Week 5 - Cardiovascular Conditions Flashcards
(55 cards)
1
Q
- Formation of fibro-fatty lesions in the intimal lining of large and medium-sized arteries
- Leading cause of CAD, stroke, peripheral arterial disease
A
Atherosclerosis
2
Q
Non-modifiable
Atherosclerosis- Risk Factors (4)
A
Increasing age
Male gender
Genetic disorders of lipid metabolism
Family history of CAD
3
Q
Modifiable
Atherosclerosis - Risk Factors (5)
A
Smoking Obesity Hypertension Hyperlipidemia Diabetes mellitus
4
Q
Atherosclerosis Lesions are of three types:
A
Fatty streak
Fibrous atheromatous plaque
Complicated lesion
5
Q
- Thin, flat, yellow discolouration of intima
- Progressively become thicker and slightly elevated
- Contain macrophages and smooth muscle cells that have become distended to form foam cells!
A
Fatty Streaks
6
Q
- Responsible for clinically significant manifestations of atherosclerosis
Lesions:
- Begin as grey to pearly white with increase thickening of the vessel intima
- Core of extracellular lipid covered by a fibrous cap of connective tissue and smooth muscle
- Lesions increases and impairs patency of arterial lumen causing decreased blood flow
A
Fibrous atheromatous plaque
7
Q
4 Stages of Atherosclerosis Development
A
- Endothelial cell injury
- Migration of inflammatory cells
- Lipid accumulation and smooth muscle cell proliferation
- Plaque structure
8
Q
- Endothelial lining normally acts as a barrier protecting underlying layers
- Agents cause endothelial cell injury and allow monocytes and platelets to adhere to vessel wall
A
1.Endothelial cell injury
9
Q
- Early development of atherosclerotic lesion
- Monocytes and other inflammatory cells bind to endothelial wall
- Monocytes migrate between endothelial cells to intima and transform into macrophages
- Macrophages engulf lipoproteins (LDL)
A
2.Migration of inflammatory cells
10
Q
- Activated macrophages release toxic oxygen species that oxidize LDL
- Oxidized LDL ingested by macrophage through a scavenger receptor resulting in foam cells
- Activated macrophages also produce growth factors which causes: migration and proliferation of smooth muscle cells (SMCs) + elaboration of the extracellular matrix (ECM)
A
3.Lipid Accumulation & Smooth Muscle Cell Proliferation
11
Q
Plaques consist of: (4)
A
aggregation of SMCs
macrophages & other leukocytes
ECM (inc. collagen & elastic fibers)
intracellular & extracellular lipids
12
Q
Superficial fibrous cap of plaque composed of (2)
A
SMCs & dense ECM
13
Q
Shoulder of plaque consists of (3)
A
macrophages, SMCs & lymphocytes
14
Q
Central core of plaque composed of (2)
A
lipid laden foam cells and fatty debris
15
Q
- Thick fibrous caps
- Partially block vessels
- Do not tend to form clots or emboli
A
Stable Plaques
16
Q
- Thin fibrous caps
- May completely block artery
- Plaque can rupture and cause a thrombus to form
- The clot may break free and become an embolus
A
Unstable Plaques
17
Q
Manifestations of Atherosclerosis
A
Depends on vessel involved & extent of obstruction
- Cardiac, cerebral, renal, lower extremities and small intestine vessels involved most often
- May produce ischemia, infarction, obstruction, thrombi, emboli or aneurysm
18
Q
- Disorders that affect arteries in the extremities are the same as those affecting coronary and cerebral arteries
- Also produce ischemia, pain, impaired function, infarction and tissue necrosis
- Arterial vs. Venous in origin
A
Peripheral Vascular Disease
19
Q
Presence of systemic atherosclerosis distal to the arch of the aorta
A
Peripheral Arterial Disease (PAD)
20
Q
Manifestations of vessel occlusion are gradual
4
A
- Intermittent claudication
- Atrophic changes/thinning skin of lower extremity
- Weak pedal pulse
- Ischemia pain
21
Q
Diagnostics of PAD: (4)
A
Inspection of limbs
Palpation of pulses
Ankle-brachial index
Ultrasound, MRI, Spiral CT, angiography
22
Q
Treatment of PAD (6)
A
Protection of affected area Walking to the point of claudication Avoidance of injury Address other CVS risk factors Drugs: antiplatelets Surgery
23
Q
- Manifested by venous HTN - a sustained increase in venous blood pressure
- Caused by reflux through incompetent veins
- Prolonged standing increases pressure and causes dilation of vessel wall
A
Peripheral Venous Disease (PVD) (aka Chronic Venous Insufficiency)
24
Q
Manifestations of PVD:
A
- Tissue congestion, edema, impairment of tissue nutrition
- Necrosis of fat deposits
- Brown pigmentation from hemosiderin deposits
- Advanced: stasis dermatitis, ulcerations
25
Treatment of PVD:
compression therapy
| dressings, bandages
26
- Also called Thrombophlebitis
- Presence of a thrombus in a vein and accompanying inflammatory response
– common in calf
Venous Thrombosis
| DVT
27
Risk factors for DVT (2)
```
1. Virchow’s Triad –
blood stasis
hyperactivity of blood coagulation
vessel wall injury
2. Increased risk with impaired cardiac function
```
28
- Usually asymptomatic
| - If symptomatic, will have pain, swelling and tenderness due to the inflammatory response
PVD
29
Dx of PVD:
U/S, d-dimer
30
Tx of PVD:
Prevention(i.e. ambulation, TEDS)
Anticoagulant (warfarin)
ICV filter
31
Complication of PVD:
Pulmonary embolism
32
Abnormal localized dilation of a blood vessel
Aneurysms
33
the aneurysm is bounded by a complete vessel wall
| Blood remains in the vascular compartment
True aneurysm
34
A localized dissection of tear in the inner wall of the artery
Extravascular hematoma
False aneurysm
35
Factors causing aneurysms (4)
Congenital defects
Atherosclerosis
Trauma
Infections
36
- Wall of artery weakens and stretches
- Risk of rupture and hemorrhage
- Risk of clot formation
Aneurysms
37
May occur in any part of the aorta, multiple aneurysm may be present.
Aortic Aneurysm
38
less common
due to atherosclerosis
usually asymptomatic
Thoracic:
39
Manifestations of Thoracic Aortic Aneurysm:
Depend on size and location
Substernal pain, back pain
Dyspnea, stridor
40
most frequent type of aortic aneurysm
Risk Factors: Age 50y+, HTN, severe atherosclerosis
Most located below the level of the renal artery
Abdominal aortic aneurysm (AAA)
41
Manifestations of Abdominal aortic aneurysm (AAA) : (4)
Most are asymptomatic
Pulsating mass
Palpable when > 4 cm
Pain, abdominal/lumbar/back
42
Diagnostics of Aortic Aneurysm:(4)
U/S, echocardiogram, CT scan, MRI
43
Treatments of Aortic Aneurysm (3)
measures to slow growth
risk factor modification
Surgical repair: synthetic graft
44
- Acute life threatening condition
- Caused by conditions that weaken the elastic and smooth muscle of the layers of the aorta
- Hemorrhage into vessel wall through longitudinal tearing
- High Mortality Rate
Aortic Dissection
45
Risk factors of Aortic Dissection (2)
1. HTN
| 2. degeneration of the medial layer of the vessel wall
46
Two types of aneurysms
Type A – involve the proximal aorta (most common)
| Type B – usually begin distal to subclavian artery
47
type of aneurysm
| – involve the proximal aorta (most common)
Type A
48
type of aneurysm
| - usually begin distal to subclavian artery
Type B
49
When aorta is involved in aneurysm & rupture occurs, the tear may impair closure of the ________
aortic valve.
50
Also, in aneurysms blood may go into the _____ and compress the heart
pericardium
51
May occlude the arteries that arise from the _____.
aortic arch
52
Symptoms of Dissection
1. Abrupt presence of excruciating pain –tearing, ripping
- Pain located to anterior chest (ascending aorta)
- Pain located to back (descending aorta)
2. Initial high BP, then unable to obtain BP and pulse in one or both arms
3. Hemiplegia, paralysis of lower extremities
4. Syncope
5. Heart failure
53
Diagnosis of Aortic Dissection:
| 6
Based on physical exam
| Aortic angiography, transesophageal echocardiography (TEE), CT scans, MRI
54
Treatment of Aortic Dissection (4)
Stabilized medically even before diagnosis is confirmed
Control of HTN and decrease the force of systolic blood ejection (beta-blockers and nitroprusside)
Pain control
Surgery
55
Surgical Tx of Aortic Dissection (2)
Resection of the involved segment and replacement with prosthetic graft
