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Cardioresp > Final > Flashcards

Final Flashcards

1
Q

Where does pleuritic pain localize to?

A

distribution of an intercostal nerve

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2
Q

T/F: Pleuritic pain may or may not be made worse by taking a deep breath

A

TRUE

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3
Q

Do shingles outbreaks occur unilaterally or bilaterally?

A

unilaterally

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4
Q

What is the first symptom of shingles?

A

pain (it can occur before rash erupts)

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5
Q

What is a key symptom for intercostal neuralgia?

A

increased pain when bending toward the side of involvement

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6
Q

What is a key symptom for pleurisy?

A

increased pain when bending away from the side of involvement

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7
Q

What can sometimes be an extremely good mimic of angina/ACS/MI?

A

non-cardiac chest pain

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8
Q

What is costochondritis?

A

aka costosternal syndrome. Intermittent unilateral pain at one or more of the costosternal junctions/costochondral junctions. Pain can radiate across the anterior chest and increases with inspiration.

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9
Q

What is Tietze’s syndrome?

A

idiopathic costochondritis with painful enlargement of the costal cartilage. Usually the 2nd costochondral junction.

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10
Q

What is sternalis syndrome?

A

pain over midline of sternum. Can radiate bilaterally. Pain is less intense but more constant than costosternal syndrome

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11
Q

What is xyphoidalgia?

A

pain over xyphoid process. Increased by lifting, deep breathing, or heavy meals

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12
Q

What is rib tip syndrome?

A

aka slipping rib. Hypermobility of anterior costal cartilage in a lower rib. Movement of rib increases pain and causes clicking or snapping sound

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13
Q

Where are most rib fractures?

A

angle of the rib via blunt trauma

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14
Q

what are the most commonly damaged ribs?

A

ribs 4 -9

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15
Q

What are some common concerns about first rib injury?

A

significant chest damage, injury to lungs, aorta, subclavian, or brachial plexus

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16
Q

What can a lower rib fx damage?

A

Liver or spleen

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17
Q

what can floating ribs damage?

A

kidneys

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18
Q

what is the main complication with rib fx?

A

compromised ventilation (more prone to hyperventilation)

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19
Q

What can fragmented rib fx lead to?

A

pneumothorax or hemothorax

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20
Q

what can flail chest lead to?

A

decreased excursion and ventilatory insufficiency

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21
Q

What are some conditions that have been associated with cervical pseudo-angina?

A

spondylolisthesis, osteophytes, discopathy involving lower Cx spine, cervical NR compression (usually c7)

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22
Q

what is cervicobrachial syndrome?

A

pain arising from a cervical spine dz, NR compression, or TOS. Might be mistaken for angina pectoris

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23
Q

what is cervicogenic angina?

A

pain that very closely resembles true cardiac angina but originates from the cervical spine

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24
Q

what must always be ruled out in a pt with cervicogenic angina?

A

coexisting CAD

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25
Q

what are the mechanisms in cervical pseudo-angina?

A
  1. radicular pain d/t NR compression 2. compression of ventral motor root 3. referred pain from ALL, PLL, disc, or facets 4. autonomic Sx mediated by sympathetic nervous system
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26
Q

what are the possible symptoms of cervical pseudo-angina?

A
  1. angina-type pain 2. autonomic/sympathetic sx (SOB, diaphoresis, dyspnea, nausea, pallor, vasoconstriction)
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27
Q

what could trigger a Prinzmetal angina?

A

vasoconstriction mediated by autonomic/sympathetic nervous system and/or pain

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28
Q

What does functional chest pain have a close association with?

A

GERD

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29
Q

What is functional chest pain?

A

characterized by recurrent episodes of unexplained chest pain that are usually midline, of visceral quality, and therefore potentially of esophageal origin. The pain is often debilitating.

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30
Q

how many americans suffer from GERD every year?

A

100 million

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31
Q

What is spontaneous passive movement of some gastric contents into the esophagus called?

A

normal asymptomatic reflux (some degree occurs in almost everyone multiple times/day)

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32
Q

What is symptomatic functional heartburn?

A

reflux symptoms are present. Acid levels are not elevated, esophageal mucosa appears normal upon endoscopy

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33
Q

What is non-erosive reflux dz?

A

reflux symptoms. Acid levels elevated. Esophageal tissue appears normal upon endoscopy

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34
Q

What is gastro-esophageal reflux dz?

A

aka erosive esophagitis. Reflux symptoms present. Acid levels elevated. Esophageal damage on endoscopy/biopsy

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35
Q

what are the physical anti-reflux barriers?

A

mucosal rosettes, gastro-esophageal angle (weak barriers)

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36
Q

what are the physiological anti-reflux barriers?

A

stronger defense mechanisms, positive pressure gradient between lower esophageal sphincter and the stomach, positive intra-abdominal pressure, appropriate LES basal tonus

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37
Q

how does weight loss affect intra-abdominal pressure?

A

decreases

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38
Q

What are the factors that decrease LES basal pressures and increase risk of reflux?

A

gastric acidification, citrus, nicotine, alcohol, fried or fatty foods, caffeine, chocolate, peppermint, spearmint. Sometimes: potatoes, tomatoes, sweet and hot peppers, eggplant, tomatillos, tamarillos, pepinos, pimentos, paprika, cayenne, tabasco.

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39
Q

what is considered the first line of Tx for GERD?

A

avoid foods that can contribute GERD

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40
Q

what has shown to consistently work better than dietary modification for GERD?

A

weight loss and elevating the head of the bed

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41
Q

along with laying down, how can LES basal pressure also be decreased?

A

pregnancy, meds, hiatal hernia

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42
Q

what is the incidence of heartburn in US adults?

A

monthly = 40% weekly = 20% daily = 10%

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43
Q

What is a typical heartburn?

A

substernal burning pain located b/t xyphoid process and episternal notch

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44
Q

where are the two places that heartburn can have referred pain?

A

midthoracic spine b/t shoulder blades = 40% of cases, left shoulder/arm = 5% of cases

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45
Q

what is acid regurgitation that can burn the throat?

A

acid brash

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46
Q

what is excess salivation?

A

water brash

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47
Q

what is the time frame for classic heartburn to occur?

A

30-60 mins after offending meal

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48
Q

what often provokes heartburn?

A

lying down or bending over after meals

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49
Q

T/F: the severity of heartburn often correlates with the degree of damage

A

false - does not correlate

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50
Q

T/F: older pts with verified GERD may not experience “heartburn”.

A

TRUE

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51
Q

in a pt with stomach problems, what might dr feel when palpating Tx spine?

A

“rubbery” between shoulder blades

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52
Q

What are the warning signs that suggest complicated GERD?

A
  1. chest pain that can mimic angina pectoris (motility disorders such as esophageal spasm) 2. dysphagia 3. odynophagia 4. weight loss 5. anemia/gastrointestinal bleeding/blood in stool
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53
Q

What should GERD pts with alarm symptoms undergo?

A

prompt endoscopy

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54
Q

what could be a concern for pts with very chronic GERD?

A

potential barretts esophagus

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55
Q

what can hyperventilation induce?

A

vasoconstriction

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56
Q

what is a common concern with hyperventilation syndrome?

A

coexisting CAD

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57
Q

what is hyperventilation syndrome classically associated with?

A

hypocalcemia

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58
Q

what are some possible nms findings for hyperventilation syndrome?

A

latent tetany or neuromuscular irritability

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59
Q

What are the 2 provocative tests for latent tetany?

A
  1. Chvostek’s sign 2. Trousseau’s sign
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60
Q

What is Chvostek’s sign?

A

facial twitching via stimulation of CN VII. (tap over TMJ/parotid gland/masseter) low sensitivity

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61
Q

What is Trousseau’s sign?

A

carpal spasm/obstetrician’s hand (inflate BP cuff until pulse disappears and hold for 5 min.) decent sensitivity, low false-positive rate

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62
Q

describe the atypical chest pain assoc. with HVS?

A

pain may last for hours, pain often relieved by exercise

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63
Q

what are the characteristics of HVS paresthesias?

A

usually bilateral, upper extremity. If unilateral, 80% are left-sided

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64
Q

what is a possible result when minute ventilation exceeds metabolic demands?

A

“perceived dyspnea”

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65
Q

what do HVS pts tend to breathe using?

A

upper thorax instead of diaphragm (can lead to chronically over-inflated lungs)

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66
Q

What causes acute primary hyperventilation?

A

no organic cause identified

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67
Q

how common is acute primary hyperventilation?

A

1% of HVS cases

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68
Q

what are 2 characteristics that make chronic/compensated primary ventilation difficult to Dx?

A
  1. no organic cause identified 2. chest wall tenderness
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69
Q

What are some of the characteristics of secondary hyperventilation?

A

organic cause identified, pain, mild bronchospasm, asthma

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70
Q

how does pursed lip respiration affect breathing?

A

slows respiration rate and reduces work of breathing

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71
Q

what is a panic disorder commonly caused by?

A

spontaneous sudden onset of fear or discomfort (seen in up to 30% of college students)

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72
Q

What does a non-productive cough during a dyspnea attack indicate?

A

advanced small airways dz

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73
Q

T/F: productive cough would be seen after airways are reopened

A

TRUE

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74
Q

what is chronic bronchitis?

A

centrilobular emphysema and increased airways resistance

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75
Q

what is classic emphysema?

A

panlobular emphysema and decreased elastic recoil

76
Q

what are the two forms of COPD?

A

chronic bronchitis (more common) and pulmonary emphysema. Most COPD pts have combination of both conditions

77
Q

What is the definition of COPD?

A

chronic, incompletely reversible airflow obstruction on forced expiration

78
Q

What is the primary risk for COPD?

A

cigarette smoking

79
Q

What is the risk involved with secondhand smoke?

A

might be a factor in pulmonary emphysema. (not considered a direct factor for chronic bronchitis)

80
Q

what is a common side effect for COPD pts?

A

more susceptible to infection (bronchitis, pneumonia, etc)

81
Q

What is the clinical definition of chronic bronchitis?

A

long term cigarette smoking and a mucus producing cough that occurs on most days and lasts for at least 3 months per year for 2 years in a row

82
Q

In end stage chronic bronchitis, what is physically obstructed?

A

greatly increased small airways resistance

83
Q

what is grade 3 dyspnea?

A

dyspnea with ADLs (common in end stage chronic bronchitis)

84
Q

what is a common complication of end stage chronic bronchitis?

A

cor pulmonale/ “right sided heart failure”

85
Q

what are some characteristics of end stage chronic bronchitis?

A
  1. prolonged expiration 2. excessive use of accessory msls of respiration 3. pursed lip respiration 4. noisy breathing
86
Q

What is a “blue bloater” associated with?

A

end stage chronic bronchitis (“can’t catch my breath and I cough all the time”)

87
Q

What are 3 common causes of pulmonary emphysema?

A
  1. inflammatory response 2. alpha-1 antitrypsin deficiency 3. relative obstruction
88
Q

What is most strongly linked to pulmonary emphysema?

A

lack of alpha-1 antitrypsin

89
Q

how does pulmonary emphysema affect respiration?

A

very prolonged expiration

90
Q

what lobes are most affected by emphysema associated with cigarette smoking?

A

upper lobes

91
Q

how can emphysema occur in a non-smoker?

A

congenital lack of AAT (more severe in lower lobes)

92
Q

What does a loss of elastic recoil lead to?

A

very prolonged expiration

93
Q

What kind of pt often presents underweight, in a tripod posture when seated, and with a possible expiratory grunt?

A

pulmonary emphysema

94
Q

what is a “pink puffer” associated with?

A

pulmonary emphysema

95
Q

what is the method of choice for dxing copd?

A

spirometry

96
Q

what is the most effective preventitive measure against chronic bronchitis?

A

smoking cessation

97
Q

what is pneumoconiosis?

A

lung dust d/t inhalation of asbestos, coal dust, or crystalline silica

98
Q

What is an important cofactor for pneumoconiosis?

A

smoking

99
Q

What is the most common pneumoconiosis in the US?

A

silicosis and “sand blasters lung”

100
Q

What is defined as an asthma-like reaction to the inhalation of cotton dust?

A

byssinosis

101
Q

what is the classic early asthmatic response?

A

a rapid-onset IgE mediated bronchoconstriction right after exposure to a specific trigger

102
Q

what is the classic late asthmatic response?

A

mucosal edema d/t inflammatory response that occurs 6-24 hours after exposure to the specific trigger

103
Q

what are activated in the lungs of asthmatic pts?

A

eosinophils

104
Q

what alteration takes place in the epithelium of chronic asthma pts?

A

increase in number of mucus secreting cells (=> dramatic increase in mucus production)

105
Q

what can inflammation and tissue alterations in asthmatic pts result in?

A

an asthmatic response upon exposure to non-specific irritants

106
Q

what is classically associated with allergic asthma?

A

exogenous/extrinsic asthma

107
Q

what are common causes of endogenous asthma?

A

GERD, viral respiratory infections, emotional stress, obesity, exposure to cold or dry air

108
Q

what are some examples of conditions that can involve wheezing?

A

asthma, bronchitis, neoplasm, pulmonary edema/CHF, respiratory foreign bodies, hyperventilation syndrome

109
Q

T/F: severity of symptoms and intensity of wheezing sounds usually correlate with the actual degree of airway obstruction

A

false - does not correlate

110
Q

what is an acute asthmatic exacerbation that’s unresponsive to bronchodilators?

A

status asthmaticus

111
Q

what are the signs of respiratory distress?

A
  1. increased RR 2. increased HR 3. diaphoresis 4. excessive use of accessory msls of respiration
112
Q

what is a commonly used benchmark for CHF?

A

left ventricle ejection fraction

113
Q

What are two types of late stage mitral stenosis?

A
  1. tight mitral stenosis (TMS) 2. pulmonary vascular dz (PVD)
114
Q

What is the most common symptom in heart failure?

A

dyspnea (usually d/t elevated left atrial pressure)

115
Q

What percentage of heart failure pts have glucose abnormalities?

A

40%

116
Q

how is neurohumoral stimulation a compensation for a failing heart?

A

sympathetic stimulation elevates HR, increases strength of cardiac contraction, and may be accompanied by diaphoresis

117
Q

what are catecholamines thought to be toxic to?

A

cardiac myocytes

118
Q

what does compensated heart failure cause?

A

hypertrophy

119
Q

what does decompensated heart failure cause?

A

apoptosis

120
Q

how does retention of sodium and water compensate for a failing heart?

A

helps maintain BP, increases preload to make use of Frank Starling mechanism

121
Q

how does cardiac remodeling compensate for a failing heart?

A

dilation of ventricle OR hypertrophy

122
Q

what is a problem associated with dilation of the ventricle during cardiac remodeling?

A

eventually stretched msl becomes weakened, leading to overt systolic dysfunction (balloon analogy)

123
Q

what is a problem associated with hypertrophy during cardiac remodeling?

A

msl becomes stiff and can no longer relax or stretch, leading to overt diastolic dysfunction

124
Q

what results in increased left atrial pressure?

A

left backward heart failure

125
Q

what is the classic symptom progression in pulmonary venous congestion?

A

exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dyspnea at rest, acute pulmonary edema

126
Q

what is the cardinal sign of left ventricular failure?

A

breathlessness

127
Q

what is the classic association with left forward heart failure?

A

fatigue and exercise intolerance

128
Q

what does left forward heart failure result in?

A

decreased cardiac output

129
Q

what is the most common cause of right heart failure?

A

left ventricular failure

130
Q

what is the second most common cause of right ventricular failure?

A

lung dz (cor pulmonale)

131
Q

what is considered a minor criterion in the dx of CHF?

A

edema

132
Q

what is compensated heart failure?

A

heart failure with a relatively normal cardiac output/ejection fraction

133
Q

what is decompensated heart failure?

A

CHF with grossly inadequate cardiac output (death)

134
Q

what is the NYHA classification of heart failure based upon?

A

amt of effort needed to produce heart failure symptoms

135
Q

what is class I CHF?

A

comfortable at rest and NO limitation of ADLs

136
Q

what is class II CHF?

A

comfortable at rest with SLIGHT limitation of ADLs

137
Q

what is class III CHF?

A

comfortable at rest with MODERATE limitation of ADLs

138
Q

what is class IV CHF?

A

Uncomfortable at rest with SEVERE limitation of ADLs (decompensation)

139
Q

what is the most common form of heart failure?

A

dilated cardiomyopathy

140
Q

Does dilated cardiomyopathy cause systolic or diastolic failure?

A

systolic

141
Q

does hypertrophic cardiomyopathy cause systolic or diastolic failure?

A

diastolic

142
Q

how may a compensated pts appear at rest?

A

comfortable

143
Q

what commonly precedes dilated cardiomyopathy?

A

systemic hypertension

144
Q

what kind of therapy is very effective in preventing the development of CHF?

A

anti-hypertensive therapy

145
Q

What is a common cause of sudden cardiac death in young competitive athletes?

A

hypertrophic cardiomyopathy

146
Q

what are some morphologic changes that occur in response to training?

A

increased left ventricular wall thickness, increased interventricular septal thickness, increased left ventricular end-diastolic dimension

147
Q

after the first week of detraining, how much physiologic hypertrophy is lost?

A

up to 60%

148
Q

within the first 3 weeks of detraining, how much does maximal cardiac output during exercise decrease?

A

8% (VO2 max decreases 8% also)

149
Q

What is the most common cause of sudden cardiac death in athletes over 35?

A

CAD

150
Q

what is the most common cause of sudden cardiac death in athletes under 35?

A

hypertrophic cardiomyopathy

151
Q

What is S1?

A

closure of the mitral and tricuspid valves. Marks start of ventricular systole

152
Q

What are the different names for mitral valve systolic murmurs?

A

mitral regurgitation, mitral imcompetence, systolic regurgitant murmurs, holosystolic murmurs

153
Q

what are the two problems with acute mitral regurgitation?

A

dyspnea and decreased systemic perfusion

154
Q

what is the key clinical feature for acute mitral regurgitation?

A

dyspnea

155
Q

What usually occurs 10 years after acute MR is dxed?

A

90% of pts die or undergo surgical procedure

156
Q

What does dilation of the left atrium imply?

A

chronic mitral regurgitation

157
Q

what does rupture of a papillary msl imply?

A

acute mitral regurgitation

158
Q

What has mitral regurgitation classically been associated with?

A

rheumatic heart dz

159
Q

what is mitral valve prolapse?

A

an abnormal upward systolic displacement of the one or both mitral valve leaflets

160
Q

what are the 3 categories of mitral valve prolapse?

A
  1. “click” 2. syndrome 3. “click-murmur”
161
Q

is mitral valve prolapse syndrome more common in men or women?

A

women

162
Q

what age range has a peak incidence of mitral valve prolapse syndrome?

A

30-40

163
Q

Is leaflet approximation good or bad in mitral valve prolapse syndrome? Why?

A

good, the valve still closes and there is no murmur or regurgitation

164
Q

How does mitral valve prolapse present in many pts?

A

benign and asymptomatic

165
Q

Describe the regurgitation associated w/ MVP click-murmur?

A

some degree of regurgitation - valve does not fully close

166
Q

What is the peak incidence for MVP click murmur?

A

45-60

167
Q

is MVP click-murmur more common in males or females?

A

males

168
Q

what are potential complications of mitral valve prolapse?

A

mitral valve regurgitation, infective endocarditis, cerebrovascular accidents

169
Q

what causes congenital aortic stenosis?

A

small/unicuspid/bicuspid aortic valve (more susceptible to wear and tear)

170
Q

with a congenital aortic stenosis, when do symptoms develop?

A

during growth spurts

171
Q

what is the first problem with adult onset aortic valve stenosis?

A

left ventricular hypertrophy and diastolic failure

172
Q

what is the eventual problem with adult onset aortic valve stenosis?

A

left ventricular dilation and overt heart failure

173
Q

what are the 2 most important clinical features of adult onset aortic stenosis?

A
  1. late appearance of symptoms 2. dyspnea on exertion
174
Q

What is S2?

A

closure of the aortic and pulmonic valves. End of ventricular systole

175
Q

what does classic chronic aortic regurgitation lead to?

A

diastolic regurgitant murmur, increased stroke volume, combined hypertrophy and dilation of left ventricle

176
Q

what is a common first symptom of chronic aortic regurgitation?

A

uncomfortable awareness of the heart beat

177
Q

what is the key feature of classic mitral stenosis?

A

elevated left atrial pressure

178
Q

what is mitral stenosis most often due to?

A

rheumatic fever

179
Q

what is the first symptom of mitral stenosis?

A

dyspnea on exertion (almost all heart valve dzs)

180
Q

When does S3 occur?

A

mid diastole during rapid passive ventricular filling

181
Q

what is the abnormal variant of S3?

A

ventricular gallop (s1, s2, s3)

182
Q

When does S4 occur?

A

late diastole during period of atrial contraction

183
Q

What does S4 imply?

A

decreased ventricular compliance/remodeling

184
Q

What is the abnormal variant of S4?

A

atrial gallop (s4, s1, s2)

185
Q

when is a “soft” s4 common?

A

in pts with no overt signs of heart dz

Cardioresp (2 decks)

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