Vascular Dx: Arterial, Lipids, Flashcards
(149 cards)
1
Q
What arteries are in the upper extremities?
A
Subclavian, axillary, Brachial/deep brachial, ulnar, radial
2
Q
What arteries are in the lower extremities?
A
Common femoral, superficial femoral, profunda femoris, Tibial arteries: Anterial tibial, perineal, posterior tibial
3
Q
Etiology fo peripheral artery disease (PAD)
A
Atherosclerotic peripheral vascular disease, arterial abolish, vasculitis, fibromuscular dysplasia (FMD)
4
Q
Risk factors for PAD
A
Age >70, M>F, family hx of early onset atherosclerosis, smoking, HTN, diabetes, hyperlipidemia, metabolic syndrome, homocysteinemia
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
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
7
Q
Si/sx of PAD
A
Extremity pain, claudication, atypical or diffuse extremity pain, ischemic rest pain, skin discoloration, gangrene, ED
8
Q
PE findings of PAD
A
Smooth and shiny skin* reduced skin temp, pallor/cyanosis/mottling, ulcers, dependent rubor, gangrene, LE neuropathy
9
Q
What is dependent rubor?
A
Found in PAD; a color change when you change the position of the leg due to gravity
10
Q
Other PE findings for PAD
A
Decreased or absent distal pulses, bruits, muscle atrophy, hair loss, thickened nails
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)
12
Q
What types of gangrene are found in PAD?
A
Dry and wet
13
Q
Pulse exam: palpate or use Doppler on which pulses?
A
Femoral, popliteal, dorsal pedal, posterior tibial
14
Q
What can be heard on auscultation if pt has PAD?
A
Bruits: turbulent flow
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
16
Q
Diagnostic of choice for PAD?
A
ABI
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
18
Q
Interpretation of ABI: 0.41-0.90 is what?
A
Mild to moderate PAD
19
Q
Interpretation of ABI: 0.00-0.40 is what?
A
Severe PAD
20
Q
What are examples of duplex imaging?
A
Segmental pressures, pulsating volume recording (PVR), toe pressures
21
Q
PAD diagnosis
A
Abnormal pulse exam, claudication, ischemic rest pain, tissue loss (ulceration or gangrene), ABI <0.90
22
Q
What are the two ways to classify PAD?
A
Fontaine and Rutherford
23
Q
What are some other ways to classify PAD?
A
LE threatened limb classification, WIFI classification, wound, ischemia, foot infection
24
Q
What is the WIFI classification of PAD?
A
Wound (degree of tissue loss), ischemia (perfusion status/ABI), foot infection (degree of infection)
25
Conservative care for PAD
Risk factor modification, smoking cessation, consistent moderate exercise routine
26
Medical management for PAD
Aspirin, statin, Cilostazole (Pletal) 100mg PO BID
| 2/3 of pts can respond with increased walking distance
27
Indications for surgical intervention for PAD
Disabling claudication, ischemic rest pain, ulceration, gangrene, surgical risk must always be considered!
28
What types of surgery can be done for treatment of PAD
Angioplasty, Steiner placement, endarterectomy, surgical open bypass procedures, amputation
29
Angioplasty: PAD
Balloon angioplasty
30
What is the TASC classification?
To determine if lesions are amenable to percuteanous intervention
31
TASC classification
Type A, B, C, or D
| Helps to delineate which procedure pts need: endovascular or open
32
Type A and B
Vascular intervention
33
Type D
Open surgical procedure recommended
34
What other candidates are good for surgical open revascularization
Type D lesions, good risk candidates with type C lesions, type B lesions that fail endovascular management
35
What are some examples of surgical open bypass procedures
Aortobifemoral bypass graft (AFBG), femoral to femoral artery bypass (fem-fem), femoropoliteal bypass (fem-pop), femoral to distal bypass, axillary femoral bypass
36
What is another way to treat PAD?
Amputations: toe, transmetatarsal, below the knee, hip disarticulation
37
Estimated outcomes at 5 years in pts with intermittent claudication:
Stable claudication 70-80%, worsening claudication 10-20%, critical limb ischemia 1-2%, nonfatal MI or stroke 20%, death in 15-30%
38
When to refer (PAD)
Progressive symptoms, short distance claudication, rest pain, ulceration or any wounds
39
What is Subclavian Steal Syndrome?
Unequal UE BP (>10-15), arm claudication, arm or hand ischemia, and neurologic symptoms
40
What neurologic symptoms can be seen with subclavian steal syndrome
Dizziness, vertigo, ataxia, diploid, nystagmus, visual changes, syncope, tinnitus, hearing loss
41
How can you diagnose subclavian steal syndrome?
Noninvasive evaluation cerebrovascular and upper extremity arterial circulation
42
What imaging studies can be used to diagnose subclavian steal syndrome?
Continuous wave Doppler, duplex ultrasonography, transcranial Doppler, MRO or CTA angiography
43
What are the treatment options for subclavian steal syndrome?
Similar to lower extremity peripheral vascular disease treatment, medical and surgical therapy if needed
44
Acute limb ischemia
Sudden decrease in limb perfusion that causes a potential threat to limb viability
45
Arterial occlusion
Results in a sudden cessation of blood supply and nutrients to the tissues in the distribution of the vessel, including skin, muscle, and nerves
46
Etiology of limb ischemia
Progression of PAD, arterial emboli, arterial thrombus, arterial trauma
47
Arterial occlusion etiology
Arterial emboli, thrombus or trauma
48
Where can an arterial thromboemboli occur?
```
Femoral: 28%
Arm: 20%
Aortoiliac: 18%
Popliteal: 17%
Visceral and other: 9% each
```
49
Arterial thrombus occurs where?
Most likely at site of atherosclerotic plaque
50
Risk factors for arterial occlusion
AFIB, recent MI, large vessel aneurysmal disease, aortic dissection risk factors, arterial trauma, DVT
51
The clinical presentation of a arterial occlusion is dependent on what?
Time course of vessel occlusion; location of vessel occlusion and the ability to recruit collateral channels
52
What are the 6 Ps of limb ischemia?
1. Pulselessness
2. Pain
3. Poikilothermia
4. Pallor
5. Paresthesia
6. Paralysis
53
Irreversible damage occurs in how long with arterial occlusion?
6 hours
54
Diagnosis of arterial occlusion
ABI, vascular imaging: urgency should be weighed against benefit of imaging
55
Arterial occlusions can be classified as what?
Viable, marginally-threatened, immediately-threatened,or irreversible (nonviable)
56
What is the treatment for an arterial occlusion?
EMERGENT or URGENT revascularization
57
What are the revascularization options for arterial occlusion treatment?
IV heparin, thrombectomy/embolectomy, endovascular surgery: angioplasty or stent, surgical intervention, thrombolytic therapy
58
What is important to do post revascularization therapy for an arterial occlusion?
Find the source of the embolus!
59
How do you find the source of the embolus?
EKG and telemetry, vascular ultrasound or legs or abdomen, hypercoagulable evaluation, cardiac evaluation with TEE, chest CT
60
What could an EKG pick up as the source of an embolus?
AFIB
61
What can a vascular ultrasound of legs or abdomen see that can cause an embolus?
Aneurysm or plaque
62
Hypercoagulable evaluation
For antiphospholipid syndrome or lupus anticoagulant
63
Blue toe syndrome
Smaller vessel occlusion, usually embolic
| Has scattered petechiae or cyanosis of soles or toes
64
What are some screening labs done for lipids?
Total cholesterol, LDL, HDL, triglycerides, and glycated hemoglobin
65
Lipids
Serve as energy stores, essential components of all cell membranes, hydrophobic
66
What two types of lipds serve as metabolic fuel?
Triglycerides and phospholipids
67
What does cholesterol serves as a precursor for?
1. Plasma membranes
2. Bile salts
3. Steroid hormones
4. Other specialized molecules
68
Triglycerides
Used in energy metabolism, combinations of 3 fatty acids
69
What are phospholipids important constituents of?
Lipoproteins, blood clotting components, myelin sheath and cell membranes
70
Not composed of fatty acids but steroid nucleus is synthesized from fatty acids
Cholesterol
71
Cholesterol can be converted to what?
Hormones or bile acids
72
Special fat-carrying proteins that encapsulate and transport cholesterol and triglycerides
Lipoproteins
73
What are the 5 types of lipoproteins?
1. Chylomicrons
2. VLDL
3. IDL
4. LDL
5. HDL
74
What is the function of chylomicrons?
Carrey exogenous triglycerides and cholesterol
75
What do very low density lipoproteins do? VLDL?
Carry endogenous triglycerides primarily, and cholesterol too
76
What is the main carrier of cholesterol, delivers it TO the cells?
LDL = BAD cholesterol
77
Acceptor of cholesterol FROM various tissues, 50% protein
HDL = GOOD cholesterol
78
What are the 2 sources of cholesterol
1. Exogenous
| 2. Endogenous
79
Exogenous cholesterol comes from what
Diet: animal sources
80
Endogenous cholesterol is made how?
1. Produced from the liver
| 2. Produced from the cells lining the GI tract
81
What is the fate of cholesterol once its in the GI tract?
Some is excreted in fevers, some is absorbed into plasma and carried by chylomicrons
82
The liver can both and and remove what from the blood?
Cholesterol
83
The synthesis of cholesterol by the liver in inhibited when?
When plasma levels of cholesterol are increased
84
When does the liver increase the synthesis of cholesterol
When plasma levels falls
85
It’s very follicular to alter plasma serum cholesterol levels by what?
By dietary modification of cholesterol’s ingestion ALONE
86
LDL is removed form circulation via two mechanisms:
1. Receptor-dependent
| 2. Non-receptor-dependent
87
What is the receptor dependent way that LDL is removed from circulation
Binds to cell surface receptors -> endocytosis
| LDL is enzymatically degraded -> cholesterol is then released into cytoplasm and excreted
88
What is the non receptor dependent way that LDL is removed from circulation?
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
When LDL levels exceed receptor availability,
An increased amount of LDL must be removed by non-receptor-dependent mechanisms causing atherosclerosis
90
Definition of dyslipidemia
LDL >160
HDL <40
Triglycerides >150
91
LDL = ?
LDL = Total cholesterol - HDL - trigylcerides
92
Is total cholesterol a risk factor for heart disease?
No, but the ratio of plasma LDL to plasma HDL is
93
What is the Friedwald equation
Measures the LDL directly
94
What are some primary causes of dyslipidemia?
Disorders of lipid metabolism, overproduction and/or impaired removal of lipoproteins
95
What are some secondary causes of dyslipidemia
T2DM, excessive alcohol, cholestatic liver disease, nephrotic syndrome, chronic renal failure, hypothyroidism, smoking, obesity, drugs
96
Who should be screened for dyslipidemia?
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
How often should these pts be screened for dyslipidemia?
Every 5 years in pts clearly above therapy threshold, every 3 years in pts near threshold
98
What are some familial disorders of LDL receptors?
Strong link to premature CAD, >200LDL receptor mutations, autosomal dominant, prevalent in French Canadian, Lebanese
99
What is the presentation of familial disorders of LD receptor?
Xa Thomas, high LDL, FHx
100
What types of diets are good treatment for dyslipidemia?
High in fruits and veggies, whole grains, lower in dairy, some alcohol, red and processed meat, low in sugar sweetened foods
101
What is another name for statins?
HMG-CoA Reductase Inhibitors
102
Statins
Most commonly used lipid-lowering drugs
103
What drug is most powerful at lowering LDL?
Statins
104
Examples of statins
Atorvastatin, Simvastatin, Pravastatin, Rosuvastatin, Fluvastatin, Lovastatin
105
What is the only lipid lowering medication proven to improve CV outcomes?
Statins
106
Who should receive statin therapy?
All pts with known atherosclerosis regardless of LDL level
107
Positive outcomes of statins
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
What are the 4 groups of people who benefit from statins?
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
Non-statin therapies do not provide risk reduction for what?
ASCVD risk reduction benefits or safety profiles comparable to statin therapy
110
What is an example of a cholesterol absorption inhibitor?
Exetimibe (Zetia)
111
What is an example of a fibric acid derivative?
Fenofibrate, Gemfibrozil
112
What is an example of a bile acid sequestrant?
Cholestyramine
113
What is an example of a PCSK9 inhibitor?
Evolucumab (Repatha)
114
Who should be on high-intensity statin therapy?
21-75YO with clinical ASVD, or with an LDL-C>190
115
Who should be on a moderate intensity statin?
21-75YO with clinical ASCVD OR someone who isn’t a candidate for high intensity statin
116
Someone with Diabetes that has an LDL-C from 70-189 aged 40-75 should be on what?
Either moderate or high intensity statin
High intensity if: estimated ASCVD risk is >7.5%
117
What is the daily dose of a high-intensity statin?
Atorvastatin 80mg
| Rosuvastatin 40mg
118
What is the daily dosing for a moderate statin?
Atorvastatin 10mg, Rosuvastatin 10mg, Simvastatin 20-40mg
119
What is the daily dosing for a low-intensity statin?
Pravastatin 10-20mg, Lovastatin 20mg
120
What is the initial evaluation prior to statin therapy consist of?
Fasting lipid panel:
| ALT< CK, consider evaluation for other 2ndary causes or conditions that may influence statin safety
121
If someone is less than 75 WITHOUT C/I or drug-drug interactions, they should be started on what statin dose?
High-intensity
122
If someone is >75YO OR has C/I to high statin therapy, they should be placed on what?
Moderate intensity statin dosing
123
Evaluate and treat laboratory abnormalities:
1. Triglycerides >500
2. LDL-C >190
- secondary causes
- If primary, screen family for FH
3. Unexplained ALT >3 times ULN
124
What are some side effects of statins?
Myopathy: rhabdomyolysis, myositis, myalgia, LFT abnormalities
125
Rhabdomyolysis
Markedly increased CK, painful
126
Myositis
Somewhat elevated CK >10x ULN, ache
127
Myalgia
Normal CK, muscle aches
128
IF unexplained SEVERE muscle symptoms or fatigue develop during statin therapy:
Promptly D/C statin, address possibility of rhabdo with:
| CK, Creatinine, Urinalysis for myoglobinuria
129
If mild-moderate muscle symptoms develop during statin therapy,
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
What are some other reasons for elevated CK?
Hypothyroid Disease, inflammatory myopathies, polymyalgia rheumatica (Age>50), injury or excessive exercise, alcohol misuse
131
Increased risk of statin intolerance
Erythromycin, cyclosporine, HIV retroviral inhibitors, grapefruit juice, combination lipid therapy: Fibrates and niacin
132
What combo if lipid therapy can give you an increased risk for statin intolerance?
Fibrates and Niacin
133
Ezetimibe
Inhibits intestinal absorption of cholesterol, in combo with statin: reduces LDL even more
134
What can be an alternative to a high dose statin?
Ezetimibe in combo with a statin (lower intensity)
135
Monitor liver function for which drug?
Cholesterol absorption inhibitor: Ezetimibe
136
Hypertriglyceridemia
Mild to moderate levels (150-1000)
| Severe >1000
137
What are you at risk for with severe hypertriglyceridemia?
Pancreatitis, Fibrates and fish oils
138
What is metabolic syndrome?
Glucose intolerance, dyslipidemia, central obesity
139
Glucose intolerance criteria for metabolic syndrome
FBG 100-125
| Hgb A1c 5.7 to 6.4%
140
What are the BP criteria for metabolic syndrome?
SBP >135 DBP >85
141
Dyslipidemia criteria for metabolic syndrome
Elevated triglycerides >150
Low HLD <40
Elevated apolipoprotein B
142
Central obesity criteria for metabolic syndrome
Waist circumference greater than 40 inches in men and 35 inches in women
143
Nonpharmacologic therapy of hypertriglyceridemia
Weight loss, aerobic exercise, avoid concentrated sugars, avoid meds that raise triglyceride levels, strict glycemic control in DM
144
Weight loss for treatment of hypertriglyceridemia
May reduce TG elves by 22% and increase HDL 9%, maintenance of large weight loss is difficult
145
Aerobic exercise for treatment fo hypertriglyceridemia
Moderate intensity 4 hours a week improves cardiorespiratory fitness
146
Avoidance of concentrated sugars for treatment of hypertriglyceridemia
Low fat diets coupled with carbs reduce LDL and HDL, diet consisting of complex carbs and mono-and polyunsaturated fats
147
Fish oil for HDL/TG
Decreases TH by 15-30%, 1-2grams a day
148
Niacin for HDL/TG
15-30% increase in HDL and 20-30% decrease in TG, lots of SEs, Flushing*
149
Fibrates for HDL/TG
15% increase in HDL and 15-20% reduction in TG
