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Cardiovascular > Vascular disease (arterial/venous insufficiencies, aortic diseases etc) > Flashcards

Vascular disease (arterial/venous insufficiencies, aortic diseases etc) Flashcards

1
Q

Definition of acute arterial occlusion/insufficiency & how many hours within do you have to treat to avoid irreversible ischaemia & myonecrosis?

A
  • acute occlusion/rupture of a peripheral artery
  • urgent management required: treat within 6 h or irreversible ischemia and myonecrosis may result
  • tends to be lower extremity > upper extremity; femoropopliteal > aortoiliac
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2
Q

What are the risk factors (congenital & acquired) for acute arterial occlusion/insufficiency?

A

Hypercoagulable state

Congenital:

  • group 1: reduced anticoagulants (antithrombin, protein C, S)
  • group 2: increased coagulants (factor V Leiden, prothrombin, factor VIII, hyperhomocysteinemia)
Acquired:
• Immobility
• Cancer
• Pregnancy/OCP
• Antiphospholipid antibody syndrome
• Inflammatory disorders (e.g. IBD)
• Myeloproliferative disorders (e.g. ET)
• Nephrotic syndrome (acquired deficit
in Protein C and S)
• Disseminated Intracascular
Coagulation (DIC)
• Heparin-Induced Thrombocytopenia
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3
Q

Clinical Px of acute arterial occlusion/insufficiency

A

6 Ps

  • Pain: absent in 20% of cases
  • Pallor: within a few hours becomes mottled cyanosis
  • Paresthesia: light touch lost first then sensory modalities
  • Paralysis/Power loss: most important, heralds impending gangrene
  • Polar/Poikilothermia (cold)
  • Pulselessness: not reliable
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4
Q

Ix of acute arterial occlusion/insufficiency

A
  • history and physical exam: depending on degree of ischemia may have to forego investigations and go straight to OR
  • ABI (ankle-brachial index): extension of physical exam, easily performed at bedside
  • ECG, troponin: rule out recent MI or arrythmia
  • CBC: rule out leukocytosis, thrombocytosis or recent drop in platelets in patients receiving heparin
  • PT/INR: patient antocoagulated/sub-therapeutic INR
  • echo: identify wall motion abnormalities, intracardiac thrombus, valvular disease, aortic dissection (type A)
  • CT angiogram: underlying athelosclerosis, aneurysm, aortic dissection
  • conventional catheter based angiography: can be obtained in OR; prelude to thrombolytics
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5
Q

Cx of acute arterial occlusion/insufficiency

A
  • compartment syndrome with prolonged ischemia; requires fasciotomy
  • renal failure and multi-organ failure due to toxic metabolites from ischemic muscle
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6
Q

Rx of acute arterial occlusion/insufficiency

A

• immediate heparinization with 5000 IU bolus and continuous infusion to maintain PTT >60 s
• if absent power and sensation: emergent revascularization
• if present power and sensation: work-up (including angiogram)
• definitive treatment
embolus: embolectomy
thrombus: thrombectomy ± bypass graft ± endovascular therapy irreversible ischemia: primary amputation
• identify and treat underlying cause
• continue heparin post-op, start warfarin post-op day 1 x 3 mo depending on underlying etiology

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7
Q

Prognosis of acute arterial occlusion/insufficiency

A
  • 12-15% mortality rate

* 5-40% morbidity rate (amputation)

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8
Q

What is the main cause of chronic arterial occlusion/insufficiency?

A

Ahterosclerosis (primarily lower extremities)

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9
Q

Risk factors for chronic arterial occlusion/insufficiency

A
  • major: smoking, DM

* minor: HTN, hyperlipidemia, family history, obesity, sedentary lifestyle

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10
Q

Px of (2) main types of chronic arterial occlusion/insufficiency

A
  1. Claudication
    - pain with exertion: usually in calves or any exercising muscle group
    - relieved by short rest: 2 to 5 min, and no postural changes necessary
    - reproducible: same distance to elicit pain, same location of pain, same amount of rest to relieve pain
  2. Critical limb ischaemia
    - includes rest pain, night pain, tissue loss (ulceration or gangrene)
    - ankle pressure
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11
Q

Ix of chronic arterial occlusion/insufficiency

A

Non-invasive
ƒƒ- routine bloodwork, fasting metabolic profile
ƒƒ- ABI: take highest brachial and highest ankle [dorsalis pedis (DP) or posterior tibial (PT)] pressures for each side generally
ŠŠ- ABI

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12
Q

DDx of claudication (vascular, neurologic, MSK)

A

Vascular
• Atherosclerotic disease
• Vasculitis (e.g. Buerger’s disease, Takayasu’s arteritis)
• Diabetic neuropathy
• Venous disease (e.g. DVT, varicose veins)
• Popliteal entrapment syndrome (e.g. Baker’s cyst, tumour)

Neurologic
• Neurospinal disease (e.g. spinal stenosis)
• Reflex sympathetic dystrophy

MSK
• Osteoarthritis
• Rhematoid arthritis/connective tissue disease
• Remote trauma

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13
Q

Rx of chronic arterial occlusion/insufficiency

A

Conservative

  • reduce RF (stop smoking, Rx HTN, HChol, DM)
  • exercise program
  • foot care

Pharm

  • antiplatelet agents (clopidogrel)
  • cilostazol (antiplatelet + vasodilator)

Surgical

  • indications: severe life impairment, vocational impairment, critical ischaemia
  • endovascular (stenting/angioplasty)
  • endarterectomy
  • bypass graft
  • chemical sympathectomy: sympathetic plexus is destroyed with EtOH injection into nerve plexus to stimulate vasodilation
  • amputation: if persistent serious infections/gangrene
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14
Q

Prognosis of chronic arterial occlusion/insufficiency

A

• claudication: conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate, 5% will require intervention within 5 yr,

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15
Q

What are signs of poor perfusion?

A

hair loss, hypertrophic nails, atrophic muscle, skin ulcerations and infections, slow capillary refill, prolonged pallor with elevation and rubor on dependency (Buerger’s test), venous troughing (collapse of superficial veins of foot)

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16
Q

Range of ankle-brachial indices

A

> 1.2: Suspect wall calcification (most common in diabetics)
0.95: Normal/no ischemia
0.50 – 0.8: Claudication range

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17
Q

Describe acute traumatic ulcers

A

failure of lesions to heal, usually due to compromised blood supply and unstable scar

usually over bony prominence ± edema ± pigmentation changes ± pain

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18
Q

Rx of acute traumatic ulcers

A
  • debridement of ulcer and compromised tissue,
  • left to heal via secondary intention with dressings,
  • may need reconstruction with local or distant flap in select cases,
  • vascular status of limb must be assessed clinically and via vascular studies (i.e. sonographically)
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19
Q

What are the major (3) types of non-traumatic chronic ulcers?

A
  1. Venous (70% of vascular ulcers)
  2. Arterial
  3. Diabetic
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20
Q

Describe venous ulcers

A
  • Cause: valvular incompetence, venous HTN
  • Hx of dependent edema, trauma
  • medial malleolus common
  • yellow exudates, granulation tissue
  • IRREGULAR margin
  • superficial depth
  • venous stasis, discolouration (brown) surrounding skin!!
  • normal distal pulses
  • moderately painful, more painful with leg dependency, no rest pain
  • Rx: leg elevation & rest, moist dressings
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21
Q

Describe arterial ulcers

A
  • secondary to small/large vessel disease
  • arteriosclerosis, claudication common
  • slow progression
  • distal locations common
  • pale/white, necrotic base
  • “punched out” appearance
  • thin SHINY dry skin, hairless, cool
  • decreased distal pulses
  • Buerger’s sign
  • extremely painful, decreased with dependency (hanging legs off the end of bed)
  • Rx: rest, no elevation
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22
Q

Describe diabetic ulcers

A
  • due to peripheral neuropathy (decreased sensation ) & atherosclerosis (decreased regional blood flow)
  • diabetes mellitus, peripheral neuropathy Hx
  • Pressure point distribution affected
  • necrotic base appearance
  • irregular OR punched out or deep appearance
  • Superficial/deep
  • thin dry skin, hyperkeratotic border
  • hypersensitive/ ischemic surrounding skin
  • decrased pulses likely
  • ABI inaccurately high due to calcifications
  • PAINLESS
  • no claudication or rest pain
  • paraesthesia, anaesthesia
  • Rx: control DM, careful wound care, foot care, orthotics, early intervention for infections
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23
Q

What % of pts with symptomatic proximal DVT develop PE?

A

50% often within days to weeks of the event

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24
Q

Risk factors for VTE

A

THROMBOSIS

  • Trauma, travel
  • Hypercoagulable, HRT
  • Recreational drugs (IVDU)
  • Old (age >60)
  • Malignancy
  • Birth control pill
  • Obesity, obstetrics
  • Surgery, smoking
  • Immobilization
  • Sickness (CHF, MI, nephrotic
    syndrome, vasculitis)

• Virchow’s triad
- alterations in blood flow (venous stasis e.g. flights)
- injury to endothelium (e.g. recent surgery)
- hypercoagulable state (including pregnancy, use of OCP, malignancy)
• clinical risk factors

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25
Q

Px of DVT

A

calf pain, leg swelling/ erythema/edema, palpable cord on exam; can be asymptomatic

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26
Q

Px of PE

A

dyspnea, pleuritic chest pain, hemoptysis, tachypnea, cyanosis, hypoxia, fever

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27
Q

Ix of DVT/PE

A
  • ECG and CXR are useful to look for other causes (e.g. ACS, pneumonia)
  • D-dimer is only useful if it is negative in low risk patients (highly sensitive)
  • ultrasound has high sensitivity and specificity for proximal clot but only 73% sensitivity for DVT below the knee (may need to repeat in 1 wk)
  • CT angiography has high sensitivity and specificity for PE, may also suggest other etiology
  • V/Q scan useful when CT angio not available, or patient unable to tolerate IV contrast (e.g. renal failure, allergy)
28
Q

Rx of DVT/PE

A

• LMWH unless patient also has renal failure (bridging warfarin)
- dalteparin 200 IU/kg SC q24h or enoxaparin 1.5 mg/kg SC q24h
• warfarin started at same time as LMWH (5 mg PO OD initially)
• LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days.

• long term anticoagulation

  • if reversible risk factor: 3-6 mo of warfarin
  • idiopathic VTE: may need longer term warfarin (5 yr or more)
29
Q

Define superficial venous thrombosis

A

erythema, induration, and tenderness along the superficial vein; usually spontaneous but can
follow venous cannulation

30
Q

Causes of superficial venous thrombosis

A
  • infectious: suppurative phlebitis (complication of IV cannulation; associated with fever/chills)
  • trauma
  • inflammatory: varicose veins, migratory superficial thrombophlebitis, Buerger’s disease, SLE
  • hematologic: polycythemia, thrombocytosis
  • neoplastic: occult malignancy (especially pancreatic)
  • idiopathic
31
Q

Px of superficial venous thrombosis

A
  • pain
  • cord like swelling
  • areas of induration, erythema, tenderness
  • most commonly in greater saphenous vein
32
Q

Ix of superficial venous thrombosis

A

non-invasive tests (e.g. Doppler) to exclude associated DVT

33
Q

Rx of superficial venous thrombosis

A

Conservative

  • moist heat, compression bandages
  • mild analgesics
  • anti inflammatory & anti-platelet, LMWH, ambulation

Surgical

  • indication: failure of conservative measures (>2wk)
  • Rx suppurative thrombophlebitis with broad spectrum IV antibiotics & excision
34
Q

Cx of superficial venous thrombosis

A
  • simultaneous DVT (
35
Q

Define chronic venous insufficiency

A

venous insufficiency and skin damage

36
Q

Causes of chronic venous insufficiency

A

• calf muscle pump dysfunction and valvular incompetence (valvular reflux) due to phlebitis,
varicosities, or DVT
• venous obstruction
• AV fistulas, venous malformations

37
Q

Px of chronic venous insufficiency

A
  • pain (most common), ankle and calf edema – relieved by foot elevation
  • pruritus, brownish hyperpigmentation (hemosiderin deposits)
  • stasis dermatitis, subcutaneous fibrosis if chronic (lipodermatosclerosis)
  • ulceration: shallow, above medial malleolus, weeping (wet), painless, irregular outline
  • signs of DVT/varicose veins/thrombophlebitis
38
Q

Ix of chronic venous insufficiency

A
  • ambulatory venous pressure measurement (gold standard)
  • Doppler U/S (most commonly used)
  • photoplethysmography
39
Q

Rx of chronic venous insufficiency

A

Conservative

  • elastic compression stockings, leg elevation, avoid prolonged sitting/standing
  • ulcers: zinc-oxide wraps, split-thickness skin grafts, ABx, debridement

Surgical
- surgical ligation of perforators in region of ulcer

40
Q

What is phlebitis?

A

inflammation of the walls of a vein

41
Q

Define lymphedema

A

obstruction of lymphatic drainage resulting in edema with high protein content

42
Q

Causes of lymphedema

A

Primary
- Milroy’s syndrome (congenital hereditary lymphedema)

Secondary

  • infection: filariasis (#1 cause worldwide), postop
  • malignant infiltration: axillary, groin or intrapelvic
  • radiation/surgery (axillary, groin lymph node removal): #1 cause in N. America
43
Q

Px of lymphedema

A
  • classically non-pitting edema

* impaired limb mobility, discomfort/pain, psychological distress

44
Q

Rx of lymphedema

A

• avoid limb injury (can precipitate or worsen lymphedema)
• skin hygiene (moisturiser, topical Rx of fungal infections)
• external supportƒƒ intensive: compression bandages
ƒƒmaintenance: lymphedema sleeve
• exercise (w/ use of compression bandage)
• massage and manual lymph drainage therapy

45
Q

Prognosis of lymphedema

A
  • if left untreated becomes resistant to treatment due to subcutaneous fibrosis
  • cellulitis causes rapid increase in swelling: can lead to sepsis and death
46
Q

What is thrombophlebitis?

A

inflammation of the wall of a vein with associated thrombosis, often occurring in the legs during pregnancy

47
Q

What is Trousseau’s sign?

A

Migratory superficial thrombophlebitis

as often a sign of underlying malignancy

48
Q

Define aortic dissection

A

tear in aortic intima allowing blood to dissect into the media;

acute 2 wk (mortality levels up to 75-80%)

49
Q

Causes of aortic dissection

A

• most common: HTN -> degenerative/cystic changes -> damage to aortic media
• other: connective tissue disease (e.g. Marfan’s, Ehlers-Danlos), cystic medial necrosis,
atherosclerosis, congenital conditions (e.g. coarctation of aorta, bicuspid aortic valves, patent ductus arteriosus), infection (e.g. syphilis), trauma, arteritis (e.g. Takayasu’s)

50
Q

Epidemiology of aortic dissection

A

Peak incidence 50-65 yr old; 20-40 yr old with connective tissue diseases

  • incidence of 5.2 in 1 000 000
  • male:female = 3.2:1
  • small increased incidence in African-Canadians (related to higher incidence of HTN)
  • lowest incidence in Asians
51
Q

Px of aortic dissection

A
  • Sudden onset, TEARING pain that radiates to the BACK

on a background of:

  • HTN
  • asymmetric BP & pulses b/w arms
  • ischaemic syndromes due to occlusion of aortic branches
  • rupture into pleura (dyspnoea, hemoptysis) or peritoneum (hypotension, shock) or pericardium (cardiac tamponade)
  • syncope
  • new diastolic murmur (20-30%)
52
Q

Ix of aortic dissection

A

• CXR
ƒƒ- pleural cap (pleural effusion in lung apices)
ƒƒ- widened mediastinum
ƒƒ- left pleural effusion with extravasation of blood
• CT (gold standard), aortography, MRA: 100% sensitive and specific
• bloodwork: lactate (r/o ischemic gut), amylase (r/o pancreatitis), troponin (r/o MI) •TEE: can visualize aortic valve and thoracic aorta but not abdominal aorta
• ECG: LVH ± ischemic changes, pericarditis, heart block

53
Q

Rx of aortic dissection

A

Pharm

  • beta blockers to lower BP & contractility
  • non dihydropyridine Ca2+ channel blocker if C/I to beta blockers
  • target sBP of 110mmHg and HR of
54
Q

Cx of aortic dissection

A
  • Post op: renal faliure, intestinal ischemia, stroke, paraplegia, persistent leg ischaemia
  • 2/3 of pts die of op or post op Cx

W/ treatment: 60% 5 year survival, 40% 10 year survival

55
Q

Describe type A & B of aortic dissection. Which is worse?

A

Type A: proximal. Involves the ascending aorta and/or aortic arch, and possibly the descending aorta

Type B: distal. Involves the descending aorta or the arch (distal to the left subclavian artery), without involvement of the ascending aorta

Type A is worse due to possible continuous tear of coronary arteries at/beyond the proximal aortic root

56
Q

Define an aneurysm

A

localized dilatation of an artery having a diameter at least 1.5 times that of the expected normal diameter

57
Q

Compare true aneurysm to false aneurysm

A

ƒƒ- true aneurysm: involving ALL vessel wall layers (intima, media, adventitia)
ƒƒ
- false aneurysm (also known as psuedo-aneurysm): disruption of the aortic wall or the anastomotic site between vessel and graft with containment of blood by a fibrous capsule made of surrounding tissue

58
Q

What can happen to aneurysms?

A

aneurysms can rupture, thrombose, embolize, erode, and fistulize

59
Q

Causes of aortic aneurysm

A
  • degenerative (atherosclerotic)
  • traumatic
  • mycotic (Salmonella, Staphylococcus, usually suprarenal aneurysms)
  • connective tissue disorder (Marfan syndrome, Ehlers-Danlos syndrome)
  • vasculitis
  • infectious (syphilis, fungal)
  • ascending thoracic aneurysms are associated with bicuspid aortic valve
60
Q

Risk factors for aortic aneurysm

A

smoking, HTN, age >70, family history

61
Q

Who is in the high risk group of aortic aneurysm?

A

• incidence 4.7 to 31.9 per 100 000 for AAA and 5.9 per 100 000 for TAA

• high risk groups
- ƒƒ65 yr and older
ƒƒ- male:female = 3.8:1
ƒƒ- PVD, CAD, CVD
ƒƒ- family history of AAA
62
Q

Px of aortic aneurysm

A

due to acute expansion or disruption of wall

  • syncope
  • pain (chest, abdo, flank, back)
  • HYPOtension
  • palpable pulsatile mass above umbilicus, pulsatile abdo mass in 2 directions (expansile)
  • airway/esophageal obstruction
  • hoarseness (left recurrent laryngeal nerve paralysis)
  • hemoptysis, hematemesis
  • distal pulse may be intact

75% asymptomatic

63
Q

What is the classic triad of ruptured AAA

A
  1. Pain
  2. Hypotension
  3. Pulsatile abdo mass
64
Q

Ix of aortic aneurysm

A
  • bloodwork: CBC, electrolytes, urea, creatinine, PTT, INR, type and cross
  • abdominal U/S (100% sensitive, up to ± 0.6 cm accuracy in size determination)
  • CT (accurate visualization, size determination)
  • MRI (accurate visualization, limited access)
  • aortogram (only for EVAR)
  • Doppler/duplex (r/o vascular tree aneurysms elsewhere, e.g. popliteal)
65
Q

Rx of aortic aneurysm

A

Conservative

  • reduce CV RF
  • exercise
  • watchful waiting. US every 6 months for 3 years

Surgical

  • if risk of rupture > = risk of surgery (>5.5cm)
  • elective AAA repair mortality 2.5%
  • Open surgery with graft replacement
  • Endovascular aneurysm repair (EVAR): decreased morbidity, mortality, procedure time, recovery time
66
Q

Rx of ruptured AAA

A 
• ABCs
• No imaging (hemodynamically
unstable)
• Straight to OR (confirm diagnosis by laparotomy)
• Crossmatch 10 units packed RBCs

Cardiovascular (3 decks)

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