Quiz 1 Flashcards

1
Q

What two factors principally determine the cardiac output?

A

Heart Rate
Stroke Volume

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2
Q

What are LVEDV and LVESV?

A

LVEDV- Left ventricular end diastolic volume

LVESV- Left ventricular end systolic volume

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3
Q

What is the formula for stroke volume?

A

SV = LVEDV - LVESV

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4
Q

What is the formula for Ejection fraction (EF)?

A

EF = SV / LVEDV

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5
Q

What is the range for a normal ejection fraction?

A

55-70%

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6
Q

What is the general definition of preload?

A
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7
Q

What is the definition of preload as it pertains to the heart? What factor primarily determines preload?

A
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8
Q

What is the definition of afterload as it pertains to the heart? What is it often approximated by?

A
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9
Q

What is contractility in the heart? What nervous system regulates contractility? What effect does it have on ESV (LVSEV)?

A
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10
Q

What is venous return?

A
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11
Q

What are the three main factors that affect venous return?

A

1) Right atrial pressure
- decreased RAP increases VR
2) Mean systemic filling pressure
- Increased MSFP increases venous return
3) Total peripheral resistance
-Decreased TPR increases venous return

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12
Q

What is right atrial pressure? What is the normal range? What can cause it to decrease/increase?

A
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13
Q

What is MSFP? What causes it to increase/decrease?

A
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14
Q

What proportion of resistance to venous return is determined by arteriolar/small artery resistance? What proportion by venous resistance?

A
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15
Q

What is the resting membrane potential for a contractile cardiac mucle cell?

A

-80 mV

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16
Q

What occurs during phase 4 of a ventricular myocyte action potential?

A
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17
Q

What occurs during phase 0 of a ventricular myocyte action potential?

A
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18
Q

What occurs during phase 1 of a ventricular myocyte action potential?

A
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19
Q

What occurs during phase 2 of a ventricular myocyte action potential?

A
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20
Q

What occurs during phase 3 of a ventricular myocyte action potential?

A
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21
Q

What occuring during phase 4 of a ventricular myocyte action potential?

A
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22
Q

What event during a cardiac myocyte action potential induces muscle contraction?

A
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23
Q

In a healthy heart, the only viable pathway for electrical signaling between the atria and the ventricles is what structure?

A

The bundle of His

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24
Q

Myocytes specializing in conduction have notably smaller levels of what two contractile proteins?

A

Myosin and Actin

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25
Q

What occurs during phase 4 of a cardiac pacemaker cell action potential?

A
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26
Q

What occurs during phase 0 of a cardiac pacemaker cell action potential?

A
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27
Q

What occurs during phase 3 of a cardiac pacemaker cell action potential?

A
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28
Q

What is the sarcolemma as found in cardiac myocytes?

A
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29
Q

What are T-tubules as found in cardiac myocytes (also present in other muscle types)?

A
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30
Q

What are L-type Ca2+ channels as found in cardiac myocytes?

A
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31
Q

What is the Ryanodine receptor? What is its function?

A
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32
Q

What elements does a couplon consist of?

A
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33
Q

What is the role of the sarcoplasmic reticulum?

A
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34
Q

What is the first step of excitation contraction coupling?

A
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35
Q

What is the second step of excitation contraction coupling?

A
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36
Q

What is the third step of excitation contraction coupling?

A
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37
Q

What is the fourth step of excitation contraction coupling?

A
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38
Q

What is the role of SERCA in step 5 of excitation contraction coupling?

A
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39
Q

What is the role of NaCaX in step 5 of excitation contraction coupling?

A
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40
Q

What is the role of the Ca2+ pump in step 5 of excitation contraction coupling?

A
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41
Q

Descrie which leads should be observed in the “quick and dirty” axis determination method:

A
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42
Q

What are three potential causes of a left axis deviation?

A
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43
Q

What are three potential causes of a right axis deviation?

A
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44
Q

STEMI localized to the LCX or diagonal branch of LAD arteries will involve which EKG leads?

A
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45
Q

STEMI localized to the RCA or LCX arteries will involve which EKG leads?

A
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46
Q

STEMI localized to the LAD will involve which EKG leads?

A
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47
Q

What is true about the relationship between ST elevations and ST depressions?

A
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48
Q

What is a hallmark on an EKG denoting a prior MI?

A
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49
Q

What is Ohm’s law?

A

I = V/R
V= IR

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50
Q

How can Ohm’s law (picture attached) be related to blood flow?

A
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51
Q

What is the formula for MAP derived from Ohm’s law?

A
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52
Q

What are two formulas for MAP using SBP and DBP?

A
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53
Q

What is the formula for calculating resistance to blood flow in a vessel?

A
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54
Q

What is the signifance of Poiseuille’s law in terms of blood flow?

A
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55
Q

Why is Poiseulle’s law referred to as a fourth power law?

A

The relationship between radius and flow (or resistance in medical applications) is massive due to r being raised to the 4th power

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56
Q

What is the most important factor determing blood flow in the CV system?

A

Vessel radius

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57
Q

How is resistance totaled when the resistors are arranged in a series?

A
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58
Q

How is resistance totaled when the resistors are arranged in parallel?

A
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59
Q

What is the formula for compliance? How is compliance different from elastance? Of arteries and veins, which are more compliant? Which are more elastance?

A
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60
Q

What are three notable causes of blood viscosity? What is a notable cause of low viscosity?

A
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61
Q

How is pulse pressure calculated? What is its relation to stroke volume and to arterial compliance?

A
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62
Q

What is the law of Laplace in context of ventricular myocardium?

A

*where h is the thickness of the ventricular myocardium

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63
Q

At what structure does an AP orginating from the SA node slow before entering the ventricles?

A

The AV node

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64
Q

Which two catecholamines are the most responsible for binding adrenergic receptors?

A

Epinephrine and Norepinephrine

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65
Q

What G protein is preferred by a-1 adrenergic receptors?

A
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66
Q

What G protein is preferred by a-2 adrenergic receptors?

A
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67
Q

What G protein is preferred by b-1 adrenergic receptors?

A
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68
Q

What G protein is preferred by b-2 adrenergic receptors?

A
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69
Q

Which alpha adrenergic receptor acts pre-synaptically, inhibiting the release of NE?

A

alpha-2 receptors

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70
Q

Which alpha receptor acts post-synaptically, stimulating phospholipase C to cause vasoconstriction and pupil dilation?

A

alpha-1 receptors

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71
Q

What effect does alpha-1 receptor activation have on associated muscle?

A
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72
Q

What three tissues are associated with alpha-1 receptors? What are the associated responses at each tissue?

A
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73
Q

Where are alpha-2 receptors found? What response is associated with receptor activation?

A
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74
Q

What two tissues are beta-1 receptors associated with?

A

The heart and kidneys

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75
Q

Which parts of the heart and kidney are beta-1 receptors associated with? What responses are associated with receptor activation?

A
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76
Q

In which five tissues are beta-2 receptors principally found? What responses are associated with activation of these receptors?

A
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77
Q

Which catecholamine has a preference for alpha receptors over beta receptors?

A

NE

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78
Q

Does EPI have a preference for alpha or beta receptors?

A

Neither; EPI stimulates alpha and beta receptors equally

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79
Q

If a tissue has only beta receptors, will EPI or NE be the effective stimulant?

A

EPI

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80
Q

T/F: NE has an 100 fold greater affinity for the beta-2 receptor than EPI

A

False; EPI has an 100 fold greater affinity for the B2 receptor relative to NE

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81
Q

What signaling molecule binds to cholinergic receptors?

A

Acetylcholine (ACh)

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82
Q

What are the two types of cholinergic receptors?

A

Nicotinic
Muscarinic

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83
Q

What are the two synapse types where muscarinic receptors are found?

A
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84
Q

What tissues are M1 receptors found in? What response is associated with receptor activation?

A
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85
Q

Which four parts of the heart are M2 receptors associated with? What are the responses to receptor activation?

A

The fourth is to decrease contractility in the ventricles

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86
Q

What six tissues/organ systems are M3 receptors associated with?

A
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87
Q

What occurs in response to M3 receptor activation in secretory glands and in sweat glands?

A
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88
Q

What three divisions of the respiratory system are associated with M3 receptors? What response is associated with receptor activation?

A
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89
Q

What 5 elements of the GI tract are associated with M3 receptors? What responses occur as a result of receptor activation?

A
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90
Q

What two elements of the urinary bladder are associated with M3 receptors? What responses are associated with receptor activation?

A
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91
Q

What three elements of the eye are associated with M3 receptors? What responses are associated with receptor activation?

A
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92
Q

What is the cell membrane permeable to?

A

Water ghosts on steroids

-H20
-Gasses (O2, CO2)
- Lipid based molecules like steroid hormones

93
Q

Which of the Starling forces has the greatest effect on fluid movement?

A

Capillary hydrostatic pressure (Pc)

94
Q

If lymphatic capillaries are blind-ended tubes, how does excess interstial fluid enter them?

A
95
Q

Using this diagram, explain how right-sided HF can lead to edema

A

Good job!

96
Q

A patient with hypoalbuminemia and edema is given an infusion of albumin with normal saline. What happens to the following:
-Plasma volume
-Interstitial volume
-Intracellular volume
-Plasma osmolality
-Cellular osmolality

A
97
Q

What would be the most likely cause of sustained dyspnea with a finding of pulmonary edema?

A

Left-sided heart failure

98
Q

Which organ produces angiotensinogen?

A
99
Q

Which is the direct action of Renin?

A
100
Q

How is angiotensin I converted to angiotensin II? In what type of capillary does the majority of this conversion take place in the body?

A
101
Q

What are the direct effects of angiotensin II in the body (besides stimulating aldosterone secretion)?

A
102
Q

What are the direct effects of aldosterone secretion? In which part of the kidneys do they exert their effect?

A
103
Q

Lymph nodes in which parts of the body drain into the thoracic duct? In which parts of the body do they drain into the right lymphatic duct?

A
104
Q

Into what structure(s) does the thoracic lymphatic duct drain?

A

Into the internal jugular vein, the subclavian vein, or the joint between the two (L. brachiocephalic vein)

105
Q

The major vein draining a tissue is partially occluded. What would be the expected effects on the following:
-Capillary hydrostatic pressure
-Interstitual fluid hydrostatic pressure
-Lymph flow rate

A
106
Q

Why does concentration of EPI matter in regards to vasoconstriction/vasodilation?

A
107
Q

What is the perfusion pressure of the coronary arteries approximated by?

A
108
Q

What three types of factors do the coronary arteries use to control their own blood flow?

A

Metabolic factors
Endothelial factors
Neural factors

109
Q

What is the main metabolic factor that coronary arteries use to control blood flow during hypoxemia? What are other metabolites that act as vasodilators?

A
110
Q

What endothelial factors can be used by coronary arteries to control their blood flow? Which factor is a vasoconstrictor?

A
111
Q

What is nitric oxide a metabolite of? How does it cause SM relaxation and vasodilation?

A
112
Q

What is NO a metabolite of? How does it cause SM relaxation and vasodilation?

A
113
Q

What are the two ANS (neural) factors that coronary arteries use to control blood flow? Which is the main contributor?

A
114
Q

How is the change in pressure calculated using Ohm’s law in context of blood flow?

A
115
Q

In Poiseuille’s law, blood flow has what relationship to vessel radius and resistance?

A
116
Q

What are the three major determinants of myocardial oxygen demand?

A
117
Q

In Laplace’s law, what relationship does wall stress have to pressure, radius and thickness?

A
118
Q

What is atherosclerosis? In what type of arteries does it occur? How common is it?

A
119
Q

What are the two types of arteriolosclerosis? In what type of arteries does it occur? How common is it?

A
120
Q

What is Monckeberg medial arteriosclerosis? How common is it? In what types of arteries does it occur?

A
121
Q

What are the top 4 locations (in descending order) that are most commonly involved in atherosclerosis?

A
122
Q

Which landmark study identified common risk factors for CVD?

A
123
Q

What are 4 nonmodifiable RF for atherosclerosis? What are 4 modifiable RF?

A
124
Q

What is the first step in the “Response to Injury” hypothesis for atherosclerosis?

A

Explain the pathogenesis using the diagram

125
Q

What is the second step in the “Response to Injury” hypothesis for atherosclerosis?

A

Explain the pathogenesis using the diagram

126
Q

What is the third step in the “Response to Injury” hypothesis for atherosclerosis?

A

Explain the pathogenesis using the diagram

127
Q

What is the fourth step in the “Response to Injury” hypothesis for atherosclerosis?

A

Explain the pathogenesis using the diagram

128
Q

What is the fifth step in the “Response to Injury” hypothesis for atherosclerosis?

A

Explain the pathogenesis using the diagram

129
Q

What pathology of early atherosclerosis can be seen here?

A

A fatty streak

130
Q

What are the color and pattern of formation of atherosclerotic plaques (gross findings)? Where are they particularly common?

A
131
Q

What are the three main differences between a vulnerable plaque and a stable plaque?

A
132
Q

What are the three stages of progression of atherosclerosis in the pre-clinical phase?

A
133
Q

What are the three major complications of atherosclerosis in the clinical phase?

A
134
Q

What is an abdominal aortic aneurysm often associated with?

A
135
Q

What sizes of an aortic mural thrombus are high risk for rupture?

A
136
Q

What atherosclerotic pathology finding is seen here?

A

Lines of Zahn

137
Q

What are lines of Zahn?

A
138
Q

Atherosclerosis complications include peripheral vascular disease (PVD) What is the progression of symptoms in PVD?

A
139
Q

T/F: Atherosclerosis is not a realistic cause of stroke

A

False

140
Q

What type of arteriosclerosis is displayed here? What is it commonly seen in?

A
141
Q

What type of arterosclerosis is displayed here? What is it seen in?

A
142
Q

What are the etiologies of hyaline arteriosclerosis and hyperplastic arteriosclerosis?

A

Hyaline art- proteins leak into damaged vessel wall (pink “glassy” material)

Hyperplastic art- proliferation of SM and BM (“onion skinning” layers of SM and BM)

143
Q

What type of arteriosclerosis is seen here? In what patient population is it often found?

A

Monckeberg’s arteriosclerosis

144
Q

What are the syndromes that compose ischmeic heart disease?

A
145
Q

How many deaths in the US are due to ischemic heart disease? After what age does risk increase?

A
146
Q

How long after 90+% of coronary flow is lost does myocyte death begin? Is it reversible?

A

20-30 minutes

It is irreversible

147
Q

What microscopic changes are seen less than four hours after an infarction?

A
148
Q

What microscopic changes are seen between 4-24 hours after an infarction?

A
149
Q

What microscopic changes are seen between 1-3 days after an infarction?

A
150
Q

What microscopic changes are seen between 4-7 days after an infarction?

A
151
Q

What microscopic changes are seen between 1-3 weeks after an infarction?

A
152
Q

What microscopic changes are seen months after an infarction?

A
153
Q

How long after an infarction is a ruptured septum, ventricular free wall, or papillary muscle seen?

A
154
Q

How long after an infarction is an aneurysm, mural thrombus, or Dressler syndrome seen?

A
155
Q

What complications are possible within the first 24 hours of an infarction?

A
156
Q

Based on the histology slide, how recently has this patient had an MI?

A

Less than four hours (normal findings)

157
Q

Based on the histology slide, how recently has this patient had an MI? What findings can be seen?

A

Between 4 and 24 hours

Necrosis (loss of nuclei)
Hemorrhage

158
Q

What is the etiology of the wavy fibers seen in this biopsy? How long after an MI can this be seen?

A
159
Q

Based on the histology slide, how recently has this patient had an MI? What findings can be seen?

A

Between 1-3 days

Inflammation of predominantly neutrophils

160
Q

Based on the histology slide, how recently has this patient had an MI? What findings can be seen?

A

Between 4-7 days

Inflammation of predominantly macrophages

161
Q

Based on the histology slide, how recently has this patient had an MI? What findings can be seen?

A

Between 1-3 weeks

162
Q

Based on the histology slide, how recently has this patient had an MI? What findings can be seen?

A

4+ weeks

163
Q

What MI complication is seen here?

A

Ventricular free-wall rupture

164
Q

What MI complication is seen here?

A

Septal rupture

165
Q

What MI complication is seen here?

A

Papillary muscle rupture

166
Q

What MI complication is seen here?

A

Fibrinous pericarditis

167
Q

What MI complication is seen here?

A

Mural thrombus

168
Q

What MI complication?

A

Aneurysm

169
Q

What is Dressler’s syndrome? How is it differentiated from fibrinous pericarditis?

A
170
Q

What are the physical symptoms associated with the following effects of myocardial ischemia?

A
171
Q

According to the Canadian cardiovascular society (CCS) What constitutes classes I- IV of chest pain?

A
172
Q

How is unstable angina defined according to the CCS?

A
173
Q

What are the three acute coronary syndromes (ACS)?

A

STEMI
NSTEMI
Unstable angina

174
Q

What five factors play a major role in diagnosis of CAD?

A
175
Q

What are the two types of stress testing? Which is always accompanied by imaging (PET, ECG, MRI)?

A

Exercise
Pharmacologic

Pharmacologic stress testing is accompanied by imaging

176
Q

What two medication regimens are used for pharmacologic stress testing?

A

Dobutamine -> increase HR and contractility

Adenosine/Dipyridamole- vasodilation

177
Q

What three questions should be asked in determing a cardiac stress test? In what situations should imaging be done?

A
178
Q

What are the three main goals of tx of angina?

A
179
Q

What does PCI stand for? What are examples of PCI?

A

Percutaneous coronary intervention

Ballon, stent, rotoblation

180
Q

What treatment for angina (CAD) can be employed if PCI is insufficient?

A

Coronary artery bypass grafting (CABG)

181
Q

What is the pathophysiology of 90% of ACS cases?

A
182
Q

After a patient history of chest pain denotes probable ACS, how is a UA/NSTEMI differentiated from a STEMI?

A
183
Q

What two areas of an ECG can help differentiate between UA/NSTEMI and a STEMI?

A
184
Q

How can a UA be differentiated from an NSTEMI?

A
185
Q

Why is troponin measured? When does it begin to be elevated? When does it peak?

A
186
Q

What is the door to balloon time for a STEMI? What is the door to lytic time? When are thrombolytics indicated?

A

DTB < 90 minutes
DTL < 30 minutes

Thrombolytics are only used for STEMI AND DTB time estimated at over 90 minutes

187
Q

When are thrombolytics used in treatment of ACS? What are two types of thrombolytics used?

A
188
Q

What two classes of drugs are used to increase blood supply apart from thrombolytics?

A
189
Q

What are three types of anticoagulants used to increase blood supply during ACS? What are 2 types of antiplatelets besides aspirin?

A
190
Q

What are three examples of P2Y12 inhibitors used to treat ACS?

A
191
Q

What are the six primary treatments used in cases of UA/NSTEMI? What secondary treatment is preferred?

A
192
Q

What specific reasons might there be for an urgent/invasive stratery in treatment of a UA/NSTEMI?

A
193
Q

A patient between what ages presenting with aortic stenosis would be most lie to have a rheumatic etiology? (95% mitral disease)

A

Ages 40-60

*also some congenital bicuspid presentations

194
Q

A patient between what ages presenting with aortic stenosis would be most likely to have a degenerative etiology?

A

70+

195
Q

A patient between what ages presenting with aortic stenosis would be most likely to have a congenital (unicuspid/bicuspid) etiology?

A

Under 30

196
Q

How common is a bicuspid aortic valve? What is the inheritance pattern? With what changes/pathologies is it associated?

A
197
Q

What are the three main symptoms of aortic stenosis?

A
198
Q

What type of murmur is expected with aortic stenosis? Which heart sound maybe absent?

A
199
Q

What is the treatment for aortic stenosis?

A
200
Q

What is a TAVR?

A
201
Q

What is the most common etiology of mitral stenosis? Is it more common in men or women?

A
202
Q

What is the hallmark of rheumatic valve disease?

A
203
Q

What are common symptoms of mitral stenosis? Why are pulmonary and right sided heart symptoms common?

A
204
Q

Between what sounds can mitral stenosis be auscultated?

A
205
Q

What treatments are available for mitral stenosis?

A
206
Q

At what point is heart disease class III or class IV according to the NYHA?

A
207
Q

What three surgical procedures are available for a mitral stenosis?

A
208
Q

How common is tricuspid stenosis? What are 2 common symptoms? How is it treated?

A
209
Q

Though rare, what are two significant causes of pulmonic stenosis? What type of heart sound abnormalities can be auscultated? What is the first line treatment?

A
210
Q

What are the four most likely causes of acute mitral regurgitation?

A
211
Q

What are the symptoms of acute mitral regurgitation?

A
212
Q

What treatments are administered for acute mitral regurgitation?

A
213
Q

What are the most likely etiologies for chronic mitral regurgitation? In what ways are etiologies different from acute MR?

A

Involvement or mitral annulus, left ventricle, and additional leaflet etiologies.

Unlikely to have rupture or involvement or papillary muscles or chordae tendinae

214
Q

How much of the population is affected by mitral valve prolapse (Barlow’s syndrome, myxomatous mitral valve)? What is the inheritance pattern? What other diseases is it associated with?

A
215
Q

What symptoms typically present with chronic mitral regurgitation? Why are symptoms associated with low CO and pulmonary congestion?

A
216
Q

Between what heart sounds can chronic mitral regurgitation be auscultated? How is it differentiated from acute mitral regurgitation?

A
217
Q

What kind of imaging can be done to diagnose chronic mitral regurgitation?

A
218
Q

What are the clinical symptoms of acute aortic regurgitation?

A
219
Q

Between what heart sounds is an acute aortic regurgitation able to be auscultated?

A
220
Q

How serious is acute aortic regurgitation? What treatments are usually given? What treatments are CI?

A
221
Q

What symptoms are common with chronic aortic regurgitation? Walk through how these symptoms relate to the pathophysiology of the disease.

A
222
Q

Between what heart sounds can chronic aortic regurgitation be auscultated?

A
223
Q

What kind of imaging is used to diagnose chronic aortic regurgitation?

A
224
Q

What three criteria are used to determine if Aortic valve replacement is necessary?

A
225
Q

Do mechanical or bioprothetic valves last longer? Which requires anticoagulative therapy?

A
226
Q

Do mitral valve or aortic valve replacements result in thrombosis more often? How is thrombosis of an artificial valve treated?

A
227
Q

How serious is prothetic valve endocarditis?

A
228
Q
A