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Patho 22, 23, 25

front 1

When preparing for the admission of a client diagnosed with bronchiectasis, the nurse will

back 1

put a sputum cup and a box of tissues on the bedside table.

front 2

A major risk factor for the development of active pulmonary tuberculosis (TB) disease is

back 2

immunosuppression.

front 3

Immunosuppressed individuals, such as those with HIV, are at high risk for active _____ _______.

back 3

TB disease

front 4

Copious amounts of foul-smelling sputum are generally associated with

back 4

bronchiectasis.

front 5

Obstructive sleep apnea would most likely be found in a patient diagnosed with

back 5

Pickwickian syndrome.

front 6

Pickwickian syndrome is _________ ________ ____ ________.

back 6

Hypoventilation caused by obesity.

front 7

A restrictive respiratory disorder is characterized by

back 7

decreased residual volume.

front 8

Obstructive disorders are associated with

back 8

Low expiratory flow rates and high residual volume.

front 9

Accumulation of fluid in the pleural space is called

back 9

pleural effusion.

front 10

Pleural effusion is accumulation of

back 10

fluid in the pleural space.

front 11

The hallmark manifestation of acute respiratory distress syndrome is

back 11

hypoxemia.

front 12

The hallmark of acute respiratory distress syndrome is hypoxemia caused by

back 12

intrapulmonary shunting of blood.

front 13

A patient has been hospitalized several times in 6 months with severe ECV depletion and hypokalemia resulting from chronic laxative abuse. Which blood gas results should be relayed to the physician?

back 13

pH in high part of normal range, PaO2 normal, PaCO2 high, bicarbonate high

front 14

A major cause of treatment failure in tuberculosis is

back 14

noncompliance.

front 15

Individuals who have chronic bronchitis most often have

back 15

A productive cough.

(for at least 3 months)

front 16

Airway obstruction in chronic bronchitis is because of

back 16

thick mucus, fibrosis, and smooth muscle hypertrophy.

front 17

After evaluation, a child’s asthma is characterized as “extrinsic.” This means that the asthma is

back 17

associated with specific allergic triggers.

front 18

To best prevent emphysema, a patient is instructed to stop smoking since cigarette smoke.

back 18

impairs α1-antitrypsin, allowing elastase to predominate.

front 19

Viral pneumonia is characterized by

back 19

a dry cough.

front 20

Cystic fibrosis is associated with

back 20

bronchiectasis.

front 21

Which complication of asthma is life threatening?

back 21

Status asthmaticus

front 22

Status asthmaticus is a

back 22

severe attack unresponsive to routine therapy and can be life threatening if not reversed.

front 23

Early manifestations of a developing metabolic acidosis include

back 23

headache.

front 24

A patient with a productive cough and parenchymal infiltrates on x-ray is demonstrating symptomology of

back 24

bacterial pneumonia.

front 25

A common characteristic of viral pneumonia is

back 25

dry cough.

front 26

Clinical manifestations of severe symptomatic hypophosphatemia are caused by

back 26

deficiency of ATP.

front 27

What age group has a larger volume of extracellular fluid than intracellular fluid?

back 27

Infants

front 28

Fully compensated respiratory acidosis is demonstrated by

back 28

pH 7.36, PaCO2 55, HCO3 – 36.

front 29

A person who has hyperparathyroidism is likely to develop

back 29

hypercalcemia.

front 30

A patient, who is 8 months pregnant, has developed eclampsia and is receiving intravenous magnesium sulfate to prevent seizures. To determine if her infusion rate is too high, you should regularly

back 30

check the patellar reflex; if it becomes weak or absent, her infusion rate probably is too high and she is at risk for respiratory depression or cardiac arrest.

front 31

Hypermagnesemia causes

back 31

decreased neuromuscular excitability

front 32

A person who overuses magnesium-aluminum antacids for a long period of time is likely to develop

back 32

hypophosphatemia.

front 33

A patient has a positive Chvostek sign. The nurse interprets this as a sign of

back 33

increased neuromuscular excitability.

front 34

A known cause of hypokalemia is

back 34

insulin overdose.

front 35

Insulin overdose causes hypokalemia by

back 35

shifting potassium into cells.

front 36

Emesis causes

back 36

metabolic alkalosis

front 37

The body compensates for metabolic alkalosis by

back 37

hypoventilation.

front 38

Clinical manifestations of extracellular fluid volume deficit include

back 38

weak pulse, low blood pressure, and increased heart rate.

front 39

The major buffer in the extracellular fluid is

back 39

bicarbonate.

front 40

Signs and symptoms of clinical dehydration include

back 40

decreased urine output.

front 41

Diarrhea causes

back 41

metabolic acidosis.

front 42

Diarrhea causes metabolic acidosis as the intestinal fluids are rich in

back 42

bicarbonate ions.

front 43

Clinical manifestations of moderate to severe hypokalemia include

back 43

muscle weakness and cardiac dysrhythmias.

front 44

The process responsible for distribution of fluid between the interstitial and intracellular compartments is

back 44

osmosis.

front 45

Filtration is responsible for the distribution of

back 45

fluid between the vascular and interstitial compartments

front 46

A person who experiences a panic attack and develops hyperventilation symptoms may experience

back 46

numbness and tingling in the extremities.

front 47

Numbness and tingling in the extremities occurs in alkalosis as a result of

back 47

increased neuromuscular irritability.

front 48

What is the most likely explanation for a diagnosis of hypernatremia in an elderly patient receiving tube feeding?

back 48

Inadequate water intake

front 49

What form of oral rehydration, bottled water or salty broth, is best suited for a patient who is demonstrating signs of clinical dehydration?

back 49

Salty soup, because it will provide some sodium to help hold the fluid in his blood vessels and interstitial fluid

front 50

Vomiting of stomach contents or continuous nasogastric suctioning may predispose to development of

back 50

Metabolic acid deficit.

front 51

Empyema is defined as an

back 51

Infection in the pleural space.

front 52

Air that enters the pleural space during inspiration but is unable to exit during expiration creates a condition called

back 52

tension pneumothorax.

front 53

An increase in the resting membrane potential (hyperpolarized) is associated with

back 53

hypokalemia.

front 54

The assessment findings of a 5-year-old with a history of asthma include extreme shortness of breath, nasal flaring, coughing, pulsus paradoxus, and use of accessory respiratory muscles. There is no wheezing and the chest is silent in many areas. How should you interpret your assessment?

back 54

The child may be having such a severe asthma episode that the airways are closed, so start oxygen and get the doctor immediately.

front 55

A patient exhibiting respiratory distress as well as a tracheal shift should be evaluated for

back 55

pneumothorax.

front 56

The most definitive diagnostic method for active tuberculosis is acquired via

back 56

sputum culture.

front 57

When exposed to inhaled allergens, a patient with asthma produces large quantities of

back 57

IgE.

front 58

Emphysema results from destruction of alveolar walls and capillaries, which is because of

back 58

release of proteolytic enzymes from immune cells.

front 59

COPD leads to a barrel chest, because it causes

back 59

air trapping.

front 60

When a client diagnosed with COPD type A asks, “Why is my chest so big and round?”, the nurse responds that

back 60

“Loss of elastic tissue in your lungs allows your airways to close and trap air, which makes your chest round.”

front 61

What is likely to lead to hyponatremia?

back 61

Frequent nasogastric tube irrigation with water

front 62

Respiratory alkalosis is caused by

back 62

hyperventilation.

front 63

How do clinical conditions that increase vascular permeability cause edema?

back 63

By allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure

front 64

The primary cause of infant respiratory distress syndrome is

back 64

lack of surfactant.

front 65

The finding of ketones in the blood suggests that a person may have

back 65

metabolic acidosis.

front 66

When a parent asks how they will know if their 2-month-old baby, who is throwing up and has frequent diarrhea, is dehydrated, the nurse’s best response is

back 66

“If the soft spot on the top of his head feels sunken in and his mouth is dry between his cheek and his gums, then he is probably dehydrated.”

front 67

The nurse provides teaching regarding dietary intake of potassium to avoid an electrolyte imbalance when a patient

back 67

has chronic heart failure that is treated with diuretics.

front 68

A patient diagnosed with chronic compensated heart failure reports that, “My feet swell if I eat salt but I don’t understand why” The nurse’s best response is

back 68

“Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell.”

front 69

Which electrolyte imbalances cause increased neuromuscular excitability?

back 69

Hypocalcemia and hypomagnesemia

front 70

How is a patient hospitalized with a malignant tumor that secretes parathyroid hormone–related peptide monitored for the resulting electrolyte imbalance?

back 70

Serum calcium, bowel function, level of consciousness

front 71

The fraction of total body water (TBW) volume contained in the intracellular space in adults is

back 71

two thirds.

front 72

Signs and symptoms of extracellular fluid volume excess include

back 72

bounding pulse

front 73

The ________ system compensates for metabolic acidosis and alkalosis.

back 73

respiratory

front 74

The arterial blood gas pH = 7.52, PaCO2 = 30 mm Hg, HCO3 – = 24 mEq/L demonstrates

back 74

respiratory alkalosis

front 75

The person at highest risk for developing hypernatremia is a person who

back 75

receives tube feedings because he or she is comatose after a stroke.

front 76

The increased anterior-posterior chest diameter associated with obstructive lung disease is caused by

back 76

Increased residual lung volumes.

front 77

What is the normal ratio for FEV1/FVC diagnostic test?

____% or ______%

back 77

75% or 80%

front 78

What do arterial blood gas (ABG) testing access?

back 78

oxygenation and acid-base status.

front 79

If the pH is <7.35 is it alkalosis or acidosis?

back 79

Acidosis

front 80

If the pH is >7.45 is it alkalosis or acidosis?

back 80

Alkalosis

front 81

What is the normal pH range?

back 81

7.35-7.45

front 82

What is the range considered lethal in pH?

back 82

Bellow 6.9 (too much acidity); higher than 7.6 (too much base).

front 83

What is acidosis?

_________ _______ _________.

back 83

Retaining carbon dioxide.

front 84

What is alkalosis?

________ __________ __________ ___________.

back 84

Too little carbon dioxide. -hyperventilating

front 85

Diagnosis of obstructive disorders

___________ FEV1

_____ FE V/FVC ratio.

__________ in FEV1 after use of bronchodilator (asthma).

____________ residual volume.

____________ functional residual capacity.
When bronchodilator is given there will be ___________ bronchodilator response.

back 85

Decreased

Low (<70%)

Improvement

Increased

Increased

Positive

front 86

Diagnosis of restrictive disorders

FEV1/FVC ratio could be ________ since both of them are reduced.

__________ in vital capacity (VC).

__________ in total lung capacity (TLC)

__________ in functional residual capacity (FRC)

__________ in residual volume (RV)

back 86

Normal

Decrease

Decrease

Decrease

Decrease

front 87

The greater the _________in the lung volume, _________ the severity of disease.

back 87

decrease, greater

front 88

Obstructive pulmonary disorders are manifested by ______________ ___________ _____ __________.

back 88

Increased resistance to airflow

front 89

TRUE or FALSE

In asthma, an airway obstruction is not reversible.

back 89

False, in asthma, airway obstruction could be reversible, but not completely in some patients.

front 90

What type of asthma?

-Non-allergic, adult-onset.

-Develops in middle age w/ less favorable prognosis.

-Respiratory infection/psychological factors.

back 90

Intrinsic

front 91

What type of asthma?

- Allergic, pediatric-onset.

-1/3 to 1/2 of asthma cases

-An IgE-mediated response- Mast cell activation (histamine)- inflammation cell infiltration (neutrophils, eosinophils, and lymphocytes)

back 91

extrinsic

front 92

Wheezing is a clinical manifestation of asthma. Is wheezing seen in the inspiratory or expiratory stage?

back 92

expiratory.

front 93

What are the clinical manifestation of asthma?

back 93

Wheezing, feeling tightness of chest, dyspnea, cough (dry or productive), hyperinflated chest seen in an x-ray, and decreased breath sounds on physical exam.

front 94

Important Clinical manifestations seen in a severe asthma attack are....

(4)

back 94

Orthopnea, agitation, tachypnea: >30 beats per/min, tachycardia >120 beats per/min.

front 95

What are the X-ray findings in asthma?

back 95

Hyperinflation with flattening of the diaphragm.

front 96

What are sputum examination findings that can indicate that someone has asthma? (3)

back 96

-Charcot-Leyden crystals (from crystalized enzymes from eosinophilic membranes)

-Eosinophils

-Curschmann spirals (mucus casts of bronchioles)

front 97

What are pulmonary function test findings in someone who has asthma?

back 97

-Forced expiratory volume decrease

-Peak expiratory flow rate (PEFR)

front 98

In asthma the ratio of FEV1/FVC before and after administration of short-acting bronchodilator will change >_____%.

back 98

greater than 15%

front 99

In asthma

ABG:

___________ during mild attack.

_________ __________ and hypoxemia as bronchospasm increases in intensity.

PaCO2__________: sign that patient is getting worse,

back 99

Normal

Respiratory alkalosis

elevation

front 100

In asthma:

CBC

____________ WBCs and eosinophils

back 100

Elevated

front 101

What is treatment/medications used for asthma-anti-type 1 hypersensitivity

back 101

Oxygen therapy, small-volume nebulizers, B2 agonists, corticoid steroids, leukotriene modifiers, and mast cell inhibitors.

front 102

Etiology of chronic bronchitis:

How long must the patient have a chronic or recurrent productive cough to be diagnosed with chronic bronchitis?

back 102

greater than 3 months, over two successive years.

front 103

What is type A COPD?

back 103

emphysema

front 104

What is type B COPD?

back 104

chronic bronchitis

front 105

TRUE or FALSE

Chronic bronchitis is irreversible when paired with emphysema.

back 105

True

front 106

What is the male to female ratio for chronic bronchitis?

back 106

1:2 male to female ratio

front 107

Pathogenesis of chronic bronchitis:

Chronic ___________________ and swelling of the bronchial mucosa resulting in _________________.

back 107

inflammation, scarring

front 108

TRUE or FALSE

Hypertrophy of bronchial mucuos gland/goblet cells happen in chronic bronchitis.

back 108

False; hyperplasia of bronchial mucous gland/goblet cells happen in chronic bronchitis.

front 109

In chronic bronchitis, pulmonary hypertension causes inflamation where?

back 109

In bronchial walls with vasoconstriction of pulmonary vessels and arteries.

front 110

In chronic bronchitis, pulmonary hypertension causes high pulmonary resistance that may lead to ________-_________ _________ ____________.

back 110

Right-sided heart failure

front 111

In chronic bronchitis, pulmonary hypertension causes inflammation in bronchial walls with vasoconstriction of pulmonary vessels and arteries, due to _______________ and activation of _________ ________ ________.

back 111

Autoregulation and activation of the sympathetic nervous system.

front 112

Clinical manifestations of chronic bronchitis:

- The typical patient is _____________.

- Commonly associated with ____________.

-____________ sputum.

- (more severe in the morning) ______________ _____________.

- evidence of excess ________ _______________.

back 112

Overweight, emphysema, excessive, chronic cough, body fluids.

front 113

What is a clinical manifestation of chronic bronchitis seen in late stages?

back 113

Cyanosis

front 114

SOB is a clinical manifestation of chronic bronchitis, why does it typically happen on expiration?

back 114

Because its an exhaling problem

front 115

Diagnosis of Bronchitis:

Chest X-Rays show:

____________ bronchial vascular markings

___________ lung fields

____________ horizontal cardiac silhouette

____________ of previous pulmonary infection

back 115

Increased, congested, enlarged, evidence.

front 116

Diagnosis of Bronchitis:

What are the three things seen in pulmonary function tests for a patient with chronic bronchitis?

back 116

Normal total lung capacity (TLC), Increased residual volume (RV), Decreased FEV1 and Decreased FEV1/FVC

front 117

Diagnosis of Bronchitis:

In a patient with chronic bronchitis what will be found in their ABG results?

back 117

Elevated PaCO2, decreased PO2

front 118

Treatment for chronic bronchitis includes a low dose O2 therapy, why?

back 118

A low dose is necessary to prevent the retention of carbon dioxide.

front 119

What etiological changes does emphysema cause?

back 119

Destructive changes of the alveolar walls without fibrosis.

front 120

TRUE or FALSE

In emphysema damage is irreversible.

back 120

True

front 121

Pathogenesis of emphysema:

Release of ____________ _______________ from _____________ and __________ leading to alveolar damage.

back 121

proteolytic enzymes, neutrophils, macrophages

front 122

Pathogenesis of emphysema:

Smoking causes alveolar damage that causes inflammation.

Inflammation leads to _________ of __________ ____________.

back 122

release of proteolytic enzymes

front 123

Pathogenesis of emphysema:

Smoking causes alveolar damage by inactivating what?

back 123

a1 -antitrypsin

front 124

Pathogenesis of emphysema:

What is lost in tissue in a patient who has emphysema?

back 124

Loss of elastic tissue in the lung, that usually holds the airway open.

front 125

What causes barrel chest in patients with emphysema?

back 125

Air that has become trapped in distal alveoli.

front 126

Clinical manifestations of emphysema

Progressive ________ ____________.

back 126

exertional dysnea

front 127

Clinical manifestations of emphysema

Will the patient be thin or overweight?

back 127

Thin; due to the increased respiratory effect, increased caloric expenditure and decreased ability to consume adequate calories.

front 128

What does barrel chest cause?

*not what causes barrel chest.

back 128

Increased total lung volume to compensate the lost lung capacity due to dead space.

front 129

What will be seen in pulmonary function tests in an emphysema patient?

(3)

back 129

Increased functional residual capacity

increased RV, TLC

Decreased FEV1, FVC

front 130

What will be seen in the X-Ray of a patient with emphysema?

back 130

Hyperventilation, low flat diaphragm, presence of blebs, narrow mediastinum, normal or small vertical heart.

front 131

In patients with emphysema what will be seen in their ABG test?

Which one is elevated in late stages?

back 131

mild decrease in PaO2 and normal PaCO2

front 132

What are the two important physical findings in a patient with emphysema?

back 132

Decreased breath sounds, lack of crackles and rhonchi, and decreased heart sounds.

front 133

Restrictive pulmonary disorders result from __________ __________ ___________.

back 133

Decreased lung expansion.

front 134

What are the two classification of restrictive pulmonary disorders?

back 134

Pulmonary and extrapulmonary

front 135

In acute (adult) respiratory distress syndrome (ARDS) damage to the alveolar capillary membrane causes _______ _______-__________ __________ ___________ and __________ ____________.

back 135

Widespread protein-rich alveolar-infiltrates and severe dyspnea.

front 136

Aveoli type II cells produce surfactants, why are surfactants important?

back 136

For fighting against surface tension to prevent lungs from collapsing.

front 137

ARDS is associated with a decline in the _______ ______ _____ ___________.

back 137

the PaO2 that is refractory.

(does not respond to supplemental oxygen therapy).

front 138

ARDS is _____________+___________________.

back 138

inflammation + fibrosis

front 139

In ARDS, atelectasis and decrease lung compliance is caused from a lack of _______________.

back 139

Surfactant

front 140

What are the important clinical manifestations in late ARDS?

back 140

Tachycardia, tachypnea, hypotension frothy secretions, crackles, and rhonchi on auscultation.

front 141

What is >40% of causes of ARDS?

What is >30% of causes of ARDS?

back 141

sepsis and aspiration of gastic acid

front 142

In ARDS, protein-rich fluids are found where? an example?

back 142

hyaline membrane, fibrosis

front 143

In ARDs Hallmark is _________ __________ to _________ levels of supplemental O2.

back 143

Hypoxemia refractory, increased

front 144

What is seen in the ABGs in a patient with ARDS?

back 144

Hypoxia, acidosis, hypercapnia

front 145

What is seen in the X-ray in a patient with ARDS?

back 145

Normal with progression to diffuse "whiteout"

front 146

ARDS Diagnosis:

PFTs:

______________ in FVC

______________ lung volume

______________ lung compliance

VA/Q ___________ with __________ right-to-left shunt.

back 146

Decreased

Decreased

Decreased

mismatch; large

front 147

What are the 4 findings from an open lung biopsy of a patient with ARDS

back 147

Atelectasis, hyaline membranes, cellular debris, interstitial and alveolar edema.

front 148

In ARDS what causes reduced oxygen usage in the heart; vasodilation-increase tissue oxygenation until inflammation resolves.

back 148

inhaled nitric oxide

front 149

TRUE/FALSE

The only treatment for ARDS are only supportive measures.

back 149

True

front 150

What type of supplemental O2 is given to patients with ARDS?

back 150

High-frequency jet ventilation (HFJV)

Inverse ratio ventilation (IRV)

PEEP- mechanical ventilation w/ positive end-expiratory pressure

front 151

What type of atelectatic disorder:

-Also called hyaline membrane disease

-syndrome of premature neonates

-associated w/ a1-antitrypsin deficiency

-Atelectasis and decrease in lung compliance from lack of surfactant

back 151

Infant respiratory distress syndrome (IRDS).

front 152

What are clinical manifestations seen in late occupational lung diseases?

back 152

Chronic hypoxemia, cor pulmonale, respiratory failure

front 153

Pneumothorax is accumulation of.....

back 153

air in the pleural space

front 154

What are 4 important clinical manifestations of pneumothorax?

back 154

Hypotension (shock), tracheal shift to contralateral (opposite) side, neck vein distension, hyperresonance.

front 155

What type of occupational lung disease:

-Caused by inhalation of inorganic dust particles.

back 155

Pneumoconiosis

front 156

What type of occupational lung disease:

-"coal miner's" lungs or "black lungs"

back 156

anthracosis

front 157

What type of occupational lung disease:

Silica inhalation

back 157

Silicosis

front 158

What type of occupational lung disease:

Asbestos inhalation

back 158

asbetosis

front 159

What findings are seen in the ABGs of a patient with pneumothorax?

back 159

Decreased PaO2, acute respiratory alkalosis (due to tachypenia)

front 160

What X-ray findings are seen in a patient with pneumothorax?

back 160

Depression of hemidiaphragm on the side of pneumothorax.

front 161

In pleural effusion is pathologic collection of .....

back 161

fluid or pus in pleural cavity as result of another disease process.

front 162

What are impotant clinical manifestations of pleural effusion?

back 162

Pleuritic pain (sharp, worsens with inspiration), dry cough, dyspnea, absence of breath sounds, contralateral trachea shift (massive effusion),

front 163

TRUE/FALSE
Is pneumothorax a medical emergency?

back 163

True

front 164

Patient with plural effusion show what sign in their X-ray?

back 164

signs of CHF

front 165

In pneumothorax a sudden chest pain on affected side is it angina or MI?

back 165

Angina - no signs of MI

front 166

TRUE/FALSE

You will hear loud sounds on the affected side in pneumothorax patients.

back 166

False, you will hear a decrease or absent breath sounds.

front 167

How are CT and Ultrasonograph test helpful to diagnose plural effusion?

back 167

Assist in complicated effusions and distinguish mass from large effusion.

front 168

Death can occur if pH falls or rises

back 168

pH falls below 6.9 and pH rises above 7.8

front 169

Normal laboratory values for acid-base parameters

PaCO2 (aterial blood) =

HCO3- (serum) =

pH (arterial blood) =

back 169

PaCO2 (aterial blood) = 36-44 mm Hg (adults), average 40

HCO3- (serum) = 22-26 mm Hg (adults), average 24

pH (arterial blood) = 7.35-7.45 (adults), average 7.40

front 170

What measures lung (respiratory) function

back 170

PaCO2

if it falls or rises < 40 >, it means that there is a problem with your lungs. It is an indicator for lung function.

front 171

What measures renal (metabolic) function

back 171

HCO3 -

If it falls or rises < 24>, it means that there is a problem with your kidneys. It is an indicator for kidney function.

front 172

What are the three major mechanisms that regulate the body's acid-base status?

back 172

- Buffers (first line of defense)

- Respiratory system (compensatory mechanism)

- Renal system (compensatory mechanism)

front 173

What chemicals help control pH of body fluids

back 173

Base: Bicarbonate ions (HCO3 -) takes up hydrogen when fluid is too acidic

Weak acid: Carbonic acid (H2CO3) release hydrogen ions when a fluid is too alkaline

front 174

What are the four types of buffers

back 174

- Bicarbonate buffers (most important )

- phosphate buffers

- hemoglobin buffers

- Protein buffers

front 175

respiratory response

Metabolic reponse

back 175

- The lungs can excrete only carbonic acid (Volatile acid)

- Lactic acid and acetoacetic acid: nonvolatile acids get excreted through the metabolic response (compensatory)

front 176

What is the respiratory response, and is it acidosis or alkalosis

Increased Paco2, decreased pH

Decreased Paco2, increased pH

Decreased pH from excess of metabolic acids

Increased pH from deficit of metabolic acids

back 176

- Acidosis, hyperventaltion

- Alkalosis, hypoventaltion

- Acidosis, hyperventilation

- Alkalosis, Hypoventilation

front 177

Renal contribution

back 177

- third line of defense against acid-base disorders

- can excrete any acid from the body except carbonic acid (solely excreted by the lungs)

- excrete metabolic acids produced continuously during normal metabolism

front 178

what does decreased HCO3 - indicate

back 178

- Indicates a relative excess of metabolic acids

front 179

What does increased HCO3 - indicate

back 179

- Indicates a relative deficit of metabolic acids

- in other words, a relative excess of base

front 180

What are the renal compensatory responses to carbonic acids imbalances

back 180

- For high carbonic acid levels, increase the excretion of metabolic acids and H+

- For low carbonic acid levels, decrease the excretion of metabolic acids and H+, excrete HCO3 -

- requires several days to be fully operative

front 181

What is the renal response, and is it acidosis or alkalosis

Decreased pH from excess of metabolic acids

increased pH from deficit of metabolic acids

Decreased pH from excess of carbonic acid

Increase of pH from deficit of carbonic acid

back 181

- Acidosis, secrete more H+ into renal tubules and make more ammonia

- Alkalosis, secrete fewer H+ into renal tubules, and excretes HCO3 -, make less ammonia

- Acidosis, Secrete more H+ into renal tubules, and make more ammonia

- Alkalosis, secrete fewer H+ into the renal tubules, excrete HCO3 -, make less ammonia

front 182

What are the (3) reasons why someone might have respiratory acidosis

back 182

- Impaired gas exchange

- inadequate neuromuscular function

- Impairment of respiratory control in the brainstem

front 183

Chronic Obstructive pulmonary disease (COPD), Pneumonia, severe asthma, Pulmonary edema, and ARDS are examples of what reason for respiratory acidosis

back 183

Impaired gas exchange

front 184

Guillian-Barre syndrome, Chest injury or surgery (pain limits breathing), Hypokalemic respiratory muscle weakness, sever kyphoscoliosis, respiratory muscle fatigue are examples of what reason for respiratory acidosis

back 184

Inadequate Neuromuscular Function

front 185

Respiratory-depressants drugs (opioids, barbiturates) are examples of what reason for respiratory acidosis

back 185

Impaired respiratory control (Brainstem)

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What condition causes respiratory alkalosis

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- any condition that tends to cause a carbonic acid deficit

  • e.g Hyperventilation

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Metabolic acidosis is caused by

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Relative excess of any acid except carbonic acid

- May be caused by

  • Increase in acid
  • excess removal or decrease in base
  • combination of increase in acid and decrease in base

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What are some examples of metabolic acidosis

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Example: starvation ketoacidosis

- caloric and glucose intake is insufficient, body begins to use fat stores for energy, fat metabolizes incompletely, ketoacids accumulate in blood, causing metabolic acidosis

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Hyperkalemia =

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Metabolic acidosis

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What causes metabolic acidosis

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any condition that tends to cause a relative deficit of any acid (except carbonic acid)

causes

- increase in base (bicarb)

-decrease in acid

-combination of the two

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What are some examples of decrease in acid

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Emesis, gastric suction, Hyperaldosteronism, Hypokalemia