Module 6 Vascular Disorders Flashcards
What is the cause, risks factors, & common sites of Peripheral Artery Disease (PAD)
Cause: •atherosclerosis (abnormal; plaque build-up. Alters blood flow by narrowing of arteries)
•gradual thickening of intima and media
Risk Factors: cigarette/tobacco smoking, DM, HTN, high cholesterol, > 60 y/o
SITES: iliac, femoral, popliteal, tibial & peroneal arteries
S/S of Peripheral Arterial Disease (PAD)
•Intermission claudication (goes away with rest)
•paresthesia (nerves- need blood supply to function- common comorbidity DM)
• visual inspection (shiny, thin, taut skin, hairless -no oxygen to the tissues)
•pallor (pale- happens when legs are elevated)
•Rubor (red skin, rush of blood to extremity)
•pain at rest (late sign)
•critical limb ischemia
What is the Progression of PAD Pain?
•intermittent claudication (caused by exercise, resolved with rest)
•rest pain (laying down, limbs are same level as heart , blood flow isn’t moving back and forth. Pt’s may sleep w/legs dangling or in chair
•critical limb ischemia (rest pain lasting more than 2 wks, non-healing ulcers)
- move bed into reverse Trendelenburg (feet lower than head for blood flow)
What are the diagnostics for PAD?
1 ultrasound
#2 find pulses (use Doppler if needed)
•Doppler
•Angiography
•Ankle/Brachial Index (Doppler on each extremity for very accurate BP)
H&P:
•Disappearing pulse
•Segmental BPs (cuff on all extremities one at a time to see if there’s a drop in lower extremity BP)
Arterial ulcer overview
•“Punched out” look
•lateral side (outside) ankle/foot/toes
•Dry
•dry dressings
•healing won’t take place if blood flow doesn’t improve
3 Medication classes for Arterial Ulcers?
ACE inhibitors
Statins
Anti-platelets
What Ace Inhibitors tx arterial ulcers?
1 Ramipril, enalapril, lisinopril
What Statins are tx for arterial ulcers?
Atorvastatin, simvastatin
Which anti-platelets are tx for arterial ulcers?
ASA, clopidogrel (Plavix)
What are the 4 pillars of collaborative care for vascular disorders?
•Lifestyle changes (smoking, nutrition, exercise)
•Drug therapy (ace inhibitors, statins, anti-platelets)
•Patient education (cleaning wounds, footwear, positioning. NO tight clothes/shoes or compression socks)
•Revascularization (interventional radiology and surgical therapy)
What are two surgeries to bypass plaque in arteries?
•“Femoral- popliteal” bypass
-Donor vein, makes a bypass for blood flow
•Femoral endovascular procedure
Common to go in one iliac side and work on affected extremity/ vessel.
-Place stent or remove plaque
What is an acute arterial occlusion?
May start in the heart (example: A-fib) and can move to systemic circulation.
Sudden without warning
•Causes: embolism, occlusion of an already narrowed artery, trauma
•Assessment: 6 Ps
•Emergent management
•Anticoagulant therapy, surgical intervention (remove clot)
What are the 6 P’s?
Pain
Pallor
Pulselessness (acute= fast, PAD= could be later sign)
Paresthesia
Paralysis (latest sign)
Poikilothermia (cool temperature)
What is the pathophysiology of Buerger’s Disease?
Pathophysiology: Inflammatory, thrombotic disorder
•Occurs only in smokers & improves once stopped. Mostly in men (25-40). •can be Familial
•Acute or chronic
What is the diagnosis and treatment of Buerger’s disease?
•Diagnosis: Based on history, symptoms, age of onset
•Treatment: Protect limb from injury (no tight or constricting clothes. Clean and treat cuts/scrapes quickly)
& stop smoking
What is the pathophysiology of Raynaud’s phenomenon? (* = test)
•Transient (comes & goes)/episodic arterial spasm of small cutaneous ARTERIES
•Contributing Factors: most common in women, lupus, thyroid disease
•Cold environment, Underlying disease
•Assoc w progressive triphasic color change of the skin from pallor, cyanosis, rubor (WHITE, BLUE, RED)
What is the patient education and medication’s for Raynaud’s phenomenon? 
Patient teaching =
•Protection from cold, avoid tobacco & caffeine, *avoid cold meds like pseudoephedrine- causes vasoconstriction/ impedes blood flow
•Medications
•CCB (relaxes vasospasms)
•Vasodilators (increase blood flow)
Explain the triphasic color change of Raynaud’s phenomenon
Phase 1: pallor (white)
• blood flow to capillaries is impeded, resulting in digital ischemia
Phase 2: cyanosis (blue)
• capillaries and venules dilate in response to ischemia, and are filled with deoxygenated blood
Phase 3: Rubor (red)
• Capillaries are still dilated, but are now carrying oxygenated blood
(blood rush)
Explain the pathophysiology causes signs and treatment of phlebitis 
Pathophysiology =
•Acute inflammation of the vein walls
•Causes = Irritation from catheter, infusion of irritating drugs, catheter location
•Signs = Pain, tenderness, warmth, erythema, swelling, palpable cord
•Treatment = #1 remove catheter*, elevate extremity (to reduce edema/pain/throbbing), apply warm/moist heat (vasodilation)
Explain the pathophysiology, signs, and diagnostics for Venous thrombosis
Pathophysiology = Virchow’s Triad – Venous stasis, Endothelial Damage, Blood Hypercoagulability
•Signs: Superficial: palpable, firm, cordlike vein. Deep veins: Unilateral edema, erythema, pain, paresthesia
•Diagnostics: Ultrasound & D-dimer
look at slide/book pg. 814 for important chart
What is a VTE? (Venous thromboembolism)
Detached thrombus results in embolus
Travels through venous system to right side of the heart and lodges in pulmonary circulation, becomes a PE
•Turbulent blood flow—major factor in embolization - it can break off and cause the clot to travel. Endothelial lining damage.
What does a vena cava interruption Device do?
Surgical procedure where they can enter through the neck or groin. It’s a basket- type device that catches clots before it returns to the heart. Blood flow is not impeded and this solution is good for people who cannot take anticoagulants. (Major fall
Risk, GI bleed*) It is permanently placed and the body will naturally break down clots. The device is just to keep them from traveling in the bloodstream.
Explain post thrombotic syndrome, pathophysiology
Pathophysiology:
•Results from chronic inflammation & venous HTN
•Damage to vein wall
•Can lead to venous ulcerations
*serious complication:
Weakened valves that lets blood flow the wrong way is called reflux .
•Symptoms: pain, aching, edema, venous dilation, reflux —-> leads to ulcerations
Pathophysiology, causes, signs, and tx of varicose veins
Pathophysiology = Dilated, tortuous (twisted) superficial veins in the lower extremities
•Causes: weakened vein walls
•Primary (women/hereditary) vs Secondary (injury, previous DVT)
•Signs = Heavy, achy feeling, burning, itching
•Treatments = Conservative management (compression socks- put on in the morning- problems are worse when standing/sitting) vs sclerotherapy (saline inj to veins. Can take 2 years to see results)
Pathophysiology, causes, signs of Chronic Venous insufficiency
Pathology = Ambulatory venous hypertension (too much pressure in leg veins when standing, blood refluxes) , chronic inflammatory changes (iron breakdown - Hemosiderin color change)
•Causes = weakness of valves/ reflux,
Hx varicose veins or post-thrombotic syndrome
•Signs = Leathery, brownish appearance, Venous ulcers
Tx of Venous leg ulcers
Treatment:
•Compression(make sure Pt does not have PVD) , avoid sitting or standing for long periods
•Wound care (wet dressings, possible wound vac)
These are generally wet, draining wounds, nutrition is important for healing (high in protein), 4-6 wks healing
What are the 10 Vascular Disorders in this module we need to know?
•Peripheral arterial disease (PAD)
•Arterial occlusion
•Buerger’s Disease
•Raynaud’s phenomenon
•Phlebitis
•Venous thrombosis/thromboembolism (VTE)
•Varicose veins
•Chronic venous insufficiency
•Arterial ulcers
•venous ulcers
What are the 6 medication classes needed to know for this module?
•Ace inhibitors (ramipril, enalapril, lisinopril)
•statins (atorvastarin, simvastatin)
•calcium Chanel blockers (nifedipine)
•Vasodilators (nitroglycerin)
•anti-platelets (ASA, Plavix/clopidogrel)
•anticoagulants (Heparin, lovenox, warfarin/Coumadin)
Ramipril (Altace) overview
Class: ACE inhibitor
MOA: inhibits ACE which is responsible for for converting Angiotensin 1 to angiotensin 2. —> BP is lowered
Side effects: fatigue, dizziness, mood changes, headache, dry cough, loss of taste, hyperkalemia, angioedema, renal impairment
Enalapril (vasotec) overview
Class: ACE Inhibitor
MOA: inhibits ACE which is responsible for converting Angiotensin 1 to angiotensin 2. —> BP is lowered
Route : PO
Side Effects: hypotension, angina, headache, fatigue, dizziness, constipation, N/V
Lisinopril (Prinivil) overview
Class: ACE inhibitor (
MOA: inhibits ACE which is responsible for for converting Angiotensin 1 to angiotensin 2. —> BP is lowered
Side effects: dizziness, hypotension, hyperkalemia, headache
Atorvostatin (Lipitor) overview
Class: cholesterol lowering drugs: statins
MOA: Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL.
Route: PO, daily, at dinner or bedtime
Side effects: UTI, hemorrhagic stroke, musculoskeletal pain, nausea, diarrhea
Simvastatin (Zocor) overview
Class: statins (lower cholesterol)
MOA: Bile acid sequestrations bind bile and prevent resorption of the bile acids from the small intestine. An insoluble bile acid and resin complex is formed, and then excreted in the stool. 
Side effects: constipation, heartburn, nausea, belching, bloating
Nifedipine (procardia) overview
Class: Calcium Channel Blocker
MOA: Preventing calcium from entering into this process, prevents muscle contraction and promotes muscle relaxation. relaxation of smooth muscles that surrounds the coronary arteries causes them to dilate. The dilation increases blood flow to the ischemic heart, which in turn, increases the oxygen supply and shifts the demand ratio back to normal.
Side effects: hypotension, palpitations, tachycardia, constipation, nausea, peripheral edema
Nitroglycerin
Class: Vadodilators
MOA: primary effects related to cardiovascular system. Expands blood vessels through vasodilation
Side effects: headache, tachycardia, postural hypotension
Heparin overview
Anticoagulant with Quick onset of action but have a shorter 1/2 life
•Given IV or SQ
•For short term use
•Monitor aPTT
•Therapeutic Range 46-70
•Antidote: Protamine Sulfate (not normally given, just wait for it to wear off)
Warfarin/Coumadin overview
• anticoagulant with Slower onset of action but Longer 1/2 life
•Given PO
•For life-long therapy
•Monitor: PT/ INR
•Therapeutic Range: 2-3 OR 2.5-3.5 for heart valve (Patient may be on heparin drip first to get to TR then stop trip)
•Antidote: Vitamin K
• consumption of vitamin K should be consistent not increasing or decreasing in patient’s diet.
Lovenox/enoxaparin overview
•Enoxaparin (Lovenox) = Anticoagulant/Low molecular weight heparin
•Administered SQ (5/8needle) , 2” from umbilicus (better absorption!)
•Pre-packed with “airlock” (seals in medication to injection site)
•Monitor platelet count before administering (if less than 100 ask if it needs to be held)
