Anticoagulants/ assessment and management of vascular disorders Flashcards
Pathophysiology of blood/lymphatic vessels
- Obstruction of blood and lymphatic vessels occur d/t atherosclerosis (plaque buildup), thrombus, embolus, or congenital malformations.
- Chemical or mechanical trauma.
- Infection or inflammation.
Remember that thrombi or emboli obstructs venous valves (reduced blood flow) and lymphatic vessels. Obstructed vessels = swelling and edema. Edematous (think edema= swelling with fluid) tissue results in injury or infection.
Arteriosclerosis vs atherosclerosis
Arteriosclerosis (think arTERIOsclerosis like deTERIOration): hardening of arteries especially with age.
Atherosclerosis: Affects intima large and medium arteries. Also caused by accumulation of lipids, calcium, blood components, carbohydrates, and fibrous tissue.
Intermittent claudication
When there is buildup in arteries, oxygen rich blood can’t get to the muscles. When walking, your leg muscles need more oxygen, but if the arteries in legs are narrowed, the lack of oxygen will cause pain and cramping when walking.
(side note: Artery build up obviously not exclusively located in legs)
Radiologic interventions
Angioplasty (PTA):
Balloon tipped catheter is inserted into an area of stenosis (narrowing). This decreases the risk of re-occlusion. The stent is used to support the walls of blood vessels and prevent collapse.
Peripheral vascular disease risk factors
Hypertension Dyslipidemia Cigarette smoking Diabetes Obesity Sedentary lifestyle Foods high in trans fats/triglycerides
Clinical manifestations of Arterial occlusion/5 Ps
Pain Pallor Pulselessness Paresthesia (pins and needles) Paralysis
Arterial insufficiency
Pain/ Intermittent claudication
Pulses- decreased or absent
Temperature- cool
Color- rubor, cyanotic, pallor
Edema- none
Gangrene (tissue death)- may develop
Venous insufficiency
Pain- none to aching
Pulse- normal
Temperature- normal
Color- brown pigmentation
Edema- present
Gangrene (tissue death)- does not develop
Cholesterol labs and foods
Total cholesterol should be less than 200!!!. To calculate:
cholesterol - HDL= total cholesterol
Ideally:
HDL ( good)- greater than 60 mg/dL
LDL (bad)- less than 150 mg/dL
Triglycerides- less than 150, better 100 mg/dL
(values from CDC)
To lower cholesterol, eat oats, whole grains, fruits, veggies, beans, fish high in omega 3 fatty acids… limit salt and alcohol.
Antilipemics/Statins/HMG-CoA reductase inhibitors
end in -STATIN.
Action:
HMG–CoA reductase inhibitors block HMG–CoA reductase from completing the synthesis of cholesterol.
Medications:
- Atorvastatin
- Simvastatin
- Lovastatin
They lower abnormal blood lipid levels.
Make sure to monitor serum liver function.
Dont eat/drink grapefuit. It may increase the level of statins and have negative adverse effects. For example, rhabdomyolysis can occur, which breaks down muscle and and releases the muscle fiber into the blood stream. It hurts the kidneys and damages cells… leading to extreme muscle pain and fatigue.
Venous Thrombus
For thrombosis to occur, you need 2 out of 3 of Virchows Triad present…
- Stasis of blood
- Vessel wall injury
- Altered blood coagulation
Platelets attach to venous walls forming an appendage which travel the direction of the blood flow, then break off and occlude veins, creating an embolic occlusion.
Medical management of thrombus
- Prevent thrombus formation by wearing elastic pressure stockings, intermittent sequential compression devices, or exercise.
- Anticoagulant therapy: Heparin sulfate:
- IV bolus of 5,000-10,000 units
- Followed by continuous heparin @ units per hour via pump, and is weight based.
Antagonist- protamine sulfate ( reverse effects of heparin)
DIagnostic:
APTT (activated partial thromboplastin time)
PTT (partial thromboplastin time)
Heparin
-Parenteral (IV). Works FAST, but only lasts a few hours!
Actions:
- enhances antithrombin III, inhibits thrombin and stops conversion of fibrinogen to fibrin.
- block the formation of thrombin from prothrombin (Book says both actions)
Heparin sulfate:
- IV bolus of 5,000-10,000 units
- Followed by continuous heparin @ units per hour via pump, and is weight based.
Antagonist- protamine sulfate ( reverse effects of heparin)
Diagnostic: APTT (activated partial thromboplastin time) or PTT (partial thromboplastin time)
APTT: time of 1.5 to 3 times the normal rate
PTT: 1.5 to 2.5 (?)
WBCT (whole blood clotting time): 2.5-3
Warfarin
Works SLOW, lasts for days!
Oral anticoagulation therapy used to PREVENT thromboembolic conditions.
Actions:
Inhibits hepatic synthesis of vitamin K, affecting clotting Factors II, VII, IX, and X. Remember vitamin K aids clotting. If it is inhibited, then you can’t clot!!
Given within 24 hours AFTER heparin therapy given concurrently.
Watch your garlic intake!
Monitor:
- PT (prothrombin time)- therapeutic range is 1.5-2.5 times the control time).
- INR (international normalized ratio)- therapeutic range 2.0-3.0
Agonist: Vitamin K aka phytonadione. Vitamin K found in green leafy veggies. Watch your intake of vitamin K when on warfarin!
Even though vit K is an antahonist, it would take 48-72 hours for clots to develop again.
Anti platelet aggregator
Decrease the formation of the platelet plug by decreasing the responsiveness of the platelets to stimuli that would cause them to stick and aggregate on a vessel wall. Antiplatelet agents inhibit platelet adhesion and aggregation by blocking receptor sites on the platelet membrane, preventing platelet–platelet interaction or the interaction of platelets with other clotting chemicals. Prevent blood clots!!!
- Aspirin (acetylsalicylic acid)
- Clopidogrel
- Ticlopidine
Rememember CLO= CLOT
Side effects are thrombocytopenia or active bleeding.
