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HLSC 222 Pathophysiology 🧫 > Chapter 24 > Flashcards

Chapter 24 Flashcards

1
Q

WHat are some diseases of the veins?

A

Varicose veins
Chronic venous Insufficiency

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2
Q

What is a varicose vein?

A

Vein where blood has pooled, producing distended and palpable vessels

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3
Q

What causes varicose veins?

A

Trauma that damages valves or gradual distension caused by the action of gravity

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4
Q

How do the valves become damaged, leading to varicose veins?

A

Increase the pressure and volume of blood under the pressure of gravity

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5
Q

What veins are typically involved in varicose veins?

A

Saphenous veins of the legs

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6
Q

What happens to the vessel wall during varicose veins?

A

Enzymes remodel vessel wall
Vein swells with increased pressure
Pressure pushes plasma through vessel wall

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7
Q

What are the risk factors associated with varicose veins?

A
  1. Standing for long hours
    2.Age
  2. Obesity
  3. Genetics
  4. Pregnancy
  5. Previous leg injury
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8
Q

How does standing for long hours cause varicose veins?

A

It diminishes the action of the muscle pump

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9
Q

How are varicose veins treated?

A

Elevated legs
Compression stockings

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10
Q

What is the invasive treatment for varicose veins?

A

Surgical ligation
-Tying up the blood vessel

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11
Q

What is chronic venous insufficiency?

A

Inadequate venous return over an extended period

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12
Q

What are the symptoms of chronic venous insufficiency?

A

Edema of lower extremities
Hyperpigmentation (discoloured and thickened) pf ankle and feet skin

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13
Q

What can chronic venous insufficiency progress to?

A

Necrosis
-Circulation is sluggish, reduced oxygen to cells

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14
Q

What is a risk associated with chronic venous insufficiency?

A

Infection

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15
Q

What can lead to chronic venous insufficiency?

A

Surgery
-reduced circulation

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16
Q

What are venous stasis ulcers?

A

Infection occurs because of poor circulation in veins and impairs delivery of oxygen causing necrosis

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17
Q

Thrombus

A

blood clot that remains attached to vessel wall

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18
Q

Thromboembolism

A

A detached thrombus

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19
Q

What kind of thrombi are more common?

A

Venous thrombi are more common than arterial thrombi
-Flow and pressure is lower in veins

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20
Q

Where do thrombi more often occur?

A

lower etremities

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21
Q

What are the three factors that promote DVT called?

A

Virchow triad

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22
Q

What are the 3 factors of the virchow triad that promote deep venous thrombosis (DVT)?

A
  1. Venous stasis (immobility, age, heart failure)
  2. Venous endothelial damage
  3. Hypercoagulable states (increased tendency of blood to thrombose)
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23
Q

What causes hypercoagulable states?

A

pregnancy
Oral contraceptives
heredity

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24
Q

How do thrombi form?

A

Accumulation of clotting factors and platelets near a venous valve= venous obstruction

Inflammation promotes further platelet aggregation= pain and redness

Thrombus obstruction creates extremity edema= ulceration of limb (break on skin surface)

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25
How are thrombi treated?
Most thrombus dissolve w/out treatment Anticoagulants (aspirin, warfarin)
26
How is a thrombus diagnosed?
Doppler ultrasonography
27
What is doppler ultrasound?
Non-invasive test that can be used to estimate blood flow through vessels by bouncing high-frequency sound waves
28
What is superior vena cava syndrome?
Progressive occlusion of superior vena cava leading to venous distention to upper extremities and head
29
What causes SVC syndrome?
Bronchogenic cancer (75% of cases) -is an oncological emergency
30
How does bronchi cancer cause SVC syndrome?
Normal lung bronchi are always touching the SVC but with bronchi cancer there's now pressure on the SVC
31
What is the result of the SVC syndrome?
Edema and venous distention in upper extremities and face
32
What is the effect of edema cause by SVC syndrome?
Tightness of shirt collars, necklaces, headache, visual disturbances
33
How is SVC syndrome diagnosed?
Chest x-ray, CT and MRI
34
What is hypertension?
Consistent elevation of systemic arterial blood pressure
35
Who is at risk for hypertension?
Increases with age Higher in diabetics
36
How can you maintain a proper blood pressure?
Exercise and proper nutrition
37
What is primary hypertension?
Essential or idiopathic 95% of cases
38
What is secondary hypertension?
Caused by a sperate underlying disorder e.g., renal disease 5% of cases
39
What is malignant hypertension?
Rapidly progressive hypertension Causes system and organ complications -Is a medical emergency
40
What are the systolic and diastolic pressures of malignant hypertension?
Systolic higher than 180 mmHg Diastolic higher than 120 mmHg
41
What are the systolic and diastolic pressures of normal hypertension?
Systolic- Less than 120 Diastolic- Less than 80
42
What are the systolic and diastolic pressures of elevated BP?
Systolic- 120-129 mmHg Diastolic- Less than 80
43
What are the systolic and diastolic pressures of hypertension STAGE 1?
Systolic- 130-139 Diastolic- 80-89
44
What are the systolic and diastolic pressures of hypertension STAGE 2?
Systolic- 140 or higher DIastolic- 90 or higher
45
What factors are associated with primary hypertension?
No specific cause (idiopathic) has been identified * combination of genetic and environmental factors * Genetic factors are associated with epigenetic changes (epigenetics: how behaviours and environment affect gene function)
46
What does hypertension result from?
Sustained increase in peripheral resistance (arterial vasoconstriction) Increase in blood volume or both
47
What are the 2 primary factors leading to primary hypertension?
1. Sympathetic nervous sytem (SNS) 2. RAAS (renin angiotensin angiotensin II aldosterone pathway)
48
How does the SNS lead to primary hypertension?
Increased SNS causes increased HR, cardiac contractility and systemic vasoconstriction therefore causing BP to rise
49
What does aldosterone part of RAAS lead to hypertension?
increased Na+ reabsorption from kidney= increased blood volume = increased BP
50
How does the angiotensin II part of RAAS lead to hypertension?
increased Vasopressin= increases vasoconstriction = increased BP
51
Sclerosis
Abnormal hardening of body tissue
52
Arteriosclerosis
generic term for vascular disease in which causes thickening and inelasticity of arteries.
53
Atherosclerosis
Dominant pattern of arteriosclerosis Characterized by formation of fatty plague with a core rich in lipids
54
Athero
From greek work Athera meaning porridge
55
How is hypertension treated?
Life style changes: diet, exercise, no smoking, losing weight Advanced: Diuretics, Angiotensin II blockers
56
What is orthostatic (postural) hypotension
Decrease in systolic BP of 20 mmHg, or a decrease in diastolic BP of 10 mmHg within three minutes of standing
57
What normally happens when standing to maintain normal BP?
baroreceptors, vasoconstriction, and heart rate adjusted to maintain normal BP -These mechanisms dysfunction causing OH
58
Orthostatic hypotension: Signs/symptoms?
dizziness, loss of vision, reduced brain blood flow
59
Orthostatic hypotension: treatment?
No curative treatment suggested: increased fluid and salt intake, wearing thigh-high stockings.
60
What is an aneurysm?
Localized dilation (out pouching) of vessel wall
61
What parts of the vessel are involved in an aneurysm?
All 3 layers of arterial wall -Vessel wall is weakened 1. Tunica adentitia 2. Tunica media 3. Tunica intima
62
What artery is the most commonly affected by aneurysms?
Aorta -Result of constant high-pressure stress
63
Aneurysms: Risk factors?
Smoking, genetics, diet
64
What is an embolism?
Vessel obstruction by an embolus (a bolus of matter circulating in bloodstream) -Embolus travels in blood stream until it reaches a vessel it can’t pass
65
What can the embolus be made up of that causes embolism?
Dislodged thrombus Aggregation of fat/cancer cells Foreign substance
66
What does an embolism cause?
Ischemia Continural obstruction = infarction (ischemia --> necrosis)
67
What is Thromboangiitis Obliterans (Buerger’s Disease)?
Inflammation of peripheral arteries -strongly associated with smoking Autoimmune disease = thrombus filled with immune cells = occlusion of smaller arteries
68
Thromboangiitis Obliterans (Buerger’s Disease): Symptoms?
reddish skin Thickened and malformed nails
69
Thromboangiitis Obliterans (Buerger’s Disease): Adavnced condition?
Gangrene Amputation
70
Thromboangiitis Obliterans (Buerger’s Disease): Treatment?
Stop smoking keep smoking = amputation
71
What is the leading cause of coronary artery disease?
Atherosclerosis
72
Atherosclerosis: Is caused by?
* Smoking, * Hypertension, * Diabetes, * increased low-density lipoproteins (LDL) * Decreased levels of high-density lipoproteins (HDL) * Autoimmune action
73
How does atherosclerosis begin?
Injury to epithelial cells lining artery wall
74
What happens after cells are injured? Atherosclerosis
THey become inflammed Inflammed cells express adhesion molecules that bind macrophages
75
What do bound macrophages do? Atherosclerosis
release cytokines and enzymes that further damage vessel wall
76
What does the inflammation do during atherosclerosis?
causes free radicals to oxidize LDL that has accumulated in vessel intima.
77
What do macrophages do to oxidized LDL?
Engulf it now called "foam cell"
78
What do foam cells do in atherosclerosis?
Accumulate and form Fatty streak
79
What does the fatty streak result in?
Recruitment of T cells -Autoimmunity -More damage to vessel wall
80
WHat do macrophages release?
Growth factors which produce collagen
81
What does collagen do to the fatty streak?
Assumaltes over it forming a fibrous plaque
82
What does the fibrous plaque do?
Protrudes into lumen and obstructs/occludes blood flow
83
What may happen to the fibrous plaques?
They can rupture -Complicated plaques
84
What do complicated plaques do?
Produce rapid thrombus formation -thrombus = ischemia/infarction
85

HLSC 222 Pathophysiology 🧫 (16 decks)

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