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Flashcards in Midterm Deck (141)
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1

What are the symptoms that are considered alarm findings that increase clinical concern when paired with chest pain?

Productive cough, syncope, evidence of systemic inflammation (joint pain, night sweats, significant wt loss)

2

Alarm findings: what are the signs that increase clinical concern when paired with chest pain?

fever, hypotension, tachycardia/tachypnea, pleural/pericardial friction rubs, rales/crackles, asymmetric lung sounds, absent lung sounds

3

What is the chest pain called that is made worse by taking a deep breath?

respirophasic

4

Is there a relationship b/t typical angina and exertion?

Yes. Classically exercise induced

5

What is exercise-induced transient abdominal pain AKA?

side stitch

6

What is believed to cause a side stitch?

stretching of ligaments that extend from diaphragm to internal organs (esp. liver)

7

If your chest is sore upon palpation, what is the most likely origin of the pain?

muscle/ribs/cartilage

8

What are the three characteristics of pleuritic pain?

1. localized to distribution of intercostal nerve 2. NOT made worse by palpation 3. may or may not be respirophasic

9

What is direct pleuritic pain?

inflammation of parietal pleura

10

What are the three main characteristics of direct pleuritic pain?

1. NOT made worse by palpation 2. is made worse by taking a deep breath 3. usually made worse by lateral flexion away from the involved side

11

What is indirect pleuritic pain?

Inflammation in the vicinity of the parietal pleura

12

What is indirect pleuritic pain most often associated with?

lung diseases

13

Which type of pleuritic pain is more likely to have alarm findings?

indirect

14

How often does pleuritic chest pain accompany myocardial infarction?

About 14%

15

How do you DDx musculoskeletal "mimics" from pleuritic pain?

pain is localized or made worse by palpation

16

What is the first step in plaque progression?

endothelial activation

17

What occurs during endothelial activation?

Endothelium becomes more permeable, which allows leukocytes and macrophages to migrate into tunica intima

18

What can be used to conservatively intervene with pts between 45 and 79 suffering from endothelial activation?

aspirin (also some Rx ACE-inhibitors)

19

T/F: decreased arterial stress is a major pathophysiologic problem

TRUE (normal laminar flow through normal artery => high arterial wall stress)

20

Why is decreased arterial stress a bad thing?

endothelium will favor vasoconstriction and platelet aggregation

21

Test question:

Most people with a strong family Hx of heart dz also have one or more of the other risk factors for CV dz. Therefore it's even more important to treat and control any other risk factors they have.

22

Can elevated BP be reversed?

Yes, partially but there is a residual risk.

23

What do sudden or abrupt increases in BP result in?

vasconstriction and inhibition of platelet reactivity

24

What is a healthy endothelium's response to sudden increases in BP?

release of nitrous oxide and prostacyclin

25

What does a damage endothelium favor?

vasconstriction and thrombus formation

26

What also induces endothelial release of vasoactive substances?

hypoxia

27

What does a pt with CV dz HAVE to avoid?

Anything that would cause a sudden spike in blood pressure

28

What can diabetes and insulin resistance lead to?

1. basement membrane thickening 2. increased permeability 3. endothelial activation/dysfunction (can occur in absence of plaque)

29

What vasculature does diabetes have more of an impact on?

capillaries and smaller arterioles

30

What does nicotine stimulate?

stimulates adrenal medulla to increase release of epinephrine => increased BP, HR, RR, and blood glucose levels

31

T/F: aggressive management of BP in diabetic pt is just as important as tight glycemic control

True

32

What is considered a strong independent risk factor for CV dz?

Tobacco smoking

33

What is the risk of CV dz proportional to (in regards to tobacco)?

proportional to number of cigarettes smoked and how deeply the smoker inhales

34

What substance increases plasma cholesterol, triglycerides, and fibrinogen?

Cigarette smoke

35

What substance enhances thromboxane producton and platelet aggregation?

Cigarette smoke

36

What effect does cigarette smoke have on HDL?

Decreases HDL

37

What effect does chronic exposure to epinephrine and norepinephrine have?

Toxic to cardiac myocytes

38

What are the most notable chemical by-products found in cigarette smoke?

carbon monoxide, various nitrogen oxides, various hydrogen cyanides, and ammonia

39

How many components of cigarette smoke are known to be carcinogenic?

About 70

40

How long does it take to fully reverse the effects of long-term smoking?

Up to 15 years

41

What are 3 independent risk factors that can lead to hypertriglyceridemia?

1. poorly controlled diabetes 2. obesity 3. excessive alcohol consumption

42

What is the purpose of aspirin in decreasing risk of CVD?

Decreases risk of thrombus formation

43

When are "uninhibited" platelets normally activated?

When they contact exposed collagen

44

How does aspirin decrease risk of thrombus formation?

irreversibly suppresses "activation" for life-span of platelet

45

How does aspirin suppress platelet activation?

competes for receptor sites

46

What is the primary concern with aspirin use?

hemorrhagic stroke

47

What are the 2 kinds of stroke?

1. hemorrhagic stroke 2. ischemic stroke

48

What percentage of strokes are hemorragic?

20%

49

What percentage of strokes are ischemic?

80%

50

What is the second concern with aspirin use?

Upper GI bleeding

51

Why is aspirin recommended for men?

decreased risk of myocardial infarction

52

Why is aspirin recommended for women?

decreased risk of ischemic stroke

53

What age group should be encouraged to use aspirin?

45-79

54

When should aspirin be recommended?

When benefit of MI/stroke reduction outweighs potential harm

55

How long should patients with existing CHD remain on aspirin therapy?

life-long

56

T/F: aspirin does not reduce mortality risk DURING an MI

FALSE

57

What dosage of aspirin should be given to a patient during an MI?

full-dose; 325 mg

58

How should the patient take aspirin during an MI?

chew the tablet

59

What is defined as "diffuse thickening of the tunica intima and deposition of extra-cellular lipids"?

Type IV atheroma

60

Do type IV atheromas result in clinical symptoms?

May or may not

61

What type of angina might type IV atheromas be associated with?

typical

62

Why is risk factor management so important?

type IV atheromas are unpredictable

63

Are type IV atheromas stable?

may or may not be

64

What is defined as "a fibrous cap that forms over an atheroma"?

Type V lesion - the fibroatheroma

65

Will type V atheromas result in symptoms?

May or may not

66

Are type V atheromas stable?

may or may not be

67

What is the ultimate goal with atheroma management?

keeping stable plaques stable

68

What is the first step in destabilizing type IV and V lesions?

oxidize excess LDLs

69

What is the second step in destabilizing type IV and V atheromas?

inflammation and cell "activation"

70

What is the third step in destabilizing type IV and V atheromas?

break down fibrous cap

71

What is defined as "surface defects in the fibrous cap"?

type VI "complicated" fibroatheroma

72

Why are type VI atheromas a bad thing?

much greater chance of hemorrhage, formation of thrombi, and subsequent ACS or MI

73

What is considered a key element in the disruption of stable plaque?

inflammation

74

What percentage of people who go to the ER with chest pain are actually having a heart attack?

10-15%

75

What percentage of people who are considered "low risk" and are sent home are actually having heart attacks?

4%

76

How soon within onset of symptoms do 60% of people with heart attacks die?

within 2 hours

77

What does chest pain of visceral origin imply?

cardiac ischemia

78

Is visceral pain made worse by taking a deep breath?

no

79

Is visceral pain made worse by changes in body position?

no

80

Is visceral pain made worse by palpation?

no

81

What percentage of MI cases present with pleuritic chest pain?

14%

82

What does "activation" of the sympathetic nervous system manifest in? (4)

diaphoresis, pallor, elevated resting HR, elevations in BP

83

What causes endogenous sympathetic activation?

response to the release of epinephrine/norephinephrine

84

When is endogenous sympathetic activation often seen?

in response to heart failure and/or hypoxia

85

What causes exogenous sympathetic activation?

response to various Rx, OTC, and recreational stimulants

86

What is an important differential for systemic activation of sympathetic nervous system?

Pain

87

What is the first clinical indication of an MI in 1/3 of male pts?

sudden cardiac death

88

T/F: the plaque responsible for ACS is often NOT critical before it rapidly evolves into an acutely threatening lesion

TRUE

89

Does the onset of acute coronary syndrome (ACS) cause symptoms before rupture?

may not

90

What do a large fraction of ACS cases appear to be triggered by?

external factors or conditions

91

What percentage of MI patients do not have chest pain?

33%

92

What is the problem with the physical exam in ACS pts?

results may be normal

93

What 2 factors increase the likelihood of ACS?

1. history 2. presence of cardiac "markers"

94

What is defined as "an abnormal localized collection of blood within soft tissue space or an organ"?

hematoma

95

What most often initiates hematoma formation?

a break or tear in a vessel's tunica intima

96

Which is more common, frank rupture of the abdominal aorta or an aortic dissection?

aortic dissection

97

What disease is classically associated with dissecting aneurysm?

Marfan's syndrome

98

What is the most important contributing risk factor for dissecting aneurysm?

hypertension

99

What percentage of pericarditis cases are idiopathic?

26-86%

100

What is the cardinal symptom of pericarditis?

chest pain

101

What usually makes pericarditis chest pain worse?

lying down flat

102

What usually makes pericarditis chest pain better?

sitting up and leaning forward

103

What sign is considered pathognomonic for acute pericarditis, even though it is not always present?

pericardial friction rub

104

What patient position is the best way to hear a friction rub?

sitting up and leaning forward

105

What is the primary factor in determining O2 consumption?

myocyte contraction

106

T/F: cardiac ischemia usually leads to frank/overt pain

FALSE

107

What is the most common trigger of typical angina?

exertion/exercise

108

What is the quality of pain in a typical angina?

poorly-localized and visceral

109

Is the location of a typical angina the same in each patient?

No - varies from pt to pt

110

Is a given individual's angina location the same every time?

Yes, usually predictable and unvarying

111

What does "umbilicus to eyebrows" mean?

suspect angina when a pt with CV risk factors describes any exercise induced, rest relieved discomfort above the waist or below the eyebrows

112

What causes dysfunctional intramyocardials?

occlusion of the "microcirculation"

113

are atypical anginas consistently precipitated by exertion and relieved by rest?

No

114

What demographics are more likely to experience atypical angina? (3)

1. older pts 2. females 3. diabetics

115

What is a Prinzmetal angina?

vasospasm in absence of plaque

116

What percentage of MI are accounted for by prinzmetal anginas?

1%

117

Why are women at high risk for heart disease? (3)

1. atypical angina more common 2. atypical chest pain more common 3. more likely to have comorbid condition (diabetes)

118

What is the leading cause of death in US women?

coronary artery dz

119

What type of chest pain might be "respirophasic", might be made worse by taking a deep breath, and is localized/dermatomal but NOT made worse by palpation?

inflammation of parietal pleura

120

What important question should you ask a pt with any lung dz?

Ask if pt is a smoker

121

How is pleurisy pain usually described?

sharp/stabbing and well-localized (course of intercostal nn.)

122

What life-threatening dzs can pleurisy be associated with? (4)

1. pneumonia 2. pulmonary emboli 3. pneumothorax 4. MI

123

Which type of pneumonia is often preceded by viral dzs such as influenza?

typical pneumonia

124

What type of pneumonia is found in a non-hospitalized, non-immunosuppressed person?

community-acquired

125

What type of pneumonia is acquired in the hospital?

nosocomial

126

What are 2 general clinical indications of lobar pneumonia in a pt with a cough and fever?

1. rales/crackles 2. bronchial breath sound

127

What is the positive LR of rales/crackles in a pt with cough and fever?

2

128

What is the positive LR of bronchial breath sound in a pt with cough and fever?

3.3

129

What is the 6th leading cause of death in the US?

pneumonia

130

What is considered "classic" lobar pneumonia history?

history of cold followed by sudden abrupt onset of fever

131

What is the time frame for early consolidation and red hepatization in lobar pneumonia?

days 3-4

132

What is the time frame for late consolidation and white hepatization in lobar pneumonia?

days 4-6

133

What is the "classic" association with a pancoast tumor?

rapid onset of shoulder/arm/brachial plexus symptoms in a middle age male smoker

134

Pulmonary emboli can arise from DVT where in the body?

anywhere

135

What is the second most common cause of sudden death?

massive pulmonary embolism

136

What type of pts is the highest incidence of PE seen in?

hospitalized pts

137

Why is the clinical presentation of PE misleading?

Sx usually sudden onset

138

What is the classic triad of PE Sx?

1. dyspnea 2. hemoptysis 3. chest pain

139

What is defined as "free air in the intra-pleural space"?

pneumothorax

140

How does tension pneumothorax present?

sudden onset of respiratory distress

141

What is "compressive atelectasis"?

collapse of previously expanded lung tissue d/t massive fluid accumulation in the intra-pleural space