Cardiology Flashcards

1
Q

Statins

  • lovastatin
  • pravastatin
  • atorvastatin
  • rosuvastatin
A

decreases synthesis of cholesterol in liver by inhibiting HMG-CoA reductase

best drug to lower LDL
increases HDL

side effects: muscle injury (test CK in any patient on a statin with muscle symptoms), hepatic dysfunction (check LFT before you start, and then again later if there is a clinical indication to do so)

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2
Q

ezetimibe

A

cholesterol absorption inhibitor

impairs dietary and biliary cholesterol absorption at the brush border of the intestine

  • does not affect TG or fat-soluble vitamin absorption
  • primarily lowers LDL
  • side effects:myalgias, increased LFTs
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3
Q

fibrates

gemfibrozil, fenofibrate

A

primary effect on triglycerides and also raise HDL 5-20%

Fibrates work primarily by reducing hepatic secretion of VLDL

Side effects: myositis and LFT elevation

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4
Q

Bile acid sequestrants
aka bile-acid binding resins

Cholestyramine, colestipol, colesevelam

A

Primarily lower LDL (10-20%)
so not as strong as an effect as is seen with high intensity statins (50%)

Can serve a dual role in diabetics, as it lowers HbA1C in these patients by 0.5%

Side effects: GI side effects, LFT elevation, bad taste

Cholestyramine can bind C.Diff toxin!

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5
Q

Niacin

A

Primary effect on HDL

Side effect: flushing, but this improves with continued use, or prevent with dose at bedtime (sleep through the side effects), aspirin/NSAID use

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6
Q

Omega-3 fatty acids

A

Primary effect on TGs
Can be added on to other treatments
side effect: fishy burp

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7
Q

SE: facial flushing

A

niacin

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8
Q

SE: elevated LFT, myositis

A

statin, fibrates, ezetimibe

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9
Q

SE: Gi discomfort, bad taste

A

bile acid binding resins

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10
Q

Best effect on HDL

A

niacin

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11
Q

Best effect on TGs

A

fibrates

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12
Q

Best effect on LDL/cholesterol

A

statins

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13
Q

Binds C. difficile toxin

A

cholestyramine

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14
Q

2013 AHA/ACC guildelines

Who should be on statins?

A
  1. Those with clinical ASCVD
    - acute coronary syndrome
    - myocardial infarction
    - stable or unstable angina
    - revascularization procedures
    - stroke or TIA
    - peripheral arterial disease
  2. Anyone with LDL>190
  3. Diabetics (type 1 and 2), and between age 40-75yo
  4. 10-year ASCVD risk of 7.5% between age 40-75 (this calculation based on diabetes, anihypertensive use, age, SBP, total cholesterol, tobacco use)
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15
Q

Angina

A

chest pain associated with myocardial ischemia

chest discomfort, pressure sensation, “like something is sitting on my chest”

  • left-sided, midsternal
  • radiates to back/jaw/left arm
  • diaphoresis, SOB, palpitations

atypical symptoms:

  • female, diabetic, older
  • abdominal pain, exercise intolerance, generalized fatigue
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16
Q

Myocardial ischemia

A
myocardial oxygen demand exceed oxygen supply
predisposing factors:
-atherosclerosis
-shock
-hypoxemia
-anemia
-coronary artery vasospasm

increased demand:

  • vigorous exertion
  • tachycardia
  • HTN
  • ventricular hypertrophy
  • increased catecholamines
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17
Q

stable (predicatable) angina

A

resolves with rest, does not occur at rest

diagnosed with exercise or pharmacologic stress test

Labs: cardiac enzymes (troponin I, CKMB)

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18
Q

How do we treat stable angina?

A
  1. Beta blockers decrease HR and contractility
  2. CCBs promote coronary and peripheral vasodilation, and decrease contractility
  3. Nitrates: promote peripheral venous vasodilation (decrease preload, which decreases oxygen demand on the heart)
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19
Q

Prinzmetal angina (variant angina)

A

Caused by coronary artery vasospasm (NOT atherosclerosis)

RF: smoking
More often in younger patients (

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20
Q

What is the major RF associated with Prinzmetal angina?

A

smoking (

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21
Q

How does Prinzmetal angina present?

A

Pain at rest occurring at night, lasting 5-15 minutes

often indistinguishable from classic angina

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22
Q

How is prinzmetal diagnosed?

A

Coronary arteriography shows no sign of high grade coronary artery stenosis

in the setting of recurrent CP at rest, and transient ST-segment elevation on ECG

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23
Q

What medication class is used first-line to treat Prinzmetal angina?

A

CCB (diltiazem) and nitrates promote vasodilation in the coronary arteries
Smoking cessation is also very important

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24
Q

Why avoid beta blockers in Prinzmetal angina?

A

they may exacerbate vasospasm

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25
Q

Causes of CP

A
MSK- costochondritis
GERD
Esophageal spasm (relieved by nitrates)
Cocaine intoxication
Hyperventilation
Herpes zoster
Aortic stenosis
Trauma
Pulmonary embolism
Pneumonia
Pericarditis
Pancreatitis
Angina
Aortic dissection
Aortic aneurysm
Infarction
Neuropsychiatric diseases
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26
Q

ST segment elevation only during brief episodes of chest pain

A

Prinzmetal angina (coronary vasospasm)

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27
Q

Patient is able to localize the pain by pointing to it, and it is tender to palpation

A

Costochondritis

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28
Q

Rapid onset sharp chest pain that radiates to the scapula

A

aortic dissection

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29
Q

Rapid onset sharp pain in a 20-year old, with associated dyspnea

A

spontaneous pneumothorax, which is more common in young males

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30
Q

occurs after heave meals and is improved by antacids

A

GERD, maybe esophageal spasm, but still needs to be worked up

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31
Q

sharp pain lasting hours-days and is somewhat relieved by sitting forward

A

pericarditis

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32
Q

pain made worse by deep breathing and/or motion

A

musculoskeletal pain, pleuritic chest pain (irritation of the lining of the lung)

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33
Q

chest pain in a dermatomal dist

A

zoster

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34
Q

MCC noncardiac chest pain

A

GERD

musculoskeletal pain

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35
Q

acute onset dyspnea, tachycardia, confusion in a hospitalized patient

A

PE

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36
Q

widened mediastinum on CXR

A

aortic dissection

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37
Q

How does nitroglycerin relieve pain?

A

dilates peripheral veins
decreases preload
reduces myocardial O2 demand

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38
Q

inhibits COX1 and COX2

A

aspirin

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39
Q

ADP receptor inhibitor

A

clopidogrel

ticlopidine

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40
Q

Glycoprotein 2b/3a inhibitor

A

TIrofiban, Eptifibatide

abciximab

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41
Q

Activates antithrombin

A

heparin. enoxaparin

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42
Q

converts plasminogen to plasmin

A

streptokinase

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43
Q

streptokinase reversal agent

A

aminocaproid acid

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44
Q

drugs that can cause type 2 heart block (Mobitz I)

A

beta blockers
digoxin
calcium channel blockers

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45
Q

Narrow QRS, rate>100

A

SVT

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46
Q

No relationship between pulses and QRS

A

complete heart block

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47
Q

3 p-wave readings, rate>100

A

MAT

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48
Q

rate

A

bradycardia

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49
Q

PR interval >0.2 second

A

first degree heart block

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50
Q

Early, wide WRS beat without p-wave

A

PVT

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51
Q

wide QRS, HR 160-240

A

ventricular tachycardia

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52
Q

PR interval becomes longer with dropped beat

A

second- degree type I heart block

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53
Q

chaotic pattern, no P wave, no QRS

A

ventricular fibrillation

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54
Q

PR normal, occasional dropped beat

A

2nd degree type 2 heart block

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55
Q

sawtooth pattern

A

atrial fibrillation

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56
Q

no p waves, narrow QRS, iregularly irregular

A

atrial fibrillation

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57
Q

sinusoidal pattern of QRS

A

torsades des pointes

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58
Q

Which heart med is associated with pulmonary fibrosis and therefore requires pre-check of PFT and diffusion capacity every 6 months?

A

amiodarone

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59
Q

contraindications to triptans

A

sulfa allergy
pregnancy
CAD
Prinzmetal angina

60
Q

which drugs block transmission through the AV node?

A

beta blockers
nondihydropyridine CCBs
digoxin
adenosine

61
Q

stones, bones, groans, and psychiatric overtones

A

hypercalcemia (consider hyperparathyroidism)

62
Q

diastolic murmur best heard at left lower sternum that increases with inspiration

A

tricuspid stenosis

63
Q

late diastolic murmur with opening snap (no change with inspiration)

A

mitral stenosis

64
Q

systolic murmur best heard in the second right interspace, parasternal

A

aortic stenosis

65
Q

late systolic murmur best heard at apex

A

mitral prolapse

66
Q

Diastolic murmur with widened pulse pressure

A

aortic regurgitation

67
Q

holosystolic murmur at the left lower sternum that is louder with inspiration

A

tricuspid regurgitation

68
Q

holosystolic murmur heart at the apex, and radiates to the axilla

A

mitral regurgitation

69
Q

systolic murmur best heard in the second left interspace, parasternal

A

pulmonic stenosis

70
Q

things that can cause acute pericarditis

A
viral infection
TB
lupus
uremia
renal failure
neoplasm
drugs (INH, hydralazine)
Post- MI inflammation (Dressler syndrome)
radiation
recent heart surgery
71
Q

Acute pericarditis H and P

A

worse when supin
better when sitting up, leaning forward
dyspnea
pericardial friction rub
pulsus peridoxus (SBP drops more than 10mmHg during inspiration)
EKG changes (global ST elevation), PR depression

The pericardial effusion is usually transudative (thin, watery, low in protein)

If exudative, consider neoplasm, fibrotic disease, TB

Acute pericarditis:
Echo- pericardial effusion
CXR- enlarged globular canteen heart

Tx: treat the underlying cause

72
Q

Constrictive pericarditis

A

diffuse thickening of pericardium
decreased diastolic filling
decreased cardiac output

most common causes are radiation and heart surgery

symptoms- consistent with heart failure, Kussmaul sign

73
Q

What causes dilated cardiomyopathy?

A
ischemic heart disease
chronic alcohol use
chronic cocaine use
doxodubicin
CoxsackieB
Beriberi
Chagas
hemochromatosis
peripartum cardiomyopathy
S3
74
Q

What causes restrictive cardiomyopathy?

A

amyloidosis
sarcoidosis
hemochromatosis

(infiltrative causes)

75
Q

What causes hypertrophic cardiomyopathy?

A
aotosomal dominant
systolic murmur
sudden death in young athlete
S4
avoid diuretics, restrict exercise
76
Q

indications for prophylactic antibiotics against infectious endocarditis

A

NOT rheumatic heart disease, and NOT GU/GI procedures
prosthetic cardiac valves
previous infective endocarditis
Some congenital heart diseases (unrepaired heart defect)
cardiac transplants with valvulopathy
unrecovered heart transplant

If indicated, give 2g amoxicillin 30-60 minutes prior to procedure

77
Q

Endocarditis predisposing factors

A

congenital heart defects
IVDA
prosthetic heart calces

78
Q

normal blood pressure

A
79
Q

prehypertension

A

120-139/ 80-89

counsel these patients to stop smoking, reduce alcohol intake, reduce sodium in their diet, and lose weight

80
Q

hypertension

A

> 140/90

3 readings on 3 separate occasions

81
Q

Essential hypertension risk factors

A
family history
high sodium diet
tobacco use
obesity
age
black> white
82
Q

MCC secondary hypertension

A

kidney diseases, such as
chronic renal insufficiency
end stage renal disease
renal artery stenosis

83
Q

How do we treat renal disease in end-stage hypertension?

A

ACEI to delay progression

84
Q

renal artery stenosis

A

MCC fibromuscular dysplasia of renal artery

85
Q

renal artery stenosis >50yo

A

MCC atherosclerosis

86
Q

signs and symptoms of renal artery stenosis

A

renal artery bruit

87
Q

What tests can be used to diagnose renal artery stenosis?

A

MRA of renal arteries- MOST FREQUENTLY used screening test

spiral CT scan of renal arteries with IV contrast

renal artery duplex scan- is time- consuming (2 hours) and requires well- trained operator

renal arteriogram- gold standard, but invasive

88
Q

Why are ACEI contraindicated in renal artery stenosis?

A

They impede renal blood flow and renal GFR, thereby accelerating renal issues

89
Q

Combination OCPs and HTN

A

obese, women, >35yo

poorly controlled HTN is a contraindication to starting OCP
-stop OCP and change to progestin-only pill if hypertensive, or use IM medroxyprogesterone

90
Q

Pheochromocytoma and HTN

A

young patients
screen for MEN

Episodic HTN
diaphoresis
tachycardia
palpitations
headache

24-hr urine: catecholamines, VMA
serum: metanephrines, normetanephrines
CT or MRI: see the tumor?

91
Q

Pheochromocytoma treatment

A

surgically remove the tumor
pharmacologic contrl of HTN, pre-operatively

Alpha- blocker before beta- blocker (labetalol would be a suitable plan B, since it blocks both alpha and beta blockers)

92
Q

Primary hyperaldosteronism: Conn syndrome

A

HTN
hypokalemia
metabolic alkalosis
high PAC: PRA ratio
Treat this with surgical removal of tumor
possibly pre-treat with an aldosterone antagonist such as spironolactone or epleronone

93
Q

Cushing syndrome

A
Cushingoid features
obesity
hirsutism
buffalo hump
glucose intolerance

Dexamethasone suppression test

94
Q

Coarctation of the aorta- focal narrowing

A
kink in the hose
associated with: 
1. Congenital aortic valve 
pathology
2. Turner syndrome
3. Patent ductus arteriosis

high BP in arms but low BP in the legs, and weak dosalis pedis pulses

Diagnosis: LVH on EKG, echocardiogram

Treatment: surgical repair

95
Q

Hyperparathyroidism

A

hypercalcemia

  • confusion ans psychosis
  • calcium kidney stones
  • constipation
96
Q

Hypertensive urgency

A

SBP>180 or higher
or DBP>120 or higher

No sumptoms, no evidence of end organ damage

If there is evidence of end organ damage then we call this hypertensive emergency

97
Q

Hypertensive emergency

A

SBP>180 or higher
or DBP>120 or higher

with signs of end organ damage:

  • renal failure
  • changes in mental status
  • papilledema
  • retinal vascular changes
  • unstable angina
  • MI
  • aortic dissection
  • pulmonary edema
98
Q

How do we treat hypertensive urgency and hypertensive emergency?

A

reduce DBP to 100mmHg
with something that will work quickly
-in the first 2 hours, initial decrease should not exceed 25% of presenting pressure

lowering it too much would risk ischemia

start maintenance oral antihypertensive

99
Q

High BP in UE but low BP in LE

A

coarctation of the aorta

100
Q

proteinuria

A

renal disease

101
Q

hypokalemia

A

Cushing disease (primary hypoaldosteronism) or renal artery stenosis

102
Q

tachycardia, diarrhea, heat intolerance

A

hyperthyroidism

103
Q

hyperkalemia

A

renal failure

104
Q

episodic sweating, tachycardia

A

pheochromocytoma

105
Q

What tests do you order when you’re trying to rule out infectious endocarditis?

A
  1. rule out infection with blood/urine cultures, UA, +/- CXR
  2. Toxicology screen
  3. Rule out pancreatitis with amylase/lipase
  4. rule out MI with EKG and cardiac enzymes x3
106
Q

Beta blockers that reduce mortality in CHF

A

bisoprolol
carvedilol
extended-release metoprolol

107
Q

antihypertensive to use in DM

A

ACEI or ARB

108
Q

antihypertensive to use in heart failure (multiple

A

ACEI, ARB, Beta- blocker, aldosterone antagonist

109
Q

antihypertensive to use in BPH

A

alpha-1 antagonists

110
Q

antihypertensive to use in left ventricular hypertrophy

A

ACE I or ARB, which lower afterload

111
Q

antihypertensive to use in hyperthyroidism

A

propanolol

112
Q

antihypertensive to use in osteoporosis

A

thiazides

113
Q

antihypertensive to use in benign essential tremor

A

beta blociers

114
Q

antihypertensive to use in postmenopausal woman

A

thiazides, which will help with retaining calcium and reduce risk of osteopososis

115
Q

migraines

A

beta blockers

116
Q

antihypertensive to with the side effect of first-does orthostatic hypertension

A

alpha blockers

117
Q

antihypertensive to with the side effect of hypertrichosis

A

minoxidil

118
Q

antihypertensive to with the side effect of dry mouth, sedation, severe rebound HTN

A

clonidine (wears off every six hours or so)

119
Q

antihypertensive to with the side effect of bradycardia, impotence, asthma exacerbation

A

Nonselective beta blockers

120
Q

antihypertensive to with the side effect of reflex tachycardia

A

vasodilators

121
Q

antihypertensive to with the side effect of cough

A

ACE-I

122
Q

antihypertensive to avoid in patients with sulfa allergy

A

thiazides and loop diuretics

123
Q

antihypertensive to with the side effect of angioedema

A

ACE-I

124
Q

antihypertensive to with the side effect of development of drug- induced lupus

A

hydralazine

125
Q

antihypertensive to with the side effect of cyanide toxicity

A

sodium nitroprusside

126
Q

consequences of longterm treatment with NE

A

ischemia/necrosis of fingertips and toes
mesenteric ischemia
renal failure

127
Q

underlying mechanism of cardiogenic shock

A

failure of the pump

128
Q

underlying mechanism of extracardiogenic shock

A

pump compression

129
Q

underlying mechanism of hypovolemic shock

A

not enough fluid to pump

130
Q

mechanism of anaphylactic shock

A

vasodilation, releaes of vasodilatory agents (histamine)

131
Q

mechanism of neurogenic shock

A

vasodilation, loss of autonomic-regulated vascular tone

132
Q

mechanism of septic shock

A

vasodilation, massive release of inflammatory mediatiors

133
Q

AAA risk factors

A
tobacco use
age>55
atherosclerosis
htn 
family history

usually asymptomatic, pulsatile abdominal mass, abdominal bruit, hypotension, severe abdominal pain

radiology: us
CT or MRI if the US is positive

134
Q

AAA screening

A

all men between 65-75 who have a history of smoking

1-time screening abdominal US

follow with
US every 6 months if
5.5cm in men or >5cm in women

or if diameter has increased by more than 0.5cm in a 6-month interval (should be having abdominal ultrasounds every 6 months)

or if the aneurysm is symptomatic (tenderness, pain in abdomen or back)

135
Q

Aortic dissection

A

key difference between aortic dissection and AAA is that dissections tend to occur in the thorax, in the aortic arch.

RIsk factors: HTN, trauma, coarctation of the aorta, syphilis, Ehlers-Danlos syndrome, Marfan syndrome

Tear in the intima of the aorta
blood forces its way into the media and forms a false lumen

Stanford A- ascending aorta
B- confined to the distal aorta, below the branches

H and P: acute ripping/tearing chest pain radiating to the back

syncope or TIA, decreased peripheral pulses

EKG:
normal
+/- LVH

Radiology: CXR (widening of the mediastinum)

CT of the chest with contrast

B/L upper and lower extremity pulses, if unequal will be indicative of aortic dissection

Treatment: stabilize BP with beta blocker that will minimize the slope of rise of BP

Stanford A- emergency surg
Stanford B- beta blocker, surgery if uncontrolled

136
Q

Peripheral vascular disease

A

atherosclerosis of peripheral arteries

HTN, DM, coronary disease

symptoms- claudication- leg pain that comes with activity and improves with rest

Skin changes- dryness, ulcers, decreased leg hair growth

erectile dysfunction

PVD- ankle-brachial index (ABI)
ratio ankle SBP: brachial SBP
ABI0.4: severe disease

137
Q

What are components of conservative medical management of peripheral artery disease?

A

smoking cessation
glucose and BP control
daily exercise to increase collateral flow
cilostazol to improve flow to LE and decrease claudication (improves flow to LE and decreases claudication, more effective than pentoxifylline which is supposed to make RBCs more bendy)
contraindicated if any heart failure, due to increased mortality

Daily aspirin or clopidogrel to reduce cardiovascular events

Statin therapy to reduce cardiovascular events and increase pain-free walking distance

138
Q

PVD surgical interventions

A

angioplasty
bypass grafting
amputate if there is prolonged ischemia

139
Q

PVD and CAD

A

screen them with cardiac stress test before surgery

140
Q

varicosities

A

dilated veins due to incompetent valves

blood pools in the veins
H and P:
enlarged veins, visible veins, palpable veins, increased skin pigmentation, edema, ulceration

141
Q

How do we treat varicose veins?

A

weight reduction, avoid prolonged standing, leg elevation

compression stockings

sclerotherapy (injection of a substance that causes injury and thrombosis)

thermal ablation (external or internal)

surgery or ligation of the vein

142
Q

AVM

A

abnormal communication between arteries and veins

palpable, warm, pulsating masses if superficial
pain
local ischemia

Treat: surgical removal or sclerosis if in brain or bowel where it might bleed

143
Q

DVT

A

blood clot in large vein
usually in the lower extremity
RF: prolonged inactivity (travel or immobilization), recent surgery

Ted hose, SCDs, heart failure, hypercoag states

Cancer, pregnancy, OCPs, tobacco use, vascular trauma

DVT: hemostasos, hypercoagulability, vascular endothelial damage

H and P:
often asymptomatic
deep leg pain
calf sweeling and warmth

Homan sign (very unreliable)
measure circumference of the calf

Labs:
D-dimer
compressive venous ultrasound

Ts: elevate the leg
LMWH or unfractionated heparin, warfarin (long-term)

IVC filter (Greenfield filter) if the patient can’t take warfarin

144
Q

Dilates veins

A

nitroglycerine

145
Q

dilates veins and arteries

A

dihydropyridine CCBs

146
Q

dilates arteries

A

hydralazine

147
Q

dilates veins and arteries

A

nitroprusside