Unit 9 Cardiovascular system: DVT, HTN, Atherosclerosis, CAD, HF, PDA-VSD, Kawasaki Disease
Terms in this set (55)
blood clot that remains attached to a vessel wall
blood clot that detatches
Which type of thrombi are more common- venous or arterial?
Venous : blood flow and pressure are lower in the veins than in arteries
Deep Vein Thrombosis (DVT)
clot formation in large veins, mostly in the lower extremities. May result in VTE (venous thromboembolism) to the pulmonary circulation.
How many estimated occurrences of VTE occur annually (according to the AHA) and how many are fatal?
What three factors promote venous thrombosis:
Triad of Virchow:
1. venous stasis (immobility, obesity,prolonged leg dependency-airplane ride, age, heart failure (HF)
2. venous endothelial damage (trauma, meds)
3.hypercoagulable states (clotting disorders, malignancy, pregnancy, birth control, hormone replacement, hyperhomocysteinemia, antiphospholipid syndrome)
What genetic abnormalities are associated with an increased risk of VTE?
*those related to hypercoagulability
*factor V Leiden mutation
*deficiencies of protein C, protein S and antithrombin
If someone develops a thrombi and doesn't have the usual risk factors, what should be suspected?
What leads to venous thrombus formation, usually near a valve?
accumulation of clotting factors and platelets
What happens when there is inflammation surrounding the thrombus?
*further platelet aggregation
*thrombus propagation and proximal growing
what happens if there is a clot deep in the vein?
there aren't clinical symptoms or signs. If there is a significant obstruction to the venous blood flow, increased pressure behind the clot can cause edema to the extremity
If untreated, a DVT can lead to what?
thromboembolization of part of the clot from the leg to the lung which leads to pulmonary embolism
In 1/3 of those with a DVT, this can happen if there is persistent venous outflow obstruction:
post thrombolytic syndrome (PTS)
What characterizes post thrombolytic syndrome?
chronic, persistent pain, edema and ulceration of affected limb
prophylactic treatment of dvt:
low molecular weight heparin
For those at high risk for a PE , this procedure is necessary to prevent one from forming:
inferior vena caval filter
diagnosis of DVT
lower extremity ultrasound
What is a DVT treated with?
unfractionated IV heparin
adjusted SQ heparin
When is thrombolytic therapy used?
when there is a large clot in the proximal vein, used to dissolve the clot quicker and reduce risk of postphlebotic syndrome
What does pharmacomechanical treatment involve?
catheter mediated removal of clots, used in select individuals
If there are no identifiable underlying conditions or unprovoked occurrence, can dvt be reversed?
YES! There is a 26% recurrence rate, 5 years after the discontinuation of of anticoagulation therapy
What can be given to individuals who stop anticoagulatants to reduce recurrence rates?
Superior Vena Cava Syndrome (SVCS)
a progressive occulsion of the superior vena cava that leads to venous distention of the upper extremities and head
What is the leading cause of SVCS?
bronchogenic cancer 70%
metastasis of other cancers
What are some benign causes of SVCS?
benign tumors such as retrosternal goiter
What can lead to acute and chronic SVCS?
invasive therapies such as pacemaker wires, central venous catheters, pulmonary artery catheters
which mainstem bronchus could be obstructed with SVCS?
THe RIGHT mainstem bronchus:
cancers occuring at this site could obstruct venus return to the right atrium
What type of node gets involved with SVC?
lymph nodes: they surround the SVC and form chains that can be involved with thoracic cancers, compressing the SVC during growth of the tumor
Clinical manifestations of SVCS:
*edema and venous distention of upper extremities & face
*fullness in the head
*c/o their shirt collar, necklaces & rings being tight
***last 3 caused by cerebral and CNS edema
*purple color of face/arms
*skin of face/arms become taut
*Prolonged cap refill time
*resp distress due to edema/compression of bronchial structures due to carcinoma
Diagnosis of SCVS:
How is SCVS treated:
As an oncologic emergency
* if malignant: radiation, chemo, diruetics, steroids, anticoagulants
*non malignant: bypass surgery w/grafts, thrombolysis, balloon angioplasty, intravascular stents
what is atherosclerosis?
thickening and hardening of a vessel that is caused by an accumulation of lipid laden macrophages within the arterial wall.
WHat does artherosclerosis lead to?
formation of plaque
What is the leading cause of coronary artery and cerebrovascular disease?
Atherosclerosis is what type of disease?
inflammatory that develops and proceeds when there is elevated serum plasma cholesterol levels present
Possible causes of endothelial injury which in turn causes atherosclerosis?
increased LDL and HDL levels
elevated C reactive protein
incrased serum fibrinogen
once injured, dysfunction and inflammation of endothelial cells lead to:
1. inability to make normal amounts of antithrombotic and vasodilating cytokines
2. release of many inflammatory cytokines ( TNF-a, IFN-y, IL-1), toxic oxygen radicals, CRP and heat shock proteins
3.adhesion of macrophages to injured endothelium
4. enzymes and toxic oxygen radicals are realeased which further injures the vessel wall
5. release of growth factors ( angiotensis II, fibroblast growth factor, TGF-b, platelet derived growth factor. This stimulates smooth muscle cell proliferation in the affected vessel.
What causes aggregated LDL to become oxidized?
activation of macrophages
What contributes to an increased LDL oxidation?
What does oxidized LDL do?
*toxic to endothelial cells
*causes smooth muscle proliferation
*increases endothelial adhesion molecule expression(this causes more monocyte/macrophage to penetrate the vessel wall)
Oxidized LDL that fill macrophages are?
Lesion formed by an accumulation of lipid laden foam cells are?
What do fatty streaks cause once formed?
immunologic and inflammatory changes, causing more progressive damage o the vessel wall.
result of smooth muscle cell proliferation and collagen production. They migrate over fatty streaks forming this.
Complications of figrous plaque
protrudes into the vessel lumen
obstructs blood flow to distal tissues (usually during exercise)
ANGINA or INTERMITTENT CLAUDICATION
may rupture before they affect the blood flow, are 'clinically silent' until they rupture
plaques that have ruptured
What happens when plaque ruptures?
*platelet adhesion to the exposed underlying tissue
*intitation of clotting cascade
*occlusion of the affected vessel may occur from rapid thrombus formation. This can result in ischemia or infarction.
What medication is given to prevent atherosclerosis?
clinical manefestation of atherosclerosis
Caused by inadequate tissue perfusion due to the vessel obstruction
* TIA's may occur due to partial vessel obstruction
What is a major cause of MI and one of the most important health issues in the US?
CAD caused by atherosclerosis
What is a major cause of stroke in the US?
atherosclerotic obstruction of the blood vessels supplying the brain
Assessment of atherosclerosis?
completel health history
arterial bruits present?
evidence of decreased blood flow to tissues?
labs tests: lipids, glucose, CRP
radiographic tests: xray, ecg, us, nuclear scanning, ct, mri, angiography
what is the current treatment focus?
to detect and treat preclinical lesions with drugs that stabilize and reverse plaque before they rupture
primary goal is manage the atherosclerosis so that adequeate blood flow is restored to the affected tissues.
Prevention tools with atherosclerosis
control of HTN/Diabetes
reduce LDL by diet or meds
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