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Cards Test 2 Flashcards

1
Q

HTN for which the cause is unknown

A

Essential hypertension

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2
Q

Normal blood pressure values

A
  • SBP: < 120 and

- DBP: < 80

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3
Q

Prehypertension blood pressure values

A

SBP: 120-139
or
DBP: 80-89

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4
Q

Stage I HTN blood pressure values

A

SBP: 140-159
or
DBP: 90-99

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5
Q

Stage II HTN blood pressure values

A

SBP: > 160
or
DBP: > 100

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6
Q

When evaluating a patient for hypertension, what should you think if you hear flank abdominal or flank bruits?

A

HTN may be caused by renovascular HTN or renal artery stenosis?

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7
Q

When evaluating a patient for hypertension, what should you think if you detect absent or diminished femoral pulses?

A

Coarctation of the aorta

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8
Q

When evaluating a patient for hypertension, what should you think if you palpate flank or abdominal masses?

A

HTN may be due to polycystic kidney disease or AAA

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9
Q

What physical signs might you expect to see in a patient with end organ damage from hypertension?

A
  • Fundoscopic exam: AV nicking, arteriolar narrowing, exudates, papilledema, hemorrhages
  • Signs of heart failure: S3, S4, laterally displaced PMI
  • Neurologic deficits
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10
Q

Most causes of death fro mHTN have to do with complications of what?

A

Atherosclerosis

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11
Q

Primary organs/tissues that suffer from HTN

A 
Heart
Brain
Kidneys
Blood vessels
Eyes
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12
Q

Lacunar stroke

A

occlusion of small penetrating brain arteries resulting in multiple tiny infarcts

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13
Q

Water-Shed stroke

A

generalized arterial narrowing that causes structural requirements for higher perfusion pressure in order to maintain adequate tissue flow; a sudden drop in BP can cause a CVA

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14
Q

Good marker for renal dysfunction in HTN

A

Microalbuninuria

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15
Q

Essential or Secondary HTN more common?

A

Essential (95%)

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16
Q

Medications that can cause hypertension

A
  • OCP
  • Glucocorticoids
  • Cyclosporine
  • Erythropoietin
  • Sympathomimetic drugs (for colds)
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17
Q

Most common cause of secondary hypertension

A

Renal parenchymal disease

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18
Q

2 common causes of renal artery stenosis

A
  • Atherosclerotic lesions

- Fibromuscular lesions

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19
Q

When evaluating a patient for hypertension, what should you think if you observe unexplained hypokalemia?

A
  • Renovascular hypertension

- Or hyperaldosteronism

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20
Q

Gold standard for diagnosing renovascular hypertension

A

Renal angiography

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21
Q

If an aorta has coarcation, where is the coarctation likely located?

A

Just distal to the origin of the left subclavian artery

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22
Q

When evaluating a patient for hypertension, what should you think if you auscultate a midsystolic murmur that’s particularly loud over the back?

A

Coarctation of the aorta

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23
Q

When evaluating a patient for hypertension, what should you think if the patient has “attacks” of severe, throbbing headaches, profuse sweating, and tachycardic palpitations?

A

Pheochromocytoma

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24
Q

When evaluating a patient for hypertension, what should you think if you observe Trousseau’s Sign?

A

Hyperaldosteronism

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25
Q

Tetanic muscle cramps of the hand distal to an inflated BP cuff

A

Trousseau’s sign

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26
Q

How do you differentiate between primary and secondary aldosteronism?

A
  • Measure renin activity
  • Low renin activity with primary
  • High renin activity with secondary
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27
Q

Why might Cushing syndrome cause secondary HTN?

A

-Excessie cortisol increases blood volume and stimulates the synthesis of RAAS components

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28
Q

Dominant long-term controller of blood pressure

A

The kidneys via pressure natriuresis (PN)

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29
Q

What do chemoreceptors detect?

A

Changes in oxygen and carbon dioxide in the blood

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30
Q

What does the CNS respond to (in terms of blood pressure control)?

A

Ischemia of the vasomotor centers int he brain (the medulla oblongata)

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31
Q

Most powerful hormone system for regulating body volumes and BP

A

RAAS

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32
Q

BP Treatment goals

A

< 140/90

of < 130/80 w/ DM or chronic kidney disease

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33
Q

When evaluating a patient for hypertension, what should you think if you hear flank abdominal or flank bruits?

A

HTN may be caused by renovascular HTN or renal artery stenosis?

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34
Q

When evaluating a patient for hypertension, what should you think if you detect absent or diminished femoral pulses?

A

Coarctation of the aorta

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35
Q

When evaluating a patient for hypertension, what should you think if you palpate flank or abdominal masses?

A

HTN may be due to polycystic kidney disease or AAA

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36
Q

What physical signs might you expect to see in a patient with end organ damage from hypertension?

A
  • Fundoscopic exam: AV nicking, arteriolar narrowing, exudates, papilledema, hemorrhages
  • Signs of heart failure: S3, S4, laterally displaced PMI
  • Neurologic deficits
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37
Q

Most causes of death fro mHTN have to do with complications of what?

A

Atherosclerosis

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38
Q

Primary organs/tissues that suffer from HTN

A 
Heart
Brain
Kidneys
Blood vessels
Eyes
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39
Q

Lacunar stroke

A

occlusion of small penetrating brain arteries resulting in multiple tiny infarcts

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40
Q

Water-Shed stroke

A

generalized arterial narrowing that causes structural requirements for higher perfusion pressure in order to maintain adequate tissue flow; a sudden drop in BP can cause a CVA

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41
Q

Good marker for renal dysfunction in HTN

A

Microalbuninuria

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42
Q

Essential or Secondary HTN more common?

A

Essential (95%)

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43
Q

Medications that can cause hypertension

A
  • OCP
  • Glucocorticoids
  • Cyclosporine
  • Erythropoietin
  • Sympathomimetic drugs (for colds)
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44
Q

Most common cause of secondary hypertension

A

Renal parenchymal disease

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45
Q

2 common causes of renal artery stenosis

A
  • Atherosclerotic lesions

- Fibromuscular lesions

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46
Q

When evaluating a patient for hypertension, what should you think if you observe unexplained hypokalemia?

A
  • Renovascular hypertension

- Or hyperaldosteronism

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47
Q

Gold standard for diagnosing renovascular hypertension

A

Renal angiography

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48
Q

If an aorta has coarcation, where is the coarctation likely located?

A

Just distal to the origin of the left subclavian artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

When evaluating a patient for hypertension, what should you think if you auscultate a midsystolic murmur that’s particularly loud over the back?

A

Coarctation of the aorta

How well did you know this?
1
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2
3
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5
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50
Q

When evaluating a patient for hypertension, what should you think if the patient has “attacks” of severe, throbbing headaches, profuse sweating, and tachycardic palpitations?

A

Pheochromocytoma

How well did you know this?
1
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2
3
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51
Q

When evaluating a patient for hypertension, what should you think if you observe Trousseau’s Sign?

A

Hyperaldosteronism

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52
Q

Tetanic muscle cramps of the hand distal to an inflated BP cuff

A

Trousseau’s sign

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53
Q

How do you differentiate between primary and secondary aldosteronism?

A
  • Measure renin activity
  • Low renin activity with primary
  • High renin activity with secondary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why might Cushing syndrome cause secondary HTN?

A

-Excessie cortisol increases blood volume and stimulates the synthesis of RAAS components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Dominant long-term controller of blood pressure

A

The kidneys via pressure natriuresis (PN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do chemoreceptors detect?

A

Changes in oxygen and carbon dioxide in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does the CNS respond to (in terms of blood pressure control)?

A

Ischemia of the vasomotor centers int he brain (the medulla oblongata)

How well did you know this?
1
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2
3
4
5
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58
Q

Most powerful hormone system for regulating body volumes and BP

A

RAAS

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59
Q

HTN for which the cause is unknown

A

Essential hypertension

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60
Q

Normal blood pressure values

A
  • SBP: < 120 and

- DBP: < 80

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3
4
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61
Q

Prehypertension blood pressure values

A

SBP: 120-139
or
DBP: 80-89

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62
Q

Stage I HTN blood pressure values

A

SBP: 140-159
or
DBP: 90-99

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63
Q

Stage II HTN blood pressure values

A

SBP: > 160
or
DBP: > 100

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64
Q

When evaluating a patient for hypertension, what should you think if you hear flank abdominal or flank bruits?

A

HTN may be caused by renovascular HTN or renal artery stenosis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

When evaluating a patient for hypertension, what should you think if you detect absent or diminished femoral pulses?

A

Coarctation of the aorta

How well did you know this?
1
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2
3
4
5
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66
Q

When evaluating a patient for hypertension, what should you think if you palpate flank or abdominal masses?

A

HTN may be due to polycystic kidney disease or AAA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What physical signs might you expect to see in a patient with end organ damage from hypertension?

A
  • Fundoscopic exam: AV nicking, arteriolar narrowing, exudates, papilledema, hemorrhages
  • Signs of heart failure: S3, S4, laterally displaced PMI
  • Neurologic deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Most causes of death fro mHTN have to do with complications of what?

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
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69
Q

Primary organs/tissues that suffer from HTN

A 
Heart
Brain
Kidneys
Blood vessels
Eyes
How well did you know this?
1
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2
3
4
5
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70
Q

Lacunar stroke

A

occlusion of small penetrating brain arteries resulting in multiple tiny infarcts

How well did you know this?
1
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2
3
4
5
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71
Q

Water-Shed stroke

A

generalized arterial narrowing that causes structural requirements for higher perfusion pressure in order to maintain adequate tissue flow; a sudden drop in BP can cause a CVA

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3
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72
Q

Good marker for renal dysfunction in HTN

A

Microalbuninuria

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73
Q

Essential or Secondary HTN more common?

A

Essential (95%)

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74
Q

Medications that can cause hypertension

A
  • OCP
  • Glucocorticoids
  • Cyclosporine
  • Erythropoietin
  • Sympathomimetic drugs (for colds)
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75
Q

Most common cause of secondary hypertension

A

Renal parenchymal disease

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76
Q

2 common causes of renal artery stenosis

A
  • Atherosclerotic lesions

- Fibromuscular lesions

How well did you know this?
1
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2
3
4
5
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77
Q

When evaluating a patient for hypertension, what should you think if you observe unexplained hypokalemia?

A
  • Renovascular hypertension

- Or hyperaldosteronism

How well did you know this?
1
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2
3
4
5
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78
Q

Gold standard for diagnosing renovascular hypertension

A

Renal angiography

79
Q

If an aorta has coarcation, where is the coarctation likely located?

A

Just distal to the origin of the left subclavian artery

80
Q

When evaluating a patient for hypertension, what should you think if you auscultate a midsystolic murmur that’s particularly loud over the back?

A

Coarctation of the aorta

81
Q

When evaluating a patient for hypertension, what should you think if the patient has “attacks” of severe, throbbing headaches, profuse sweating, and tachycardic palpitations?

A

Pheochromocytoma

82
Q

When evaluating a patient for hypertension, what should you think if you observe Trousseau’s Sign?

A

Hyperaldosteronism

83
Q

Tetanic muscle cramps of the hand distal to an inflated BP cuff

A

Trousseau’s sign

84
Q

How do you differentiate between primary and secondary aldosteronism?

A
  • Measure renin activity
  • Low renin activity with primary
  • High renin activity with secondary
85
Q

Why might Cushing syndrome cause secondary HTN?

A

-Excessie cortisol increases blood volume and stimulates the synthesis of RAAS components

86
Q

Dominant long-term controller of blood pressure

A

The kidneys via pressure natriuresis (PN)

87
Q

What do chemoreceptors detect?

A

Changes in oxygen and carbon dioxide in the blood

88
Q

What does the CNS respond to (in terms of blood pressure control)?

A

Ischemia of the vasomotor centers int he brain (the medulla oblongata)

89
Q

Most powerful hormone system for regulating body volumes and BP

90
Q

Cornerstone for antihypertensive therapy

A

Thiazide diuretics

91
Q

Number one cause of resistant hypertension

A

compliance

92
Q

Definition of hypertensive emergency

A

BP > 220/120 with signs and symptoms of:

  • encephalopathy
  • acute MI
  • stroke
  • pulmonary edema
  • aortic dissection
93
Q

BP reduction time frame for patient in HTN emergency

94
Q

Most common cause of hypertensive emergency

A

Something to do with kidneys

95
Q

Hypertensive urgency definition

A

BP >220/120 with minimal or no symptoms

96
Q

Blood pressure reduction time frame in patient in hypertensive urgency

97
Q

Good drug for hypertensive urgency

A

IV Labetalol

98
Q

Most common cause of orthostatic hypertension

A

hypovolemia secondary to diuretic use

99
Q

What does the endothelial intima release when it’s injured?

100
Q

Chemical irritants that can injure vessel endothelium

A

Nicotine, elevated lipids, elevated sugars in diabetcs

101
Q

Formula for LDL if it’s not directly measured

A

LDL = total cholesterol - HDL - TG/5

102
Q

Desirable total cholesterol

103
Q

Borderline high total cholesterol

104
Q

high total cholesterol

105
Q

low (bad) HDL

106
Q

high (good) HDL

107
Q

desirable LDL levels

108
Q

near or above optimal LDL levels

109
Q

borderline high LDL levels

110
Q

high LDL leels

111
Q

Very high LDL levels

112
Q

normal TG levels

113
Q

Borderline high TG levels

114
Q

High TG levels

115
Q

Very high TG levels

116
Q

LDL goal < 2 risk factors

117
Q

LDL goal with 2 or more risk factors

118
Q

LDL goal with CAD, Diabetes, or Established atherosclerosis

A

< 100mg/dL

119
Q

LDL goal with acute coronary syndrome, multiple risk factors, metabolic syndrome, and tobacco usage

A

< 70 mg/dL

120
Q

Although LDLs are the primary treatment goal, at what point should TG be the primary goal of treatment and why?

A

When TG > 500 because of pancreatitis risk

121
Q

Characteristics of metabolic syndrome

A
  • abdominal obesity
  • atherogenic dyslipidemia
  • elevated BP
  • insulin resistance or glucose intolerance
  • prothrombotic state
  • proinflammatory state
  • low HDL
122
Q

Wast circumference defining level for metabolic syndrome

A

> 102cm (40in) for men

> 88 cm (35in) for women

123
Q

Most common manifestation of ischemic heart disease

A

Angina pectoris

124
Q

Most patients with chronic ischemic heart disease have what?

A

coronary atherosclerosis

125
Q

How do we estimate perfusion pressure?

A

By measuring aortic diastolic pressure

126
Q

Relationship of wall stress to afterload

A

directly proportional

127
Q

Relationship of wall stress to LV radius

A

directly proportional

128
Q

relationship of wall stress to LV thickness

A

inversely proportional

129
Q

Evidence of ischemia on EKG

A

Horizontal or down-sloping ST depression

130
Q

Equation for maximal predicted HR

131
Q

Target HR for stress testing

A

85% of maximal predicted HR (220 - age)

132
Q

How much ST depression is considered a positive stress test?

133
Q

How much ST depression is considered a markedly positive stress test

134
Q

Gold standard for evaluating the anatomy of the coronary artery tree

A

Contrast coronary angiography

135
Q

Where does cardiac catheterization measure pressures?

A

LV and aorta

136
Q

Screening test that you’d perform on someone with risk factors for CAD, but no symptoms

A

Electron beam computed tomography (EBCT)

137
Q

What test is indicated when a patient has a positive stress test?

A

coronary angiography

138
Q

What test should you perform if the patient presents as unstable or has profound symptoms?

A

Proceed directly with coronary angiography

139
Q

Typical angina symptoms with no evidence of significant atherosclerotic coronary stenosis on angiogram

A

Syndrome X

140
Q

Single most important coronary artery risk factor

A

Tobacco exposure

141
Q

If you were a little RBC wanting to get to the diaphragmatic surface of the left ventricle, which coronary would you flow through?

142
Q

If you were a little RBC wanting to get to the posterior aspect of the LV, through which coronary would you travel?

A

The posterior descending branch of the RCA or possibly the circumflex, if it was posterolateral

143
Q

If you were a little RBC wanting to get to the AV node, through which coronary would you travel?

144
Q

What causes > 90% of UA and STEMIs?

A

Disruption of atherosclerotic plaque with subsequent platelet aggregation and intracoronary thrombus formation

145
Q

Role of Antithrombin III

A

Irreversibly binds to thrombin, inactivating it

146
Q

Role of prostacyclin

A

Inhibits platelet activation and aggregation; potent vasodilator

147
Q

Role of NO

A

Inhibits platelet activation; potent vasodilator

148
Q

Role of tissue plasminogen activator (tPA)

A
  • cleaves plasminogen to form plasmin

- plasmin degrades fibrin clots

149
Q

Role of thrombin

A

Helps to form a fibrin clot

150
Q

Two hemostatic “players” that are involved in clot degradation or prevention of formation?

A

Antithrombin III

tPA

151
Q

Primary difference between UA and NSTEMI

A

UA has no evidence of necrosis, while NSTEMI does

152
Q

Pattern of pain associated with UA

A

Crescendo pattern of chest pain

153
Q

What should you think if you have elevated cardiac markers without evolution of Q waves?

154
Q

How long can Troponin levels stay elevated?

A

10-14 days

155
Q

How long can CK and CK-MB levels stay elevated?

156
Q

Biochemical marker of choice in the evaluation of myonecrosis and diagnosis

157
Q

Cornerstone of therapy for UA and NSTEMI

158
Q

How is unfractionated heparin administered?

159
Q

How is LMWH administered?

A

SQ injection

160
Q

Sign of hand over the chest indicating an MI

A

Levine Sign

161
Q

What should you think if you have elevated JVPs and the lungs sound clear?

A

IWMI with right-sided failure

162
Q

How would you treat an IWMI with right heart failure?

163
Q

What should you think if you ahve elevated JVPs and the lungs have rales?

A

Left heart failure

164
Q

How would you treat left heart failure (as opposed to right heart failure)?

165
Q

How long after patient arrival with chest pain do you have to perform an EKG?

A

10 minutes

166
Q

Where would you have ST elevation with an anteroseptal wall MI?

A

V1, V2, V3, and V4

167
Q

Where would you have ST elevation with an anterior wall MI?

168
Q

EKG changes associated with a lateral wall MI

A

ST elevation in I, aVL, V5 and V6

Reciprocal ST depression in II, III, and aVF

169
Q

EKG changes associated with an inferior wall MI

A
  • ST elevation in II, III, and aVF

- Reciprocal ST depression in I and aVL (high lateral leads

170
Q

EKG changes with a RV infarct

A

> 1mm ST elevation in lead V4R

171
Q

EKG changes with a posterior wall MI

A

Large R waves in V1 and V2

ST depression in V1 and V2

172
Q

Door-to-balloon time

A

90 minutes

173
Q

door-to-needle time (fibrinolytic therapy)

A

30 minutes

174
Q

Revascularization time limit after STEMI symptom onset

175
Q

Best drug for ischemia in HF patients

176
Q

What type of murmur would you hear if someone developed a VSD after an MI?

A

pansystolic on the LSB

177
Q

Uncommon form of pericarditis that occurs several weeks after an MI

A

Dressler Syndrome

178
Q

Normal aorta diameter at the base of the heart

179
Q

descending aorta diameter

180
Q

AAA that’s distal to the renal arteries

A

Infrarenal abdominal aortic syndrome

181
Q

Most useful mode of diagnosis for aortic aneurysm

A

Ultrasound

182
Q

When would you repair an ascending aortic aneurysm?

183
Q

When would you repair a descending aortic aneurysm?

184
Q

When would you repair an AAA?

185
Q

Where are aortic dissections most common?

A

Ascending thoracic aorta

186
Q

Type A aortic dissection

A

proximal to the left subclavian artery

187
Q

Type B aortic dissection

A

distal to the left subclavian artery

188
Q

In which type of aortic dissection is early surgical correction indicated?

189
Q

Ankle-brachial index is useful in assessing which pathology?

190
Q

What is often the origin of the embolus that causes acute aortic arterial occlusion?

191
Q

primary treatment for superficial thrombophlebitis

A

local heat

192
Q

Virchow’s triad

A
  • stasis
  • hypercoagulability
  • vascular damage
193
Q

Homans Sign

A

calf pain produced by dorsiflexion of the foot

Cardiology (8 decks)

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