pyridium?

A

Is a urinary analgesic.
Local analgesic effect in bladder wall.
Relieves UT pain and symptoms.

81
Q

What are adverse effects of pyridium?

A

Will cause tinted urine -> normal finding!

82
Q

Define Acute Cystitis

A

Inflammation of the bladder.

83
Q

What are the clinical manifestations of acute cystitis?

A

a. Frequency
b. Dysuria
c. Urgency
d. Lower abdominal and/or Suprapubic pain

84
Q

What are the treatment options for acute cystitis?

A

a. Amoxicillin
b. Cephalosporins
c. Ciprofloxacin or Levofloxacin
d. Doxycycline
e. Nitrofurantoin (Macorbid)
f. Sulfonamides (Bactrim)

85
Q

Define acute pyelonephritis

A

a. Infection of the renal pelvis and interstitium.

86
Q

What are the clinical Manifestations of acute pyelonephritis?

A

a. Acute onset of symptoms
b. Fever/chills
c. Flank/groin pain
d. N/V
e. Symptoms of UTI

87
Q

What is the Pathophysiology of acute pyelonephritis?

A

a. Check Exam 2: Urinary Tract Disorders on Brainscape for Pathophysiology

88
Q

What drugs are used to treat acute pyelonephritis?

A

a. *Fluoroquinolones (Levofloxacin or Ciprofloxacin)
b. *Sulfonamides (Bactrim DS)
c. PCNs
d. Cephalosporins
e. Aminoglycosides (Gentamycin)

89
Q

What are the contraindications of sulfonamides?

A

Sulfa allergy

Pregnant women and infants younger than 2 months of age.

90
Q

What are contraindications of fluorquinolones?

A

Allergy to quinolone

91
Q

Urinalysis indicates

A

i. Specific Gravity
ii. Urinary pH
iii. Hematuria
iv. Proteinuria
v. Glycosuria
vi. Ketonuria
vii. Nitrates
viii. Leukocytes

92
Q

What is specific gravity?

A

Patient’s hydration status.

93
Q

Normal range for specific gravity.

A

1.003-1.030

94
Q

Specific Gravity: Dehydration Range

A

> 1.020

95
Q

Urinary pH is used to diagnose

A

Dx UTIs, calculi and renal tubular acidosis.
UTI with alkaline = struvite calculi
Acidic = uric acid calculi
Bacteria creates alkaline urine

96
Q

What are the cause of hematuria?

A

Hematuria has various causes: glomerular, renal, and urologic (calculi, infections).

97
Q

What causes proteinuria?

A

..

98
Q

Renal Regulation

A

a. Kidneys regulate fluid volume, electrolytes and acid-base balance.

99
Q

Kidneys secrete

A

renin, erythropoietin and calcitrol

100
Q

Calcitrol

A

Is an active form of Vitamin D for homeostasis.

101
Q

What is the purpose of nephrons?

A

a. Functional unit of the kidney that forms the final urine product.

102
Q

Functions of the nephron include:

A

i. Filters plasma at glomerulus.
ii. Reabsorption and secretion of different substances along the tubular structures.
iii. Forms a filtrate of protein-free fluid.
iv. Regulates the filtrate to maintain body fluid volume, electrolyte composition and pH.

103
Q

What is the purpose of the glomerulus?

A

Tuft of capillaries that loop into Bowman’s Capsule. Forms primary urine.

104
Q

Glomerular filtration membrane

A

Filters blood.

105
Q

What are the renal function tests?

A

a. Estimated Glomerular Filtration Rate
b. Plasma Creatine
c. Blood Urea Nitrogen
d. Potassium (serum)

106
Q

What is eGFR?

A

Best estimate of functioning renal tissues.

107
Q

As GFR decreases, what happens to plasma creatinine?

A

It increases.

108
Q

When GFR decreases, what happens to BUN?

A

It increases.

109
Q

Glomerular Disorders

A

a. Affects kidney function by attacking the glomeruli (where blood is cleaned).

110
Q

Glomerular Disorders include

A

Glomerulonephritis and Glomerulosclerosis

111
Q

What can cause glomerular disorders?

A

i. Acute post-streptococcal glomerulonephritis
ii. Bacterial endocarditis
iii. Diabetes: diabetic neuropathy
iv. SLE

112
Q

What is glomerulonephritis?

A

a. A group of disease that injure the part of the kidney that filters blood (glomeruli).

113
Q

What are the clinical manifestations of acute glomerulonephritis?

A

i. Infection in throat or on skin
ii. Puffiness of face in the morning
iii. Blood in urine (or brown urine)
iv. Urinating less than usual.
v. SOB and cough (d/t excess fluid in lungs)

114
Q

What are the clinical Manifestations of chronic glomerulonephritis?

A

i. May develop without symptoms over several years. Often leads to complete kidney failure.
ii. Hematuria and proteinuria
iii. Decreased urine output accompanies decreased eGFR
iv. Fluid retention: High BP and Edema
v. Frequent urination at night (nocturia)
vi. Very bubbly or foamy urine
vii. Lack of appetite
viii. N/V
ix. Fatigue
x. Difficulty sleeping
xi. Dry/itchy skin
xii. Nighttime muscle cramps

115
Q

What is the Pathophysiology of glomerulonephritis?

A

Injury to the body ->
Forms antibody against antigen ->
But instead of antibody breaking down the antigen ->
Formation of antigen-antibody complexes ->
Complexes deposit within glomerular membranes ->
Damage of glomerular network ->
Loss of function

116
Q

Define Nephrotic Syndrome

A

a. AKA Nephrosis
b. Happens when the kidneys start losing large amounts of protein in urine.
c. Includes an excretion of > 3.5 g or more of protein in the urine per day

117
Q

What are the clinical manifestations of nephrotic syndrome?

A

a. Hypoalbuminemia
b. Edema
c. Hyperlipidemia
d. Proteinuria
e. Vitamin D Deficiency

118
Q

What is the Pathophysiology of nephrotic syndrome?

A

Disturbance in the glomerular basement membrane -> increases permeability of protein and loss of electrical negative charge -> hyperalbuminemia (d/t urinary loss of albumin and diminished synthesis of replacement albumin in the liver)

119
Q

What is used to treat nephrotic syndrome?

A

a. Normal Protein Diet (1g/kg/day)
b. Low fat, Low salt diet
c. Treat HTN and Edema (Diuretics, CCB, ACEI, ARBs, corticosteroids)

120
Q

Define Acute Renal Failure/Acute Kidney Injury

A

a. Sudden decline in kidney function.
b. Decrease in GFR.
c. Accumulation of waste products in the blood.

121
Q

What is prerenal AKI?

A

a. Most common cause of AKI.
b. Decreased renal function with increased BUN and creatinine. (Caused by impaired renal blood flow)
c. GFR declines (d/t decrease in filtration pressure)

122
Q

What are the causes of prerenal AKI?

A

i. Hypovolemia
ii. Hypotension
iii. Shock
iv. Hemorrhage
v. MI with poor cardiac output
vi. Left ventricular failure

123
Q

What is intrarenal AKI?

A

a. Caused by impaired blood flow within the kidney.

b. Is a result of direct damage to the kidney including ischemia or inflammatory damage.

124
Q

What is the most common cause of intrarenal AKI?

A

Acute tubular necrosis

125
Q

Other causes of intrarenal AKI include:

A

i. Glomerulonephritis
ii. Malignant HTN
iii. Disseminated Intravascular Coagulation (DIC)
iv. Renal Vasculitis

126
Q

What is the postrenal AKI?

A

a. Caused by impaired outflow from the kidney.
b. Urine is unable to pass d/t obstruction (urine backs up into the renal pelvis and changing pressures within the kidney)

127
Q

What are causes of postrenal AKI?

A

i. Kidney stones
ii. Bladder outlet obstruction
iii. Enlarged prostate

128
Q

What are examples of nephrotoxic?

A 
Aminoglycosides
Amphotericin B
ACE Inhibitors*
NSAIDs*
Cyclosporine/Tacrolimus
Foscarnet
Pentamidine
Radiographic contrast agents*
Cisplatin/carboplatin
129
Q

Define Chronic Renal Failure/Chronic Kidney Disease

A

a. The irreversible loss of renal function that affects nearly all organ systems.
b. Includes conditions that damage the kidneys and decrease their ability to keep you healthy.

130
Q

What is the pathophysiology of chronic kidney failure?

A
  • Injury -> irreversible d/t already lost nephrons
  • Loss of nephrons -> Ang 2 and renin release
  • High Ang 2 levels lead to -> vasoconstriction
  • HTN in kidneys -> increased permeability
  • Injury to kidney -> scarring -> fibrosis
131
Q

What are the clinical Manifestations of chronic kidney failure?

A

a. Fatigue
b. Trouble concentration
c. Poor appetite
d. Trouble sleeping
e. Muscle cramps at night
f. Swollen feet/ankles
g. Puffiness around eyes especially in the morning
h. Dry/itchy skin
i. Needs to urinate more often especially at night

132
Q

What are Complications of renal failure?

A
  • Fatigue, weakness
  • Fractures (d/t decrease in Vitamin D not bein able to absorb calcium)
  • HTN, edema
  • Decrease EPO -> anemia
  • Weak immunity
  • Ammonia, urea and nitrogenous substances have affinity to CNS
  • Irritation -> neuropathy -> if severe -> confusion and decreased LOC
  • N/V, Not eating well
  • Crystal formation on skin
133
Q

What is the pathophysiology of complications of renal failure?

A

..

134
Q

What is the treatment used to manage complications of renal failure?

A
  • Attempt to cure causes of dysfunction (can cure acute but NOT chronic)
  • Diuretics to increase urine output
  • Cardiovascular drugs to treat HTN and HF
  • Dietary Management: Restriction of protein, salt and water; Reduction of Na, K, phosphorus and Mg
135
Q

What are diuretic classes used to treat renal failure?

A

a. Potassium Sparing Diuretics: Spironolactone and Aldactone
b. Loop Diuretics: Furosemide
c. Thiazide Diuretics: Hydrochlorothiazide

136
Q

Define loop diuretic - furosemide.

A

Increases rate of urine flow. Excretion of excess fluid.

137
Q

Define potassium-sparing diuretics.

A

a. Diuresis without affecting blood potassium levels.

b. Used to significantly reduce mortality in heart failure.

138
Q

Define thiazide diuretics

A

Used to treat mild to moderate HTN. Also indicated to reduce edema associated with HF, severe renal and hepatic failure.

139
Q

Define mannitol

A

Osmotic diuretic

Given for pt. With head trauma and cerebral edema. (Decreases ICP)

140
Q

What is the MOA of loop diuretics?

A

Acts in the loop of Henle and prevents reabsorption of Na and water in the kidneys.

141
Q

What is the MOA of potassium-sparing diuretics?

A

Either by blocking sodium or by blocking aldosterone.

142
Q

What is the MOA of thiazide diuretics?

A

Blocks sodium absorption in distal convoluted tubule of nephron.

143
Q

What are the adverse effects of loop diuretics?

A

a. Orthostatic Hypotension
b. Hypokalemia - dysrhythmias
c. Hyponatremia
d. Polyuria
e. Rash or pruritus
f. Ototoxicity

144
Q

What are the adverse effects of potassium-sparing diuretics?

A

Hyperkalemia

145
Q

What are the adverse effects of thiazide diuretics?

A

a. Dehydration
b. Orthostatic Hypotension
c. Hypokalemia

146
Q

What are the nursing implications for loop diuretics?

A

a. Take medications in the morning
b. Change positions slowly
c. Monitor weight
d. Take potassium supplements and consume potassium rich foods.

147
Q

What are the nursing implications for potassium-sparing diuretics?

A

a. Spironolactone may decrease effectiveness of anticoagulants
b. Clients taking lithium or digoxin may be at increased risk for toxicity.
c. Report S&S of hyperkalemia.

148
Q

What are the nursing implications of thiazide diuretics?

A

a. Use sunscreen to decrease photosensitivity.
b. Take K+ supplements as ordered; consume K+ rich foods
c. Report any tenderness or pain in joints (may cause hyperuricemia.. gout like conditions)

149
Q

Methotrexate

A

Inhibits lymphocyte multiplication.

Can be used to treat psoriasis and RA.

150
Q

Entanercept

A

b. Treats psoriasis and RA.

c. PATIENTS MUST BE SCREEN FOR LATEX ALLERGY. SOME DOSAGE FORMS MAY CONTAIN LATEX.

151
Q

Side effects of Mannitol

A 
Electrolyte Disturbances
Fatigue, N/V
Dizziness
Hyponatremia
Edema
Convulsions
Tachycardia
152
Q

Triamterine is contraindicated in

A

Lactating women

153
Q

Adverse effects of Amantadine

A 
Insomnia 
Nervousness
Lightheaded ness
Anorexia, Nausea
Anticholinergic Effects
Orthostatic Hypotension
Blurred vision

NURS 320 (28 decks)

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