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CARDIO > CARDIO MIDTERM EXAM > Flashcards

CARDIO MIDTERM EXAM Flashcards

1
Q

It is characterized bv an elevation in mean pulmonary arterial pressure greater than 25 mmlic at rest or 30 mmHa during exercise. increased pulmonarv vascular resistance, and normal left heart ventricular function in the absence of other secondarv causes.

A

Pulmonary Hypertension

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2
Q

Pulmonary Hypertension associated with:

A

Congenital Heart Disease, Collagen vascular disease, liver cirrhosis,
viral infection
drug effects

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3
Q

more common among women than in men, with a ratio of 3 to 1.

A

Primary pulmonary hypertension

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4
Q

rare and can occur at any age, although it is more common in the third and fourth decades.

A

Primary pulmonary hypertension

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5
Q

Primarv pulmonarv hvpertension is characterized by:

A

Dyspnea
Angina
Syncope
Cough, hemoptysis, hoarseness and Raynaud phenomenon

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6
Q

most common symptoms

A

Dyspnea (60% of patients)

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7
Q

probably due to underpeftusion of the Right ventricle or stretching of the large pulmonary arteries

A

Angina (50% of patients)

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8
Q

an early symptoms of PH

A

Syncope ( 8% of patients)

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9
Q

Most important non-invasive test.

A

V/O scan

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10
Q

Useful to determine the degree of hemodynamic impairment, the presence of vasoreactivity and the prognosis or patents win LAn.

A

Pulmonary artery catheterization

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11
Q

Useful to rule out the presence of significant restrictive or obstructive airway disease

A

Pulmonary Function Test

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12
Q

Rule out associated etiologies and evaluate patients with chronic interstitial disease and
normal chest radiographs.

A

High-resolution CT

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13
Q

life-threatening and
has poor prognosis

A

IPAH

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14
Q

improves survival. > Recommended target IN is approximately 1.5:2.5 (average 2).

A

Oral anticoagulations

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15
Q

indicated for Right ventricular volume overload ( pulmonary congestion ana pedal edema)

A

Diuretics

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16
Q

reserved for patients with refractory ventricular failure and for rate control in atrial fllutter or fibrillation

A

Digoxin

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17
Q

Refers to a disease state characterized by the presence of incompletely reversible airflow obstruction.

A

chronic obstructive pulmonary disease
(COPD), or

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18
Q

proposes a definition that focuses on the
progressive nature of airflow limitation and its association with abnormal inflammatory response of the lungs to various noxious particles or gases, primarily causes by smoking

A

Global Initiative for Chronic Obstructive Lung Disease (GOLD)

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19
Q

COPD is “a disease state characterized by airflow limitation that is not fully reversible.”

A

GOLD document

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20
Q

The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal destruction (emphysema),

A

The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal destruction (emphysema),

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21
Q

TWO MAJOR DISEASES THAT MAKE UP COPD

A

Emphysema
Chronic Bronchitis

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22
Q

defined in condition characterized by abnormal, permanent enlargement of the airspaces beyond the terminal bronchiole, accompanied by destruction of the walls of the airspaces and loss of elastance

A

Emphysema

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23
Q

defined in clinical terms as a condition in which chronic productive cough is present for at least 3 months per year for at least 2 consecutive years.

A

Chronic bronchitis

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24
Q

Common denominator of the 3 diseases:

A

Airflow Obstruction

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25
Q

asthma is no longer conventionally considered to be part of the spectrum of COPD, the diagram shows that there is overlap between asthma and COPD.

A

asthma is no longer conventionally considered to be part of the spectrum of COPD, the diagram shows that there is overlap between asthma and COPD.

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26
Q

In actual practice, it may not be possible to distinguish between individuals with a history of asthma but with incompletely reversible airflow obstruction and individuals with COPD. Recently, this overlap has been recognized with the term ________________

A

“asthma-COPD overlap” syndrome (ACOS)

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27
Q

Pink puffer
Cachexia

A

EMPHYSEMA

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28
Q

Blue bloater
Barrel chested

A

BRONCHITIS

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29
Q

one of the most frequent causes of morbidity and mortality worldwide.

A

COPD

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30
Q

will become the fifth most prevalent disease in the world and the third leading cause of worldwide mortality by 2030.

A

COPD

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31
Q

COPD prevalence increases with aging, with a five-fold. Increased risk for adults older than 65 years.

A

COPD prevalence increases with aging, with a five-fold. Increased risk for adults older than 65 years.

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32
Q

is the third leading cause of death worldwide, causing 3.23 million deaths in 2019. WHO

A

Chronic Bronchitis

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33
Q

Nearly 90% of COPD deaths in those under 70 years of age occur in low- and middle-income countries.

A

Nearly 90% of COPD deaths in those under 70 years of age occur in low- and middle-income countries.

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34
Q

Common Causes (COPD):

A

Cigarette smoking
Alpha-1 antitrypsin (AAT) deficiency
Outdoor air pollution
Long-standing asthma
Biomass and occupational exposure

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35
Q

a Genetic condition (symptoms; trouble breathing, jaundiced or yellow skin). Which can cause COPD at a young age and also damage lungs and liver.

A

alpha-1 antitrypsin (AAT) deficiency

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36
Q

chronic asthma

A

Long-standing asthma

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37
Q

Risk factors COPD

A

COPD is prevalent w/aging such as 65 years old, except for COPD brought by AAT because it is genetic and may occur in younger people.

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38
Q

the main component of cigarette that is mainly
causing COPD

A

Nicotine

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39
Q

Prevents the attack of neutrophil elastase

A

ALPHA 1 – ANTITRYPSIN

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40
Q

released by neutrophil, when this elastase break off from neutrophil, it destroys the bacteria and can also destroys the lungs

A

Neutrophil elastase

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41
Q

in the absence of a1-antitrypsin, the neutrophil elastase is increased, and the lungs is being continuously damaged and this can even invades the liver

A

in the absence of a1-antitrypsin, the neutrophil elastase is increased, and the lungs is being continuously damaged and this can even invades the liver

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42
Q

a condition that features a reduced amount of the protein
AAT

A

GENETIC EMPHYSEMA OR Α-1 ANTIPROTEASE DEFICIENCY

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43
Q

May result in the early onset of emphysema
and which is inherited

A

autosomal codominant condition..

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44
Q

The importance of early identification is emphasized by the need to test (by simply sending a serum level for a1- antitrypsin testing) first-degree relatives (e.g., siblings, parents, children), by the favorable effect of primary prevention of smoking among individuals identified early, and by the availability of a specific therapy

A

intravenous (IV) augmentation therapy

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45
Q

a major structural protein that supports the alveolar walls of the lung, is normally protected by a1-antitrypsin, a protein that opposes the degradative threat of neutrophil elastase.

A

lung elastin

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46
Q

a protein contained within neutrophils that is disgorged when neutrophils are attracted to the lung during inflammation or infection.

A

Neutrophil elastase

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47
Q

individuals with established emphysema,
consideration can be given to available specific therapy

A

intravenous (IV) augmentation therapy

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48
Q

COPD may also occur without active cigarette smoking or AAT deficiency. Factors such as: may contribute to airflow obstruction that is not reversible.

A

1.passive smoking
2.air pollution
3.occupational exposure
4.airway hyperresponsiveness

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49
Q

CLINICAL SIGNS AND SYMPTOMS (COPD)

A

cough
phlegm production
wheezing
shortness of breath

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50
Q

often slow “but progressive in onset and occurs later in the course of the disease, characteristically in the late sixth or seventh decade of life.

A

Dyspnea

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51
Q

in which dyspnea begins sooner (mean age, approximately 45).

A

a1-antitrypsin deficiency

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52
Q

may show wheezing or diminished breath sounds
early

A

COPD

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53
Q

may be evident (i.e., increased anteroposterior diameter (sometimes called barrel chest),

A

hyperinflation

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54
Q

diaphragm flattening, and dimpling inward of the chest wall at the level of the diaphragm on inspiration

A

Hoover’s sign

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55
Q

is not caused by COPD alone, even if hypoxemia is present. Clubbing in a patient with COPD warrants consideration of another cause (e.g., bronchogenic cancer, bronchiectasis)

A

Digital clubbing

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56
Q

because of cor pulmonale

A

Bipedal edema

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57
Q

Other late signs of COPD include:

A

the use of accessory muscles of respiration,
o edema resulting from cor pulmonale,
o mental status changes caused by hypercapnia
(especially if acute, as in acute exacerbations
of chronic, severe disease),
o or asterixis (i.e., involuntary flapping of the
hands when held in an extended position, as in
“stopping traffic”).

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58
Q

The goal of management is to relieve the bronchoconstriction

A

The goal of management is to relieve the
bronchoconstriction

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59
Q

In managing patients with chronic, stable COPD, the following goals must guide the clinician:

A

-Establish the diagnosis of COPD.
– Optimize lung function.
– Maximize the patient’s ability to perform daily
activities.
– Simplify the medical treatment program as
much as possible.
– Avoid exacerbations of COPD.
– Prolong survival

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60
Q

In cases of emphysema and part of the lungs is severely damaged then the patient can undergo surgical procedure, which is removal of the damaged lung portion or lobe.

A

In cases of emphysema and part of the lungs is severely damaged then the patient can undergo surgical procedure, which is removal of the damaged lung portion or lobe.

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61
Q

If the ordinary nasal or face mask is not effective on patient, CPAP or BIPAP is used to expel the excessive CO2 instead of intubating the patient.

A

If the ordinary nasal or face mask is not effective on patient, CPAP or BIPAP is used to expel the excessive CO2 instead of intubating the patient.

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62
Q

The major challenge facing the clinician who encounters a patient with airflow obstruction is to distinguish COPD (i.e., emphysema or chronic bronchitis or both) from
asthma.

A

The major challenge facing the clinician who encounters a patient with airflow obstruction is to distinguish COPD (i.e., emphysema or chronic bronchitis or both) from
asthma.

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63
Q

Features that tend to favor COPD include chronic daily phlegm production, which establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph (called hyperlucency); and a decreased diffusing capacity.

A

Features that tend to favor COPD include chronic daily phlegm production, which establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph (called hyperlucency); and a decreased diffusing capacity.

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64
Q

establishes the diagnosis of chronic bronchitis; diminished vascular shadows on the chest radiograph

A

hyperlucency

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65
Q

The diagnosis of asthma is favored if the diminished FEV obtained on spirometry returns to normal after bronchodilator treatment.

A

The diagnosis of asthma is favored if the diminished FEV obtained on spirometry returns to normal after bronchodilator treatment.

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66
Q

a secondary issue is for the clinician to consider whether the patient has an unusual cause for COPD, such as a1- antitrypsin deficiency or another etiology. Such underlying etiologies will be present in fewer than 5 % of patients with COPD, with a1-antitrypsin deficiency the most common.

A

a secondary issue is for the clinician to consider whether the patient has an unusual cause for COPD, such as a1- antitrypsin deficiency or another etiology. Such underlying etiologies will be present in fewer than 5 % of patients with COPD, with a1-antitrypsin deficiency the most common.

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67
Q

Pulmonary Disease Strategies during acute exacerbations of COPD (MEDICAL MANAGEMENT)

A

inhaled bronchodilators
antibiotics
corticosteroids
anti-inflammatory mediators
supplemental oxygen

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68
Q

especially beta-2 agonists

A

inhaled bronchodilators

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69
Q

if there’s an infection(e.g., trimethoprim-sulfamethoxazole, amoxicillin, or doxycycline)

A

antibiotics

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70
Q

to reduce inflammation and improve lung function (e.g., trimethoprim-sulfamethoxazole, amoxicillin, or doxycycline)

A

corticosteroids

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71
Q

theophylline

A

anti-inflammatory mediators

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72
Q

theophylline

A

anti-inflammatory mediators

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73
Q

to maintain arterial saturation at greater than 90%, inhaled bronchodilators, oral antibiotics, and a brief course of systemic corticosteroids

A

supplemental oxygen (O2)

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74
Q

recommended for px with COPD

A

Bronchodilator therapy

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75
Q

produce smooth muscle relaxation, resulting in improved airflow obstruction, improved
symptoms and exercise tolerance, and decrease in the frequency and severity of exacerbations, but they do not enhance survival

A

Bronchodilators

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76
Q

can improve airflow in patients with COPD, although many clinicians favor an inhaled

A

anticholinergic and sympathomimetic bronchodilators

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77
Q

first-line therapy (COPD)

A

anticholinergic medication (e.g., ipratropium bromide)

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78
Q

Controlled trials do show lessened dyspnea in methylxanthine recipients despite lack of measurable increases in airflow.18 Side effects of methylxanthines include anxiety, tremulousness, nausea, cardiac arrhythmias, and seizures. To minimize the chance of
toxicity, current recommendations suggest maintaining serum theophylline levels at 8 to 10 ug/mL.

A

Controlled trials do show lessened dyspnea in methylxanthine recipients despite lack of measurable increases in airflow.18 Side effects of methylxanthines include anxiety, tremulousness, nausea, cardiac arrhythmias, and seizures. To minimize the chance of
toxicity, current recommendations suggest maintaining serum theophylline levels at 8 to 10 ug/mL.

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78
Q

The addition of a sympathomimetic bronchodilator (e.g., a p2-agonist) may offer additive bronchodilation.

A

The addition of a sympathomimetic bronchodilator (e.g., a p2-agonist) may offer additive bronchodilation.

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79
Q

offers little additional bronchodilation in patients on inhaled bronchodilators and generally is reserved for patients with debilitating symptoms from stable COPD despite optimal inhaled bronchodilator therapy.

A

Methylxanthine therapy

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80
Q

recommend the use of short-acting β-adrenergic agents (≤6 hours) for symptomatic management of all patients with COPD.

A

GOLD guidelines

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81
Q

can lessen the frequency of acute exacerbations of COPD.

A

long-acting β agonist (e.g., salmeterol) or a long-acting anticholinergic drug (e.g., tiotropium)

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82
Q

Strategies to improve lung function in acute exacerbations of COPD generally include inhaled bronchodilators (especially (32-agonists) and systemic corticosteroids. An early randomized, controlled trial of IV methylprednisolone for patients with acute exacerbations has shown accelerated improvement in FEV1 within 72 hours.

A

Strategies to improve lung function in acute exacerbations of COPD generally include inhaled bronchodilators (especially (32-agonists) and systemic corticosteroids. An early randomized, controlled trial of IV methylprednisolone for patients with acute exacerbations has shown accelerated improvement in FEV1 within 72 hours.

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83
Q

offer little benefit in the setting of acute exacerbations of COPD and have fallen into disfavor in this setting

A

IV methylxanthines

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84
Q

For patients with purulent phlegm as an underlying feature of their acute exacerbation, oral antibiotics (e.g., trimethoprim-sulfamethoxazole, amoxicillin, doxycycline) administered for 7 to 10 days have produced accelerated improvement of peak flow rates compared with the rates of placebo recipients.

A

For patients with purulent phlegm as an underlying feature of their acute exacerbation, oral antibiotics (e.g., trimethoprim-sulfamethoxazole, amoxicillin, doxycycline) administered for 7 to 10 days have produced accelerated improvement of peak flow rates compared with the rates of placebo recipients.

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85
Q

Criteria defining candidacy for noninvasive ventilation include:

A

-acute respiratory acidosis (without frank
respiratory arrest);
-hemodynamic stability;
-ability to tolerate the interface needed for
noninvasive ventilation;
-ability to protect the airway;
-and lack of craniofacial trauma or burns,
copious secretions, or massive obesity.

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86
Q

PREVENTING PROGRESSION OF COPD AND ENHANCING SURVIVAL

A

-Stop smoking
-Take regular exercise
-Get vaccinated

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87
Q

maximize patients ability to perform daily activities concerns COPD and other neuromuscular disease

A

pulmonary rehabilitation

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88
Q

IMPORTANT AREAS OF PULMONARY REHABILITATION

A

Exercise
Psychological counselling
Appropriate therapy/treatment

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89
Q

involving strengthening the respiratory
muscles

A

Exercise

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90
Q

strengthening the patients
morale

A

Psychological counselling

91
Q

Asthma in childhood is reversible, but asthma in adulthood is not fully reversible and may lead to COPD

A

Asthma in childhood is reversible, but asthma in adulthood is not fully reversible and may lead to COPD

92
Q

COPD AND ASTHMA SIMILARITIES

A

Same pathophysiology:
- Inflammation
- bronchoconstriction

93
Q

COPD AND ASTHMA DIFFERENCES

A

Triggering factors and risk factors
- COPD: smoking cigarette
- Asthma: allergen

94
Q

classification for asthma

A

GINA guidelines

95
Q

classification for COPD

A

GOLD

96
Q

The point of origin of pulmonary emboli is found in only one half of patients.

A

The point of origin of pulmonary emboli is found in only one half of patients.

97
Q

arise from detached portions of venous thrombi that form, in most cases, in deep veins
of the lower extremities or pelvis (86%).

A

Pulmonary emboli

98
Q

A small percentage of pulmonary emboli arise from the right heart chambers (3.15%) or the superior vena cava (3%).

A

A small percentage of pulmonary emboli arise from the right heart chambers (3.15%) or the superior vena cava (3%).

99
Q

CAUSES OF PULMONARY EMBOLISM:

A

-Thrombus formation occurs by blood stasis, the presence of hypercoagulable states, or vessel wall abnormalities.
-The causes of stasis include local pressure, venous obstruction, and immobilization.
-Other causes of stasis include congestive heart failure, shock and dehydration, varicose veins, and enlargement of the right heart chambers.

99
Q

RISK FACTORS OF THE VIRCHOWS TRIAD HYPERCOAGULABILITY

A

-Malignancy (cancer patient)
- Major surgery
-Infection and sepsis
-Estrogen
-dehydration

100
Q

RISK FACTORS OF DVT FORMATION

A
  • Dehydration – lack of water cause the blood to become thick
  • Long flight (immobilization)
  • Bedridden
    *Stroke
    *Coma
    *Lower extremity disorder
  • Pregnancy
  • Obesity
  • Blood extraction especially during searching
  • Invasive catheter
101
Q

VASCULAR DAMAGE

A
  • thrombophlebitis
  • Indwelling catheter
  • actual or direct trauma
102
Q

BLOOD STASIS

A
  • Immobilization
  • bradycardia (low heart rate)
  • inadequate blood volume
103
Q

an important factor for the formation of DVT, is rarely the only risk factor.

A

Stasis

104
Q

Deposition of platelets and fibrin in the venous valve cups of the lower extremities occurs as a result of stasis

A

Deposition of platelets and fibrin in the venous valve cups of the lower extremities occurs as a result of stasis

105
Q

Most PEs originate as thrombi in the deep veins (DVT) due to deposition of platelets and fibrin in the venous valve cusps of the lower extremities.

A

Most PEs originate as thrombi in the deep veins (DVT) due to deposition of platelets and fibrin in the venous valve cusps of the lower extremities.

106
Q

most frequently in the calf veins, then femoropopliteal veins, and less frequently in the iliac veins.

A

site of thrombosis

107
Q

Emboli detach from their point of origin and travel through the systemic venous system, through the right sided chambers of the heart, and lodge in the pulmonary arterial system.

A

Emboli detach from their point of origin and travel through the systemic venous system, through the right sided chambers of the heart, and lodge in the pulmonary arterial system.

108
Q

occur more frequently in the lower lobes and often found in right lung

A

Pulmonary emboli

109
Q

Embolic obstruction of the pulmonary artery increases the alveolar dead space, causes bronchoconstriction, and decreases the production of alveolar surfactant

A

Embolic obstruction of the pulmonary artery increases the alveolar dead space, causes bronchoconstriction, and decreases the production of alveolar surfactant

110
Q

areas occur because of the presence of ventilated but nonperfused lung parenchyma.

A

Wasted or dead space

111
Q

The response is to increase total ventilation (V). The increased V contributes to the sensation of dyspnea that accompanies pulmonary embolism.

A

The response is to increase total ventilation (V). The increased V contributes to the sensation of dyspnea that accompanies pulmonary embolism.

112
Q

Not all patients with pulmonary embolism have arterial hypoxemia, but the presence of a wide alveolararterial oxygen tension gradient andreduced arterial oxygen tension (Pa02) are common

A

Not all patients with pulmonary embolism have arterial hypoxemia, but the presence of a wide alveolararterial oxygen tension gradient and a reduced arterial oxygen tension (Pa02) are common

113
Q

develops because of high and low V/Q mismatch, intrapulmonary shunt, or cardiogenic shock

A

Hypoxemia

114
Q

caused by obstruction of the pulmonary vasculature by massive emboli or by numerous small emboli in the presence of cardiopulmonary disease

A

Shock

115
Q

resulting to venous oxygen desaturation

A

Cardiac output decreases, and oxygen delivery falls

116
Q

may develop because of the presence of a patent foramen ovale

A

intracardiac shunt

117
Q

no specific signs or symptoms indicate the presence of venous thromboembolic disease, although most patients with DVT have pain or swelling, or both, of the extremity

A

no specific signs or symptoms indicate the presence of venous thromboembolic disease, although most patients with DVT have pain or swelling, or both, of the extremity

118
Q

In patients who have swelling above and below the knee, fever, and a history of immobility and cancer, the likelihood of finding DVT on a venogram is only 42% .

A

In patients who have swelling above and below the knee, fever, and a history of immobility and cancer, the likelihood of finding DVT on a venogram is only 42% .

119
Q

PHYSICAL FINDINGS OF DVT IN LOWER EXTREMITIES

A
  • Erythema
  • Warm skin
  • Swelling and tenderness
120
Q

SIGNS AND SYMPTOMS (PVD)

A

1) Dyspnea
2) Pleuritic chest pain
3) Cough
4) Apprehension
5) Leg swelling and Pain
6) hemoptysis
7) hypoxemia
8) tachypnea
9) tachycardia
10) wheezing
11) angina-like pain

121
Q

The combination of dyspnea of sudden onset, fainting, and chest pain should raise suspicion of pulmonary embolism

A

The combination of dyspnea of sudden onset, fainting, and chest pain should raise suspicion of pulmonary embolism

122
Q

When a pulmonary embolism is possible, the most commonly used tool to predict the clinical probability of a pulmonary embolism is the modified

A

Wells Scoring System

123
Q

Chest Radiograph for PVC by itself is helpful to rule out other potentially life-threatening conditions, such as pneumothorax

A

Chest Radiograph for PVC by itself is helpful to rule out other potentially life-threatening conditions, such as pneumothorax

124
Q

a normal chest radiograph may be a clue to the presence of pulmonary embolism.

A

Dyspneic patients

125
Q

enlargement of the right descending pulmonary artery (66%)

A

Palla’s sign

126
Q

enlargement of the heart shadow (55%)

A

Cardiomegaly

127
Q

present in patients who have infarction or atelectasis

A

Parenchymal densities

128
Q

Other less common findings include: PVC

A

Westermark sign
Hampton hump

129
Q

helpful to rule out other diagnoses, such as acute myocardial infarction and
pericarditis

A

electrocardiogram

130
Q

are the mosT common findings in PVC

A

tachycardia and ST-segment depression

131
Q

Most patients with acute pulmonary embolism have _________

A

hypoxemia
hypocapnia

132
Q

In an intubated patient or in patient with COPD, a decrease in PaO2 and increase in arterial carbon dioxide content should raise suspicion of pulmonary embolism

A

In an intubated patient or in patient with COPD, a decrease in PaO2 and increase in arterial carbon dioxide content should raise suspicion of pulmonary embolism

133
Q

The utility of measuring ABGs is to document hypoxemia and direct oxygen supplementation. In the care of patients with limited cardiopulmonary reserve, ABG levels are used to document the level of carbon dioxide.

A

The utility of measuring ABGs is to document hypoxemia and direct oxygen supplementation. In the care of patients with limited cardiopulmonary reserve,
ABG levels are used to document the level of carbon dioxide.

134
Q

Measurement of fibrin split products (D-dimers), products of cross-linked fibrin, has been found sensitive for ______________

A

acute venous thromboembolism

135
Q

The most standard test is the It helps to see the segmental defect.

A

V/Q scan

136
Q

involves the inhalation of a radiolabeled gas (usually xenon-133, xenon-127,
krypton-181m, or technetium-99m) and the intravenous injection of macroaggregated albumin tagged with a gamma-emitting radioisotope

A

Ventilation/perfusion scanning

137
Q

The distribution of lung V and lung Q is studied, and areas of mismatch where Q is less than V are sought

A

The distribution of lung V and lung Q is studied, and areas of mismatch where Q is less than V are sought

138
Q

The presence of mismatches most often indicates embolic occlusion of the blood vessel

A

The presence of mismatches most often indicates embolic occlusion of the blood vessel

139
Q

TREATMENT FOR PVC

A

Prophylactic therapy
Pharmacological choices
Mechanical measures

140
Q

reduces the risk of venous thromboembolism in patients at risk. Preventive measures especially if there is an identified risk.

A

Prophylactic therapy

141
Q

for prophylaxis include lowdose subcutaneous heparin, warfarin, low-molecularweight heparin, heparinoids, and dextran

A

Pharmacological choices

142
Q

should monitor the dosage because
too much can cause massive bleeding, or GI
bleeding

A

Heparin

143
Q

Simplest treatment for PVC

A

Aspirin

144
Q

To reduce venous stasis include
early ambulation, wearing elastic stockings
(compressive stocking to help the muscle to contract),
pneumatic calf compression, and electrical stimulation
of calf muscles.

A

Mechanical measures

145
Q

the standard therapy for
venous thromboembolic disease; it has an immediate
action and is relatively safe

A

Heparin (anticoagulant)

146
Q

It potentiates the action of antithrombin and heparin
cofactor 2

A

It potentiates the action of antithrombin and heparin
cofactor 2

147
Q

Clinical recurrence of DVT and PE is rare when heparin
is infused at doses of at least ___________

A

1250 units per hour

148
Q

Complication of IV heparin administration includes

A

major bleeding
thrombocytopenia

149
Q

Most commonly used oral anticoagulant in PVC

A

racemic warfarin sodium

150
Q

MANAGEMENT OF PULMONARY EMBOLISM

A

Therapy with heparin followed by oral coumarin is the modality of choice
Supplemental oxygen
Analgesics
Resuscitation with fluids and vasopressor agent

151
Q

for patients who are hypotensive and in shock

A

Resuscitation with fluids and vasopressor agent –

152
Q

In the care of patients with severe hypoxemia, acute right heart failure, or shock, thrombolytic therapy may be administered for lysis of the emboli.

A

In the care of patients with severe hypoxemia, acute right heart failure, or shock, thrombolytic therapy may be administered for lysis of the emboli.

153
Q

For massive pulmonary embolism:

A

Pulmonary Embolectomy
Catheter tip embolectomy Catheter tip fragmentation
Inferior vena caval filter

154
Q

Surgical removal of the embolus

A

Pulmonary Embolectomy

155
Q

A medical condition which causes the airway path of the lungs to swell and narrow

A

ASTHMA

156
Q

hyperreactive airway disease

A

ASTHMA

157
Q

a clinical syndrome characterized by airway obstruction, which is partially or completely reversible either spontaneously or with treatment; airway inflammation; and airway hyperresponsiveness (AHR) to various stimuli

A

Asthma

158
Q

In the genetically susceptible host, allergens, respiratory infections, certain occupational and environmental exposures, and many unknown hosts or environmental stimuli can produce the full spectrum of asthma, with persistent airway inflammation, bronchial hyperreactivity, and consequent airflow obstruction.

A

In the genetically susceptible host, allergens, respiratory infections, certain occupational and environmental exposures, and many unknown hosts or environmental stimuli can produce the full spectrum of asthma, with persistent airway inflammation, bronchial hyperreactivity, and consequent airflow obstruction.

159
Q

When inflammation and bronchial hyperreactivity are present, asthma can be triggered by additional factors, including exercise; inhalation of cold, dry air; hyperventilation; cigarette smoke; physical or emotional stress; inhalation of irritants; and pharmacologic agents, such as methacholine and histamine.

A

When inflammation and bronchial hyperreactivity are present, asthma can be triggered by additional factors, including exercise; inhalation of cold, dry air; hyperventilation; cigarette smoke; physical or emotional stress; inhalation of irritants; and pharmacologic agents, such as methacholine and histamine.

160
Q

When a patient with asthma inhales an allergen to which he or she is sensitized, the antigen cross-links to specific immuno- globulin E (IgE) molecules attached to the surface of mast cells in the bronchial mucosa and submucosa.

A

When a patient with asthma inhales an allergen to which he or she is sensitized, the antigen cross-links to specific immuno- globulin E (IgE) molecules attached to the surface of mast cells in the bronchial mucosa and submucosa.

161
Q

Early (acute) asthmatic response an immediate hypersensitivity reaction that usually subsides in approximately 30 to 60 minutes

A

Early (acute) asthmatic response an immediate hypersensitivity reaction that usually subsides in approximately 30 to 60 minutes

162
Q

The mast cells degranulate rapidly (within 30 minutes), releasing multiple mediators including leukotrienes

A

slow-reacting substance of anaphylaxis [SRS-A])

163
Q

Late asthmatic response

A
  • usually more severe and lasts longer than the early asthmatic response
  • late asthmatic response is characterized by increasing influx and activation of inflammatory cells such as mast cells, eosinophils, and lymphocytes.
164
Q

particularly involved in the pathophysiology of asthma

A

T lymphocytes

165
Q

stimulated by microbes or allergens and assist B cells transform into plasma cells that produce immunoglobulin E (lgE).

A

Th 1 cells

166
Q

attract mast cells, eosinophils, and basophils, which promote inflammation.

A

Th2 cells

167
Q

binds to mast cells and provokes their degranulation, which releases mediators such as histamine and leukotrienes.

A

IgE

168
Q

responsible for the development of bronchoconstriction, bronchial hyperreactivity, edema, and eosinophilia.

A

Leukotrienes

169
Q

contributes to bronchospasm and inflammation

A

Histamine

170
Q

Supposedly asthma is only common during childhood

A

Supposedly asthma is only common during childhood

171
Q

CATEGORY OF ASTHMA

A

Intermittent (green zone)
Mild Persistent (green zone)
Moderate persistent (yellow zone)
Severe persistent (red zone)

172
Q

The attacks are not frequent and the duration
- Not recognized early

A

Intermittent (green zone)

173
Q
  • 2 times a week, or symptoms at least once per week,
    -Symptoms is relief after medication
A

Mild Persistent (green zone)

174
Q
  • Daily symptoms
  • Relieve after medication
  • Daily use of short-acting B2-aginist
A

Moderate persistent (yellow zone)

175
Q
  • Continuous symptoms
  • Go to ER immediately
A

Severe persistent (red zone)

176
Q

TRIGGERING FACTORS OF ASTHMA:

A

Allergen
Infection
Season
Exercised-induced
Stress (intrinsic)
Skin asthma
Environment (such as chemical prone places)

177
Q

The diagnosis of asthma requires a two-pronged approach of clinical assessment supported by laboratory evaluation

A

The diagnosis of asthma requires a two-pronged approach of clinical assessment supported by laboratory evaluation

178
Q

physical examination can be entirely normal between episodes, the history plays a key role in suggesting

A

physical examination can be entirely normal between episodes, the history plays a key role in suggesting

179
Q

Laboratory Findings for ASTHMA

A

Spirometry
Peakflow
Methacholine challenge
Imaging tests
Allergy testing
Nitric oxide test
Provocative testing for exercise and cold- induced asthma

180
Q

The severity of the symptoms depends on the degree of bronchial hyperresponsiveness and reversibility of the bronchial obstruction

A

The severity of the symptoms depends on the degree of bronchial hyperresponsiveness and reversibility of the bronchial obstruction

181
Q

classic symptoms of asthma are

A

episodic wheezing,
shortness of breath, dyspnea
chest tightness
cough

182
Q

Patients going into respiratory failure caused by marked airway constriction have inaudible breath sounds and a repetitive, hacking cough.

A

Patients going into respiratory failure caused by marked airway constriction have inaudible breath sounds and a repetitive, hacking cough.

183
Q

may be present if larger bronchial airways are involved.

A

Rhonchi

184
Q

If the asthma is related to allergies, signs of chronic rhinitis may be present, including nasal edema, nasal polyps, rhinorrhea, and oropharyngeal erythema

A

If the asthma is related to allergies, signs of chronic rhinitis may be present, including nasal edema, nasal polyps, rhinorrhea, and oropharyngeal erythema

185
Q

asthma requires demonstration of a component of reversible airflow obstruction

A

asthma requires demonstration of a component of reversible airflow obstruction

186
Q

PFTs may be normal in asymptomatic patients with asthma, but more commonly they reveal some degree of airway obstruction manifested by a decreased FEV1 and FEV1/FVC ratio

A

PFTs may be normal in asymptomatic patients with asthma, but more commonly they reveal some degree of airway obstruction manifested by a decreased FEV1 and FEV1/FVC ratio

187
Q

RADIOGRAPHY (CHEST X-RAY) ASTHMA

A

Usually shows normal
Hyperinflation or flattening of diaphragm

188
Q

improvement in the FEV1 by at least 12% and 200 mL after administration of a short-acting bronchodilator is considered evidence of reversibility.

A

improvement in the FEV1 by at least 12% and 200 mL after administration of a short-acting bronchodilator is considered evidence of reversibility.

189
Q

Spontaneous variation in self-recorded PEFR by 15% or more can also provide evidence of reversibility of airway obstruction.

A

Spontaneous variation in self-recorded PEFR by 15% or more can also provide evidence of reversibility of airway obstruction.

190
Q

Elevated values of exhaled nitric oxide can also be used to support the diagnosis of asthma when eosinophilic inflammation is present.

A

Elevated values of exhaled nitric oxide can also be used to support the diagnosis of asthma when eosinophilic inflammation is present.

191
Q

a well-established method to detect and quantify AHR.

A

Bronchoprovocation

192
Q

Pharmacologic agents (ASTHMA):

A

acetylcholine, methacholine, histamine, cysteinyl leukotrienes, and prostaglandins, and physical stimuli such as exercise and isocapnic hyperventilation with cold, dry air have been used to detect, quantify, and characterize nonspecific AHR in asthma

193
Q

The goal of asthma management is to maintain a high quality of life for the patient, uninterrupted by asthma symptoms, side effects from medications, or limitations on the job or during exercise.

A

The goal of asthma management is to maintain a high quality of life for the patient, uninterrupted by asthma symptoms, side effects from medications, or limitations on the job or during exercise.

194
Q

Asthma management relies on the following four important components recommended by the National Asthma Education Program (NAEP) expert panel:

A

1) Objective measurements and monitoring of lung function
2) Pharmacologic therapy
3) Environmental control
4) Patient education

195
Q

LONG-TERM ASTHMA CONTROL MEDICATIONS: keep asthma under control on a day-to-day basis and make it less likely you’ll have an asthma attack

A

Inhaled corticosteroids Leukotriene modifiers Combination inhalers Theophylline

196
Q

recommended as part of the initial assessment of all patients being evaluated for asthma and peri- odically thereafter as needed.

A

Spirometry

197
Q

recommend that home PEFR measurement be used for patients with moderate to severe asthma

A

NAEP guidelines

198
Q

the baseline diagnosis for ASTHMA

A

PFT

199
Q

Simple device used in emergency setting

A

peak
flow meter (portable spirometer) or asthma meter

200
Q

the best personal blow

A

Personal best

201
Q

used for promoting deep breathing exercise especially for patient who undergone surgical procedure in thorax or abdomen

A

Incentive spirometry

202
Q

Get the baseline pre and post the medication using the peak flow meter. After medications there should be an improvement.

A

Get the baseline pre and post the medication using the peak flow meter. After medications there should be an improvement.

203
Q

-to monitor if the O2 saturation is good
* to see if there is an evident increase of CO2
o revealing hypoxia or hypercapnia

A

ABG ANALYSIS

204
Q

PHARMACOTHERAPY (ASTHMA)

A

anti-inflammatory agents
Bronchodilators
inhalation therapy
Inhaled therapy
Spacer devices

205
Q

corticosteroids that suppress the primary disease process and its resultant airway hyperreactivity

A

anti-inflammatory agents

206
Q

β-2–adrenergic agonists and anticholinergics relieve asthma symptoms

A

Bronchodilators

207
Q

preferred to oral or other systemic therapy

A

inhalation therapy

208
Q

using metered dose inhalers or dry powder inhalers allows high concentration of the medication to be delivered directly to the airways, resulting in fewer systemic side effects

A

Inhaled therapy

209
Q

used to improve delivery of inhaled medication, but training and coordination are still required for patients using metered dose inhalers

A

Spacer devices

210
Q

Step-by-step treatment: ASTHMA

A

1) If the medication did not work combine with other medication
2) If still not responding to any medication then the patient may be status asthmaticus
* This is the time you intubate the patient

211
Q

plays a key role in the pathogenesis of asthma, and many asthmatic patients have elevated levels of IgE.

A

IgE

212
Q

Studies have shown that treatment with omalizumab allows reduction of the dose of inhaled glucocorticoids required to control symptoms and also a decrease in the number of asthma exacerbation episodes

A

Studies have shown that treatment with omalizumab allows reduction of the dose of inhaled glucocorticoids required to control symptoms and also a decrease in the number of asthma exacerbation episodes

213
Q

recommend that omalizumab should be considered as adjunctive therapy for patients with severe persistent asthma

A

NAEP asthma guidelines

214
Q

a cytokine that promotes eosinophilic inflammation of the airway

A

IL-5

215
Q

Shown to decrease oral corticosteroid use and reduce exacerbations in patients with severe persistent asthma and an eosinophilic phenotype

A

Mepolizumab

216
Q

Works in a slightly different way than the other two drugs, in that it blocks the IL-5 receptor on immune cells and is considered to be more effective in lowering the number of eosinophils.

A

Benralizumab

217
Q

Emergency management of acute asthma should include early and frequent administration of aerosolized β-2 agonists and therapy with systemic corticosteroids.

A

Emergency management of acute asthma should include early and frequent administration of aerosolized β-2 agonists and therapy with systemic corticosteroids.

218
Q

an approved addition to treatment options for adults whose asthma remains uncontrolled despite use of inhaled steroids and long- acting β agonists.

A

Bronchial thermoplasty

219
Q

procedure in which a probe is introduced into the central airways through a bronchoscope and heat is applied (through radiofrequency waves) to airways of 3 to 10 mm diameter with the goal to reduce the airway smooth muscle mass, reducing the ability of the airways to constrict.

A

Bronchial thermoplasty

220
Q

based on the theoretical rationale that part of the immunologic response to an administered allergen is the production of an IgG-specific antibody to the allergen injected

A

Immunotherapy (called “allergy shots” by patients)

221
Q

environmental control measures to reduce exposure to indoor and outdoor allergens and irritants are essential

A

environmental control measures to reduce exposure to indoor and outdoor allergens and irritants are essential

222
Q

Patients should be advised to avoid outdoor antigens, primarily ragweed, grass, pollens, and molds.

A

Patients should be advised to avoid outdoor antigens, primarily ragweed, grass, pollens, and molds.

223
Q

Exposure to outdoor allergens is best reduced by staying indoors with the windows closed, in an air- conditioned environment, particularly during the midday and afternoon, when pollen and some mold counts are highest

A

Exposure to outdoor allergens is best reduced by staying indoors with the windows closed, in an air- conditioned environment, particularly during the midday and afternoon, when pollen and some mold counts are highest

CARDIO (2 decks)

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