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Clin Med 2 > Vascular Dx: Arterial, Lipids, > Flashcards

Vascular Dx: Arterial, Lipids, Flashcards

1
Q

What arteries are in the upper extremities?

A

Subclavian, axillary, Brachial/deep brachial, ulnar, radial

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2
Q

What arteries are in the lower extremities?

A

Common femoral, superficial femoral, profunda femoris, Tibial arteries: Anterial tibial, perineal, posterior tibial

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3
Q

Etiology fo peripheral artery disease (PAD)

A

Atherosclerotic peripheral vascular disease, arterial abolish, vasculitis, fibromuscular dysplasia (FMD)

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4
Q

Risk factors for PAD

A

Age >70, M>F, family hx of early onset atherosclerosis, smoking, HTN, diabetes, hyperlipidemia, metabolic syndrome, homocysteinemia

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5
Q

At risk population for PAD

A

> 70YO, 50-69 with smoking or diabetes, 40-49 with diabetes and at least one other risk factor for atherosclerosis, leg symptoms suggestive of intermittent claudication or ischemic rest pain, abnormal LE pulse examination, known atherosclerosis

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6
Q

Intermittent claudication

A

Exertional pain: causes a person to stop walking, and resolves within 10 minutes of rest
-can be in buttock, hip, thigh, calf, foot

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7
Q

Si/sx of PAD

A

Extremity pain, claudication, atypical or diffuse extremity pain, ischemic rest pain, skin discoloration, gangrene, ED

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8
Q

PE findings of PAD

A

Smooth and shiny skin* reduced skin temp, pallor/cyanosis/mottling, ulcers, dependent rubor, gangrene, LE neuropathy

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9
Q

What is dependent rubor?

A

Found in PAD; a color change when you change the position of the leg due to gravity

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10
Q

Other PE findings for PAD

A

Decreased or absent distal pulses, bruits, muscle atrophy, hair loss, thickened nails

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11
Q

What is the Buerger test?

A

Have the pt lay flat and raise leg up 90 degrees, if they have PAD, the affected leg will change color (turn pale)

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12
Q

What types of gangrene are found in PAD?

A

Dry and wet

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13
Q

Pulse exam: palpate or use Doppler on which pulses?

A

Femoral, popliteal, dorsal pedal, posterior tibial

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14
Q

What can be heard on auscultation if pt has PAD?

A

Bruits: turbulent flow

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15
Q

Diagnostic studies for PAD

A

Ankle brachial index* exercise ABI, arterial duplex, segmental pressures, toe pressure, CT angiography, magnetic resonance angiography MRA, angiography

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16
Q

Diagnostic of choice for PAD?

A

ABI

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17
Q

ABI ankle-brachial index

A

Simple and inexpensive, compares SBP at the ankle with systolic brachial pressure in the arm
Ratio defines index, measure severity of PAD

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18
Q

Interpretation of ABI: 0.41-0.90 is what?

A

Mild to moderate PAD

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19
Q

Interpretation of ABI: 0.00-0.40 is what?

A

Severe PAD

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20
Q

What are examples of duplex imaging?

A

Segmental pressures, pulsating volume recording (PVR), toe pressures

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21
Q

PAD diagnosis

A

Abnormal pulse exam, claudication, ischemic rest pain, tissue loss (ulceration or gangrene), ABI <0.90

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22
Q

What are the two ways to classify PAD?

A

Fontaine and Rutherford

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23
Q

What are some other ways to classify PAD?

A

LE threatened limb classification, WIFI classification, wound, ischemia, foot infection

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24
Q

What is the WIFI classification of PAD?

A

Wound (degree of tissue loss), ischemia (perfusion status/ABI), foot infection (degree of infection)

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25
Q

Conservative care for PAD

A

Risk factor modification, smoking cessation, consistent moderate exercise routine

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26
Q

Medical management for PAD

A

Aspirin, statin, Cilostazole (Pletal) 100mg PO BID

2/3 of pts can respond with increased walking distance

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27
Q

Indications for surgical intervention for PAD

A

Disabling claudication, ischemic rest pain, ulceration, gangrene, surgical risk must always be considered!

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28
Q

What types of surgery can be done for treatment of PAD

A

Angioplasty, Steiner placement, endarterectomy, surgical open bypass procedures, amputation

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29
Q

Angioplasty: PAD

A

Balloon angioplasty

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30
Q

What is the TASC classification?

A

To determine if lesions are amenable to percuteanous intervention

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31
Q

TASC classification

A

Type A, B, C, or D

Helps to delineate which procedure pts need: endovascular or open

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32
Q

Type A and B

A

Vascular intervention

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33
Q

Type D

A

Open surgical procedure recommended

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34
Q

What other candidates are good for surgical open revascularization

A

Type D lesions, good risk candidates with type C lesions, type B lesions that fail endovascular management

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35
Q

What are some examples of surgical open bypass procedures

A

Aortobifemoral bypass graft (AFBG), femoral to femoral artery bypass (fem-fem), femoropoliteal bypass (fem-pop), femoral to distal bypass, axillary femoral bypass

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36
Q

What is another way to treat PAD?

A

Amputations: toe, transmetatarsal, below the knee, hip disarticulation

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37
Q

Estimated outcomes at 5 years in pts with intermittent claudication:

A

Stable claudication 70-80%, worsening claudication 10-20%, critical limb ischemia 1-2%, nonfatal MI or stroke 20%, death in 15-30%

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38
Q

When to refer (PAD)

A

Progressive symptoms, short distance claudication, rest pain, ulceration or any wounds

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39
Q

What is Subclavian Steal Syndrome?

A

Unequal UE BP (>10-15), arm claudication, arm or hand ischemia, and neurologic symptoms

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40
Q

What neurologic symptoms can be seen with subclavian steal syndrome

A

Dizziness, vertigo, ataxia, diploid, nystagmus, visual changes, syncope, tinnitus, hearing loss

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41
Q

How can you diagnose subclavian steal syndrome?

A

Noninvasive evaluation cerebrovascular and upper extremity arterial circulation

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42
Q

What imaging studies can be used to diagnose subclavian steal syndrome?

A

Continuous wave Doppler, duplex ultrasonography, transcranial Doppler, MRO or CTA angiography

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43
Q

What are the treatment options for subclavian steal syndrome?

A

Similar to lower extremity peripheral vascular disease treatment, medical and surgical therapy if needed

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44
Q

Acute limb ischemia

A

Sudden decrease in limb perfusion that causes a potential threat to limb viability

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45
Q

Arterial occlusion

A

Results in a sudden cessation of blood supply and nutrients to the tissues in the distribution of the vessel, including skin, muscle, and nerves

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46
Q

Etiology of limb ischemia

A

Progression of PAD, arterial emboli, arterial thrombus, arterial trauma

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47
Q

Arterial occlusion etiology

A

Arterial emboli, thrombus or trauma

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48
Q

Where can an arterial thromboemboli occur?

A 
Femoral: 28%
Arm: 20%
Aortoiliac: 18%
Popliteal: 17%
Visceral and other: 9% each
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49
Q

Arterial thrombus occurs where?

A

Most likely at site of atherosclerotic plaque

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50
Q

Risk factors for arterial occlusion

A

AFIB, recent MI, large vessel aneurysmal disease, aortic dissection risk factors, arterial trauma, DVT

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51
Q

The clinical presentation of a arterial occlusion is dependent on what?

A

Time course of vessel occlusion; location of vessel occlusion and the ability to recruit collateral channels

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52
Q

What are the 6 Ps of limb ischemia?

A
  1. Pulselessness
  2. Pain
  3. Poikilothermia
  4. Pallor
  5. Paresthesia
  6. Paralysis
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53
Q

Irreversible damage occurs in how long with arterial occlusion?

A

6 hours

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54
Q

Diagnosis of arterial occlusion

A

ABI, vascular imaging: urgency should be weighed against benefit of imaging

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55
Q

Arterial occlusions can be classified as what?

A

Viable, marginally-threatened, immediately-threatened,or irreversible (nonviable)

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56
Q

What is the treatment for an arterial occlusion?

A

EMERGENT or URGENT revascularization

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57
Q

What are the revascularization options for arterial occlusion treatment?

A

IV heparin, thrombectomy/embolectomy, endovascular surgery: angioplasty or stent, surgical intervention, thrombolytic therapy

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58
Q

What is important to do post revascularization therapy for an arterial occlusion?

A

Find the source of the embolus!

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59
Q

How do you find the source of the embolus?

A

EKG and telemetry, vascular ultrasound or legs or abdomen, hypercoagulable evaluation, cardiac evaluation with TEE, chest CT

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60
Q

What could an EKG pick up as the source of an embolus?

A

AFIB

61
Q

What can a vascular ultrasound of legs or abdomen see that can cause an embolus?

A

Aneurysm or plaque

62
Q

Hypercoagulable evaluation

A

For antiphospholipid syndrome or lupus anticoagulant

63
Q

Blue toe syndrome

A

Smaller vessel occlusion, usually embolic

Has scattered petechiae or cyanosis of soles or toes

64
Q

What are some screening labs done for lipids?

A

Total cholesterol, LDL, HDL, triglycerides, and glycated hemoglobin

65
Q

Lipids

A

Serve as energy stores, essential components of all cell membranes, hydrophobic

66
Q

What two types of lipds serve as metabolic fuel?

A

Triglycerides and phospholipids

67
Q

What does cholesterol serves as a precursor for?

A
  1. Plasma membranes
  2. Bile salts
  3. Steroid hormones
  4. Other specialized molecules
68
Q

Triglycerides

A

Used in energy metabolism, combinations of 3 fatty acids

69
Q

What are phospholipids important constituents of?

A

Lipoproteins, blood clotting components, myelin sheath and cell membranes

70
Q

Not composed of fatty acids but steroid nucleus is synthesized from fatty acids

A

Cholesterol

71
Q

Cholesterol can be converted to what?

A

Hormones or bile acids

72
Q

Special fat-carrying proteins that encapsulate and transport cholesterol and triglycerides

A

Lipoproteins

73
Q

What are the 5 types of lipoproteins?

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
74
Q

What is the function of chylomicrons?

A

Carrey exogenous triglycerides and cholesterol

75
Q

What do very low density lipoproteins do? VLDL?

A

Carry endogenous triglycerides primarily, and cholesterol too

76
Q

What is the main carrier of cholesterol, delivers it TO the cells?

A

LDL = BAD cholesterol

77
Q

Acceptor of cholesterol FROM various tissues, 50% protein

A

HDL = GOOD cholesterol

78
Q

What are the 2 sources of cholesterol

A
  1. Exogenous

2. Endogenous

79
Q

Exogenous cholesterol comes from what

A

Diet: animal sources

80
Q

Endogenous cholesterol is made how?

A
  1. Produced from the liver

2. Produced from the cells lining the GI tract

81
Q

What is the fate of cholesterol once its in the GI tract?

A

Some is excreted in fevers, some is absorbed into plasma and carried by chylomicrons

82
Q

The liver can both and and remove what from the blood?

A

Cholesterol

83
Q

The synthesis of cholesterol by the liver in inhibited when?

A

When plasma levels of cholesterol are increased

84
Q

When does the liver increase the synthesis of cholesterol

A

When plasma levels falls

85
Q

It’s very follicular to alter plasma serum cholesterol levels by what?

A

By dietary modification of cholesterol’s ingestion ALONE

86
Q

LDL is removed form circulation via two mechanisms:

A
  1. Receptor-dependent

2. Non-receptor-dependent

87
Q

What is the receptor dependent way that LDL is removed from circulation

A

Binds to cell surface receptors -> endocytosis

LDL is enzymatically degraded -> cholesterol is then released into cytoplasm and excreted

88
Q

What is the non receptor dependent way that LDL is removed from circulation?

A

Ingestion by phagocytic monocytes
Macrophage uptake of LDL in arterial wall can result in accumulation of insoluble cholesterol esters -> formation of foam cells -> development of atherosclerosis

89
Q

When LDL levels exceed receptor availability,

A

An increased amount of LDL must be removed by non-receptor-dependent mechanisms causing atherosclerosis

90
Q

Definition of dyslipidemia

A

LDL >160
HDL <40
Triglycerides >150

91
Q

LDL = ?

A

LDL = Total cholesterol - HDL - trigylcerides

92
Q

Is total cholesterol a risk factor for heart disease?

A

No, but the ratio of plasma LDL to plasma HDL is

93
Q

What is the Friedwald equation

A

Measures the LDL directly

94
Q

What are some primary causes of dyslipidemia?

A

Disorders of lipid metabolism, overproduction and/or impaired removal of lipoproteins

95
Q

What are some secondary causes of dyslipidemia

A

T2DM, excessive alcohol, cholestatic liver disease, nephrotic syndrome, chronic renal failure, hypothyroidism, smoking, obesity, drugs

96
Q

Who should be screened for dyslipidemia?

A

M>35, F>45, M>25 with CV risks, F>35 with CV risks, pts with DM, pts with 1st degree relative with premature CAD

97
Q

How often should these pts be screened for dyslipidemia?

A

Every 5 years in pts clearly above therapy threshold, every 3 years in pts near threshold

98
Q

What are some familial disorders of LDL receptors?

A

Strong link to premature CAD, >200LDL receptor mutations, autosomal dominant, prevalent in French Canadian, Lebanese

99
Q

What is the presentation of familial disorders of LD receptor?

A

Xa Thomas, high LDL, FHx

100
Q

What types of diets are good treatment for dyslipidemia?

A

High in fruits and veggies, whole grains, lower in dairy, some alcohol, red and processed meat, low in sugar sweetened foods

101
Q

What is another name for statins?

A

HMG-CoA Reductase Inhibitors

102
Q

Statins

A

Most commonly used lipid-lowering drugs

103
Q

What drug is most powerful at lowering LDL?

A

Statins

104
Q

Examples of statins

A

Atorvastatin, Simvastatin, Pravastatin, Rosuvastatin, Fluvastatin, Lovastatin

105
Q

What is the only lipid lowering medication proven to improve CV outcomes?

A

Statins

106
Q

Who should receive statin therapy?

A

All pts with known atherosclerosis regardless of LDL level

107
Q

Positive outcomes of statins

A

Lowers risk of death by 15-20% and lowers risk of non fatal CVE , improves all cause mortality
Do this is short and long term therapy

108
Q

What are the 4 groups of people who benefit from statins?

A
  1. ASCVD
  2. LDL-C>190, age >21
  3. Primary prevention: DM: 40-75YO LDL-C 70-189
  4. Primary prevention: No DM: >7.5% 10-year ASCVD risk, 40-75YO, LDL-C 70-189
109
Q

Non-statin therapies do not provide risk reduction for what?

A

ASCVD risk reduction benefits or safety profiles comparable to statin therapy

110
Q

What is an example of a cholesterol absorption inhibitor?

A

Exetimibe (Zetia)

111
Q

What is an example of a fibric acid derivative?

A

Fenofibrate, Gemfibrozil

112
Q

What is an example of a bile acid sequestrant?

A

Cholestyramine

113
Q

What is an example of a PCSK9 inhibitor?

A

Evolucumab (Repatha)

114
Q

Who should be on high-intensity statin therapy?

A

21-75YO with clinical ASVD, or with an LDL-C>190

115
Q

Who should be on a moderate intensity statin?

A

21-75YO with clinical ASCVD OR someone who isn’t a candidate for high intensity statin

116
Q

Someone with Diabetes that has an LDL-C from 70-189 aged 40-75 should be on what?

A

Either moderate or high intensity statin

High intensity if: estimated ASCVD risk is >7.5%

117
Q

What is the daily dose of a high-intensity statin?

A

Atorvastatin 80mg

Rosuvastatin 40mg

118
Q

What is the daily dosing for a moderate statin?

A

Atorvastatin 10mg, Rosuvastatin 10mg, Simvastatin 20-40mg

119
Q

What is the daily dosing for a low-intensity statin?

A

Pravastatin 10-20mg, Lovastatin 20mg

120
Q

What is the initial evaluation prior to statin therapy consist of?

A

Fasting lipid panel:

ALT< CK, consider evaluation for other 2ndary causes or conditions that may influence statin safety

121
Q

If someone is less than 75 WITHOUT C/I or drug-drug interactions, they should be started on what statin dose?

A

High-intensity

122
Q

If someone is >75YO OR has C/I to high statin therapy, they should be placed on what?

A

Moderate intensity statin dosing

123
Q

Evaluate and treat laboratory abnormalities:

A
  1. Triglycerides >500
  2. LDL-C >190
    - secondary causes
    - If primary, screen family for FH
  3. Unexplained ALT >3 times ULN
124
Q

What are some side effects of statins?

A

Myopathy: rhabdomyolysis, myositis, myalgia, LFT abnormalities

125
Q

Rhabdomyolysis

A

Markedly increased CK, painful

126
Q

Myositis

A

Somewhat elevated CK >10x ULN, ache

127
Q

Myalgia

A

Normal CK, muscle aches

128
Q

IF unexplained SEVERE muscle symptoms or fatigue develop during statin therapy:

A

Promptly D/C statin, address possibility of rhabdo with:

CK, Creatinine, Urinalysis for myoglobinuria

129
Q

If mild-moderate muscle symptoms develop during statin therapy,

A

D/C the statin until symptoms are evaluated, evaluate pt for other conditions that may increase risk for muscle symptoms, if after 2mos muscle symptoms do not improve, consider other causes*

130
Q

What are some other reasons for elevated CK?

A

Hypothyroid Disease, inflammatory myopathies, polymyalgia rheumatica (Age>50), injury or excessive exercise, alcohol misuse

131
Q

Increased risk of statin intolerance

A

Erythromycin, cyclosporine, HIV retroviral inhibitors, grapefruit juice, combination lipid therapy: Fibrates and niacin

132
Q

What combo if lipid therapy can give you an increased risk for statin intolerance?

A

Fibrates and Niacin

133
Q

Ezetimibe

A

Inhibits intestinal absorption of cholesterol, in combo with statin: reduces LDL even more

134
Q

What can be an alternative to a high dose statin?

A

Ezetimibe in combo with a statin (lower intensity)

135
Q

Monitor liver function for which drug?

A

Cholesterol absorption inhibitor: Ezetimibe

136
Q

Hypertriglyceridemia

A

Mild to moderate levels (150-1000)

Severe >1000

137
Q

What are you at risk for with severe hypertriglyceridemia?

A

Pancreatitis, Fibrates and fish oils

138
Q

What is metabolic syndrome?

A

Glucose intolerance, dyslipidemia, central obesity

139
Q

Glucose intolerance criteria for metabolic syndrome

A

FBG 100-125

Hgb A1c 5.7 to 6.4%

140
Q

What are the BP criteria for metabolic syndrome?

A

SBP >135 DBP >85

141
Q

Dyslipidemia criteria for metabolic syndrome

A

Elevated triglycerides >150
Low HLD <40
Elevated apolipoprotein B

142
Q

Central obesity criteria for metabolic syndrome

A

Waist circumference greater than 40 inches in men and 35 inches in women

143
Q

Nonpharmacologic therapy of hypertriglyceridemia

A

Weight loss, aerobic exercise, avoid concentrated sugars, avoid meds that raise triglyceride levels, strict glycemic control in DM

144
Q

Weight loss for treatment of hypertriglyceridemia

A

May reduce TG elves by 22% and increase HDL 9%, maintenance of large weight loss is difficult

145
Q

Aerobic exercise for treatment fo hypertriglyceridemia

A

Moderate intensity 4 hours a week improves cardiorespiratory fitness

146
Q

Avoidance of concentrated sugars for treatment of hypertriglyceridemia

A

Low fat diets coupled with carbs reduce LDL and HDL, diet consisting of complex carbs and mono-and polyunsaturated fats

147
Q

Fish oil for HDL/TG

A

Decreases TH by 15-30%, 1-2grams a day

148
Q

Niacin for HDL/TG

A

15-30% increase in HDL and 20-30% decrease in TG, lots of SEs, Flushing*

149
Q

Fibrates for HDL/TG

A

15% increase in HDL and 15-20% reduction in TG

Clin Med 2 (4 decks)

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