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adn semester 2 > CH 37 Vascular Disorder > Flashcards

CH 37 Vascular Disorder Flashcards

1
Q

include disorders of the arteries, veins, and lymphatic vessels.

A

Problems of the vascular system

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2
Q

coronary, cerebral, peripheral, mesenteric, and renal artery disease

A

Atherosclerotic vascular disease is divided into

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3
Q

involves thickening of artery walls.

A

Peripheral artery disease (PAD)

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4
Q

results in a progressive narrowing of the arteries of the upper and lower extremities.

A

Peripheral artery disease (PAD) pathophysiology

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5
Q

is a marker of advanced systemic atherosclerosis

A

PAD

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6
Q

atherosclerosis, a gradual thickening of the intima (the innermost layer of the arterial wall) and media (middle layer of the arterial wall). This results from cholesterol and lipids deposited within the vessel walls and leads to narrowing of the artery

A

leading cause of PAD is

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7
Q

are tobacco use (most important), diabetes, hypertension, high cholesterol, and age over 60.

A

risk factors for PADg

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8
Q

are tobacco use (most important), diabetes, hypertension, high cholesterol, and age over 60

A

Important risk factors for PAD

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9
Q

Lower extremity PAD may affect the iliac, femoral, popliteal, tibial, or peroneal arteries, or any combination of these arteries

A

PAD of lower extremity affected

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10
Q

femoral popliteal area is the

A

most common site in nondiabetic patients (PAD affected)

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11
Q

the arteries below the knee.

A

Patients with diabetes tend to develop PAD in

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12
Q

Those with advanced PAD often have multiple arterial occlusions.

A

advanced PAD

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13
Q

depends on the site and extent of the blockage and the amount of collateral circulation

A

severity of PAD symptoms

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14
Q

is intermittent claudication

A

classic symptom of lower extremity PAD

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15
Q

This ischemic muscle pain is caused by exercise, resolves within 10 minutes or less with rest, and is reproducible. The ischemic pain is due to the buildup of lactic acid from anaerobic metabolism.

A

PAD is intermittent claudication.

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16
Q

claudication in the buttocks and thighs

A

PAD of the iliac arteries causes

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17
Q

femoral or popliteal artery involvement.

A

Calf pain indicates

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18
Q

in erectile dysfunction.

A

PAD involving the internal iliac arteries may result

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19
Q

(numbness or tingling) in the toes or feet may result from nerve tissue ischemia. True peripheral neuropathy occurs more often in patients with diabetes (see Chapter 48) and in those with long-standing ischemia. Neuropathy causes severe shooting or burning pain in the extremity. It does not follow particular nerve roots and may be present near ulcerated areas. Gradual, reduced blood flow to neurons causes loss of pressure and deep pain sensations. So, patients may not notice lower extremity injuries.

A

Paresthesia (diabetic PAD)

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20
Q

burning, heaviness, pressure, soreness, tightness, weakness) in atypical locations (e.g., ankle, foot, hamstring, hip, knee, shin). PAD involving the internal iliac arteries may result in erectile dysfunction.
- skin becomes thin, shiny, and taut.

A

symptoms of PAD

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21
Q

n becomes thin, shiny, and taut. The lower legs lose their hair. Pedal, popliteal, or femoral pulses are decreased or absent. Pallor (blanching of the foot) develops when the leg is elevated (elevation pallor). Conversely, reactive hyperemia (redness of the foot) develops when the limb is in a dependent position (dependent rubor)

A

symptoms of PAD and reactions

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22
Q

Rest pain most often occurs in the foot or toes. It is worse with limb elevation.

A

PAD painful when resting

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23
Q

Patients often try to achieve pain relief by gravity, dangling the leg over the side of the bed or sleeping in a chair.

A

PAD helpful tips improve pain

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24
Q

Critical limb ischemia (CLI) is a condition characterized by chronic ischemic rest pain lasting more than 2 weeks, nonhealing arterial leg ulcers, or gangrene of the leg from PAD. Patients with PAD who have diabetes, heart failure (HF), and a history of a stroke are at increased risk for CLI

A

Critical limb ischemia (CLI) (less common symptoms of PAD)

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25
Q

maps blood flow throughout the entire region of an artery

A

Doppler ultrasound with duplex imaging

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26
Q

than 30 mm Hg suggests PAD. Angiography

A

drop in segmental BP of greater

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27
Q

show the location and extent of PAD

A

magnetic resonance angiography (PAD)

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28
Q

is a PAD screening tool. It is done using a hand-held Doppler.

A

ankle-brachial index (ABI)

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29
Q

by dividing the ankle systolic BPs (SBPs) by the higher of the left and right brachial SBPs

A

(ankle-brachial index ) ABI is calculated

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30
Q

Calcified and stiff arteries in older patients and those with diabetes often show a falsely elevated ABI.

A

(ankle-brachial index ) ABI is show falsely

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31
Q

and increases the risk for amputation. Patients with diabetes should maintain a glycosylated hemoglobin (A1C) below 7.0% and, optimally, as near as possible to 6.0

A

Diabetes is a major risk factor for PAD

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32
Q

• Antiplatelet effect of clopidogrel is reduced by about half when given with omeprazole.
• This reduced effect increases the risk for myocardial infarction (MI) and stroke.

A

Clopidogrel (Plavix) and Omeprazole (Prilosec)

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33
Q

cilostazol and pentoxifylline. Cilostazol, a phosphodiesterase inhibitor, inhibits platelet aggregation and increases vasodilation. Pentoxifylline, a xanthine derivative, improves the flexibility of RBCs and WBCs and decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity. It is not as effective as cilostazol

A

Two drugs are available to treat intermittent claudication:

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34
Q

• Contraindicated in patients with HF.

A

Cilostazol drug alert

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35
Q

less than 25 kg/m2 and a waist circumference less than 40 inches for men and less than 35 inches for women

A

body mass index (BMI)

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36
Q

via bypass surgery using an autogenous (native) vein. An alternative is percutaneous transluminal angioplasty (PTA).3,8 Patients with CLI who are not candidates for surgery or PTA may receive IV prostanoids (e.g., iloprost [Ventavis])
-However, the FDA has not approved this drug for CLI treatment.3,8 Patients with CLI should continue optimal drug therapy (e.g., statin, antiplatelet, ACE inhibitor, β-blocker) to reduce the risk for a CVD event.

A

CLI is revascularization treatment

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37
Q

dramatic increase in pain, loss of previously palpable pulses, extremity pallor or cyanosis, numbness or tingling, or a cold extremity suggests

A

graft or stent blockage

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38
Q

Discourage prolonged sitting with legs lowered, since it may cause pain and edema, increase the risk for venous thrombosis, and place stress on the suture lines.

A

post operation for PAD alerts/teaching

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39
Q

(i.e., below the knee) using synthetic graft materials receive dual antiplatelet therapy (clopidogrel plus aspirin) for 1 to 3 months, followed by lifelong single antiplatelet therapy

A

Patients having distal peripheral bypass surgery treatment

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40
Q

is a sudden interruption in the arterial blood supply to a tissue, an organ, or an extremity that, if left untreated, can result in tissue death. It is caused by embolism, thrombosis of an atherosclerotic artery, or trauma.

A

Acute arterial ischemia

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41
Q

Embolization of a thrombus from the heart is the

A

most frequent cause of acute arterial occlusion

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42
Q

Hypovolemia (e.g., shock), hyperviscosity (e.g., polycythemia), and hypercoagulability (e.g., chemotherapy)

A

predispose a person to thrombotic arterial occlusion.

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43
Q

vessels branch (e.g., iliofemoral, popliteal, tibial) or narrow.

A

Most emboli block an artery of the leg where

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44
Q

pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia (adaptation of the limb to the environmental temperature, most often cool)

A

acute arterial ischemia include the 6 Ps:

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45
Q

Paralysis is a

A

late sign of acute arterial ischemia

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46
Q

is started to prevent thrombus growth and inhibit further embolization

A

Anticoagulant therapy with IV unfractionated heparin (UH) (

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47
Q

is a nonatherosclerotic, segmental, recurrent inflammatory disorder of the small and medium arteries and veins of the arms and legs

A

Thromboangiitis obliterans (Buerger’s disease) (not athercloris its from smoking=narrow veins and arteries)

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48
Q

e.g., scleroderma). Patients may have intermittent claudication of the feet, hands, or arms. As the disease progresses, rest pain and ischemic ulcerations develop. Other signs and symptoms may include color and temperature changes of the limbs, paresthesia, superficial vein thrombosis, and cold sensitivity.

A

Thromboangiitis obliterans (Buerger’s disease) symptoms mimic PAD

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49
Q

IV iloprost (Ventavis), a prostaglandin analog that promotes vasodilation, is used to manage rest pain, promote healing of ischemic ulcers, and decrease the need for amputation.
- Surgical options include lumbar sympathectomy (transection of a nerve, ganglion, and/or plexus of the sympathetic nervous system), implanting a spinal cord stimulator, microsurgical flap and omental transfer, bypass surgery, and stem cell therapy.11

A

treatment for Thromboangiitis obliterans (Buerger’s disease)

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50
Q

promotes ulcer healing, new blood vessel formation, and nerve cell regeneration.11

A

Stem cell therapy

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51
Q

is an episodic vasospastic disorder of small cutaneous arteries, most often involving the fingers and toes. It occurs more often in women, especially those between 15 and 40 years of age. The pathogenesis of Raynaud’s phenomenon is due to abnormalities in the vascular, intravascular, and neuronal mechanisms that cause vasodilation

A

Raynaud’s phenomenon

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52
Q

is characterized by vasospasm-induced color changes of fingers, toes, ears, and nose (white, blue, and red).

A

Raynaud’s phenomenon

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53
Q

Sustained-release calcium channel blockers (e.g., nifedipine [Procardia]) are the first-line drug therapy

A

1st line therapy treatment for Raynaud’s phenomenon

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54
Q

prostacyclin infusion therapy (e.g., iloprost), antibiotics, analgesics, and surgical debridement of necrotic tissue. Botulinum toxin A and statins may lessen the severity of Raynaud’s phenomenon.1

A

patients with digital ulceration or critical ischemia from Raynaud’s phenomenon treatment

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55
Q

The aorta is the largest artery and supplies O2, nutrients, and blood to all vital organs.

A

Aorta

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56
Q

One of the most common problems affecting the aorta is an aneurysm, which is a permanent, localized outpouching or dilation of the vessel wall.

A

Aorta aneurysms

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57
Q

below the renal arteries.

A

Most abdominal aortic aneurysms (AAAs) occur

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58
Q

degenerative, congenital, mechanical (e.g., penetrating or blunt trauma), inflammatory (e.g., aortitis [Takayasu’s arteritis]), or infectious (e.g., aortitis [Chlamydia pneumoniae, human immunodeficiency virus]).

A

main causes are classified as

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59
Q

include age, male gender, hypertension, CAD, family history, tobacco use, high cholesterol, lower extremity PAD, carotid artery disease, previous stroke, and obesity.

A

Risk factors for aortic aneurysms

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60
Q

is one in which the wall of the artery forms the aneurysm, with at least 1 vessel layer still intact. types.

A

true aneurysm

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61
Q

into fusiform and saccular

A

True aneurysms are subdivided

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62
Q

is circumferential and relatively uniform in shape.

A

A fusiform aneurysm

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63
Q

is pouchlike with a narrow neck connecting the bulge to 1 side of the arterial wall.

A

A saccular aneurysm

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64
Q

, is not an aneurysm. It is a disruption of all arterial wall layers with bleeding that is contained by surrounding anatomic structures.

A

false aneurysm, or pseudoaneurysm

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65
Q

trauma, infection, peripheral artery bypass graft surgery (at the site of the graft-to-artery anastomosis), or arterial leakage after removal of cannulae (e.g., femoral artery catheters, intraaortic balloon pump devices).

A

False aneurysms may result from

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66
Q

deep, diffuse chest pain that may extend to the interscapular area

A

Thoracic aortic aneurysms (TAAs) are often asymptomatic. but signs include

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67
Q

(1) angina from decreased blood flow to the coronary arteries; (2) transient ischemic attacks from decreased blood flow to the carotid arteries; and (3) coughing, shortness of breath, hoarseness, and/or difficulty swallowing from pressure on the laryngeal nerve. If the aneurysm presses on the superior vena cava, decreased venous return can result in jugular venous distention and edema of the face and arms.

A

Ascending aorta and aortic arch aneurysms can cause

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68
Q

pulsatile mass in the periumbilical area slightly to the left of the midline may be present. Bruits may be auscultated over the aneurysm. Physical findings may be hard to detect in obese persons

A

AAA signs and symptoms

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69
Q

(1) cuts into the diseased aortic segment, (2) removes any thrombus or plaque, (3) sutures a synthetic graft to the aorta proximal and distal to the aneurysm, and (4) sutures the native aortic wall around the graft to act as a protective cover

A

Open aneurysm repair (OAR) involves a large abdominal incision through which the surgeon

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70
Q

for select patients. Eligibility criteria include iliofemoral vessels that allow for safe graft insertion and vessels of sufficient length and width to support the graft.

A

Minimally invasive endovascular aneurysm repair (EVAR) is an alternative to OAR

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71
Q

the placement of a sutureless aortic graft into the abdominal aorta inside the aneurysm via the femoral artery. Grafts are made of various materials, such as a Dacron cylinder consisting of several sections, and supported with multiple rings of flexible wire.

A

EVAR involves

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72
Q

EVAR is less invasive than OAR and requires a shorter hospital stay. EVAR also has fewer complications, such as paraplegia and death.

A

EVAR better than OAR

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73
Q

endoleak, the seepage of blood back into the old aneurysm. This may result from an inadequate seal at either graft end, a tear through the graft fabric, or leakage between overlapping graft segments. Repair may require coil embolization (insertion of beads) for hemostasis.

A

most common complication of AAA repair is

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74
Q

is the development of intraabdominal hypertension (IAH) with associated abdominal compartment syndrome.

A

potentially lethal complication in an emergency repair of a ruptured AAA

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75
Q

reduces blood flow to the viscera.

A

Persistent IAH/intraabdominal hypertension

76
Q

to the impaired organ perfusion caused by IAH and resulting multisystem organ failure. IAH is confirmed by measuring the patient’s intraabdominal pressure indirectly through a catheter and transducer system.

A

Abdominal compartment syndrome refers

77
Q

control of situations that lead to IAH. Interventions include open (surgical) decompression, percutaneous drainage, and percutaneous drainage combined with a thrombolytic infusion. Conservative measures, such as intubation, ventilation, patient positioning, gastric decompression, cautious fluid resuscitation, pain management, and temporary hemofiltration, are used.

A

Treatment goals include

78
Q

, often misnamed “dissecting aneurysm,” is not a type of aneurysm

A

Aortic dissection

79
Q

the creation of a false lumen between the intima (inner lining) and the media (middle layer) of arterial wall . Aortic dissection is classified based on the location of the dissection and duration of onset.

A

dissection results from

80
Q

affects the ascending aorta and arch, requiring emergency surgery

A

Type A dissection

81
Q

begins in the descending aorta, allowing for potential conservative management

A

Type B dissection

82
Q

as acute (first 14 days), subacute (14 to 90 days), or chronic (greater than 90 days) based on symptom onset.14,15

A

describe dissections (duration)

83
Q

weakened elastic fibers in the arterial wall. Chronic hypertension hastens this process. In aortic dissection, a tear develops in the inner layer of the aorta. Blood surges through this tear into the middle layer of the aorta, causing the inner and middle layers to separate (dissect). If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal.

A

Nontraumatic aortic dissection is caused by

84
Q

, each pulsation increases the pressure on the damaged area and worsens the dissection. Extension of the dissection may cut off blood supply to the brain, kidneys, spinal cord, and extremities. The false lumen may remain patent, become thrombosed (clotted), rejoin the true lumen by way of a distal tear, or rupture.

A

As the heart contracts in dissection

85
Q

Hypertension is the most important risk factor for aortic dissection.15 Other predisposing factors include age, aortic diseases (e.g., aortitis, coarctation, arch hypoplasia), atherosclerosis, blunt trauma, tobacco use, cocaine or methamphetamine use, congenital heart disease (e.g., bicuspid aortic valve), connective tissue disorders (e.g., Marfan’s syndrome), family history, history of heart surgery, and pregnancy.15

A

risks of aortic dissection

86
Q

About 80% of patients with an acute Type A aortic dissection report an abrupt onset of severe anterior chest or back pain.

A

signs of aortic dissection Type A

87
Q

are more likely to report pain in their back, abdomen, or legs. Pain location may overlap between Type A and B dissections. The pain may be described as “sharp” and “worst ever,” or as “tearing,” “ripping,” or “stabbing.”

A

Patients with acute Type B aortic dissection sign n symptoms

88
Q

disrupts blood flow in the coronary arteries and causes aortic valve insufficiency. When either subclavian artery is involved, the radial, ulnar, and brachial pulse quality and BP readings may be different between the left and right arms. As the dissection progresses down the aorta, the abdominal organs and lower extremities show evidence of decreased tissue perfusion.

A

A aortic dissection usually

89
Q

of an acute ascending aortic dissection is cardiac tamponade

A

severe and life-threatening complication Type A dissecting aorta

90
Q

. This occurs when blood from the dissection leaks into the pericardial sac.

A

acute ascending aortic dissection is cardiac tamponade

91
Q

include hypotension, narrowed pulse pressure, jugular venous distention, muffled heart sounds, and pulsus paradoxus

A

tamponade signs

92
Q

. Hemorrhage may occur into the mediastinal, pleural, or abdominal cavities

A

aorta weakened by dissection may rupture

93
Q

Spinal cord ischemia leads to weakness and decreased sensation and rarely to complete lower extremity paralysis. Renal ischemia can lead to renal failure. Abdominal (mesenteric) ischemia can occur and cause abdominal pain, decreased bowel sounds, altered bowel function, and bowel necrosis.

A

Aortic dissection can lead to occlusion of the blood supply to vital organs.

94
Q

is titrated to a target HR under 60 beats/min or SBP between 100 and 110 mm Hg.

A

An IV β-blocker (e.g., esmolol [Brevibloc]) -1st line treatment for hr

95
Q

can be used to lower HR if a β-blocker is contraindicated.

A

calcium channel blocker (e.g., diltiazem) if Beta blocker contraindicated

96
Q

is similar to EVAR. Fewer postsurgical complications occur with TEVAR. However, TEVAR does not prevent the risk for renal failure, paraplegia, or stroke

A

Thoracic endovascular aortic repair (TEVAR) (endocascular for aortic dissection)// type A dissection

97
Q

β-Blockers are used to control HR and BP and decrease myocardial contractility. ACE inhibitors (e.g., lisinopril [Zestril]) are given if the patient cannot tolerate β-blockers

A

Aortic dissection 1st line treatment is Beta blocker, 2nd is ACE (type A)

98
Q

is an acute inflammation of the walls of small cannulated veins of the hand or arm. Manifestations include pain, tenderness, warmth, erythema, swelling, and a palpable cord

A

Phlebitis

99
Q

are mechanical irritation from the catheter, infusion of irritating drugs, and catheter location

A

Risk factors for phlibitis

100
Q

is more likely to occur in areas of flexion (e.g.,wrist and antecubital area).

A

Severe phlebitis

101
Q

If edema is present, elevate the extremity to promote reabsorption of fluid. Apply warm, moist heat and give oral NSAIDs (e.g., ibuprofen) or topical NSAIDs (e.g.,diclofenac gel) to relieve pain and inflammation.

A

treatment for phlebitis

102
Q

involves the formation of a thrombus (blood clot) with vein inflammation

A

Venous thrombosis

103
Q

is the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein.

A

Superficial vein thrombosis

104
Q

involves a thrombus in a deep vein, most often the iliac and/or femoral veins

A

Deep vein thrombosis (DVT)

105
Q

is the preferred terminology. It represents the spectrum from DVT to pulmonary embolism (PE)

A

Venous thromboembolism (VTE)

106
Q

(1) venous stasis, (2) damage of the endothelium (inner lining of the vein), and (3) hypercoagulability of the blood

A

3 key factors (called Virchow’s triad) that cause venous thrombosis are

107
Q

Tenderness, itchiness, redness, warmth, pain, inflammation, and induration along the course of superficial vein. Vein appears as a palpable cord. Edema rarely occurs.

A

Superficial Vein Thrombosis sight and symptoms

108
Q

enderness to pressure over involved vein, induration of overlying muscle, venous distention. Edema. May have mild to moderate pain, deep reddish color to area caused by venous congestion. Some have no obvious physical changes in the affected extremity.

A

Venous Thromboembolism (VTE)

109
Q

Normal venous blood flow depends on the action of muscles in the extremities and the function of venous valves, which allow flow in one direction. Venous stasis occurs when the valves are dysfunctional or the muscles of the extremities are inactive.

A

Venous stasis pathophysiology

110
Q

Venous stasis occurs most often in people who are obese or pregnant, have chronic HF or atrial fibrillation, have been traveling on long trips without regular exercise, have a prolonged surgical procedure, or are immobile for long periods (e.g., spinal cord injury, fractured hip, limb paralysis).17

A

risk for Venous stasis

111
Q

direct (e.g., surgery, intravascular catheterization, trauma, burns, prior VTE) or indirect (chemotherapy, diabetes, sepsis) injury.

A

Damage to the endothelium of the vein may be caused by

112
Q

anemias, polycythemia, cancers (e.g., breast, brain, pancreas, GI tract); nephrotic syndrome; high homocysteine levels; and protein C, protein S, and antithrombin deficiency.17 A patient with sepsis is predisposed to hypercoagulability because of endotoxins released from bacteria. Some drugs (e.g., corticosteroids, estrogens) predispose a patient to thrombus formation.

A

Blood hypercoagulability

113
Q

are PE, chronic thromboembolic pulmonary hypertension, post-thrombotic syndrome, and phlegmasia cerulea dolens

A

most serious complications of VTE

114
Q

occurs in 8% to 70% of patients. It results from chronic inflammation and chronic venous hypertension.

A

Post-thrombotic syndrome (PTS)

115
Q

is caused by vein wall and vein valve damage (from acute inflammation and thrombus reorganization), venous valve reflux, and persistent venous (outflow) obstruction

A

Chronic venous hypertension

116
Q

Symptoms include pain, aching, fatigue, heaviness, sensation of swelling, cramps, pruritus, tingling, paresthesia, bursting pain with exercise, and venous claudication.19

A

Symptoms Chronic venous hypertension

117
Q

include persistent edema, spider veins (telangiectasia), venous dilation (ectasia), redness, cyanosis, increased pigmentation, eczema, pain during compression, atrophie blanche (white scar tissue), and lipodermatosclerosis

A

Manifestations Chronic venous hypertension

118
Q

Venous ulceration can occur with severe PTS. Signs of PTS typically begin within a few months to a few years of a VTE

A

Post-thrombotic syndrome (PTS)

119
Q

Risk factors include persistent leg symptoms 1 month after VTE, proximal VTE location (e.g., near the iliofemoral junction), extensive VTE, recurrent ipsilateral (same side) VTE, residual thrombus, obesity, older age, poor INR control, daily tobacco use before pregnancy, increased D-dimer levels, elevated inflammatory markers, varicose veins, and asymptomatic VTE

A

Risk factors Post-thrombotic syndrome (PTS)

120
Q

(swollen, blue, painful leg) is a rare complication of a severe lower extremity VTE(s).

A

Phlegmasia cerulea dolens

121
Q

(e.g., thromboembolic deterrent [TED] hose) are a part of VTE prevention in hospitalized patients

A

Graduated compression stockings

122
Q

is enhanced if the stockings are used along with anticoagulation

A

VTE prevention

123
Q

use inflatable sleeves or boots to compress the calf and thigh and/or foot and ankle to improve venous return

A

Intermittent pneumatic compression devices (IPCs)

124
Q

(1) vitamin K antagonists (VKAs), (2) thrombin inhibitors (both indirect and direct), and (3) factor Xa inhibitors

A

3 major classes of anticoagulants available are

125
Q

if its too high then antithrombin isn’t working

A

Fibrin monomer complex

126
Q

oral anticoagulant for long-term or extended anticoagulation is warfarin, a VKA. Warfarin inhibits activation of the vitamin K–dependent coagulation factors II, VII, IX, and X and the anticoagulant proteins C and S.

A

warfrin

127
Q

is a standardized system of reporting prothrombin time (PT)

A

The INR

128
Q

Do not give antiplatelet drug or NSAIDs with warfarin as these increase bleeding risk

A

Warfarin drug alert

129
Q

UH and LMWHs. UH (e.g., heparin) affects both the intrinsic and common pathways of blood coagulation by way of the plasma antithrombin.

A

2 major classes of indirect thrombin inhibitors:

130
Q

can be given subcutaneously for VTE prevention or by continuous IV infusion for VTE treatment.

A

Heparin

131
Q

is heparin-induced thrombocytopenia (HIT). HIT is an immune reaction to heparin. It causes a severe, sudden reduction in the platelet count along with a paradoxical increase in venous or arterial thrombosis.
-Another side effect of long-term heparin therapy is osteoporosis.

A

One serious side effect of heparin

132
Q

(e.g., enoxaparin [Lovenox]) are derived from UH

A

LMWHs

133
Q

are less likely to cause HIT and osteoporosis. LMWHs typically do not require ongoing anticoagulant monitoring and dose adjustment. Their antiinflammatory properties may help prevent PTS and venous ulcer development.2

A

LMWHs benefits

134
Q

hirudin derivatives or synthetic thrombin inhibitors

A

Direct thrombin inhibitors are classified as

135
Q

is made using recombinant deoxyribonucleic acid (DNA) technology. It binds specifically with thrombin and directly inhibits its function without causing plasma protein and platelet interactions

A

Hirudin-NO ANTIDOTE

136
Q

are given by continuous IV infusion. Bivalirudin is approved for patients with or at risk for HIT having a percutaneous coronary intervention. Anticoagulant activity is monitored using aPTT or activated clotting time (ACT)

A

Hirudin derivatives (e.g., bivalirudin [Angiomax])- NO ANTIDOTE

137
Q

, a synthetic direct thrombin inhibitor, hinders thrombin

A

Argatroban (alternative for heparin cuz HIT)

138
Q

effect of argatroban is not reversible. Its anticoagulant effect is monitored using aPTT or ACT.

A

Argatroban (alternative for heparin cuz HIT)

139
Q

is an oral direct thrombin inhibitor. It is used for VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE.
-Idarucizumab (Praxbind) neutralizes the effect of dabigatran.

A

Dabigatran (Pradaxa)

140
Q

rapid onset, no need to monitor anticoagulation, few drug-food interactions, lower risk for major bleeding, and predictable dose response.

A

Dabigatran has 5 major advantages compared to warfarin:

141
Q

inhibit factor Xa directly or indirectly, producing rapid anticoagulation
-fondaparinux (Arixtra), rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa). All are used for both VTE prevention and treatment

A

Factor Xa inhibitors

142
Q

is given subcutaneously. It is contraindicated in patients with severe renal disease.

A

Fondaparinux

143
Q

. Although coagulation monitoring or dose adjustment is not needed, the drug’s anticoagulant activity can be measured using anti-Xa assays

A

Rivaroxaban, apixaban, and edoxaban are oral drugs

144
Q

thrombosis who is not bleeding, low-dose UH, LMWH, or fondaparinux is used.

A

For VTE prevention in the hospitalized medical patient at risk for

145
Q

with either LMWH, UH, or an oral factor Xa drug. Oral VKA therapy may be an option.

A

Patients with confirmed VTE should receive initial treatment

146
Q

It dissolves the clot(s), reduces the acute symptoms, improves deep venous flow, reduces valvular reflux, and may help to decrease the incidence of PTS.

A

Another treatment option for patients with a thrombus is catheter-directed administration of a thrombolytic drug (e.g., urokinase, tPA).

147
Q

who are at a low bleeding risk and present with an acute, extensive, symptomatic, proximal VTE

A

Catheter-directed thrombolysis is an option for select patients

148
Q

involves the removal of a clot through a vein incision. Anticoagulant therapy is used after venous thrombectomy.

A

Venous thrombectomy

149
Q

(e.g., Greenfield, Vena Tech, TrapEase filters) can be placed percutaneously through the right femoral or right internal jugular veins

A

Vena cava interruption devices

150
Q

on (1) maintaining catheter systems (if continuous infusions); (2) monitoring for bleeding, embolization, and impaired perfusion; and (3) VTE prevention teaching.17

A

Postprocedure nursing care focuses

151
Q

are at increased risk for bleeding

A

Patients receiving warfarin with an INR of 5.0 or more

152
Q

Tell patients to avoid taking aspirin, NSAIDs, fish oil supplements, garlic supplements, ginkgo biloba, and certain antibiotics (e.g., sulfamethoxazole and trimethoprim [Bactrim]).

A

DRUG ALERT with anticouagulant therapy

153
Q

, are dilated (3 mm or larger in diameter), tortuous superficial veins often found in the saphenous vein system

A

Varicose veins, or varicosities

154
Q

may be small and harmless or large and bulging.

A

Varicosities

155
Q

(idiopathic) are due to a weakness of the vein walls.

A

Primary varicose veins

156
Q

result from direct injury, a previous VTE, or excessive vein distention.

A

Secondary varicose vein

157
Q

may occur in the esophagus (esophageal varices), vulva, spermatic cords (varicoceles), and anorectal area (hemorrhoids), and as abnormal arteriovenous (AV) connections.

A

Secondary varicose veins

158
Q

from chromosomal defects that cause abnormal development of the venous system.

A

Congenital varicose veins result

159
Q

are smaller varicose veins that appear flat, less tortuous, and blue-green in color.

A

Reticular veins

160
Q

are small visible vessels (generally less than 1 mm in diameter) that appear bluish black, purple, or red.

A

Telangiectasias (often called spider veins)

161
Q

in the lower extremities become dilated and tortuous in response to backward (retrograde) blood flow and increased venous pressure.

A

Superficial veins

162
Q

include family history of chronic venous disease, weak vein structure, female gender, tobacco use, increasing age, obesity, multiparity, history of VTE, venous obstruction resulting from extrinsic pressure by tumors, thrombophilia, phlebitis, previous leg injury, and occupations that require prolonged standing or sitting.22,23

A

Risk factors Superficial veins

163
Q

, weak vein walls allow the vein valve ring to enlarge, so the leaflets no longer fit together properly (incompetent). Incompetent vein valves allow backward blood flow, particularly when the patient is standing.

A

In primary varicose veins

164
Q

include a heavy, achy feeling or pain after prolonged standing or sitting, which is relieved by walking or limb elevation.

A

most common symptoms varicose veins

165
Q

pressure or an itchy, burning, tingling, throbbing, or cramp-like leg sensation. Swelling, restless or tired legs, fatigue, and nocturnal leg cramps may occur.

A

symptoms varicose veins

166
Q

Conservative treatment involves rest with limb elevation; graduated compression stockings; leg strengthening exercise, such as walking; and weight loss, if indicated.

A

treatment Superficial varicose veins

167
Q

Venoactive drugs, derived from plant extracts, are powerful antioxidants that work by stimulating release of chemicals within the vein walls to strengthen the circulation and reduce inflammation and edema.

A

treatment Superficial varicose veins

168
Q

These include micronized purified flavonoid fraction, rutosides (e.g., horse chestnut seed extract [Aesculus hippocastanum]), proanthocyanidins (from grapes and apples), and Ruscus (butcher’s broom).23

A

treat varicose veins and advanced chronic venous disease.

169
Q

• May interact with lithium and antidiabetes, antiplatelet, and anticoagulant drugs.
• Should not be taken by persons with liver or kidney disease or with a latex allergy.

A

Horse Chestnut Seed Extract (Aesculus hippocastanum) DRUG ALERT

170
Q

involves the direct IV injection of a liquid or foam sclerosing substance (e.g., hypertonic saline, polidocanol, glycerin) that chemically ablates (destroys) the treated veins.

A

Sclerotherapy

171
Q

can be used on telangiectasias, perforator veins, reticular veins, varicose veins 5 mm in diameter or smaller, and venous malformations

A

Sclerotherapy

172
Q

are residual pigmentation, matting (new telangiectasias develop in the area), thrombophlebitis, and ulcers.23 After injection, a graduated compression stocking or compression bandage is worn. Patients should not travel long distances during the first week after sclerotherapy to minimize the risk for a VTE.

A

most common complications of sclerotherapy

173
Q

is used for patients in whom sclerotherapy is contraindicated or has been ineffective.

A

Transcutaneous laser or light therapy

174
Q

heating the hemoglobin in the vessels, resulting in vessel sclerosis. Complications of these therapies include pain, blistering, hyperpigmentation, and superficial erosions.

A

Vascular lasers work by

175
Q

using thermal energy from radiofrequency or laser therapy. The HCP inserts a catheter into the vein to heat the vein wall, which then causes the vein to collapse.

A

minimally invasive treatment option for saphenous vein reflux is endovenous ablation

176
Q

This involves pulling the varicosity through a “stab” incision followed by excision of the vein

A

ambulatory phlebectomy.

177
Q

involves the use of a tissue resector to destroy clusters of varicosities and removes the pieces via aspiration.

A

Transilluminated powered phlebectomy

178
Q

which promotes venous return. Check the extremities regularly for color, movement, sensation, temperature, edema, and quality of pedal pulses

A

After vein ligation surgery, encourage the patient to deep breathe,

179
Q

describes abnormalities of the venous system that result in advanced signs and symptoms, such as edema, skin changes, and/or venous leg ulcers.22 CVI can lead to venous leg ulcers (formerly called venous stasis ulcers or varicose ulcers)

A

Chronic venous insufficiency (CVI)

180
Q

causes serous fluid and RBCs to leak from the capillaries and venules into the tissue. This causes edema and chronic inflammatory changes. Enzymes in the tissue eventually break down RBCs, causing the release of hemosiderin, which causes a brownish skin discoloration

A

Ambulatory venous hypertension

181
Q

(e.g., meat, beans, cheese, tofu),

A

Foods high in protein

182
Q

(green leafy vegetables),

A

vitamin A

183
Q

(citrus fruits, tomatoes, cantaloupe), and

A

vitamin C

184
Q

(meat, seafood) are most important for healing.

A

zinc

185
Q

minimizes WBC activation and adhesion to capillary endothelium and decreases oxidative stress. Micronized purified flavonoid fraction acts on WBCs to decrease inflammation and edema

A

Pentoxifylline

adn semester 2 (19 decks)

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