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2120 Health and Illness Concepts II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Acid-Base Balance definition

A

The process of regulating the pH, bicarbonate concentration, and partial pressure of carbon dioxide of body fluids

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2
Q

Acid

A

a substance that releases hydrogen ions

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3
Q

Base

A

a substance that takes up hydrogen ions

Bicarbonate is the most important base in the body

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4
Q

pH of a solution

A

a measure of its degree of acidity

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5
Q

Low pH

A

solution is acidic (<7.35)

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6
Q

High pH

A

solution is alkaline (>7.45)

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7
Q

Buffers

A

pairs of chemicals that take up hydrogen or release it to keep the pH in the normal range

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8
Q

Metabolic acidosis is caused by…

A
  1. noncarbonic acids increase
  2. bicarbonate is lost from the extracellular fluid
  3. cannot be regenerated by the kidney
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9
Q

Clinical manifestations of metabolic acidosis

A

Kussmaul respirations (deep, rapid respirations), anorexia, nausea, vomiting, diarrhea, abdominal pain

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10
Q

Early symptoms of metabolic acidosis

A

headache and lethargy

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11
Q

Severe symptoms of metabolic acidosis

A

life threatening arrhythmias and hypotension

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12
Q

Treatment of metabolic acidosis

A

treat underlying cause; if severe, administer bicarbonate IVP

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13
Q

Metabolic alkalosis is caused by…

A

increased bicarbonate due to excessive loss of metabolic acids

  • prolonged vomiting
  • GI suctioning
  • excessive bicarbonate intake (antacids(
  • diuretic therapy
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14
Q

Clinical manifestations of metabolic alkalosis

A

weakness, muscle cramps, hyperactive reflexes r/t volume depletion and electrolyte loss; respirations are slow and shallow;

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15
Q

Severe symptoms of metabolic alkalosis

A

confusion and seizures, tachycardia, arrhythmias

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16
Q

Treatment of metabolic alkalosis

A

treat underlying cause, sodium chloride for volume depletion, and potassium replacement

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17
Q

Respiratory acidosis can be caused by…

A
  1. alveolar hypoventilation
  2. airway obstruction
  3. COPD
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18
Q

Clinical manifestations of respiratory acidosis

A

headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, seizures, coma

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19
Q

Treatment of respiratory acidosis

A

treat underlying cause, possible mechanical ventilation, bronchodilators, oxygen

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20
Q

Respiratory alkalosis can be caused by:

A
  1. alveolar hyperventilation and decreased plasma CO2

2. pulmonary disease, congestive HF

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21
Q

Clinical manifestations of respiratory alkalosis

A

dizziness, confusion, tingling of extremities, seizures, coma

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22
Q

Treatment of respiratory alkalosis

A

treat underlying cause, possible mechanical ventilation

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23
Q

Interventions for neurologic changes

A

reorient x3, safety, work with family or other loved ones

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24
Q

Interventions for respiratory changes

A

bipap mask, ventilator

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25
Interventions for GI changes
reglan (metoclopramide), H2 antagonists to control stomach acid, prevent stress ulcers
26
Interventions for arrhythmias
antiarrhythmics (amiodarone), Ca channel blockers (verapamil, diltiazem), beta blockers (metropolol)
27
Interventions for hypotension
vasopressor agents, dopamine, Ca channel blockers, levophed as last result
28
Base excess: (-2 to +2 mmol/L) measures
how well are the buffers managing metabolic acid
29
BE < -2 mmol/L
too much metabolic acid
30
BE > +2 mmol/L
too little metabolic acid
31
Infiltrate
alveoli filled with fluid
32
Consolidation
Lung tissue filled with fluid causing swelling/hardening of normally soft tissue
33
Pulmonary edema
a life threatening condition associated with left ventricular failure that severely impairs gas exchange
34
Clinical manifestations of pulmonary edema
crackles, dyspnea at rest, disorientation, tachycardia, hypertension or hypotension, reduced urinary output, cough, pink tinged sputum, PVs and other dysrhythmias, anxiety, restlessness
35
Crackles
opening of alveoli which has collapsed from fluids
36
Classic sign of pulmonary edema
pink, tinged sputum
37
Nitroglycerin
Give every 5 minutes, up to 3 times | It decreases preload and afterload
38
Emphysema
loss of lung elasticity, and hyperinflation of the lung | "pink bloaters"
39
Chronic bronchitis
inflammation of the bronchi and brochioles
40
Risk factors for COPD
active & passive smoking is greatest
41
Complications of COPD
hypoxemia and acidosis, respiratory infection, and cardiac failure
42
Medications for COPD
corticosteroids for inflammation, inhalors, mucolytics, nebulizor treatments
43
Guillain-Barre Syndrome
an acute inflammatory demyelinating disease that affects the peripheral nervous system causing motor weakness and sensory abnormalities
44
Clinical manifestations of Guillain-Barre Syndrome
ascending weakness, partial or total immobility, paralyzed respiratory muscles
45
Three stages of Guillain-Barre Syndrome
1. acute or initial period (1-4 weeks): begins with onset of symptom and ends with no further symptoms 2. plateau period (several days to 2 weeks): ascending weakness stops 3. recovery phase (4-6 months, maybe 2 years): descending weakness until there is recovery
46
Drug for Guillain-Barre Syndrome
IgA: effective in ambulatory patients early on in disease Plasmapheresis: for paralysis, it removes circulating antibodies
47
Clotting
a physiologic process in which blood is converted from a liquid to a semi-solid gel
48
Risk factors for clotting
Age, genetics, immobility, and smoking
49
Thrombocytopenia
a reduction in the number of platelets
50
Platelet count <30,000
susceptible to uncontrolled bleeding with injury
51
Platelet count <6,000
susceptible to spontaneous bleeding in the brain
52
Polycythemia
production and presence of too many RBCs
53
Prothrombin time (PT)
11-12.5 seconds Extrinsic pathway for cumadin (warfarin)
54
INR
1.1-1.2 therapeutic: 2.5-3.5 for cumadin (warfarin)
55
Partial thromboplastin time (PTT)
30-40 seconds therapeutic: 1.5-2.5 Intrinsic for heparin
56
Clopidogrel (plavix)
Antiplatelet | adverse effect: brain hemorrhage
57
Streptokinase t-PA
given in ER for stroke unless there is active bleeding in the brain (need CT scan) 3hr window from when symptoms started
58
DIC
widespread clotting uses up existing clotting factors and platelets
59
clinical manifestations of DIC
pain, stroke like symptoms, dyspnea, tachycardia, decreased kidney function, bowel necrosis
60
medication therapy for DIC
ampheteracin B
61
Sickle cell disease
a genetic disorder that results in chronic anemia, pain, disability, organ damage, risk for infection and early death
62
How many alpha and beta chains of amino acids does a healthy adult have?
2 alpha chains, and 2 beta chains
63
What percentage of hemoglobin A does a healthy adult have?
98-99%
64
What percentage of hemoglobin S does a person with sickle cell disease have?
40%
65
Clinical manifestations of sickle cell disease
Pain (due to block of blood flow), pallor or cyanosis, jaundice from RBC destruction, hepatomegay, splenomegaly, kidney damage
66
Number one nursing intervention for sickle cell disease
Pain management
67
Hemophilia
Hemophilia A is more common -deficiency of facto VII Hemophilia B -deficiency of factor IX
68
Clinical manifestations of hemophilia
abnormal bleeding, bruising easily

2120 Health and Illness Concepts II (3 decks)

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