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Cardioresp > Midterm > Flashcards

Midterm Flashcards

1
Q

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

A

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

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2
Q

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

A

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

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3
Q

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

A

respirophasic

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4
Q

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

A

Yes. Classically exercise induced

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5
Q

What is exercise-induced transient abdominal pain AKA?

A

side stitch

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6
Q

What is believed to cause a side stitch?

A

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

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7
Q

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

A

muscle/ribs/cartilage

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8
Q

What are the three characteristics of pleuritic pain?

A
  1. localized to distribution of intercostal nerve 2. NOT made worse by palpation 3. may or may not be respirophasic
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9
Q

What is direct pleuritic pain?

A

inflammation of parietal pleura

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10
Q

What are the three main characteristics of direct pleuritic pain?

A
  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
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11
Q

What is indirect pleuritic pain?

A

Inflammation in the vicinity of the parietal pleura

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12
Q

What is indirect pleuritic pain most often associated with?

A

lung diseases

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13
Q

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

A

indirect

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14
Q

How often does pleuritic chest pain accompany myocardial infarction?

A

About 14%

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15
Q

How do you DDx musculoskeletal “mimics” from pleuritic pain?

A

pain is localized or made worse by palpation

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16
Q

What is the first step in plaque progression?

A

endothelial activation

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17
Q

What occurs during endothelial activation?

A

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

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18
Q

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

A

aspirin (also some Rx ACE-inhibitors)

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19
Q

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

A

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

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20
Q

Why is decreased arterial stress a bad thing?

A

endothelium will favor vasoconstriction and platelet aggregation

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21
Q

Test question:

A

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.

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22
Q

Can elevated BP be reversed?

A

Yes, partially but there is a residual risk.

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23
Q

What do sudden or abrupt increases in BP result in?

A

vasconstriction and inhibition of platelet reactivity

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24
Q

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

A

release of nitrous oxide and prostacyclin

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25
Q

What does a damage endothelium favor?

A

vasconstriction and thrombus formation

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26
Q

What also induces endothelial release of vasoactive substances?

A

hypoxia

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27
Q

What does a pt with CV dz HAVE to avoid?

A

Anything that would cause a sudden spike in blood pressure

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28
Q

What can diabetes and insulin resistance lead to?

A
  1. basement membrane thickening 2. increased permeability 3. endothelial activation/dysfunction (can occur in absence of plaque)
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29
Q

What vasculature does diabetes have more of an impact on?

A

capillaries and smaller arterioles

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30
Q

What does nicotine stimulate?

A

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

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31
Q

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

A

True

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32
Q

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

A

Tobacco smoking

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33
Q

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

A

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

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34
Q

What substance increases plasma cholesterol, triglycerides, and fibrinogen?

A

Cigarette smoke

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35
Q

What substance enhances thromboxane producton and platelet aggregation?

A

Cigarette smoke

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36
Q

What effect does cigarette smoke have on HDL?

A

Decreases HDL

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37
Q

What effect does chronic exposure to epinephrine and norepinephrine have?

A

Toxic to cardiac myocytes

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38
Q

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

A

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

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39
Q

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

A

About 70

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40
Q

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

A

Up to 15 years

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41
Q

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

A
  1. poorly controlled diabetes 2. obesity 3. excessive alcohol consumption
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42
Q

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

A

Decreases risk of thrombus formation

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43
Q

When are “uninhibited” platelets normally activated?

A

When they contact exposed collagen

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44
Q

How does aspirin decrease risk of thrombus formation?

A

irreversibly suppresses “activation” for life-span of platelet

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45
Q

How does aspirin suppress platelet activation?

A

competes for receptor sites

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46
Q

What is the primary concern with aspirin use?

A

hemorrhagic stroke

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47
Q

What are the 2 kinds of stroke?

A
  1. hemorrhagic stroke 2. ischemic stroke
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48
Q

What percentage of strokes are hemorragic?

A

20%

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49
Q

What percentage of strokes are ischemic?

A

80%

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50
Q

What is the second concern with aspirin use?

A

Upper GI bleeding

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51
Q

Why is aspirin recommended for men?

A

decreased risk of myocardial infarction

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52
Q

Why is aspirin recommended for women?

A

decreased risk of ischemic stroke

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53
Q

What age group should be encouraged to use aspirin?

A

45-79

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54
Q

When should aspirin be recommended?

A

When benefit of MI/stroke reduction outweighs potential harm

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55
Q

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

A

life-long

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56
Q

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

A

FALSE

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57
Q

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

A

full-dose; 325 mg

58
Q

How should the patient take aspirin during an MI?

A

chew the tablet

59
Q

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

A

Type IV atheroma

60
Q

Do type IV atheromas result in clinical symptoms?

A

May or may not

61
Q

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

A

typical

62
Q

Why is risk factor management so important?

A

type IV atheromas are unpredictable

63
Q

Are type IV atheromas stable?

A

may or may not be

64
Q

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

A

Type V lesion - the fibroatheroma

65
Q

Will type V atheromas result in symptoms?

A

May or may not

66
Q

Are type V atheromas stable?

A

may or may not be

67
Q

What is the ultimate goal with atheroma management?

A

keeping stable plaques stable

68
Q

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

A

oxidize excess LDLs

69
Q

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

A

inflammation and cell “activation”

70
Q

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

A

break down fibrous cap

71
Q

What is defined as “surface defects in the fibrous cap”?

A

type VI “complicated” fibroatheroma

72
Q

Why are type VI atheromas a bad thing?

A

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

73
Q

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

A

inflammation

74
Q

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

A

10-15%

75
Q

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

A

4%

76
Q

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

A

within 2 hours

77
Q

What does chest pain of visceral origin imply?

A

cardiac ischemia

78
Q

Is visceral pain made worse by taking a deep breath?

A

no

79
Q

Is visceral pain made worse by changes in body position?

A

no

80
Q

Is visceral pain made worse by palpation?

A

no

81
Q

What percentage of MI cases present with pleuritic chest pain?

A

14%

82
Q

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

A

diaphoresis, pallor, elevated resting HR, elevations in BP

83
Q

What causes endogenous sympathetic activation?

A

response to the release of epinephrine/norephinephrine

84
Q

When is endogenous sympathetic activation often seen?

A

in response to heart failure and/or hypoxia

85
Q

What causes exogenous sympathetic activation?

A

response to various Rx, OTC, and recreational stimulants

86
Q

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

A

Pain

87
Q

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

A

sudden cardiac death

88
Q

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

A

TRUE

89
Q

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

A

may not

90
Q

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

A

external factors or conditions

91
Q

What percentage of MI patients do not have chest pain?

A

33%

92
Q

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

A

results may be normal

93
Q

What 2 factors increase the likelihood of ACS?

A
  1. history 2. presence of cardiac “markers”
94
Q

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

A

hematoma

95
Q

What most often initiates hematoma formation?

A

a break or tear in a vessel’s tunica intima

96
Q

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

A

aortic dissection

97
Q

What disease is classically associated with dissecting aneurysm?

A

Marfan’s syndrome

98
Q

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

A

hypertension

99
Q

What percentage of pericarditis cases are idiopathic?

A

26-86%

100
Q

What is the cardinal symptom of pericarditis?

A

chest pain

101
Q

What usually makes pericarditis chest pain worse?

A

lying down flat

102
Q

What usually makes pericarditis chest pain better?

A

sitting up and leaning forward

103
Q

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

A

pericardial friction rub

104
Q

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

A

sitting up and leaning forward

105
Q

What is the primary factor in determining O2 consumption?

A

myocyte contraction

106
Q

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

A

FALSE

107
Q

What is the most common trigger of typical angina?

A

exertion/exercise

108
Q

What is the quality of pain in a typical angina?

A

poorly-localized and visceral

109
Q

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

A

No - varies from pt to pt

110
Q

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

A

Yes, usually predictable and unvarying

111
Q

What does “umbilicus to eyebrows” mean?

A

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

112
Q

What causes dysfunctional intramyocardials?

A

occlusion of the “microcirculation”

113
Q

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

A

No

114
Q

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

A
  1. older pts 2. females 3. diabetics
115
Q

What is a Prinzmetal angina?

A

vasospasm in absence of plaque

116
Q

What percentage of MI are accounted for by prinzmetal anginas?

A

1%

117
Q

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

A
  1. atypical angina more common 2. atypical chest pain more common 3. more likely to have comorbid condition (diabetes)
118
Q

What is the leading cause of death in US women?

A

coronary artery dz

119
Q

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?

A

inflammation of parietal pleura

120
Q

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

A

Ask if pt is a smoker

121
Q

How is pleurisy pain usually described?

A

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

122
Q

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

A
  1. pneumonia 2. pulmonary emboli 3. pneumothorax 4. MI
123
Q

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

A

typical pneumonia

124
Q

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

A

community-acquired

125
Q

What type of pneumonia is acquired in the hospital?

A

nosocomial

126
Q

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

A
  1. rales/crackles 2. bronchial breath sound
127
Q

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

A

2

128
Q

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

A

3.3

129
Q

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

A

pneumonia

130
Q

What is considered “classic” lobar pneumonia history?

A

history of cold followed by sudden abrupt onset of fever

131
Q

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

A

days 3-4

132
Q

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

A

days 4-6

133
Q

What is the “classic” association with a pancoast tumor?

A

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

134
Q

Pulmonary emboli can arise from DVT where in the body?

A

anywhere

135
Q

What is the second most common cause of sudden death?

A

massive pulmonary embolism

136
Q

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

A

hospitalized pts

137
Q

Why is the clinical presentation of PE misleading?

A

Sx usually sudden onset

138
Q

What is the classic triad of PE Sx?

A
  1. dyspnea 2. hemoptysis 3. chest pain
139
Q

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

A

pneumothorax

140
Q

How does tension pneumothorax present?

A

sudden onset of respiratory distress

141
Q

What is “compressive atelectasis”?

A

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

Cardioresp (2 decks)

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