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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
Q

How are thrombi treated?

A

Most thrombus dissolve w/out treatment
Anticoagulants (aspirin, warfarin)

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26
Q

How is a thrombus diagnosed?

A

Doppler ultrasonography

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27
Q

What is doppler ultrasound?

A

Non-invasive test that can be used to estimate blood flow through vessels by bouncing high-frequency sound waves

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28
Q

What is superior vena cava syndrome?

A

Progressive occlusion of superior vena cava leading to venous distention to upper extremities and head

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29
Q

What causes SVC syndrome?

A

Bronchogenic cancer (75% of cases)
-is an oncological emergency

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30
Q

How does bronchi cancer cause SVC syndrome?

A

Normal lung bronchi are always touching the SVC but with bronchi cancer there’s now pressure on the SVC

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31
Q

What is the result of the SVC syndrome?

A

Edema and venous distention in upper extremities and face

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32
Q

What is the effect of edema cause by SVC syndrome?

A

Tightness of shirt collars, necklaces, headache, visual disturbances

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33
Q

How is SVC syndrome diagnosed?

A

Chest x-ray, CT and MRI

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34
Q

What is hypertension?

A

Consistent elevation of systemic arterial blood pressure

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35
Q

Who is at risk for hypertension?

A

Increases with age
Higher in diabetics

36
Q

How can you maintain a proper blood pressure?

A

Exercise and proper nutrition

37
Q

What is primary hypertension?

A

Essential or idiopathic
95% of cases

38
Q

What is secondary hypertension?

A

Caused by a sperate underlying disorder
e.g., renal disease
5% of cases

39
Q

What is malignant hypertension?

A

Rapidly progressive hypertension
Causes system and organ complications
-Is a medical emergency

40
Q

What are the systolic and diastolic pressures of malignant hypertension?

A

Systolic higher than 180 mmHg
Diastolic higher than 120 mmHg

41
Q

What are the systolic and diastolic pressures of normal hypertension?

A

Systolic- Less than 120
Diastolic- Less than 80

42
Q

What are the systolic and diastolic pressures of elevated BP?

A

Systolic- 120-129 mmHg
Diastolic- Less than 80

43
Q

What are the systolic and diastolic pressures of hypertension STAGE 1?

A

Systolic- 130-139
Diastolic- 80-89

44
Q

What are the systolic and diastolic pressures of hypertension STAGE 2?

A

Systolic- 140 or higher
DIastolic- 90 or higher

45
Q

What factors are associated with primary hypertension?

A

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
Q

What does hypertension result from?

A

Sustained increase in peripheral resistance (arterial vasoconstriction)
Increase in blood volume
or both

47
Q

What are the 2 primary factors leading to primary hypertension?

A
  1. Sympathetic nervous sytem (SNS)
  2. RAAS (renin angiotensin angiotensin II aldosterone pathway)
48
Q

How does the SNS lead to primary hypertension?

A

Increased SNS causes increased HR, cardiac contractility and systemic vasoconstriction therefore causing BP to rise

49
Q

What does aldosterone part of RAAS lead to hypertension?

A

increased Na+ reabsorption from kidney= increased blood volume = increased BP

50
Q

How does the angiotensin II part of RAAS lead to hypertension?

A

increased Vasopressin= increases vasoconstriction = increased BP

51
Q

Sclerosis

A

Abnormal hardening of body tissue

52
Q

Arteriosclerosis

A

generic term for vascular disease in which causes thickening and inelasticity of arteries.

53
Q

Atherosclerosis

A

Dominant pattern of arteriosclerosis
Characterized by formation of fatty plague with a core rich in lipids

54
Q

Athero

A

From greek work Athera meaning porridge

55
Q

How is hypertension treated?

A

Life style changes: diet, exercise, no smoking, losing weight
Advanced: Diuretics, Angiotensin II blockers

56
Q

What is orthostatic (postural) hypotension

A

Decrease in systolic BP of 20 mmHg, or a decrease in diastolic BP of 10 mmHg within three minutes of standing

57
Q

What normally happens when standing to maintain normal BP?

A

baroreceptors, vasoconstriction, and heart rate adjusted to maintain normal BP
-These mechanisms dysfunction causing OH

58
Q

Orthostatic hypotension: Signs/symptoms?

A

dizziness, loss of vision, reduced
brain blood flow

59
Q

Orthostatic hypotension: treatment?

A

No curative treatment
suggested: increased fluid and salt intake, wearing thigh-high stockings.

60
Q

What is an aneurysm?

A

Localized dilation (out pouching) of vessel wall

61
Q

What parts of the vessel are involved in an aneurysm?

A

All 3 layers of arterial wall
-Vessel wall is weakened
1. Tunica adentitia
2. Tunica media
3. Tunica intima

62
Q

What artery is the most commonly affected by aneurysms?

A

Aorta
-Result of constant high-pressure stress

63
Q

Aneurysms: Risk factors?

A

Smoking, genetics, diet

64
Q

What is an embolism?

A

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
Q

What can the embolus be made up of that causes embolism?

A

Dislodged thrombus
Aggregation of fat/cancer cells
Foreign substance

66
Q

What does an embolism cause?

A

Ischemia
Continural obstruction = infarction (ischemia –> necrosis)

67
Q

What is Thromboangiitis Obliterans (Buerger’s
Disease)?

A

Inflammation of peripheral arteries
-strongly associated with smoking

Autoimmune disease = thrombus filled with immune cells = occlusion of smaller arteries

68
Q

Thromboangiitis Obliterans (Buerger’s
Disease): Symptoms?

A

reddish skin
Thickened and malformed nails

69
Q

Thromboangiitis Obliterans (Buerger’s
Disease): Adavnced condition?

A

Gangrene
Amputation

70
Q

Thromboangiitis Obliterans (Buerger’s
Disease): Treatment?

A

Stop smoking
keep smoking = amputation

71
Q

What is the leading cause of coronary artery disease?

A

Atherosclerosis

72
Q

Atherosclerosis: Is caused by?

A
  • Smoking,
  • Hypertension,
  • Diabetes,
  • increased low-density lipoproteins (LDL)
  • Decreased levels of high-density lipoproteins (HDL)
  • Autoimmune action
73
Q

How does atherosclerosis begin?

A

Injury to epithelial cells lining artery wall

74
Q

What happens after cells are injured? Atherosclerosis

A

THey become inflammed
Inflammed cells express adhesion molecules that bind macrophages

75
Q

What do bound macrophages do? Atherosclerosis

A

release cytokines and enzymes that further damage vessel wall

76
Q

What does the inflammation do during atherosclerosis?

A

causes free radicals to oxidize LDL that has accumulated in vessel intima.

77
Q

What do macrophages do to oxidized LDL?

A

Engulf it
now called “foam cell”

78
Q

What do foam cells do in atherosclerosis?

A

Accumulate and form Fatty streak

79
Q

What does the fatty streak result in?

A

Recruitment of T cells
-Autoimmunity
-More damage to vessel wall

80
Q

WHat do macrophages release?

A

Growth factors which produce collagen

81
Q

What does collagen do to the fatty streak?

A

Assumaltes over it forming a fibrous plaque

82
Q

What does the fibrous plaque do?

A

Protrudes into lumen and obstructs/occludes blood flow

83
Q

What may happen to the fibrous plaques?

A

They can rupture
-Complicated plaques

84
Q

What do complicated plaques do?

A

Produce rapid thrombus formation
-thrombus = ischemia/infarction

85
Q
A

HLSC 222 Pathophysiology 🧫 (16 decks)

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