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NURS 311: Pathophysiology > Exam 2: 7-10 > Flashcards

Exam 2: 7-10 Flashcards

1
Q

What are the clinical manifestations of fluid volume deficit

A

o Thirst
o Dry Mucous Membranes
o Weight loss
o Flattened neck veins
o Diminished skin turgor
o Prolonged cap refill (more than 3 seconds)
o Decreased urine output
o Increased heart rate
o Decreased blood pressure
o Altered LOC

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2
Q

Hypovolemia is known as what?

A

o Decreased vascular volume, i.e – fluid volume deficit

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3
Q

What is a common cause of Hypovolemia

A

o Excessive body fluid loss (ie. Hemorrhage, excessive sweating, etc)
o Reduction of fluid intake (ie. Dehydration)
o Excessive excretion
o Loss of fluid to third space (results in decrease extracellular fluid volume)

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4
Q

With decreased intravascular volume, what two things might be interrupted

A

o Blood circulation
o Transportation of oxygen and nutrients to tissues

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5
Q

What are some of the physiologic responses to counter the manifestations of hypovolemia?

A

o Decreased blood flow to kidneys triggers RAAS: increases sodium and water reabsorption w/ aldosterone release

o Decreased BP stimulates sympathetic nervous system to increase HR, constrict arteries, and increase contractility of heart

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6
Q

What are some nursing managements associated with fluid volume deficit

A

o Measure all fluids that enter / leave body (I/O)
o Check electrolyte, CBC, and urine-specific gravity
o Assess for hypotension and weak pulses
o Assess respiratory system and tissue perfusion
o Check orientation, vision, hearing, reflexes, muscle strength
o Perform daily weights

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7
Q

What lab testing can be done to help provide insight into fluid volume status and guide treatment strategies

A

o Hemoglobin - increase w/ hypovolemic
o Hematocrit - increase w/ hypovolemic
o BUN - elevated w/ hypovolemic
o Creatinine - elevated w/ hypovolemic
o Urine-specific gravity - elevated w/ dehydration
o Blood glucose
o Electrolyte panel
o Plasma proteins

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8
Q

What are the clinical manifestations of fluid volume excess (Hypervolemia)

A

o JVD
o Bounding pulses
o Edema
o Increased weight
o Increased blood pressure

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9
Q

What are some causes of Hypervolemia

A

o Heart Failure
o Cirrhosis of liver
o Kidney failure
o Excessive fluid replacement

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10
Q

What are some treatments for Hypervolemia

A

o Loop diuretics
o Limiting water intake

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11
Q

Sodium loss typically occurs how?

A

**o Vomiting and diarrhea **
o GI suctioning
o Inadequate salt intake (not common)
o Diuretics

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12
Q

What are the normal ranges for sodium?

A

135 - 145

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13
Q

What does Na+ help maintain

A

o Blood pressure,
o blood volume
o pH balance

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14
Q

Altered ____ function can lead to N&V, lethargy, confusion, seizures, and coma with hyponatremia

A

o Neuronal

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15
Q

Excessive intake of _ and loss of body _ are the primary causes of hypernatremia

A

Sodium
Water

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16
Q

What are some clinical manifestations of hyponatremia?

A

FROM FLUID SHIFTING OUT OF ECF AND INTO CELLS = SWELLING
* Headache
* Irritiability
* Difficulty concentrating
* Vomiting, confusion, seizure -> severe
* Tachycardia, thready pulse
* Postural hypotension
* Dry membranes

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17
Q

What is the function of sodium in the body

A

conduct nerve impulses,
maintain the proper balance of water and minerals

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18
Q

What electrolyte is the primary determinant of blood osmolality?

A

Sodium

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19
Q

What is the nursing management associated w/ Hyponatremia

A

o 24 I/O record
o Check Specific urine gravity, will be less than 1.010
o Assess for bounding pulses and bulging neck veins
o Assess for putting edema w/ fluid excess
o Monitor daily weights
o Assess for BP and respiratory changes

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20
Q

Where is potassium mostly found?

A

o In muscles –> total body K+ determined in large by body size & muscle mass

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21
Q

What is primary function of potassium?

A

Major factor in resting membrane potential of nerve and muscle cells

Imbalances affect neuromuscular and cardiac function

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22
Q

What are some possible causes of Hypokalemia

A

o Excessive fluid loss / electrolyte loss
o Severe vomiting or diarrhea
o Diet low in K+
o DKA

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23
Q

How does Aldosterone affect K+?

A

o Adds Na+, which means and loses K

High aldosterone means low k+

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24
Q

What are the normal ranges for Potassium?

A

3.5 - 5

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25
Q

What are some clinical manifestations of hypokalemia

A

HYPERPOLARIZATION AND IMPAIRED MUSCLE CONTRACTION

  • Skeletal muscle weakness, parestheisias
  • Severe: paralysis
  • Shallow breathing, arrest -> weakened muscles
  • Decreased GI motility -> constipation, paralytic ileus)
  • Weak, irregular pulse
  • Hyperglycemia
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26
Q

What function does calcium have in the body?

A

o Blood clotting
o Generation of action potentials
o Muscle contraction

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27
Q

What is the normal range of calcium?

A

8.5 - 10

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28
Q

What are some common clinical manifestations of Hypercalcemia?

A

Decreased neuromuscular excitiability caused by increased threshold

  • Lethargy, weakness, fatigue
  • Decreased memory
  • Depressed DTR
  • Increased BP
  • Confusion
  • Anorexia, N&V
  • Bone pain, fx
  • Polyuria, dehydration
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29
Q

What are some causes of Hypercalcemia

A
  • Excessive bone breakdown
  • Thyroid disorders
  • Excessive intake of calcium
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30
Q

Magnesium has functions similar to what other electrolytes

A
  • Ca+
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31
Q

What are some clinical manifestations of hypomagnesia

A

Confusion
Muscle cramps, tremors
Hyperactive DTR
Chvostek’s sign
Trousseau’s sign
Dysrythmias

SIMILAR TO Ca+

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32
Q

What are some common causes of hypomagensia

A

o Inadequate intake of Mg due to malnutrition
o Malabsorption syndromes
o Severe burns
o Alcoholism
o Diuretic use

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33
Q

Hypomagnesia occurs in associated with what two other electrolyte imbalances

A

o Hypokalemia
o Hypocalcemia

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34
Q

What is the normal range for magnesium?

A

1.5 - 2.5

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35
Q

Pharm options for fluid excess

A

Diuretic ->
o Loop diuretic
o Thiazide diuretics
o Potassium-sparing diuretics

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36
Q

What medication increases urine production and causes decreased sodium reabsorption (resulting in water loss)

A

o Diuretics

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37
Q

What type of diuretic am i:

Reduces the reabsorption of sodium in the ascending loop of henle

A

o Loop diuretic

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38
Q

What type of diuretic am I:

Prevents NaCl reabsorption in the **distal convoluted tubule **

A

o Thiazide

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39
Q

What type of diuretic am i:

Reduces sodium reabsorption in the **distal tubule and collecting duce **

A

o Potassium-sparing

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40
Q

What are some clinical manifestations of dehydration

A

o Decreased LOC
o Prolonged cap refill
o Dry mucous membranes
o Decreased / absent tears
o VS changes
o Depressed fontanel, sunken eyes
o Decreased or absent urine output

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41
Q

What electrolyte is affected by hypoparathyroidism

A

Calcium

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42
Q

Parathyroid glands are responsible for regulation of what

A

o Blood calcium

‘Think “PC” – Parathyroid Calcium

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43
Q

If parathyroid hormone low, what does this mean blood calcium levels will be

A

o Low (less than 8.5)

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44
Q

How does the negative feedback loop work w/ the parathyroid?

A

o When parathyroid (and calcium) is low, PTH will be stimulated to increase Ca

o Calcium levels will rise until reaches appropriate levels -> PTH production stops

“PTH” -> puts the calcium high

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45
Q

What are the clinical manifestations of hypoparathyroidism?

A

o Trousseau’s sign – blood pressure cuff
o Chvostek’s sign - smile
o Diarrhea
o Circumoral tingling

THOSE OF LOW CALCIUM

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46
Q

What are the causes of hypoparathyrodism

A

o Hypomagnesium (Mg + Ca are bff’s)
o Autoimmune -> body attacks parathyroid
o Thyroidectomy -> complete removal of thyroid
o Radiation – can damage parathyroids

“HATR”

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47
Q

What is the purpose of the sodium-potassium pump

A

o To transport K+ into cells and transport Na+ out -> Requires ATP energy

o Done to provide energy for cell and help remove acid from body

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48
Q

____ are substances that donate hydrogen ions

A

Acids

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49
Q

__ are substances that accept hydrogen ions

A

Bases

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50
Q

What is the clinical measurement of the acid to base ratio called?

A

pH

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51
Q

What are the three types of buffer systems?

A

o Plasma
o Respiratory
o Renal

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52
Q

Of the three buffer systems, which is the quickest to react

A

o Plasma -> reacts in seconds to hydrogen ion level

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53
Q

Which buffer system reacts in minutes to excrete C02

A

Respiratory

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54
Q

Of the three buffer system, which takes the longest to respond?

A

o Renal -> **reacts in hours to days **to produce, absorb, and excrete acids/bases/ions

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55
Q

What is the purpose of the buffer systems?

A

o Mix acids and bases to resist pH change

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56
Q

What is the normal range for pH?

A

o 7.35 – 7.45

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57
Q

What is the normal range for PaCO2?

A

o 35 – 45

58
Q

What is the normal range of HC03?

A

22 - 28

59
Q

What ABG is associated w/ respiratory?

A

PaCO2

** NOT LOOKED AT W/ METABOLIC **

60
Q

What ABG is associated w/ metabolic?

A

HCO3

** NOT LOOK AT W/ RESPIRATORY **

61
Q

In Metabolic acidosis, what do the ABGs look like

A

o pH less than 7.35
o HCO03 less than 22

62
Q

What are contributing mechanisms of Metabolic Acidosis?

A

o Increased production of nonvolatile acids (fasting, ketoacidosis, lactic acidosis)

o Decreased secretion of acids by kidneys -> leads to renal failure

o Increased loss of bicarbonate (HC03) – caused by diarrhea and GI suction

o Increase in chloride

63
Q

What are some of the clinical manifestations associated with Metabolic Acidosis

A

o Anorexia
o N&V
o Weakness, Lethargy
o Confusion
o Coma
o Vasodilation
o Decreased h/r
o Flushed skin

64
Q

What are some contributing mechanisms of Metabolic Alkalosis?

A

o Decreased H+ ions
o Increased HCO3 ions
o Loss of Cl- ions

65
Q

What do ABGs look like in Metabolic Alkalosis?

A

o pH above 7.45
o HCO3 above 28

66
Q

What is the difference between benign and malignant tumors?

A

o Benign: non-cancerous, remain localized, *closely resemble tissue origin *

o Malignant: cancerous, invasive, proliferate rapidly, potential to spread, *do not resemble tissue origin *

67
Q

What are carcinogens?

A

o Agents that interfere w/ molecular pathway and cause tumors to form in the body

68
Q

What are the two types of carcinogens?

A

o Direct: cause modifications in DNA and cell function

o Indirect: induce immunosuppression or chronic inflammation

69
Q

What are some substances that can cause or promote cellular mutations?

A

o Radiation: gamma rays, x-rays, UV rays
o Hormones
o Chemicals – asbestos, insecticides, etc.
o Tobacco
o Microbes – viral infections: HPV, hepatitis -> leads to neoplasia and can alter genes or proteins

70
Q

Carcinogens: Hormones

A

o Can be cancer tx
o Removing organs or tissues that secrete specific hormones can directly kill tumor cells
o Tamoxifen – estrogen modulator, blocks action of estrogen & inhibits tumor growth (used in breast cancer)

71
Q

What is the initiation-promotion-progression theory?

A

o Steps involved in the development of neoplasms

72
Q

Step 1 in the initiation-promotion-progression theory is what?

A

o Initiation: exposure event of cells to a carcinogenic agent, causes a mutation of a cell

73
Q

Step 2 in initiation-promotion-progression theory is what?

A

o Promotion: promoter agent activates oncogene -> Mutated cells expand, grow, and reproduce

74
Q

Step 3 in initiation-promotion-progression theory is what?

A

Progression: independent growth occurs, considered cancerous at this step

75
Q

What are some general manifestations of cancer?

A

o Lymphadenopathy: enlarged lymph nodes throughout the body

o Unexplained Fever- results from the release of pyrogens from cancer cells

o Anorexia & taste receptor changes - present within the inflammatory response caused by the presence of circulating chemical mediators

o Cachexia- a result of feelings of fullness when eating coupled with release of chemical mediators

o PAINLESS palpable mass

o Loss of tissue function (depending on location)

76
Q

What are the three goals of cancer treatment?

A

o Eradicate the neoplasm
o Control the growth and spread
o Reduce symptoms w/ curing the cancer

77
Q

What are the risk factors for colon cancer?

A

o Age: over 50 years of age
o Family history
o Smoking
o Alcohol use
o Bowel disease
o Obesity, inactivity
o High-fat diet

78
Q

What are some common clinical manifestations of colon cancer?

A

o Change in bowel habits
o Occult or frank blood in stool (cancer in ascending colon)
o Abdominal pain
o Visible blood in stool (cancer in descending colon)
o Bowel obstruction (w/ descending and rectum cancer)
o Anemia – may be first clue

79
Q

What are some clinical manifestations associated with lung cancer?

A

o Persistent cough
o Hemoptysis (bloody sputum)
o Chest pain
o SOB

80
Q

What are the common causes of lung cancer?

A

o Result of environmental exposures to particular toxins (i.e, smoke) combined w/ genetic susceptibility

81
Q

What are the stages of lung cancer?

A

o Stage 1: cancer located only in lungs, not spread to lymph nodes

o Stage 2: cancer in lungs and nearby lymph nodes

o Stage 3: cancer in lungs, lymph nodes, and middle of chest

o Stage 4: cancer in both lungs, fluid around the lungs, and/or other organs

82
Q

Treatment for lung cancer depends on what?

A

Cancer type
o Small cell: chemotherapy
o Non-small cell: surgery if possible, radiation for local control

83
Q

What are the diagnostic tests associated with colon cancer?

A

o CBC
o Liver function tests (common place for spreading)
o Serum carcinoembryonic antigen (SCA) -> protein, will be high with cancer
o Colonoscopy
o Sigmoidoscopy
o Bx of suspicious lesions

84
Q

How often should patients get colonoscopies?

A

o Every 10 years beginning at age 50

85
Q

What is the treatment with colon cancer?

A

o Surgical resection with localized tumors
o Drug combination of chemotherapy, biological agents, and radiation for unresectable, locally advanced, or metastatic disease

86
Q

Brain cancer is commonly a result of what?

A

o Metastatic spread from another site

87
Q

What are the clinical manifestations of brain cancer?

A

o Depend on size and location of tumor

o Neurologic deficits from tumor eroding functional neurons -> vision changes,
numbness, weakness, or paralysis

o Cognitive, behavioral, personality changes: irritability, forgetfulness, depression

o Pressure increases: headaches (later sign), vomiting

o Seizures from irritation and disorderly discharge of neurons

88
Q

What are the common diagnostic tests for brain cancer?

A

o Complete neurologic examination -> testing cranial nerves, reflexes, sensory function, motor function

o Direct visualization: radiographs, CT, MRI, cerebral angiography

89
Q

What are the diagnostic tests for acute leukemia?

A

o Patient history and physical exam
o CBC – will show blasts (immature wbc) greater than 20%
o Microscopic examination of blood

90
Q

Acute lymphocytotic leukemia (ALL) is most commonly seen in who?

A

Children

91
Q

Acute myeloid leukemia (AML) is most commonly seen in who?

A

Adults

92
Q

What are some clinical manifestations of acute leukemia?

A

Sudden onset:
o Immaturity of WBC and other cells originating in bone marrow
o Growing of leukemic cells in bone marrow
o Infiltration of leukemic cells in the CNS, lymph nodes, liver and spleen

93
Q

What is the difference between Hodgkin’s and Non-Hodgkin’s Lymphoma?

A

Hodgkin’s has “Reed-Sternberg” cells, when they are not present it is classified as Non-Hodgkin’s

94
Q

What are some clinical manifestations of Hodgkin’s Lymphoma?

A

**o Presentation of non-tender enlarged lymph node or group of nodes in neck **
o Low grade fever
o Fatigue
o Weight loss
o Pruritus
o Drenching night sweats
o *Mass @ mediastinum that is greater than 1/3 of chest diameter *
o Possible: enlarged spleen and liver

95
Q

What are some diagnostic tests associated with Hodgkin’s Lymphoma?

A

o Patient hx, physical exam, lab studies
o Thoracic and abdominal studies
o **MOST SIGNIFICANT FEATURE: presence of Reed-Sternberg cells **

96
Q

How is Hodgkin’s Lymphoma staged?

A

With Ann Arbor classification

o Stage 1: **single lymph node area **single extranodal site (ie. Spleen, pharyngeal lymphatic ring)
o Stage 2: **2 or more lymph node areas **on the **same side **of diaphragm
o Stage 3: lymph nodes on both side of diaphragm
o Stage 4: disseminated or **multiple involvement of the extranodal organs **

97
Q

What are some clinical manifestations of Non-Hodgkin’s lymphoma?

A

o Painless and slowly progressive enlargement of lymph nodes (same as HL)
o Systemic: fever, night sweats, weight loss, increased risk for infection,
o *Paraneoplastic syndromes (group of disorders trigged by abnormal immune response -> peripheral neuropathy, MG *

98
Q

What are the diagnostic tests associated w/ Non-Hodgkin’s Lymphoma?

A

**o Lymph node biopsy **
o Chest and abdominal CT scan -> visualize tumor and location
o CSF fluid can be positive for metastasis with aggressive NHL

99
Q

What am i:

Liver disease characterized by interference of local blood flow and hepatocyte damage

A

Cirrhosis

100
Q

What is the most common complication of cirrhosis?

A

o Ascites – accumulation of fluid in the peritoneal cavity

101
Q

What are some clinical manifestations of cirrhosis?

A

o Moderate to severe abdominal discomfort
o Increase abdominal girth
o Increased weight
o Severe sodium retention
o Renal failure (oliguria and increase creatinine)

102
Q

What is the diagnostic criteria for cirrhosis?

A

o Liver, renal, and cardiac function – determines systemic damage
o Physical exam and changes in body weight – to diagnose ascites
o Measurement of abdominal girth circumference

103
Q

Why does cirrhosis result in ascites?

A

o Blood flow is slowed thru liver -> increases pressure in vein that brings blood to liver from intestines and spleen (portal vein)

o Increased pressure causes fluid to accumulate in legs and abdomen

104
Q

What are some treatments for cirrhosis?

A

o Diuretics to promote fluid loss, balance Na
o Paracentesis: removal of ascitic fluid via cannula

105
Q

What is Hydrocephalus?

A

o Fluid buildup in the ventricles deep within the brain

106
Q

What causes Hydrocephalus?

A

o an imbalance between the amount of fluid produced and the rate of fluid reabsorption

o accumulation of CSF leads to ventricular enlargement and increased ICP.

107
Q

How is hydrocephalus classified when CSF flow is obstructed?

A

o Noncommunicating

108
Q

How is hydrocephalus classified when CSF absorption is impaired?

A

o Communicating

109
Q

What are some causes of hydrocephalus?

A

o Intraventricular hemorrhage
o Neural tube defect (i.e, spina bifida)
o Meningitis
o TBI
o CSF flow obstruction
o Impaired CSF absorption

110
Q

What are some clinical manifestations of hydrocephalus in infants?

A

o Enlarged head w/ bulging fontanels
o Scalp vein distention
o Difficulty feeding
**o High, shrill cry **

111
Q

What are some clinical manifestations of hydrocephalus in older children / adults?

A

o Impaired motor and cognitive function
o Incontinence
o Death can result due to increased ICP

112
Q

What are some diagnostic criteria for hydrocephalus?

A

o Head circumference measurement
o **Transillumination: shining light against head to see accumulation of fluid in tissue **
o Imaging studies: Ultrasound, CT, MRI, skull radiograph to see separation of skull bones

113
Q

What is a pressure injury and how does it differ from an ischemic neuronal injury?

A

o Pressure injury occurs from increased CSF volume -> i.e, tumor, inflammation

o Ischemic injury is from inadequate perfusion to neurologic tissue, resulting in impaired oxygenation (i.e, stroke)

114
Q

What type of injuries lead to coup/countercoup?

A

o Head trauma from a blunt force injury (when head strikes a hard surface from front and bounces back -> damage to both sides

115
Q

Clinical manifestations of C1-C2 injuries

A

o Loss of involuntary function -> sweating, BP regulation, body temp regulation
o Requires respiratory support
o Above C4 may require respiratory support- ventilator

116
Q

Clinical manifestations of C7-T1 injuries

A

o can straighten arms, may not have fine motor control
o Paraplegia usually results from injuries at the thoracic level
o Trunk and lower body control are lost at T1 (returns @ T9)

117
Q

What clinical manifestations are present at T9-T12 injuries?

A

o return of sitting balance and abdominal muscle control

118
Q

Quadriplegia occurs with injuries within what range of the spine?

paralysis of all four limbs;

A

o C1-C7/T1

119
Q

Paraplegia occurs with injuries within what range of the spine?

paralysis of the legs and lower body

A

o injuries from the thoracic level -> T1-T12

120
Q

When there is damage to the lumbar and sacral segments of the spine, what clinical manifestations can be present?

A

o loss of control of lower extremities -> bowel, bladder, sexual function may be affected

121
Q

What is the cause of renal tubulopathy w/ maternal hydramnios?

A

o Excessive amniotic fluid because of increased fetal urine output -> Can complicate fetal life in first 28 days of life:

  • increased urine output
  • hypercalciuria (calcium in urine) leads to electrolyte imbalance
122
Q

What are clinical manifestations of renal tubulopathy w/ maternal hydramnios?

A

o Fever
o Vomiting
o Diarrhea
o Metabolic alkalosis - associated with contracted extracellular fluid because of sodium chloride loss

123
Q

What is the pathophysiology of cerebral palsy?

A

o Exact cause is not known, but central control of movement is altered

  • Cerebral anoxia (interruption of o2 to brain), hemorrhage, or other neurologic insults
124
Q

What is cerebral palsy?

A

o Group of disorders that result from damage to upper motor neurons (responsible for carrying out electrical impulses -> initiate and modulate movement)

o Stems from event that occurs in prenatal, perinatal, or post-natal period

o Symptoms appear during first few years of life

125
Q

What are some clinical manifestations of cerebral palsy?

A

Delay in reaching milestones:
o Reaching for toy: 3-4 months
o Sitting: 6-7 months
o Walking: 10 to 14 months

o Development of seizures

o Impairments in motor dysfunction during physical activity (i.e, running)

o Trouble w/ fine motor skills, coordination w/ balance and walking

126
Q

How is cerebral palsy classified?

A

o Based on type of motor dysfunction or by anatomy affected

127
Q

What are some of the motor dysfunction classifications of cerebral palsy?

A

Spastic: inability of muscles to relax
o Hemiplegia: one arm and one leg on same side of body is involved
o Diplegia: both legs involved
o Quadriplegia: involving all 4 extremities, trunk, and neck muscles

o Athetoid / Dyskinetic: inability to control muscle movement

o Ataxic: inability to control balance or coordination

128
Q

What are some diagnostic criteria for cerebral palsy?

A

o Apgar score of less than 7 at 5 minutes after birth (measures h/r, respiratory effort, color, reflexes, muscle tone)

o Metabolic acidosis – determined from analysis of umbilical cord

o Evidence of cerebral hypoxic-ischemic injury via MRI

o Organ system failure (renal, liver, cardiac, GI) due to hypoxic-ischemic encephalopathy (alteration of brain function)

129
Q

What are some treatments for Cerebral Palsy?

A

o No cure
o Botox can be used to help loosen muscle
o Anti-seizure meds
o PT, OT, Braces

130
Q

What are some clinical manifestations of Parkinson’s Disease?

A

TRAP!
o Tremors
o Rigidity (cog-well)
o Akinesia / Bradykinesia -> slowed / lack of movement
o Postural instability

131
Q

What are some pharmacologic options for Parkinson’s disease?

A

o Levodopa-Carbidopa
o Entacapone + Levodopa-Carbidopa
o Amantadine alone or in combo w/ anticholinergic
o Dopamine agonists

132
Q

Pharmacologic options for Parkinson’s disease: Levodopa-Carbidopa

A

Levodopa replaces dopamine, Carbidopa delays conversion of Levodopa until crosses BBB

Prolonged use = lose effectiveness. Higher doses needed, has more S/E

133
Q

Pharmacologic options for Parkinson’s disease: Entacapone + Levodopa-Carbidopa

A

extends duration of action of Levodopa

134
Q

Pharmacologic options for Parkinson’s disease: Amantadine alone or in combo w/ anticholinergic

A

can help reduce PD symptoms and decrease dyskinesia from Levodopa use

  • should be reserved for younger due to anticholinergic effects (dry mouth, blurred vision, urinary retention)
135
Q

Dopamine agonists

bromocriptine, pramipexole, rotigotine, ropinorole

A

activate DA receptors

136
Q

What is the pathophysiology of MS?

A

Recurrent bouts of CNS inflammation results in damage to both the myelin sheath and axons -> slows nerve conduction impulses down the axon

137
Q

What are some clinical manifestations of MS?

A

Specific nerves are affected at different times, contributing to variations seen in the course, s/s of disease

  • Unilateral vision loss, cognitive loss, bladder dysfunction, gait and balance alterations, spasticity, paresthesia, slurred speech, fatigue, pain
  • Presentation of signs/symptoms can depend on which pattern pt has
138
Q

A MS exacerbation can be defined as what?

A

Demyelinating event of at 24 hrs with **NO fever or infection **

139
Q

What are the 4 patterns of MS?

A

1.CIS: initial presentation of symptoms

  1. Relapse-remitting: periods of acute neurologic symptoms alternating w/ periods of symptom relief / return of neurologic function
  2. Primary progressive: slow, chronic deterioration of neurologic function -> not associated w/ exacerbations or remissions
  3. Secondary progressive: initial presentation of R/R (has exacerbations and remissions) followed by a pattern of slow, chronic deterioration as seen in PP
140
Q

What are some diagnostic criteria of MS?

A

o Presence of s/s consistent with disease

o Complete medical history assessment and thorough neuro exam

o MRI to detect scarring or plaques in CNS

o CNS response to peripheral sensory stimuli **(evoked potentials test) **-> can indicate abnormal nervous system function

o Lumbar puncture – evaluate CSF for presence of IgG

NURS 311: Pathophysiology (2 decks)

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