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CMS200 > Week 10- PAD > Flashcards

Week 10- PAD Flashcards

1
Q

arteriosclerosis

A

a general term for several disorders that cause thickening and loss of elasticity in the arterial wall

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2
Q

atherosclerosis as a form of arteriosclerosis , can cause

A

Causes coronary artery disease and cerebrovascular disease

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3
Q

atherosclerosis can effect large and medium arteries including

A
  • Coronary, carotid, and cerebral arteries
  • Aorta and its branches
  • Major arteries of the extremities
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4
Q

atherosclerosis epidemiology

A
  • Atherosclerotic vascular disease is a leading cause of morbidity and mortality worldwide
  • Atherosclerosis is considered a major cause of cardiovascular diseases
  • Atherosclerosis is rapidly increasing in prevalence in low- and middle-income countries, and as people live longer, incidence will increase
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5
Q

symptoms of atherosclerosis

A

predominantly asymptomatic

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6
Q

atherosclerotic cardiovascular disease

A

mainly involves the heart and brain: ischemic heart disease (IHD) and ischemic stroke

  • IHD and stroke are the world’s first and fifth causes of death respectively, and major cause of long-term disability in adults in the US
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7
Q

how many deaths in US from heart disease

A

1/4

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8
Q

in canada Atherosclerotic Cardiovascular Disease (ASCVD) is what cause of death

A

in Canada, ASCVD is the second leading cause of death and the 10-year risk of a CV event is 8.9%

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9
Q

atherosclerotic stenosis of what arteries cause up to 15% of strokes

A

internal carotid or intracranial arteries

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10
Q

PAD effects how many people in USA

A

Peripheral artery disease affects up to one in five people in the United States who are 60 years and older and nearly one-half of those who are 85 years and older

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11
Q

renal artery stenosis

A

may affect up to 5% of people with isolated hypertension and up to 40% of people with other atherosclerotic diseases

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12
Q

what % of acute myocardial infarctions occur from plaque rupture

A

75%

  • Incidenceinmen>45years
  • Incidenceinwomen,>50years
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13
Q

atherosclerosis characteristics

A

fatty streak, foam cells, fibrous plaque, complicated lesion/ rupture, stenosis, thrombus, aneurism

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14
Q

non modifiable risk factors of atheroscleorsis

A

-male gender (decrease estrogen mediated atheroprotection), decrease HDL and increase LDL

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15
Q

modifiable risk factors of atherosclerosis

A

-lifestyle (sedentary, diet)
-dyslipidemia (LDL)
-hypertension
-tobacco smoking
-diabetes (LDL, glycation, endothelial dysfunction)
-obesity (insulin resistance, hypertension, dyslipidemia)

Other risk factors:
Chlamydia pneumoniae infection, elevated levels of homocysteine, and elevated levels of lipoprotein-a (Lpa)

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16
Q

atherosclerosis progression and complications

A
  1. calcification
    -renal artery stenosis
    -angina
    -peripheral vascular disease
  2. rupture
    -myocardial infarction
    -thrombotic stroke
  3. hemorrhage
  4. embolization
    -embolic stroke
  5. aneuysm
    -AAA
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17
Q

CHART on slide 9

A
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18
Q

symptoms in coronary heart disease

A

angina/chest pain, cold sweats, dizziness, extreme tiredness, heart palpitations, shortness of breath, nausea and weakness

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19
Q

symptoms in PAD

A

Pain, aching, heaviness, or cramping in the legs when walking or climbing stairs that may be relieved by rest

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20
Q

symptoms in vertebral artery disease/ TIA

A

memory issues, weakness or numbness on one side of the body or face, and vision trouble are all early symptoms of vertebral artery disease.

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21
Q

symptoms in mesenteric artery ischemia

A

Severe pain following meals, weight loss, and diarrhea

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22
Q

general symptoms of atherosclerosis

A

stroke, fatigue and dizziness, SOB, chest pain, lower back pain, erectile dysfunction, pain numb or cold hands and feet

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23
Q

physical exams for atherosclerosis

A
  • Blood pressure
  • Peripheral pulses
  • Carotid or abdominal artery bruits
  • Abdominal palpation
  • Cardiovascular and Peripheral vascular exam * Respiratory exam
  • Skin exam - xanthomas
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24
Q

labs for atherosclerosis

A
  • Lipid profile (LDL-cholesterol)
  • Plasma glucose
  • High-sensitivity C-reactive protein (hsCRP)(in certain instances)
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25
Q

imaging in atherosclerosis

A
  • Ultrasound of the abdomen to screen for an abdominal aneurysm (ASCVD, elderly)
  • Doppler device – measure ankle-brachial index (normal 1.0 to 1.40) (PAD – as a marker for ASCVD in other beds (coronary artery disease [CAD], cerebrovascular disease, among others)
  • Sonography of the carotids (Coronary artery stenosis, a carotid bruit)
  • Electrocardiogram (ECG), stress ECG
  • Electron beam computed tomography (EBCT) (to confirm ASCVD, determines calcium score, interpreted according to age, establishes plaque burden)
  • Angiography - primary method for imaging atherosclerotic lesions in the coronary circulation, invasive procedure, reserve for high-risk patients or those with symptomatology; Not a screening test.
  • Computed Tomography (CT) angiography – in ASCVD used to detect the presence of low-attenuated plaques and in predicting future acute coronary events. noninvasive assessment
  • Cardiovascular Magnetic Resonance Imaging (cardiac MRI) - costly
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26
Q

complications of atherosclerosis

A
  1. occlusion of vessel
  2. disruption of plaque
  3. emboli
  4. aneurysm
  5. peripheral vascular disease
    a. claudication
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27
Q

disruption of plaque

A

Hemorrhage within plaque or rupture or ulceration of plaque (with exposure
of the thrombogenic components) can result in thrombus formation.

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28
Q

emboli

A

Plaque can break free and be carried in the blood stream farther down the vessel.

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29
Q

aneurysm

A

Atherosclerosis begins as an intimal process, but over time the thickened intima puts pressure on and causes atrophy of the media, often resulting in an aneurysm (i.e., dilation or saccular outpouching of the vessel).
- can lead to rupture of the vessel and resultant hemorrhage

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30
Q

peripheral artery disease- claudication

A
  1. Claudication, which is characterized by ache or cramping in the extremities with exertion that is relieved by standing still. Patients also have cool extremities, diminished distal pulses, and shiny, hairless skin. Patients with severe peripheral vascular disease have pain at rest. Ischemic ulcerations are a common cause of morbidity.
  2. Cause: Atherosclerosis of vessels of the lower extremities.
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31
Q

complications of ASCVD (Atherosclerotic Cardiovascular Disease)

A

can present as coronary artery disease (CAD), cerebrovascular disease (CVA), transient ischemic attack (TIA), peripheral artery disease (PAD), abdominal aneurysms, renal artery stenosis, mesenteric artery ischemia

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32
Q

prognosis of ASCVD (Atherosclerotic Cardiovascular Disease)

A

may be very good with management of risk factors such as LDL- cholesterol with statin therapy, BP, diabetes, smoking cessation, exercising regularly, and adhering to a prudent diet

  • Worse with full-blown, end-organ disease such as heart failure, ischemic stroke with paralysis and impaired cognition and gangrene necessitating amputation and rupture of an abdominal aneurysm
  • Pre-existing ASCVD has been shown to predict recurrent CV events – in patients with acute coronary syndromes (ACS) found that the rate of subsequent CV events over 8–17 months was 7.5%–19.9%
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33
Q

promote preventative measures for atherosclerosis

A
  • Educate patients on regular exercise, discontinue smoking, maintain a healthy body weight, eat a healthy diet and use medications used to lower lipids when indicated
  • Evidence shows these can significantly reduce the risk of adverse cardiac events and stroke
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34
Q

management of atherosclerosis

A
  • Treat risk factors such as elevated LDL-C, blood pressure, diabetes, obesity
  • Medications: statins, antihypertensives (ACEs, ARBs, diuretics, beta-blockers, CCB, vasodilators), diabetes therapies, thrombolysis therapies
  • Exercise and healthy diet low in saturated and trans fats, reduce salt intake, increase monounsaturated fats, fatty fish, fruits, vegetables, maintain healthy body weight
  • Stop smoking
  • Revascularization procedures: angioplasty, bypass, etc.
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35
Q

peripheral vascular disease

A

narrowing of arteries other than heart or brain

risks: old, smoking, hypertension, hyperlipidemia, diabetic, metabolic syndrome

mechanism: atherosclerosis

causes: pain, ulceration, gangrene

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36
Q

peripheral vascular disease; definition? what does it affect?

A

an overarching term that encompasses vascular diseases that result from circulatory dysfunction caused by damage to arteries or veins

  • may affect any blood vessel outside of the heart including arteries, veins and lymphatic vessels
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37
Q

what are the most common types of peripheral vascular disease

A

peripheral artery disease (PAD), chronic venous insufficiency (CVI), and deep vein thrombosis (DVT)

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38
Q

what causes peripheral vascular disease

A

primarily driven by progressive atherosclerotic disease resulting in the reduction of major organ blood flow and end-organ ischemia

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39
Q

what is peripheral artery disease AKA

A

lower extremity occlusive disease

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40
Q

peripheral arterial disease definition

A

is a chronic progressive atherosclerotic disease leading to partial or total peripheral vascular occlusion of the major arteries distal to the aortic arch

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41
Q

what body parts are involved in peripheral arterial disease

A
  • can involve both the upper and lower extremities
  • typically affects the abdominal aorta, iliac arteries, lower limbs to the level of the tibial arteries at the foot, and occasionally the upper extremities i.e. in carotid artery stenosis
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42
Q

what does the progressive occlusion in PAD result in

A

arterial stenosis, reduced blood flow, and claudication

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43
Q

prevalence of PAD

A

*American Heart Association estimates 8 to 12 million Americans have PAD-prevalence of 3%to 10%
* Study: 29% in those aged >70, and between ages of 50-69 with a history of smoking or diabetes * Increased to nearly 50% in those >85 yoa

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44
Q

PVD (peripheral vascular disease) prevalence

A

15% to 20% in those >70 yoa

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45
Q

demographics in PAD/PVD

A

-older, male, African American, low SES

  • Age: prevalence increases with age with up to 20% of people older than 75 years
  • Sex: male gender is risk factor
  • Race/ethnicity: non-Hispanic black race (African Americans to have an odds ratio of2.12)
  • Socioeconomic:
  • lower poverty-income ratios (PIR) have an early 2-fold increase in the risk of PAD compared to higher PIR
  • lower educational level to be significantly associated with PAD
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46
Q

who’s most at risk for PAD/PVD

A

over 50 yrs old
obesity
family member with heart disease
smoking or tobacco products
diabetes, high cholesterol, high blood pressure
coronary artery disease (CAD)

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47
Q

risk factors for PVD/PAD

A
  • Advanced age, male gender, and positive family history
  • Prior history of coronary artery disease, sedentary lifestyle
  • Cigarette smoking history
  • Study: >80% of patients with PAD were current or former smokers
  • Increases odds for PVD by 1.4 for every 10 cigarettes smoked/ day and by 2.6 in patients
    with diabetes
  • Cardiovascular mortality rates of current smokers with PAD are more than double that of those with PAD who have never smoked
  • Diabetes mellitus
  • Smoking and diabetes are associated with the highest relative risk for developing lower- extremity PAD
  • Hypertension
  • Hyperlipidemia
  • Patients with other vascular disease have a high prevalence of PAD (19% in patients with ischemic heart disease and 26% in patients with stroke)
  • Low High-density lipoprotein (HDL) cholesterol (<1.04mmol/L[40mg/dL] in men and< 1.29 mmol/L [50 mg/dL] in women
  • Chronic kidney disease/ renal insufficiency (eGFR<60mL/minute/1.73m2)
  • *NHANES:Most significant risk factors- hyperlipidemia, hypertension, diabetes mellitus, chronic kidney disease, and smoking;
  • Odds of having PAD increase with each additional risk factor, from a 1.5-fold increase with one risk factor to a 10-fold increased risk with three or more risk factors
  • In one series from the Netherlands, the likelihood of a patient having PVD (as defined by an ankle-brachial index [ABI] of less than 0.9) was increased by:
  • being male (odds ratio[OR]1.6)
  • being older than 60 years (OR4.1)
  • having hypercholesterolemia (OR1.9)
  • having a history of ischemic heart disease (OR3.5), cerebrovascular disease (OR3.6), diabetes mellitus (OR 2.5), or intermittent claudication (OR 5.6)
  • smoking(OR1.6)
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48
Q

classic/intermittent claudication is a symptom of PVD/PAD. What is it? how often does it occur?

A

Classic/intermittent claudication= defined as fatigue, muscle discomfort, cramping, or pain of vascular origin in the lower limbs (primarily in the calves and buttocks) that is consistently induced by exercise (i.e. after walking a fixed distance) and is consistently relieved by rest within 10 minutes
* Occurs in only 10-30% of patients with PAD
* Approximately 42% area symptomatic (no leg pain)
* Others have a typical (non-classical) symptoms of leg pain(47%)
* Symptoms may include exertional pain that does not stop the individual from walking, does not involve the calves, or does not resolve within 10 minutes of rest –> potentially related to comorbid musculoskeletal or neuropathic conditions
–> The presence of classic claudication has an LR+ 3.30 –> The absence of classic claudication has an LR− 0.89

  • History-include an estimate of the walking distance
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49
Q

classic/intermittent claudication

A

fatigue or pain in lower limbs induced by exercise and relieved by rest (in PVD/PAD)

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50
Q

more symptoms of PVD/PAD

A

*Additional non-classical symptoms
* Leg pains or sensations
* Skin, hair, nail changes
* Nonhealing wounds/ulcers
* Edema

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51
Q

PAD symptoms

A

-leg pain or cramping while walking
-leg numbness or weakness
-sores on toes, feet or legs that won’t heal
-coldness on the lower leg or foot
-changes in the colour of legs, texture or temperature
-slow toenail growth

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52
Q

PVD symptoms

A

-swelling in the feet, legs, or ankles
-presence of spider veins or varicose veins
-tired feeling in the legs
-difficulty standing for very long
-burning, numbness, or tingling in the thighs or calves
-itchy, dry skin on the legs

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53
Q

Edinburgh claudication questionnaire- PVD diagnosis

A

to diagnose intermittent claudication; 6 questions and pain diagram; LR+ 11

i.e. do you get pain in legs while you walk? what happens if you stand still (pain goes away in 10 mins)? where do you get the pain (calf, thigh, butt)? etc

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54
Q

physical exam for PAD

A

Vitals– Blood pressure

  • Inspection/Palpation:
    *Gait: Impaired walking function/ Intermittent
    claudication –> ischemic rest pain * Observe skin on lower extremities:
  • Non healing lower extremity wound
  • Arterial ulcerations -well-demarcated, “punched-out” lesions
  • feet inspection for ulcers between the toes (“kissing ulcers”) and ulcers related to ill-fitting footwear
  • Lower extremity gangrene
  • Observe skin perfusion:
  • Pallor on leg elevation or dependent rubor followed by pallor or blanching of the extremity with elevation
  • Inspection/Palpation:
  • Skin temperature: Cool skin
  • Nails: Dystrophic nail changes
  • Capillary refill: Abnormal capillary refill time
  • Hair: Hair loss on toes and distal ankles, shiny skin, and muscle atrophy
  • Pulses (grade): Diminished lower extremity pulses
  • Abdominal palpation: abdominal aortic aneurysm
  • Auscultation: vascular bruits–aortic, carotid, femoral, iliac and popliteal
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55
Q

Most reliable physical findings in PAD

A

diminished or absent pedal pulses, presence of femoral artery bruit, abnormal skin color, and cool skin – however their absence does not preclude PVD

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56
Q

physical findings in PAD

A

vascular bruit, cool skin, bad nails, abnormal capillary refill, hair loss, diminished lower limb pulses, pallor skin, ulcer, gangrene

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57
Q

high LR+ for PAD physical examination

A

-cool skin, foot ulcer
-iliac, femoral or popliteal bruit
-abnormal femoral pulse
-abnormal posterior tibial pulse
-abnormal dorsalis pedis pulse

58
Q

PVD highest LR+

A

DP and PT pulses absent LR+=44.6

posterior tibial pulse
dorsalis pedis pulse

59
Q

what is the ankle brachial index

A

for screening and diagnosing PVD/PAD in the primary care or hospital setting

  • inexpensive and reproducible method for assessing lower extremity hemodynamics
  • test on one or both extremities
  • requires a blood pressure cuff and a Doppler device with a probe for detecting arterial pulses
  • calculate the ratio of the highest systolic pressure in each leg (obtained at the dorsalis pedis and posterior tibial recurrent arteries using a Doppler probe), to the higher of the right or left arm brachial artery pressures
60
Q

what is the ankle bridal index value for PVD

A

less than 0.9

61
Q

what does doing the ankle bridal index for PAD/PVD not exclude

A

AB will not exclude proximal aneurysms or
arterial disease distal to the ankle

62
Q

when added to the framingham risk score, what does an ankle brachial index of less than 0.9 double the risk of

A

overall mortality, cardiovascular mortality, and major coronary events in each Framingham Risk Score category

63
Q

patients at increased risk of PAD

A
  • 65 yrs old +

-50-64 yrs with risk factors for atherosclerosis (hypertension, diabetes, hyperlipidemia, history of smoking) or family history of PAD

  • younger than 50 plus diabetes and one additional risk factor for atherosclerosis

-individuals with known atherosclerotic disease in another vascular bed (i.e. abdominal aorta, carotid, coronary, mesenteric, renal, or subclavian)

64
Q

what does USPSTF say for routine screening for PAD

A

insufficient evidence if asymptomatic patients

due to lack of evidence that screening improves outcomes such as cardiovascular morbidity or mortality

65
Q

what does American heart association say for PAD screening

A

guidelines - recommends patients at increased risk of PAD should be assessed for exertional leg symptoms, ischemic rest pain, and nonhealing wounds

66
Q

when to screen for PAD with ABI (ankle bradial index) via American heart association

A

ABI screening
for patients with history or examination findings suggestive of PAD
* Patients at increased risk of PAD, but without suggestive history or examination findings,
resting ABI testing is considered reasonable
* Guideline does not recommend ABI screening in patients who are not at increased risk of PAD

67
Q

what does American diabetes association recommend for screening with ABI for PAD

A

recommends ABI screening in all patients with diabetes who are older than 50 years

  • Normal results –> repeat screening every five years
  • Patients with diabetes <50years –> screen if risk factors present (e.g., smoking, hypertension,
    hyperlipidemia, duration of diabetes more than 10 years)
68
Q

Trans-AtlanticInter-Society Consensus guidelines recommend screening in patients with a 10-year Framingham cardiovascular risk score of ____%

A

10-20%

  • Combining the results of ABI screening with Framingham risk scores can improve 10-year cardiovascular risk prediction and alter risk factor modification goals in some patients
  • However USPSTF found inadequate evidence to assess balance of benefits and harms of ABI in risk assessment of CVD in asymptomatic adults to prevent CVD events
69
Q

what % of PVD/PAD patient have critical limb ischemia?

how many patients that have intermittent claudication may progress to CLI?

A

1-2%

21%

70
Q

how does critical limb ishcemia develop

A

develops through gradual ischemic conditioning which promotes the development of collateral vessels that maintain limb perfusion

71
Q

critical limb ischemia is a more severe presentation of

A

PAD

72
Q

risk factors for critical limb ischemia

A

most significant for development of CLI are diabetes, renal failure, heart failure, and prior stroke

73
Q

what does critical limb ischemia increase the risk of

A

Increased risk for limb loss –> CLI also referred to as chronic limb-threatening ischemia (CLTI)

74
Q

symptoms of critical limb ischemia

A

chronic (more than two weeks) ischemic rest pain, ischemic wounds or tissue loss, or gangrene in one or both legs

  • Nocturnal/ischemic rest pain - symptoms worsen at night when the patient is supine
  • Patients awakened by burning pain, cramping, coldness, numbness or pain in the forefoot or toes
  • Symptoms relieved by hanging the limb over the side of the bed, triggering dependent rubor of the foot
  • *Requires urgent referral to a vascular surgeon
75
Q

what does critical limb ischemia require

A

urgent referral to vascular surgeous

76
Q

differential diagnosis for critical limb ischemia? what’s a common comorbidity?

A

DDx: Diabetic neuropathic pain – a common comorbidity
*

  • neuropathy is experienced as pins and needles along the entire sole of the foot
77
Q

mortality rate for critical limb ischemia

A
  • Mortality rate - 25% in patients with CLI
78
Q

acute limb ischemia is

A

abrupt interruption of arterial blood flow to an extremity

79
Q

symptoms of acute limb ischemia

A

cold, painful, and pale extremity with diminished or absent pulses, motor weakness, and sensory impairment

80
Q
A
81
Q

what to do in acute limb ischemia

A
  • Acute disruption of arterial flow threatens limb integrity unless prompt revascularization is undertaken
  • *A medical emergency – evaluation by a vascular subspecialist on an emergency basis
82
Q

differential diagnosis for acute limb ischemia

A
  1. CHF, superimposed on chronic arterial disease
  2. deep venous thrombosis, acute
  3. acute spinal cord compression
83
Q

SLIDE 50 chart for DDX of acute limb ischemia

A
84
Q

PVD labs

A
  • complete blood count with platelet count
  • electrolytes
  • fasting glucose or A1C
  • fasting lipid profile
  • kidney function tests
    * serum creatinine
    * urinalysis for glucosuria and proteinuria

*although elevated homocysteine, C-reactive protein, and lipoprotein A levels are risk factors for PVD, there are no outcomes studies to demonstrate that lowering these levels leads to clinical benefit for patients with PVD

85
Q

imaging for PVD/PAD

A

Duplex ultrasonography (DUS)/Doppler ultrasonography

Magnetic resonance angiography (MRA) or computed tomography angiography (CTA)

Digital subtraction angiography (DSA) and catheter-based angiography

Transcutaneous oximetry

ECG

86
Q

Duplex ultrasonography (DUS)/Doppler ultrasonography

A

safe and cost-effective method of determining PAD location, stenosis severity, and length of stenosis or occlusion

  • Sensitivity and specificity depend on presence of calcium in the arterial wall, location or depth of the vessel, and the presence of multiple occlusions at different locations
  • Doppler ultrasonography - used in routine follow-up post-procedure for surveillance of patency, can assist in decision-making when further intervention is contemplated
87
Q

Magnetic resonance angiography (MRA) or computed tomography angiography (CTA)

A

excellent high-quality vascular imaging, useful for determining candidacy for bypass surgery versus angioplasty

MRA - identify small runoff vessels that sometimes may not be seen with digital subtraction angiography (DSA)

88
Q

Digital subtraction angiography (DSA) and catheter-based angiography

A

for determining lesion localization, best used when invasive or surgical intervention (endovascular revascularization) may be indicated

  • Catheter-based angiography the gold standard for diagnosing PAD
89
Q

Transcutaneous oximetry

A

a rapid method of assessing perfusion in patients with ulcers

90
Q

ECG

A

may reveal the presence of an arrhythmia which may be the cause of an embolic event

91
Q

what is the gold standard for diagnosing PAD

A

Catheter-based angiography

92
Q

CHART slide 55

A
93
Q

differential diagnosis for claudication

A

musculoskeletal
-arthritis
-chronic compartment syndrome
-medial tibial stress syndrome
-muscle strain
-symptomatic baker cyst

neurologic
-nerve entrapment
-nerve root compression
-peripheral neuropathy
-spinal stenosis

vascular
-deep venous thrombosis
-popliteal artery entrapment
-vasculitis
-venous insufficiency

94
Q

neurogenic claudication (spinal stenosis)

A
  • Compression of the spinal nerves or nerve roots, especially in the lumbar vertebrae
  • Caused by the narrowing of the central canal, the lateral recess, or neural foramen
  • most commonly is caused by degenerative osteoarthritis of the spine or spondylosis
  • also disc protrusion or bulging (i.e.,caused by progressive disc degeneration with aging or trauma), loss of disc height, facet joint arthropathy, osteophyte formation,
    or ligamentum flavum hypertrophy
95
Q

risk factors of neurogenic claudication (spinal stenosis)

A

obesity or family history of spinal stenosis

96
Q

what happens in neurogenic claudication (spinal stenosis)

A

Combination of low back pain, leg pain, numbness and motor weakness that starts or intensifies on standing or walking and is eased by sitting or lying down

97
Q

signs and symptoms of neurogenic claudication (spinal stenosis)

A

combination of low back pain, leg pain, numbness/parasthesia and motor weakness that starts or intensifies with ambulation (i.e. pseudoclaudication)
*
* Radiating leg pain may be down entire leg, bilaterally/asymmetrically
* Difficulty walking and gait disturbances

  • Lumbar extension increases, and flexion decreases pain
  • Pain worse:walking, standing, or upright exercises
  • Pain better: sitting or forward flexion at the waist (squatting, leaning forward), or lying down
98
Q

neurological exam for Neurogenic Claudication (Spinal Stenosis)

A

focal weakness, absent deep tendon reflexes, or sensory loss

99
Q

symptom categorization for Neurogenic Claudication (Spinal Stenosis)

A

categorized as mild, moderate, or severe, based on the extent of leg pain and pain- related disability

  • Severe symptoms - exercise intolerance, greatly restricted walking capacity, may have bladder dysfunction (i.e., urinary incontinence)

*
Maybe asymptomatic when inactive

100
Q

what makes pain better or worse in Neurogenic Claudication (Spinal Stenosis)

A
  • Lumbar extension increases, and flexion decreases pain
  • Pain worse:walking, standing, or upright exercises
  • Pain better: sitting or forward flexion at the waist (squatting, leaning forward), or lying down
101
Q

what group of people is Neurogenic Claudication (Spinal Stenosis) common in

A

elderly adults

102
Q

what can Neurogenic Claudication (Spinal Stenosis) lead to

A

cauda equina syndrome

103
Q

treatment options for Neurogenic Claudication (Spinal Stenosis)

A
  • Conservative treatment-pain-relieving agents for mild symptoms
  • Decompressive surgery - to remove the bone and ligaments around the stenosis for severe symptoms
  • Varies – for moderate symptoms
104
Q

significant morbidity and quality of life effects in Neurogenic Claudication (Spinal Stenosis)

A

Can lead to chronic pain and muscle weakness, may interfere with activities of daily living and result in progressive disability

105
Q

what are the 2 things that venous thromboembolism includes

A

Venous thromboembolism (VTE) is a blood clotting condition and includes deep-venous thrombosis (DVT) and pulmonary embolism (PE)

  • ~1/3 of patients present with PE
  • ~2/3 of patients present with DVT
106
Q

what is the 3rd most common life threatening cardiovascular disease in the US

A

Venous Thromboembolism

after MI and stroke

107
Q

what does Venous Thromboembolism cause

A

Causes cardiovascular death, chronic disability, and emotional distress

108
Q

CDC statistics for venous thromboembolism

A
  • Annual incidence of VTE is one or two per 1,000 persons
  • Overall mortality rate is between 60,000 and 100,000 annually
  • One-half of patients with DVT will have long-term complications, including post-thrombotic syndrome and venous ulcers
  • PE is more often fatal, has a higher recurrence rate, and is associated with more serious long-term complications
  • One-third of patients with VTE will have a recurrence within 10 years
109
Q

deep vein thrombosis vs pulmonary embolism [both part of venous thromboembolism]

A

DVT: blood clot forms in deep vein, most often leg

–>symptoms: pain, swelling, redness in the area, dilation of the surface veins, skin warm to touch

PE: clot blocks blood supply to part of the lung AND part of blood clot breaks off and travels to lungs

–>symptoms: SOB, chest pain, rapid HR, coughing blood, lightheaded

110
Q

what is the Virchow triad

A
  1. hyper coagulability (blood)
  2. circulatory stasis (flow)
  3. vascular damage (vessel)
111
Q

DIAGRAM SLIDE 61

A
112
Q

vascular damage

A

I.e.
thrombophlebitis
cellulitits
atherosclerosis

from physical trauma or micro trauma to vessel

113
Q

circulatory stasis

A

i.e. varicose veins, atrial fibrillation, venous obstruction

from low heart rate low BP or congenital abnormalities

114
Q

hyper coagulability

A

I.e. pregnancy, infection, IBD, autoimmune, malignancy

from estrogen therapy, inflammation,, dehydration

115
Q

what % of patients with proximal lower extremity deep vein thrombosis develop a pulmonary embolism

A

50-60%

116
Q

what is hypoxemia (in a pulmonary embolism)

A

Vascular obstruction leading to dead space ventilation, right-to-left shunting, and
decreased cardiac output

117
Q

what are the symptoms of pulmonary embolism

A
  • *Dyspnea
  • Pleuritic chest pain
  • Tachypnea
  • Cough
  • Syncope
  • Less common: tachycardia, hemoptysis, hypoxia, hypotension, fever, cyanosis, shock (alone or in combination)
  • May have concomitant signs/symptoms of DVT
118
Q

deep vein thrombosis symptoms

A

Classic clinical presentation: swelling, pain, warmth, and redness in the involved extremity

  • May be asymptomatic
  • Individual symptoms are neither sensitive nor specific for DVT
119
Q

differential diagnosis for deep vein thrombosis

A

trauma, infection, peripheral artery disease, and other venous diseases

  • DVT can coexist with any of these disease processes
120
Q

well’s score clinical prediction rule for pulmonary embolism

A

SLIDE 64

i.e. alterative diagnosis less likely that PE, clinical signs and symptoms of DVT = give higher score for pretest probability

121
Q

Wells’ score clinical prediction rule for DVT
SLIDE 65

A

i.e. add a point if have active cancer, paralysis of lower extremities, bed ridden = all increase pre test probability

122
Q

what is risk stratification for in pulmonary embolism

A
  • Massive (high-risk) PE - 5–10% of patients, systemic arterial hypotension and extensive thrombosis affecting at least half of the pulmonary vasculature
  • Dyspnea, syncope, hypotension, and cyanosis
  • May present in cardiogenic shock and can die from multisystem organ failure
  • Submassive (intermediate-risk) PE - 20–25% of patients, RV dysfunction despite normal systemic arterial pressure - high risk of clinical deterioration
  • Low-risk PE - 65–75% of patients, have an excellent prognosis
123
Q

lower extremity DVT

A

usually begins in the calf and can propagate proximally to the popliteal, femoral, and iliac veins

124
Q

upper extremity DVT

A

often precipitated by placement of pacemakers, internal cardiac defibrillators, or indwelling central venous catheters

125
Q

what’s more common, lower or upper extremity DVT

A

lower leg DVT is 10x more common

126
Q

superficial venous thrombosis

A

usually presents with erythema, tenderness, and a “palpable cord.” Patients are at risk for extension of the superficial vein thrombosis to the deep-venous system.

127
Q
A
128
Q

prevalence of AAA

A

Study of 210 patients with PAD and an average age of 65 years, the prevalence of abdominal aortic aneurysm was 9.0%, rising to 15.8% in patients older than 75 years

  • The prevalence of abdominal aortic aneurysm in the general population is only 4% to 7.6%
129
Q

symptoms of AAA

A

majority of AAA remains asymptomatic until which time rupture or less commonly rapid expansion occurs leading to severe and unrelenting abdominal pain radiating to the back or a pulsatile abdominal mass

130
Q

imaging for AAA?

A

ultrasonography for abdominal aortic aneurysm is reasonable in patients with symptomatic PAD

131
Q

PVD/PAD rate of disease progression

A

rate of disease progression to rest pain (severe ischemic pain due to insufficient arterial inflow), critical limb ischemia (gangrene, ulceration, or tissue loss), and subsequent amputation is low—on the order of 10% over 10 years or 2.5% annually

132
Q

over 5 years in patients with PAD

A
  • 70-80% have stable claudication
  • 10-20% have worsening claudication with rate of disease progression to rest pain (severe ischemic pain due to insufficient arterial inflow)
  • 1-2% may progress to acute or critical limb ischemia (gangrene, ulceration, or tissue loss) and subsequent amputation
133
Q

rate of limb amputation in 5 years with those with PAD

A

1-4%

134
Q

complications of PAD

A
  • Ischemia/Gangrene
  • Amputation
  • Infection
  • Ulceration
  • Coronary artery disease and myocardial infarction
  • Stroke
  • Blood clots
  • Erectile Dysfunction
  • Depression
135
Q

ABI testing and prognosis in PAD

A
  • Repeat ABI testing with any changes in functional status, order further testing, or refer the patient to a vascular subspecialist
  • ABI < 0.9 associated with a two-fourfold relative risk increase for cardiovascular events and all-cause mortality
  • Systematic review: ABI measured at baseline and tracked coronary heart disease, stroke, and all-cause mortality in patients who had not had a previous myocardial infarction or stroke
  • a low ABI was 92.7% specific for predicting incident coronary heart disease
  • At five years, 20% of patients with PAD had a nonfatal myocardial infarction, and 15% to 30% died; three-fourths of these were cardiovascular deaths
136
Q

prognosis of PVD

A

higher mortality rate

  • Study: 1,592 patients (men and women) from Scotland who were followed prospectively for five years with PVD
  • all-cause mortality rate of 3.8%/year for patients with PVD and claudication and 6.1%/year for patients with PVD and no symptoms, compared to 2.0%/year in the control group
  • No data to demonstrate that early identification of patients with PVD is beneficial in terms of mortality or morbidity reduction
137
Q

10 year mortality rate in those with PAD

A

risk factors: renal dysfunction, heart failure, age>65, hypercholestemia, etc… increase risk of mortality

138
Q

medication for PAD/PVD

A

statin and either aspirin or cilostazol

139
Q

surgery and emergency for PAD/PVD

A
  • Surgical revascularization should be considered in patients with lifestyle-limiting claudication symptoms that do not respond to exercise and pharmacologic treatment
  • Emergent consultation for arterial reconstruction is indicated in patients with critical limb ischemia
140
Q

health care team for PAD/PVD

A
  • Healthcare team: family doctor, nurses and pharmacists, vascular specialist/surgeon, endocrinologist interventional radiologist
  • Ensure that the patient is not on any medications that can lead to vasoconstriction
  • Educate about basic foot hygiene and wear protective shoe wear
  • Educate on signs of vascular disease and seek assistance if any changes occur
141
Q

prevention is key for PAD/PVD

A
  • Changes in lifestyle can significantly decrease the rate of progression of the disease and improve the quality of life
  • Primary prevention of PVD - encourage smoking cessation, maintain a healthy weight and control blood sugars, exercise, control blood pressure and cholesterol
  • *Smoking is the most significant modifiable risk factor
  • Exercise has been shown to increase walking time of patients with claudication by 150%
  • Aspirin reduces risk of serious vascular events - with doses of 75-150 mg being as effective as higher doses
  • Treat hypercholesterolemia with appropriate dietary modification and lipid- lowering agents, as needed.
  • Pursue aggressive blood pressure reduction
142
Q
A

CMS200 (18 decks)

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