Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Review > Cardiology (PANCE PEARLS) > Flashcards

Cardiology (PANCE PEARLS) Flashcards

1
Q

Heart failure (Systolic/Left) - how do you identify it best?

A

Echo

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

Heart failure (Systolic/Left) - how do you identify it best?

A

Echo

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

Heart failure (Systolic/Left) - what will you see? Hear?

A

Decreased ejection fraction (

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

Heart failure (Systolic/Left) - Buzz

A

Pink frothy sputum

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

Main goals for HF

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Every HF patient (unless contraindicated) should be on what?

A

An ACE and a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MOA of ACE

A

Decreased aldosterone production degreasing angiotensin II leading to decrease water retention. Bradykinin is also affected and can cause dry coughing and angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Does ACE affect mortality?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SE of ACE

A

Hypotension with first dose. Renal insufficiency (with Cr > 3 or CrCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Heart failure (Systolic/Left) - what will you see? Hear?

A

Decreased ejection fraction (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Heart failure (Systolic/Left) - Buzz

A

Pink frothy sputum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Main goals for HF

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Every HF patient (unless contraindicated) should be on what?

A

An ACE and a diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MOA of ACE

A

Decreased aldosterone production degreasing angiotensin II leading to decrease water retention. Bradykinin is also affected and can cause dry coughing and angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does ACE affect mortality?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SE of ACE

A

Hypotension with first dose. Renal insufficiency (with Cr > 3 or CrCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why give an ARB instead?

A

This only blocks the effects of angiotensin II not the creation of it and doesn’t affect bradykinin which won’t lead to cough.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do you remember ACE drugs?

A

PRIL (aces (pilots) are PRIcks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do you remember ARBS?

A

Sartans (spartans don’t eat cARBS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What do you want to be careful of when adding a beta blocker with HF?

A

It can decrease EF transiently so DON’T give with decompensated HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When do you add a beta blocker?

A

Usually after an ACE or ARB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the MOA of hydralazine?

A

Vasodilator (decreases afterload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name 3 loops

A

Furosemide, Bumetanide, Torsemide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MOA of loops.

A

They inhibit water transfer across the loop of henle. They get rid of water, chloride, Na, K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the two main SE of potassium sparing diuretics?

A

Hyperkalemia and gynecomastia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the P’s of pericarditis?

A

Persistent, pleuritic, postural, pain, pericardial friction rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Dresslers syndrome

A

Post MI pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Becks triad

A

Associated with tamponade. Becky’s tampon. Distant heart sounds, JVP, hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment for pericarditis?

A

NSAIDS, ASA, Colchicine, corticosteroids if persistent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What two complications of pericarditis?

A

Effusion (common), tamponade (less common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Kerley B lines

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Batwing/Butterfly pattern

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What might you see on ECG in pericardial effusion?

A

Low voltage QRS complexes! You may also electric alternans implying the heart is “swinging in fluid”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How will the heart look on CXR with pericardial effusion?

A

Cardiomegaly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Distant heart sounds with auscultation of suspected pericardial effusion?

A

Yes. Its in water. Low sound conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Becks triad

A

Distant heart sounds, JVP, hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is Kussmaul’s sign

A

Increased JVD during inspiration due to impaired filling of RV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When do you see Kussmaul’s sign?

A

During constrictive pericarditis as well as restrictive cardiomyopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment for constrictive pericarditis?

A

Pericardiectomy. Gotta remove that crappy pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

PR elevation and ST depression in AVR

A

Acute pericarditis. “knuckle sign”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What will you see in the V leads with acute pericarditis?

A

PR depression in V3-V5 and ST elevation in V1-V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Pulsus paradoxis is commonly seen in what?

A

Tamponade and constrictive pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Most common cause of myocarditis?

A

Viral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Whats the difference between children and adults with myocarditis?

A

Children often present in florid HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Most common viral cause of myocarditis?

A

Coxsackie B. Other causes are adenovirus, parvovirus, herpes simplex 6, EBV, HIV, VZV. think “my oh my you have a pretty coxsackie”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the bacterial causes of myocarditis?

A

Lyme disease, Rocky mountain spotted fever, Q fever (Rickettsial). Think “my oh my you have a pretty mouth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What south/central american bacterial cause of myocarditis is common?

A

Chagas of course. He’s “breaking hearts” all over south america.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What will you see on CXR with myocarditis?

A

Cardiomegally.

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

How will a patient with viral myocarditis look?

A

Fever, myalgias, malaise with on onset of HF symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

CKMB and troponin will do what with myocarditis?

A

Elevate but not due to blockage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the GOLD STANDARD for diagnosis myocarditis?

A

Endomyocardial biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do you want to treat myocarditis?

A

Same as HF. Diuretics, afterload reducing agents (ACE), increase contractility (dopamine, dobutamine, milrinone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What 3 things will you see on echo of dilated cardiomyopathy?

A

Left ventricular dilation (thin walls and large chamber), decreased EF, regional or global hypokinesis (shit doesn’t work)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treatment for dilated cardiomyopathy?

A

Same as HF.

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

What the hell is broken heart syndrome?

A

Tako-Tsubo were two japanese lovers. Tako flew away in a “balloon” when Tsubo started menopause and the surge of catacholamines broke her heart.

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

Most common type of cardiomyopathy?

A

Dilated (95%), Hypertrophic (4%), Restrictive (1%).

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

What is the most common cause of restrictive cardiomyopathy?

A

Amyloidosis (Amy restricts the heart). Sarcoidosis too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the trademark of restrictive cardiomyopathy?

A

Impaired diastolic function with preserved contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What if you saw bright speckled myocardium on echo?

A

Amyloidosis present and likely causing cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Difference on echo between dilated and restrictive?

A

Dilated ventricle on the first but dilated atria on the other.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What part of the heart is most commonly affected with hypertrophic cardiomyopathy.

A

Septal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What kind of murmur with hypertrophic cardiomyopathy?

A

Harsh systolic crescendo-decrescendo murmur best heard at left upper sternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Why does the murmur on hypertrophic cardiomyopathy go quite with squatting or lying down?

A

Increased blood return which pushes septum out of the way and decreases SAM (systolic anterior motion). Helps the blood go the right direction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How do you measure the ankle brachial index?

A

Highest ankle pressure over highest arm pressure (both arms). You calculate the index. 1 to 1.4 is normal. 0.5 to 0.8 to 1 the pt has PAD.

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

What two arteries do you use with ankle brachial index?

A

Dorsalis pedis, posterior tibial (just behind medial maliolus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

First line treatment for hypertrophic cardiomyopathy?

A

Beta blockers.

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

What causes rheumatic fever?

A

GABHS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What valve is most affected?

A

Mitral then aortic

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

Jones MAJOR criteria for RF. Must have 2 major or 1 major and 2 minor.

A

Polyarthralgia, carditis, chorea, subcutaneous nodules, erythema marginatam.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Jones Minor criteria for RF.

A

Fever (101 to 104), arthralgias, elevated labs (ESR, CRP, leukocytosis), prolonged PR. Supporting evidence of recent GABHS infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Where are the nodules seen?

A

Nodules seen over extensor surfaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Whats the difference between arthralgias and polyarthragias (minor/major criteria?)

A

Heat, redness, swelling, severe tenderness MUST be present for polyarthralgias (multiple joints more conclusive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How do you treat the chorea of RF?

A

Haldol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does the rash look like with RF?

A

Macular, erythematous, NON pruritic ANNULAR lesions with well defined borders and some possible central clearing. Appears on TRUNK and EXTREMITIES (not the face).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How do you treat RF?

A

PCN G (erythromycin if PCN allergic).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What other drug should RF patients possibly get for 2-6 weeks?

A

ASA with a taper.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What can cause a split of S2?

A

Normal would be inspiration. This would be transient only during inspiration. Abnormal would be fixed. Commonly seen with ASD or VSD or pulmonary HTN or MS. Delayed closure of pulmonary valve. Paradoxical split (during exhalation) you will see it with delayed emptying of ventricle where aortic portion is later than pulmonic. Seen with LBBB or severe aortic stenosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

When would you hear an ejection click?

A

Mitral valve prolapse where the chordae tendonae pull the valve shut rapidly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

S3.

A

Lub de bub. Rapid filling of ventricle. You hear S1 then S2 then S3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

S4.

A

Belup dub. Atria contracting into stiff ventricle. S4 then S1 then S2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Stenosis leads to what?

A

Pressure overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Regurgitation leads to what?

A

Volume overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Harsh murmurs are usually ____

A

Stenotic (forward flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Blowing murmurs are usually ____

A

Regurgitation (back flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Systolic murmurs

A

Mitral and tricuspid regurgitation AND Aortic and pulmonic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Diastolic murmurs

A

Mitral and tricuspid stenosis AND Aortic and pulmonic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Where does aortic stenosis radiate to?

A

Carotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Where does mitral regurgitation radiate to?

A

Axilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Where does aortic regurgitation radiate to?

A

L upper sternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

In was pt position can you best hear a mitral murmur?

A

Decubitus (lying left side)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

In was pt position can you best hear an aortic murmur?

A

Pt seated up leaning forward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

With the exception of hypertrophic cardiomyopathy, increasing venous return does what to murmurs?

A

Makes them louder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the classic triad of transposition of the great vessels?

A

It’s a right to left shunt (which causes what in newborns? CYANOSIS!!!) CXR will show 1) Egg on a string sign. 2) Pulmonary vascular congestion. 3) Mild cardiomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Most common type of cardiac defect?

A

VSD - V=Very common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

When would you see cyanosis? What kind of shunting?

A

Right to left (no oxygenation of blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Murmur. Harsh holosystolic murmur at left sternal border. Management?

A

VSD. 35% close. Surgery possible. Give diuretic and digoxin early if necessary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Pulmonary stenosis. What disease of the young causes it?

A

Congenital RUBELLA syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Murmur. Harsh midsystolic crescendo-decrescendo murmur at upper left sternal border radiating into the neck.

A

Pulmonary stenosis. May have WIDE split of S2 as blood can’t get out for the pulmonary valve to close.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Mid systolic click is virtually diagnostic for what?

A

Mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Early diastolic murmur with decrescendo shape?

A

Aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Opening diastolic snap with mid mid diastolic rumble with presystolic accentuation.

A

Mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Volume overload can cause what sound?

A

S3. During rapid filling phase of diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Pressure overload can cause what sound?

A

S4. It’s the atrial kick against a bad ventricular wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

A pt has a lower BP in his legs than in his arms and delayed weak femoral pulses

A

Coarctation of the Aorta

105
Q

What sign might you see with coarctation of the aorta?

A

3 sign or backward E sign.

106
Q

Infantile coarctation is ____ ductal

A

Pre

107
Q

Adult coarctation is ____ ductal

A

Post

108
Q

What is rib notching? Another name for it?

A

Roesler sign. Dilated, tortuous vessels erode the rib walls as collateral vasculature forms to feed the aorta downstream from stenosis

109
Q

How do you test for coarctation of the aorta?

A

Angiogram

110
Q

How do you treat coarctation of the aorta?

A

Balloon angioplasty

111
Q

Cyanotic or not? PDA

A

Not. Left to right shunt

112
Q

Cyanotic or not? Tetrology of fallot

A

Cyanotic. Right to left shunt

113
Q

The production of what continues to keep a PDA patent?

A

PG E2

114
Q

What will you hear with PDA

A

Continual “machine murmur” over pulmonic area. You will also see WIDE PULSE PRESSURE and bounding peripheral pulses. This is because blood is running off from the aorta into the pulmonic valve

115
Q

What syndrome can occur with PDA

A

Eisenmenger syndrome. Pulm HTN causes shunt from L to R to R to L. Bad.

116
Q

What is the treatment for PDA in a preterm infant?

A

Indomethacin (it closes the duct). Surgery if not preterm.

117
Q

Amiloride, epleronone

A

Potassium sparing diuretics with spironolactone (inhibit aldosterone mediated water/Na absorption). These cause gynecomastia in addition to hyperkalemia.

118
Q

If pt has HTN and it is refractory to antihypertesives…

A

Think 2ndary cause.

119
Q

Abdominal bruit?

A

Renal artery stenosis

120
Q

What finding on PE signifies advanced stage of malignant HTN?

A

Papilledema

121
Q

What are 3 diuretics commonly used as first line in HTN?

A

HCTZ, chlorthalidone, metolazone

122
Q

Where do thiazides work?

A

Distal tubule. Prevents sodium and thus water reabsorption there.

123
Q

Loop diuretics get rid of water, Na, Cl, and K

A

True

124
Q

What diuretics are contraindicated in sulfa allergy?

A

Loops. Furosemide and bumetanide

125
Q

HTN emergency is what? How would you treat it?

A

220/120 + with signs of organ damage. Eyes, brain, kidneys, heart damage. You want 10% reduction in MAP within first hour and an additional 15% reduction over next 2-3 hours. using IV agents.

126
Q

ARBS are contraindicated in what?

A

Pregnancy

127
Q

When do you use dyhydroperidine CCB’s and non-dyhydroperidine CCB’s? And what are the?

A

Dyhydroperidines (dipine) are good for HTN alone. Non-dyhydroperidines (verapamil, diltiazem) good for HTN and A-fib. (they work on contractility and conduction AND vasodilation (the dipines only work on vasodilation).

128
Q

Should beta blockers be used as first line mono therapy in HTN?

A

NO

129
Q

What does a beta blocker do?

A

Blocks adrenergic renin release.

130
Q

When would you use an alpha blocker? What is the first SE?

A

On a dude who wants to be the alpha male but has HTN and BPH. He will probably faint the first time he takes it.

131
Q

Zosin drugs

A

Alpha 1 blockers. A=Zosin

132
Q

HTN emergency is what? How would you treat it?

A

220/120 + with signs of organ damage. Eyes, brain, kidneys, heart damage. You want 10% reduction in BP within first hour and an additional 15% reduction over next 2-3 hours. using IV agents.

133
Q

HTN urgency is what? How would you treat it?

A

Elevated BP without signs of organ damage. You want to decrease MAP by 25% in first 24-48 hours using PO agents

134
Q

What are the 4 main oral drugs used for HTN urgency and their side effects?

A

Clonidine (Alpha 2 agonist - dry mouth, headache, tachycardia, N/V, sedation, fatigue). Captopril (ACE - andioedema, renal failure). Labetalol (Alpha 1/Beta 1/2 blocker - COPD, heart block, heart failure exacerbation). Nicardipine (CCB - reflex tachycardia, HA, N/V, flushing)

135
Q

What class of medication do you NOT want to give to an asthmatic?

A

Beta blocker. Lebetalol for example.

136
Q

What is the DRUG OF CHOICE for HTN emergency?

A

Sodium nitroprusside

137
Q

Is sodium nitroprusside ok for pregnancy?

A

NO

138
Q

What should you give a pregnant patient in a HTN emergency? What class drug is it?

A

Methyldopa. Alpha 2 agonist.

139
Q

What would you give a pt who is in HTN emergency and is having an aortic dissection due to it?

A

Labetalol, NTP + esmolol

140
Q

Patients over 60 BP goals?

A

150/90

141
Q

Pt with CKD and HTN goals?

A

140/90

142
Q

A non-african american with uncomplicated HTN can have which drugs?

A

Thiazide type diuretic, ACE, ARB, BB, or CCB

143
Q

Main causes of hypercholesterolemia?

A

Hypothyroid, pregnancy, kidney failure

144
Q

Main causes of hypertriglyceridemia

A

DM, obesity, steroids, ETOH, estrogen

145
Q

What is one finding that is common with hypercholesterolemia

A

Xanthomas (around eyelids, achilles tendon)

146
Q

What abdominal issue does hypertriglyceridemia sometimes cause?

A

Pancreatitis

147
Q

Common bacteria with IV drug abuse endocarditis?

A

MRSA, pseudomonas, candida (fungal)

148
Q

Common cause of acute bacterial endocarditis?

A

Staph. A

149
Q

Common cause of prosthetic valve endocarditis?

A

Staph epidermis

150
Q

What is the infection of normal valves?

A

Acute bacterial endocarditis.

151
Q

Common cause of subacute bacterial endocarditis (abnormal valves)

A

Strep viridans

152
Q

What are the 5 organisms responsible for large endocarditis vegetations?

A

HACEK. Haemophilus, actinobacillus, cardiobacterium, eikenella, klingella

153
Q

How might a person with infective endocarditis present?

A

Fever, weight loss, fatigue, EKG abnormalities.

154
Q

What might you find on skin exam?

A

Janeway lesions (painless palms), Osler nodes (painful pads), Roth spots (retinal hemorrhage with pale center), petechiae (palate, conjunctiva), Splinter hemorrhages, clubbing, hepatosplenomegally, septic emboli.

155
Q

What do you want to do if you suspect it?

A

Blood culture (before ABX), EKG, echo (TTE before TEE), CBC,

156
Q

What criteria is used for infective endocarditis?

A

DUKE

157
Q

What are the major Duke criteria?

A

Bactermia (2 cultures positive), Endocardial involvement (either positive echo or new MR or AR murmur)

158
Q

Empiric treatment for NATIVE VALVE ACUTE infective endocarditis?

A

Nafcillin + gentamicin 4-6 weeks. If PCN allergy or if you suspect MRSA use Vancomycin and gentamicin

159
Q

Empiric treatment for NATIVE VALVE SUBACUTE infective endocarditis?

A

PCN/Ampicillin + gentamicin. If IVDA use Vancomycin with gentamicin

160
Q

Empiric treatment for PROSTHETIC VALVE infective endocarditis?

A

Vancomycin + gentamicin + rifampin (for staph A)

161
Q

Empiric treatment for fungal infective endocarditis?

A

Amphotericin B or Capsofungin if severe

162
Q

Prophy treatment is what before procedures for pts with what?

A

Amoxicillin 2g 30-60minute before surgery OR clindamycin 600mg (if PCN allergy). Dental work, respiratory surgery, or procedures involving skin (includes I&D)

163
Q

Whats the most common presentation of PAD?

A

Intermittent claudication. Pain with activity relieved by rest.

164
Q

Most common arteries involved with PAD claudication

A

Femoral and branches and popliteal

165
Q

What if there is resting leg pain with PAD?

A

Advanced disease

166
Q

What are the s/s of acute arteriole emboli?

A

6 P’s. Parathesias, pain, pallor, pulselessness, paralysis, poikilothermia

167
Q

If there is arterial occlusion, what can happen?

A

Gangrene (wet and dry) Wet is gross and dry is mummy

168
Q

What skin findings will you have with PAD?

A

Atrophic changes. muscle atrophy, thin/shiny skin, hair loss, nail thickening, cool limbs, possible necrotic areas.

169
Q

What color will the skin be?

A

Dependent rub or with paleness on elevation.

170
Q

Where are some common ulcers of PAD?

A

Lateral maleolar ulcers.

171
Q

How do you screen/dx PAD?

A

Ankle brachial index (ABI).

172
Q

Normal value for ABI?

A

1-1.2

173
Q

PAD dx with an ABI of what?

A
174
Q

Severe PAD with ABI of what?

A
175
Q

What ABI would you need to heal diabetic ulcers?

A

At least 0.85

176
Q

What is the GOLD standard for PAD testing?

A

Arteriography

177
Q

How would you treat PAD?

A

Cilostazol is the mainstay as it’s a vasodilator and ADP inhibitor.

178
Q

What other drugs would you use for PAD?

A

ASA and clopidogrel (plavix).

179
Q

An aneurysm greater than what is considered aneurysmal?

A

3.0cm

180
Q

Where do AAA usually occur?

A

Infrarenally.

181
Q

Give me the picture of an AAA candidate?

A

Atherosclerosis (#1 cause) >60 MALE SMOKER who is WHITE

182
Q

What law says that wall tension = pressure x radiates and as the wall dilates the force on the wall increases causing more dilation making larger aneurysms expand more rapidly than small ones.

A

Laplace’s law

183
Q

Ripping chest pain is indicative of what?

A

Thoracic dissection

184
Q

Dx of AAA

A

Abdominal US

185
Q

DX of thoracic aneurysms

A

CT scan

186
Q

What is the gold standard for AAA dx

A

Angiography

187
Q

When do you operate on an AAA?

A

> or equal to 5cm or 0.5cm expansion in 6 months (remember Laplace’s law!!!)

188
Q

When do you refer?

A

> 4.5cm

189
Q

AAA 4.0 to 4.5cm

A

US monitoring every 6 months

190
Q

AAA 3.0 to 4.0cm

A

US monitoring every year

191
Q

What drug helps reduce sheering forces?

A

Beta blockers!!! Non selective (labetalol) and add nitroprusside if needed.

192
Q

Where does an aortic dissector most commonly occur and in what layer of the aorta?

A

Ascending aorta (60%) and in the INTIMA layer

193
Q

What is the most common predisposing factor to aortic dissection?

A

HTN

194
Q

What syndrome predisposes people to AAA and aortic dissection while young?

A

Marfan syndrome

195
Q

What is the aortic dissection pain like?

A

Severe, tearing, knife like ripping chest/upper back pain

196
Q

Where do the ascending aorta, aortic arch, descending aorta dissections pain radiate to?

A

Anterior chest, neck/jaw, intrascapular

197
Q

What pulse changes might you see with aortic dissection?

A

Variation of pulses between arms of more than 20mm/hg

198
Q

If pt is hemodynamically stable, how might you diagnose this?

A

Angiography (gold standard) or TEE

199
Q

How is this dx urgently?

A

CXR showing widening mediastinum and CT scan with contrast (CT 3-D is happening now too)

200
Q

A pt presents with new onset localized headache and scalp tenderness and fevers. He has noticed some pain after chewing and some jaw muscle spasms (truisms) as well. While in clinic he suddenly has feels as though a shade came down and covered one of his eyes causing monocular blindness or amaurosis fugax. What is it? How will you know? What will you do?

A

Temporal arteritis. Clinical diagnosis though ESR and CRP will likely be elevated. Treat with high dose corticosteroids 40-60mg/day for 6 weeks with tapering. You can try methotrexate or azathioprine if refractory to steroids.

201
Q

Temporal arteritis is generally a ____ disease?

A

Autoimmune sparked by a virus

202
Q

Another name for temporal arteritis

A

Giant cell arteritis

203
Q

A pt presents with very tender nodules following venous distribution. There is claudication and even some ulcers forming on the distal extremities. What are you thinking? What else might you see?

A

Thromboantiitis obliterans (buerger disease). I think the fingers, toes, ears, nose, and tongue could worsen with cold, SMOKING, or emotional stress (Raynaud’s phenomenon).

204
Q

How would you know it’s Buerger disease and how would you treat it?

A

You would not see atherosclerosis

205
Q

Young smoker with numb digits going from pale, to blue, to red in the vasospasm tricolor classic presentation of what?

A

Buerger disease

206
Q

What test may be abnormal with Buerger disease?

A

Allen test

207
Q

What is the only definitive management of buerger disease?

A

Smoking cessation

208
Q

What is the medication treatment for buerger disease?

A

Dyhydroperidine CCB. “DIPINE” Nifedipine, nicardipine, amlodipine

209
Q

What is the triad for clot development?

A

Virchow’s triad. 1) Damage (trauma, infection, inflammation 2) Stasis (sitting, surgery) 3) Hypercoagulability (factor V leiden, oral contraception)

210
Q

What is migratory thrombophlebitis?

A

Trousseau’s sign. Associated mostly with malignancy or vasculitis.

211
Q

A pt presents with tenderness, pain, induration, edema, and erythema along a palpable cord of superficial vein. How will you confirm what you suspect and how will you treat it?

A

Confirm by venous duplex US. You will see a non compressible vein with a clot. Do a hypercoag workup (factor 5, protein C, S, lupus, factor 7, homocysteine). Treatment is supportive. Elevation, warm compresses, NSAIDS, compression stockings.

212
Q

When would you consider heparin and warfarin with superficial thrombophlebitis?

A

If in saphenofemoral junction (may throw clot)

213
Q

What if the superficial thrombophlebitis is septic?

A

If they have fever or it’s purulent. Treat with PCN + aminoglycoside.

214
Q

Pt presents with unilateral leg swelling, calf pain, and noticeable phlebitis. What are you thinking? How will you know? How will you treat?

A

DVT. Venous duplex US. Also a D-dimer may be helpful. But the GOLD STANDARD is venography. The main goal is to prevent PE. Heparin/LMWH then Warfarin for 3-6 months is the mainstay of treatment.

215
Q

Where do most DVT clots that throw to a PE originate?

A

Calf

216
Q

When would you consider lifelong warfarin treatment?

A

Pts with protein C, S or antithrombin III deficiency or factor 5 leiden.

217
Q

How does heparin work?

A

Potentiates antithrombin III and coagulation factors of the INTRINSIC pathway.

218
Q

How would you treat heparin toxicity?

A

Protamine sulfate.

219
Q

What should the PTT goal be for a pt on heparin?

A

1.5-2 x the normal value

220
Q

What is the trade name for LMWH and what is the advantage of it? How is it given and when should it be avoided.

A

Enoxaparin. No need to monitor PTT. Given SQ and lasts 12 hours so patients can go home. Don’t give in renal disease (Cr > 2.0) or in thrombocytopenia.

221
Q

How does warfarin (coumadin work)?

A

Inhibits vitamin K dependent coagulation in EXTRINSIC pathway.

222
Q

What coagulation factors are affected by coumadin?

A

2, 7, 9, 10, and protein C and S.

223
Q

Should coumadin be overlapped with heparin?

A

YES. For at least 5 days.

224
Q

What is the goal INR for warfarin patients?

A

2.0-3.0

225
Q

What is the antidote for warfarin overload?

A

Vitamin K

226
Q

Talk through unlikely DVT workup

A

Low clinical probability? D-dimer. If negative then DVT is excluded. If positive then do venous US. If negative, then DVT is excluded. . If positive then DVT is dx.

227
Q

Talk through likely DVT workup

A

Intermediate or high probability? Venous US. If positive then DVT is dx. If negative then do D-dimer. If negative then DVT is excluded. If positive then do serial US. If positive then DVT is dx. If negative then DVT is excluded.

228
Q

What are the features of the DVT ____ Criteria?

A

Wells criteria. 1) Cancer 2) Paralysis, paresis, or immobilization of lower extremity 3) Bedridden for more than 3 days 4) Localized tenderness along deep vein distribution 5) Entire leg swollen 6) Unilateral calf swelling > 3cm 7) Unilateral pitting edema 8) Collateral superficial veins 8) Alternative diagnosis as likely or more likely than DVT (-2)

229
Q

What has the higher risk of heparin induced thrombocytopenia?

A

Unfractionated heparin

230
Q

Redness with dependency (PVD/PAD)

A

PAD

231
Q

Pain worse with dependency (PVD/PAD)

A

PVD

232
Q

Pain better with walking (PVD/PAD)

A

PVD

233
Q

Pain better with dependency (PVD/PAD)

A

PAD

234
Q

Pain worse with walking (PVD/PAD)

A

PAD

235
Q

Lateral Malleolus ulcers (PVD/PAD)

A

PAD

236
Q

Medial Malleolus ulcers (PVD/PAD)

A

PVD

237
Q

Unclear margins of ulcers (PVD/PAD)

A

PVD

238
Q

Clear margins of ulcers (PVD/PAD)

A

PAD

239
Q

Cyanosis with dependency

A

PVD

240
Q

Stasis dermatitis with thickening of skin and brown pigmentation (PVD/PAD)

A

PVD

241
Q

Limited edema (PVD/PAD)

A

PAD

242
Q

Lots of edema (PVD/PAD)

A

PVD

243
Q

Thin shiny skin with loss of hair and muscle, pallor, thickened nails (PVD/PAD)

A

PAD

244
Q

Livedo reticularis (PVD/PAD)

A

PAD. This is that mottled appearance

245
Q

Pulses and temp in lower extremities normal (PVD/PAD)

A

PVD

246
Q

Pulses and temp in lower extremities cool and diminshed (PVD/PAD)

A

PAD

247
Q

Who gets varicose veins?

A

People with increased estrogen, OCP’s pregnancy, obesity, prolonged standing. Treat with stockings and elevation.

248
Q

What kind of shock is this? Pt is in severe respiratory distress and appears cool and clammy. Pt has decreased CO and increased PCWP and increased systemic vascular resistance

A

This could be cardiogenic or obstructive

249
Q

What are the common causes of cardiogenic shock?

A

MI, myocarditis, valvular disease, cardiomyopathy, arrhythmias

250
Q

What are the common causes of obstructive shock?

A

Tamponade, PE, tension pneumo, aortic dissection

251
Q

What kind of shot is this? Increased cardiac output

A

Septic shock (distributive)

252
Q

In what shock might you see hypotension without tachycardia?

A

Neurogenic (distributive)

253
Q

What are the causes of distributive shock?

A

Sepsis, neurogenic, anaphylactic, hypoadrenal

254
Q

Treatment for adrenal insufficiency shock

A

Hydrocortisone 100mg.

255
Q

Sepsis treatment initial?

A

Zosyn + rocephin or imipenem

256
Q

What if you suspect pseudomonas for your sepsis?

A

Gentamicin

257
Q

What if you suspect MRSA for your sepsis?

A

Vancomycin

258
Q

What if it’s an intrabdominal source for your sepsis?

A

Clindamycin or metronidazole.

259
Q

What if the patient has not spleen and they are septic?

A

Rocephin to cover N meningitides and H. Flu.

Board Review (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions