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Flashcards in Exam 2 Deck (68):
1

Acid-Base Balance definition

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

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Acid

a substance that releases hydrogen ions

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Base

a substance that takes up hydrogen ions
Bicarbonate is the most important base in the body

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pH of a solution

a measure of its degree of acidity

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Low pH

solution is acidic (<7.35)

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High pH

solution is alkaline (>7.45)

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Buffers

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

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Metabolic acidosis is caused by...

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

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Clinical manifestations of metabolic acidosis

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

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Early symptoms of metabolic acidosis

headache and lethargy

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Severe symptoms of metabolic acidosis

life threatening arrhythmias and hypotension

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Treatment of metabolic acidosis

treat underlying cause; if severe, administer bicarbonate IVP

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Metabolic alkalosis is caused by...

increased bicarbonate due to excessive loss of metabolic acids
-prolonged vomiting
-GI suctioning
-excessive bicarbonate intake (antacids(
-diuretic therapy

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Clinical manifestations of metabolic alkalosis

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

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Severe symptoms of metabolic alkalosis

confusion and seizures, tachycardia, arrhythmias

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Treatment of metabolic alkalosis

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

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Respiratory acidosis can be caused by...

1. alveolar hypoventilation
2. airway obstruction
3. COPD

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Clinical manifestations of respiratory acidosis

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

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Treatment of respiratory acidosis

treat underlying cause, possible mechanical ventilation, bronchodilators, oxygen

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Respiratory alkalosis can be caused by:

1. alveolar hyperventilation and decreased plasma CO2
2. pulmonary disease, congestive HF

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Clinical manifestations of respiratory alkalosis

dizziness, confusion, tingling of extremities, seizures, coma

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Treatment of respiratory alkalosis

treat underlying cause, possible mechanical ventilation

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Interventions for neurologic changes

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

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Interventions for respiratory changes

bipap mask, ventilator

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Interventions for GI changes

reglan (metoclopramide), H2 antagonists to control stomach acid, prevent stress ulcers

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Interventions for arrhythmias

antiarrhythmics (amiodarone), Ca channel blockers (verapamil, diltiazem), beta blockers (metropolol)

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Interventions for hypotension

vasopressor agents, dopamine, Ca channel blockers, levophed as last result

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Base excess: (-2 to +2 mmol/L) measures

how well are the buffers managing metabolic acid

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BE < -2 mmol/L

too much metabolic acid

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BE > +2 mmol/L

too little metabolic acid

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Infiltrate

alveoli filled with fluid

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Consolidation

Lung tissue filled with fluid causing swelling/hardening of normally soft tissue

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Pulmonary edema

a life threatening condition associated with left ventricular failure that severely impairs gas exchange

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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

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Crackles

opening of alveoli which has collapsed from fluids

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Classic sign of pulmonary edema

pink, tinged sputum

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Nitroglycerin

Give every 5 minutes, up to 3 times
It decreases preload and afterload

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Emphysema

loss of lung elasticity, and hyperinflation of the lung
"pink bloaters"

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Chronic bronchitis

inflammation of the bronchi and brochioles

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Risk factors for COPD

active & passive smoking is greatest

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Complications of COPD

hypoxemia and acidosis, respiratory infection, and cardiac failure

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Medications for COPD

corticosteroids for inflammation, inhalors, mucolytics, nebulizor treatments

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Guillain-Barre Syndrome

an acute inflammatory demyelinating disease that affects the peripheral nervous system causing motor weakness and sensory abnormalities

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Clinical manifestations of Guillain-Barre Syndrome

ascending weakness, partial or total immobility, paralyzed respiratory muscles

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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

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Drug for Guillain-Barre Syndrome

IgA: effective in ambulatory patients early on in disease
Plasmapheresis: for paralysis, it removes circulating antibodies

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Clotting

a physiologic process in which blood is converted from a liquid to a semi-solid gel

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Risk factors for clotting

Age, genetics, immobility, and smoking

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Thrombocytopenia

a reduction in the number of platelets

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Platelet count <30,000

susceptible to uncontrolled bleeding with injury

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Platelet count <6,000

susceptible to spontaneous bleeding in the brain

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Polycythemia

production and presence of too many RBCs

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Prothrombin time (PT)

11-12.5 seconds
Extrinsic pathway
for cumadin (warfarin)

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INR

1.1-1.2
therapeutic: 2.5-3.5
for cumadin (warfarin)

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Partial thromboplastin time (PTT)

30-40 seconds
therapeutic: 1.5-2.5
Intrinsic
for heparin

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Clopidogrel (plavix)

Antiplatelet
adverse effect: brain hemorrhage

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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

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DIC

widespread clotting uses up existing clotting factors and platelets

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clinical manifestations of DIC

pain, stroke like symptoms, dyspnea, tachycardia, decreased kidney function, bowel necrosis

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medication therapy for DIC

ampheteracin B

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Sickle cell disease

a genetic disorder that results in chronic anemia, pain, disability, organ damage, risk for infection and early death

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How many alpha and beta chains of amino acids does a healthy adult have?

2 alpha chains, and 2 beta chains

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What percentage of hemoglobin A does a healthy adult have?

98-99%

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What percentage of hemoglobin S does a person with sickle cell disease have?

40%

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Clinical manifestations of sickle cell disease

Pain (due to block of blood flow), pallor or cyanosis, jaundice from RBC destruction, hepatomegay, splenomegaly, kidney damage

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Number one nursing intervention for sickle cell disease

Pain management

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Hemophilia

Hemophilia A is more common
-deficiency of facto VII
Hemophilia B
-deficiency of factor IX

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Clinical manifestations of hemophilia

abnormal bleeding, bruising easily