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Internal Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the most common cause of CHF

A

Coronary Artery Disease (CAD)

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2
Q

What are the 3 forms of CHF

A
  1. Left vs. Right Sided
  2. Systolic vs. Diastolic
  3. High vs. Low Outlet
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3
Q

What are common causes of left and right sided heart failure

A

Left sided: CAD and HTN

Right sided: Left HF, pulmonary disease

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4
Q

What are the 3 compensatory mechanisms for HF

A

Increased preload
Increased afterload
Decreased contractility

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5
Q

What happens to the kidneys in CHF

A

Decreased renal perfusion so they compensate

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6
Q

How do the kidneys compensate with CHF and why

A

The kidneys aren’t getting enough blood, so they think the body is dehydrated
They stimulate the renin-angiotensin-aldosterone and ADH system
That results in fluid and sodium retention and fluid overload (central and peripheral) EDEMA

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7
Q

What happens to the ventricles when preload increases (volume overload)

A

Ventricles dilate (leads to increase in BNP)

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8
Q

List the steps in cycle resulting from poor cardiac function and fluid accumulation in the lung with hypoxemia

A

Acute LV systolic Dysfunction
Decreased myocardial contractility and CO
Catecholamine production (increases HR and BP)
Increase in SVR (Afterload) and BP
Increased myocardial wall tension and O2 demands
Leads to diastolic dysfunction, increased pulmonary artery and capillary hydrostatic pressures, hypoxia, and increases myocardial ischemia

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9
Q

What disease processes are associated with low output HF

A 
CAD
Severe HTN
Valvular disease
Cardiomyopathy
Dysrhythmias
Massive PE
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10
Q

What disease process are associated with high output HF

A

Increased metabolic demands

Thyroxicosis, severe anemia, AV fistula, Beriberi (thiamine deficiency), Paget’s Disease

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11
Q

What symptoms are noted with Left HF

A

*Think about things that would result from fluid buildup in lungs due to increased pulmonary venous pressure**
Dyspnea, Orthopnea, paroxysmal nocturnal dyspnea, weakness, fatigue, tachycardia, basilar rales, Cheyne Stoke’s breathing

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12
Q

What symptoms are noted with Right HF

A

JVSD, Peripheral edema, RUQ pain, Ascites, Hepatomegaly

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13
Q

What is the most useful diagnostic test for CHF. What do you see?

A

Echo

Systolic and diastolic function, ventricular hypertrophy, wall motion abnormalities, valvular disorders

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14
Q

What is the most important determinant in prognosis for CHF and how do you measure it.

A

Ejection Fraction, measured by Echo
Normal EF is 55-60
EF

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15
Q

What are two other methods to Dx HF

A

CXR: Cardiomegaly, Cephalization, Kerley B lines, pleural effusions

BNP: Released due to volume overload

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16
Q

What should all patients with CHF be placed on. Why?

A

Ace-I and Diuretic

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17
Q

What two therapies have proven to improve OUTCOMES in CHF

A

Ace-I and Beta-Blocker

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18
Q

What two therapies improve Sx in CHF

A

Nitrates and diuretics (loop or thiazide)

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19
Q

What do Nitrates and diuretics do?

A

Decrease preload

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20
Q

What do Ace-I do?

A

Decrease afterload and improve CO and improve renal perfusion
Decrease aldosterone production and potentiate other vasodilators

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21
Q

What do Beta-Blockers do?

A

Decrease catecholamines

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22
Q

What are examples of Positive Inotropes or Sympathomimetics

A

Digoxin, Dobutamine, Dopamine

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23
Q

Management of CHF

think LMNOP

A 
Lasix (Ace-I)
Morphine
Nitrates
Oxygen
Position (place upright to decrease venous return)

Also, Nesiritide which is a synthetic BNP and decreases RAAS activation which leads to sodium excretion

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24
Q

What is the most common type of Cardiomyopathy

A

Dilated Cardiomyopathy

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25
Q

What results with dilated cardiomyopathy

A

Systolic dysfunction
Ventricles can’t contract well so there is poor EF
Heart compensates by dilating

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26
Q

What are some causes of dilated cardiomyopathy

A

Idiopathic
Viral (Enterovirus like Coxsackie and Echovirus), Parvovirus
Alcohol abuse, Cocain
Pregnancy

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27
Q

What are some sx of dilated cardiomyopathy

A

HF sx: Weakness, SOB, peripheral edema, Crackles, S3, JVD

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28
Q

Dx of dilated cardiomyopathy

A

Echo: See LV dilation, reduced EF, regional or global LV hypokinesis
CXR: Cardiomegaly, curly B-lines

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29
Q

Tx of dilated cardiomyopathy

A

Think CHF

Ace-I, Diuretics, Digoxin, Beta-Blockers

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30
Q

What do you do in dilated cardiomyopathy if EF

A

Add implantable defibrillator

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31
Q

What results in Restrictive Cardiomyopathy

A

Diastolic Dysfunction
Problem with filling
Fibrosis or infiltration of heart muscle, stiff, inflexible

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32
Q

What happens with EF in Restrictive Cardiomyopathy

A

Normal or near normal

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33
Q

What are causes of Restrictive Cardiomyopathy

A

Infiltrative Diseases like Amyloidosis, sarcoidosis

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34
Q

What are sx of Restrictive Cardiomyopathy

A

Think CHF

Kussmaul’s sign (increased JVP)

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35
Q

Dx of Restrictive Cardiomyopathy

A

Echo: Nondilated ventricles with normal wall thickness, some dilation of atria
CXR: Normal size heart or small

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36
Q

Tx of Restrictive Cardiomyopathy

A

Treat sx: Diuretics and vasodilators

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37
Q

What is happening in Hypertrophic Cardiomyopathy

A 
Thickened ventricles (usually left)
Has components of both systolic and diastolic dysfunction
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38
Q

Sx of Hypertrophic CArdiomyopathy

A

Sometimes none! Could result in sudden cardiac death (due to V.fib)
Dyspnea, Angina, Syncope, Arrhythmias

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39
Q

How can you increase the sound of a murmur

A

Valsalva maneuver

It decreases the volume in the LV while creating turbulent flow

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40
Q

How can you decrease the sound of a murmur

A

Squatting, First Clench

Increases peripheral vascular resistance so dilates aorta and creates less turbulent flow

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41
Q

Dx of Hypertrophic Cardiomyopathy

A

Echo: Assymetric wall thickness, especially septal, systolic anterior motion of mitral valve
EKG: LVH
CXR: Cardiomegaly

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42
Q

Tx of Hypertrophic Cardiomyopathy

A 
Avoid strenuous exercise
Beta Blockers are 1st line
CCB, Disopyramide (all 3 are negative inotropes)
Surgery: Myomectomy
Alcohol Septal Ablation
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43
Q

What is P-Wave

A

The beat goes through the atrium

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44
Q

What is the PR segment

A

Beat goes through the AV node

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45
Q

What is QRS

A

Rapid contraction through ventricle

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46
Q

What is a T wave

A

Ventricular Repolarization

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47
Q

What is a normal sinus rate

A

> 60bpm

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48
Q

What is Atrial Fibrillation

A

Irregularly Irregular Rhythm

No P waves seen

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49
Q

Tx for A.Fib

A

Rate control: Vagal maneuver, CCB or B-Blocker

Cardioversion may be done BUT need to anticoagulate for 3-4 weeks before doing so so they don’t throw a clot

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50
Q

What are the components of the CHADS2 criteria, and what is it measuring. Tx based on score.

A 
Measuring stroke risk
C: CHF
H: HTN
A: Age>75
D: DM
S2: Stroke, TIA, Thrombus (2points)
High risk: >2 need to place on Warfarin
Moderate risk: 1. Warfarin or ASA
Low Risk: 0. No tx or ASA
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51
Q

What are the EKG findings for a 1st degree AV block

A

1 p for every QRS

PR intervals are prolonged but they are constant

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52
Q

Tx for 1st degree AV block

A

Nothing. They’re usually age related, effects of meds, myocarditis, etc.

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53
Q

What are the EKG findings for a Type I 2nd degree AV block, and what is another name for this type of block

A

Mobitz I, Wenkebach
P-waves are constant
PR intervals gradually increase and eventually lead to a dropped QRS complex

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54
Q

What causes a Type I 2nd degree AV block

A

Heightened vagal tone, normal variant, inferior wall ischemia, tends to be transient

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55
Q

Tx for Type I 2nd degree AV block

A

Atropine, Epinephrine, Pacer

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56
Q

What are the EKG findings for a Type II 2nd degree AV block, and what is another name for this type of block

A

Mobitz II
P-waves are constant
PR intervals are constant but there is a dropped QRS complex
Random drop in QRS complex

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57
Q

What causes a Type II 2nd degree AV block

A

MI, usually anterior MI

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58
Q

Tx for Type II 2nd degree AV block

A

Pacer

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59
Q

What are the EKG findings for a 3rd degree AV block, and what type of block is this

A

Complete heart block
P waves are not related to QRS
All P’s are not followed by QRS (results in reduced CO)
PR intervals vary - no apparent association with P-waves and QRS complexes

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60
Q

What are causes of 3rd degree AV block

A

MI, usually inferior (narrow QRS), or anterior (wider QRS)

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61
Q

What does the QRS complex tell you in the a 3rd degree AV block regarding prognosis

A

Narrow QRS: Good prognosis

Wide QRS: Worse prognosis

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62
Q

Tx for a 3rd degree AV block

A

Pacer

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63
Q

Summarize 1st, 2nd, and 3rd degree heart blocks

A

1st degree: A p-wave is being conducted but slower than we would want. This is ok because every signal is making it through at a predictable manner, so no tx.
2nd degree: Most P-waves are being conducted
2nd degree Type I: QRS is dropped due to progressive elongation of PR intervals. This is in a predictable manner, so not as concerning. Tx is Atropine and Pacer
2nd degree Type II: QRS is dropped randomly, PR intervals are all the same size. Random pacing means poor perfusion. This needs to be tx with a pacer
3rd degree heart block: No p-waves are making it through, meaning conduction system is relying on AV node or ventricles, which is too slow to perfuse appropriately. Tx is pacer

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64
Q

What is the risk with Atrial Fibrilliation

A

The atrial are not contracting, so blood is stagnant there and CLOTS can form

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65
Q

What is the definitive tx for A.Fib

A

Catheter ablation to get rid of the accessory pathways

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66
Q

What is Ventricular Fibrillation

A

Ventricles are not contracting
No QRS
This is incompatible with life

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67
Q

Tx for V.Fib

A

Shock, Cardiovert

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68
Q

What is Torsades de Pointes and how do you treat.

A

Sin curve seen on EKG
Precursor to V.Fib if not tx
Tx: IV magnesium

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69
Q

What can you see with Torsades de Pointes on EKG

A

QT Prolongation

Sin-curve

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70
Q

What is Atrial Flutter. What do you see on EKG

A

When the atrium is contracting too quickly
Both Atrium and Ventricle contract
EKG: Saw-tooth waves, no P-waves

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71
Q

What is a risk with Atrial Flutter

A

Clots

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72
Q

TX for Atrial Flutter. Definitive Tx

A

Vagal maneuvers, CCB, Beta-Blockers

Definitive: Ablation

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73
Q

What is Wolff-Parkinson-White

A

Accessory signal present that is not allowing appropriate repolarization before the next depolarization signal comes through

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74
Q

What do you see on EKG with WPW

A

Delta Waves

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75
Q

What is a risk with WPW

A

Arrhythmia

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76
Q

What is happening in Supraventricular Tachycardia

A

A signal is coming from above the ventricles, so could be the AV node or the Atria

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77
Q

What do you see in SVT

A

Narrow QRS

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78
Q

Tx for SVT

A

Valsalva
Drugs: Beta-Blockers or CCB
They shut down the parasympatehtic conduction at AV node

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79
Q

What is the difference between ischemia and infarct and how do each look on an EKG

A

Ischemia: Tissue Obstruction. ST depressions
Infarct: Tissue Death. ST Elevation

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80
Q

What is a RBBB and what do you see on EKG

A

Delay in electrical signal at right side of bundle branch

See Wide Positive QRS in Leads V1, V2

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81
Q

What is LBBB and what do you see on EKG

A

Delay in electrical signal at left side of bundle branch

See Wide Negative QRS in leads V4-V6. Also see a notch or “fork” at the top of the QRS complex in V6

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82
Q

What do you see on EKG with LVH

A

Large QRS Complex (tall peaks)

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83
Q

What is a murmur

A

An extra sound during the cardiac cycle associated with TURBULENT FLOW

84
Q

What is happening in Aortic Stenosis and what are some problems associated with it

A

LV outflow obstruction

Can lead to LVH

85
Q

Describe the murmur heard

A

Systolic Ejection Crescendo-Decrescendo at the Right Upper Sternal Border

86
Q

Where does an aortic stenosis murmur radiate to

A

Carotid Arteries

87
Q

What are sx associated with Aortic Stenosis

A

Angina, Syncope, CHF

88
Q

Tx for Aortic Stenosis

A

Surveillance if no sx

If sx, aortic valve replacement

89
Q

What is Mitral Regurgitation and what are complications

A

Backflow from the LV to LA

Can lead to LV volume overload, so decreased CO

90
Q

What type of murmur is heard with Mitral Regurgitation

A

Blowing holosystolic Murmur heard best at the Apex

91
Q

Where does a Mitral Regurgitation murmur radiate to

A

Axilla

92
Q

Sx with Mitral Regurgitation

A

Acute: Pulmonary Edema, Dyspnea
Chronic: A.Fib, CHF

93
Q

What are maneuvers to increase/decrease the sound of a murmur associated with Mitral Regurgitation

A

Increase: Handgrip
Decrease: Amyl Nitrate

94
Q

Tx for Mitral Regurgitation

A

Meds: Ace-I (vasodilators that decrease afterload and can increase forward flow)
Surgery: Valve repair

95
Q

What is happening in Mitral Valve Prolapse

A

Degeneration of the mitral valve which makes it floppy

96
Q

What type of murmur is heard with a Mitral Valve Prolapse

A

Missystolic Ejection Click at the Apex

97
Q

How can you increase/decrease the sound of a murmur with Mitral Valve Prolapse

A

Decrease Venous Return via Valsalva, Standing, or Inspiration causes longer murmur duration

98
Q

Sx with Mitral Valve Prolapse

A

Most are asymptomatic
Autonomic Dysfxn: Chest pain, Panic Attacks, Arrhythmias
If Progresses: Fatigue, dyspnea, CHF

99
Q

What happens in Mitral Stenosis

A

Obstruction from LA to LV

Leads to LA Enlargement and increases LA pressure, results in Pulmonary HTN

100
Q

What type of murmur is heard with Mitral Stenosis

A

Diastolic Rumble at the Apex, may be preceded by opening snap

101
Q

Sx with Mitral Stenosis

A

R-sided HF, Pulmonary HTN, A.Fib, Mitral Facies

102
Q

Tx with Mitral Stenosis

A

Valvotomy in young people if rheumatic heart disease is cause
Valve repair in adults

103
Q

What is happening with Aortic Regurgitation

A

Backflow from the aorta to LV

Leads to LV volume overload

104
Q

What murmur is heard with Aortic Regurgitation

A

Diastolic Decrescendo Blowing at Left Upper Sternal Border

105
Q

What do you decrease/increase the sounds of a murmur in Aortic Regurgitation

A

Increase the murmur with handgrip

Decrease the murmur with Amyl Nitrate

106
Q

Where does an Aortic Regurgitation murmur radiate to

A

Left Sternal Border

107
Q

Sx of Aortic Regurgitation

A

Left Sided HF (Pulmonary HTN)

108
Q

Tx of Aortic Regurgitation

A

Vasodilators that will decrease afterload and increase forward flow (Ace-I)
Surgery

109
Q

What is happening with Atrial Septal Defect

A

Hole in the atrial septum

110
Q

What shunt results in ASD, is there cyanosis

A

Left to right shunt

No Cyanosis

111
Q

What type of murmur is heard with ASD

A

Systolic ejection crescendo-decrescendo flow at Pulmonic area (LUSB)

112
Q

Sx of ASD

A

Asymptomatic until adulthood usually
Kids: Recurrent URI
Adults: Exertional dyspnea, easy fatigability, palpitations, syncope, HF

113
Q

Tx of ASD

A

Surgical Correction

Spontaneous Closure

114
Q

Where is the area of infarct with ST elevations in V1-V4. What artery is involved

A

Anterior

Left Anterior Descending

115
Q

Where is the area of infarct with ST elevations in I, aVL, V5 and V6. What artery is involved

A

Lateral

Circumflex

116
Q

Where is the area of infarct with ST elevations in I, aVL, V4, V5, V6. What artery is involved

A

Anterolateral

Mid LAD or Circumflex

117
Q

Where is the area of infarct with ST elevations in II, III, aVF. What artery is involved

A

Inferior

Right Coronary Artery

118
Q

Where is the area of infarct with ST DEPRESSIONS in V1-V2. What artery is involved

A

Posterior

RCA, Circumflex

119
Q

What causes atherosclerosis

A

Lipid deposition, calcification, plaque formation in vessels

120
Q

What are modifiable risk factors with atherosclerosis

A

Diabetes
Cigarette Smoking
HTN
Hyperlipidemia

121
Q

What constitute a dx for Metabolic syndrome

A 
3 or more
Abdominal obesity
Trg>150
HDL110
HTN
122
Q

What falls under Acute Coronary Syndromes

A

Unstable Angina
NSTEMI
STEMI

123
Q

What is Angina

A

Imbalance between myocardial oxygen demand and myocardial oxygen delivery

124
Q

Sx of Angina

A

Subseternal chest pain, Chest tightness, Radiation to neck or Jaw, Dyspnea, Nausea/Vomiting, Diaphoresis, Levine’s Sign

125
Q

What is Stable Angina

A

Regular pattern of angina exacerbated by physical or emotional stress
Relieved with rest within minutes
Relieved with NTG within minutes

126
Q

Dx of Stable Angina

A

History

127
Q

Tx of Stable Angina

A

Modify RF, low fat low cholesterol diet

Meds: Nitrates, Beta-Blockers, CCB

128
Q

What is first line acute management for Stable Angina

A

NTG

129
Q

What is first line chronic management for Stable Angina

A

Beta-Blockers

130
Q

What is the classic regimen for someone with Angina

A

Daily ASA, Sublingual NTG as needed for pain, Daily Beta-Blockers, and Statin if LDL is increased

131
Q

What causes Acute Coronary Syndrome

A

Ruptured coronary plaques that lead to bleeding, platelet aggregation, and thrombus formation
May slo be caused by cocain-induced or prinzmetal’s variant angina

132
Q

What is Unstable Angina

A

New onset of angina symptoms
Increased intensity of stable angina
Increased frequency of angina
Subtotal occlusion of vessels that lead to severe sx without infarction

133
Q

What is an MI

A

Complete occlusions of vessels

NSTEMI and STEMI

134
Q

Sx of an MI

A

Pain is more prolonged, not relieved with rest or NTG
Note that 1/3 of pts don’t have pain, instead only come in with dyspnea, diaphoresis, nausea, weakness (Diabetics, women, obses pts)
Tachycardia, bradycardia, CHF, Hypotension, new murmur
Post-MI Pericarditis with friction rub may occur after 24 hours

135
Q

What are some common EKG findings with an MI

A 
T-Wave Abnormalities
ST-segment depression:Ischemia
ST-Segment elevation:Infarction
Q-waves: Infarction
V1-V2: Septal or Posterior
V3-V4: Anterior
V5-V6, I, aVL: Lateral
II, III, aVF: Inferior
V1-V2 with depressions:Posterior
136
Q

What are common biomarkers seen in MI

A

Myglobin
CPK-MB
Troponin, Troponin, Troponin!

137
Q

When does Troponin rise, peak, and normalize

A

Rise: 4-6 hours
Peak: 18-24 hours
Normalizes: 7-10 days

138
Q

What is the gold standard for an MI workup

A

Coronary Angiography

139
Q

What other dx modalities can be used in MI

A

CXR, Echo, Stress testing

140
Q

TX of Unstable Angina and NSTEMI

A
  1. Antithrombotic Therapy

2. Adjunctive Therapy

141
Q

Tx for STEMI

A
  1. Reperfusion Therapy
  2. Antithrombotic Therapy
  3. Adjunctive Therapy
142
Q

What is part of Antithrombotic Therapy

A 
These PREVENT clots
ASA: prevents platelet aggregation
Heparine
Clopidogrel: 
Glycoprotein (for people going cath lab)
143
Q

What are common Adjunctive Therapies

A

Beta Blockers: Metoprolol
Nitrates
Morphine
CCB

144
Q

What is a common Reperfusion Therapy in STEMI. And how soon should they be started

A

Primary Percutaneous Coronary Intervention - do it if it’s within 90 minutes
Fibrinolytics - Do within 30 minutes

145
Q

What are common Thrombolytic Therapies (Fibrinolytic)

A

These DISSOLVE clots
Tissue Plasminogen Activators: Alteplase (rTPA)
Streptokinase

146
Q

What is common Adjunctive Therapy in STEMI

A 
Beta-Blockers
Ace-I
Nitrates
Morphine
Statin therapy if high LDL
147
Q

What is a complication of MI

A

Heart Failure
Ventricular Fibrillation
Dressler’s Syndrome: Post-MI pericarditis (1-2 months after) associated with fever and pulmonary infiltrates

148
Q

What is an anuerysm

A

Abnormal dilation of the aorta

149
Q

What is the most common cause for an aneurysm

A

Atherosclerosis

150
Q

What are 2 common RF for Anuerysms

A

Smoking and COPD

151
Q

Sx of Anuerysm

A

Asymptomatic until large or rupture
Scenario: Older male with severe back pain or abdominal pain who presents with syncope or hypotension with tender pulsatile abdominal mass
Flank Ecchymosis

152
Q

Dx of Aneurysms

A

Abdominal ultrasound
CT scan for thoracic
Angiography

153
Q

What is the gold standard for dx of Anuerysms

A

Angiography

154
Q

Tx of Aneurysms. What is definitive tx.

A

Definitive: Surgery
3-4cm: monitor every year with ultrasound
4-4.5cm: Monitor every 6 months
>4.5: Vascular surgeon referral
>5.5 or expansion in 6 months: Immediate surgery

155
Q

What is an Aortic Dissection

A

Tear in the innermost layer of aorta

156
Q

What is RF for aortic dissection

A

HTN, Age, Connective Tissue Disease (Marfans)

157
Q

Sx of Aortic Dissection

A

Acute onset
Severe tearing ripping pain in upper chest or back
Decreased peripheral pulses: Variation in pulses between left and right arm

158
Q

Dx of Aortic Dissection. What is the gold standard

A

Gold Standard: MRI Angiography

CXR, CT with contrast

159
Q

Tx for Type A vs. Type B

A

Type A: Tear in ascending and descending. Tx: Surgery

Type B: Tear in descending only. Tx: Meds with Beta Blockers (Labetalol) with sodium nitropurisside if needed

160
Q

What causes Peripheral Artery Disease

A

Atherosclerosis

161
Q

Sx of Peripheral Artery Disease

A

Pain with exertion (walking), intermittent claudication, Ulcerations

162
Q

What happens with an arterial embolism/thrombosis

A

Acute occlusion of an artery

163
Q

What are common sources for emobli or thrombi

A

Heart and Aorta

164
Q

Tx for emboli/thrombosis

A

Revascularize

165
Q

What are sx for Acute Occlusion (6 P’s)

A

Pain, Pallor, Pulselessness, Paresthesias, Poikilothermia, Paralysis

166
Q

Dx for Acute Occlusion

A

Arterial Duplex, MRA, CTA, ABI, Angiography

167
Q

What is Giant Cell Arteritis

A

Vessel Inflammation of medium/larger arteries

168
Q

What is Giant Cell Arteritis commonly associated with

A

Polymyalgia Rheumatica

169
Q

What is another name for Giant Cell Arteritis

A

Temporal ARteritis

170
Q

Sx with Giant Cell Arteritis

A

Headache, scalp tendernes, jaw claudication, sore throat, visual loss

171
Q

Dx of Giant Cell Arteritis

A

Elevated ESR/CRP
Temporal Artery Biopsy: see mononuclear lymphocyte infiltration, multinucleated giant cells
Clinical DX!

172
Q

Tx of Giant Cell Arteritis

A

Steroids and referral to ENT

173
Q

What is a complication of Giant Cell Arteritis

A

Blindness

174
Q

What is Phlebitis/Thrombophlebitis

A

Inflammation of the superficial vein and venous occlusion/inflmmation

175
Q

What is Phlebitis associated with

A

IV cath, Trauma, Pregnancy

176
Q

Sx of Phlebitis

A

Pain, Tenderness, Edema, Redness, Induration, Palpable Cord

177
Q

Dx of Phlebitis

A

Venous Duplex Ultrasound

178
Q

Tx of Phelbitis

A

Supportive: Elevation, warm compress, NSAIDS, Compression stocking
If Septic: Abx
Vein Ligation/Excision

179
Q

What are Varicose Veins

A

Dilated, Tortuous superficial veins seen with increased estrogen like OCP or pregnancy

180
Q

Sx of Varicose Veins

A

Asymptomatic or mild ache

181
Q

Tx of Varicose Veins

A

Stockings, Elevation, Intervention techniques

182
Q

What is Chronic Venous Insufficiency

A

Vascular incompetency of either deep and/or superficial veins

183
Q

When does Chronic Venous Insufficiency usually occur

A

DVT or Trauma

184
Q

Sx of Chronic Venous Insufficiency

A

Leg pain worse with prolonged sitting, improved with leg elevation or walking
Edema, Stasis, Dermatitis
VENOUS STASIS ULCER: usually at MEDIAL malleolus
Atrophic Blanche

185
Q

Dx of Chronic Venous Insufficiency

A

Ankle/Brachial Index

Trendelenburg Test, Ultrasound

186
Q

Tx of Chronic Venous Insufficiency

A

Compression: Leg elevation, stockings, exercise, Una boot
If ulcers: wet to dry dressings, skin grafting, hyperbaric O2
Venous valve transplant

187
Q

What is a Venous Thrombus

A

DVT

188
Q

What are RF for DVT

A

Virchow’s Triad: Venous stasis, endothelial damage, hypercoagulability

189
Q

Sx of DVT

A

Unilateral swelling/edema of lower extremity

Calf Tenderness, Phlebitis (local warmth, erythema, palpable cord)

190
Q

Dx of DVT

A

Venous Duplex Ultrasound is #1
D-Dimer
Venograph is Gold Standard

191
Q

RF of DVT

A

Surgery, Travel, Genetics, Pregnancy

192
Q

Tx of DVT

A

Anticoagulation Therapy: Heparin, LMWH, Warfarin for 3-6 months

193
Q

What is a TIA

A

Sudden onset focal neurologic deficits, usually due to emobuls

194
Q

Sx of TIA

A

Short interval of vision, speech, weakness, sensory abnormalities
Internal Carotid: Monocular visual loss, temporary “lamp shade” over one eye, weakness in contralateral hand

195
Q

Dx of TIA

A

CT

Carotid Doppler, CT Angiography, Serum Glucose

196
Q

Tx of TIA

A

ASA Plavix (antiplatelet therapy), No Thrombolytics, Place supine to increase cerebral perfusion

197
Q

What is a Stroke

A

Neruologic deficits due to ischemia or hemorrhage

198
Q

Sx of Ischemic Stroke

A

Correlate with vessel involved (anterior vs. posterior circulation)

199
Q

Dx of Ischemic Stroke

A

Noncontrast CT
MRA/MRI
CT Perfusion/CTA
CBC, Coag studies, EKG

200
Q

Tx of Ischemic Stroke

A 
Reverse Ischemia/Salvage brain tissue
Thrombolytic therapy (tPA) within 3 hours
Antiplatelet Therapy (ASA, Plavix)
201
Q

Most common cuase for Hemorrhagic stroke

A

HTN

202
Q

Dx of Hemorrhagic Stroke

A

Noncontrast CT

203
Q

Tx of Hemorrhagic Stroke

A

Supportive, BP control

204
Q

Sx of Subarachnoid Hemorrhage

A

Acute onset “worst headache of my life”, syncope, nausea/vomiting, nuchal rigidity

205
Q

Dx of Subarachnoid Hemorrhage

A

CT

If CT negative but high suspicion do LP

206
Q

Tx of Subarachnoid Hemorrhage

A

Supportive (no exertion, stool softener, anti-anxiety meds)

Internal Medicine (16 decks)

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