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Pathophysiology > Class 1 chapter 18 > Flashcards

Class 1 chapter 18 Flashcards

1
Q

Hyperlipidemia

A

Cholesterol and triglycerides (dietary lipids) are insoluble in plasma as encapsulated by lipoproteins

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2
Q

Types of lipoproteins

A 
Chylomicrons
VLDL (very low density)
LDL 
IDL (intermediate density)
HDL
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3
Q

LDL

A

Main carrier of cholesterol but leaves some behind for uptake in arterial wall
Low protein
High triglycerides

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4
Q

HDL

A

Carries cholesterol but remove it from tissues and take to liver for disposal
High protein
Low triglycerides

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5
Q

Lipid blood levels raised by

A

Nutrition (high-calorie diet increases production of VLDL and it’s conversion to LDL)
Genetics
Comorbid conditions/diseases
Medication

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6
Q

Atherosclerosis non modifiable risk factors

A 
Increasing age
Male
Post-menopausal women
Family hx of premature CAD
Genetically determined alterations in lipoprotein and cholesterol metabolism
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7
Q

Atherosclerosis modifiable risk factors

A 
Cigarette smoking
Obesity
Htn
Hyperlipidemia
Diabetes mellitus
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8
Q

What increases risk of atherosclerosis if you have high levels?

A

C-reactive protein
Hyperhomocystinemia
Increased serum lipoprotein

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9
Q

Tobacco use

A 
Increases blood lipid levels
Damages endothelium
Enhances thrombosis formation
Increases blood viscosity
Increases circulating catecholamines (get a rush off it - increases epinephrine and norepinephrine)
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10
Q

Arteriosclerosis

A

Hardening of medium to large arteries

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11
Q

Arteriolosclerosis

A

Hardening of small arteries

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12
Q

Atherosclerosis

A

Hardening d/t atheromatous plaque (inside layer of vascular arteries)

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13
Q

What happens during atherosclerosis?

A

Inflammation is a key factor in the development of atherosclerosis
As LDL cholesterol accumulates in the arterial wall, it undergoes chemical changes and signals to endothelial cells to latch onto WBCs circulating in the blood
Immune cells penetrate the intima and trigger an inflammatory response, devouring LDLs to become fat-laden “foam cells”
Form a fatty streak, the earliest stage of atherosclerotic plaque
Plaque continues to grow and forms a fibrous cap
Substances released by foam cells can eventually destabilize the cap, allowing it to rupture, causing a blood clot which can block blood flow and trigger a heart attack

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14
Q

Stable plaques

A

Thick fibrous caps
Partially block vessels
Don’t tend to form clots/emboli

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15
Q

Unstable plaques

A

Thin fibrous caps
May rupture causing clot formation
May completely block artery (that part will not get block and become ischemic leading to necrosis)
Clot may break free (pulmonary embolsis)

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16
Q

Sites of atherosclerosis - arteries

A

Abdominal aorta
Proximal coronary (first part of all coronary arteries)
Thoracic aorta
Femoral & popliteal
Tend to form at branches (turbulence is what creates clots)

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17
Q

Types of atherosclerotic lesions

A

Fatty streak
Fibrous atheromatous plaque
Complicated lesion

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18
Q

Fatty streak

A

Found in all ages, geographic areas, race and lifestyle

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19
Q

Fibrous atheromatous plaque

A

Lipids, smooth muscle, scar tissue

Predispose to thrombus formation

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20
Q

Complicated lesion

A

Clots on it already

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21
Q

Peripheral artery disease

A

Atherosclerosis distal to the aortic arch

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22
Q

Peripheral artery disease risk factors

A

Male
>60 years old
Smokers
Diabetes Mellitus

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23
Q

Peripheral artery disease manifestations

A

Intermittent claudication (in legs - pain when walking - stops when you stop walking)
Thinning of skin and SC tissue
Gradual atrophy of muscles

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24
Q

What does decreased blood supply in peripheral artery disease lead to?

A 
Weak/absent pulses
Cool extremities
Brittle toenails, hair loss
Pallor
Dependant rubor (when legs are down – red because blood collects in artery and isn’t able to move it properly)
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25
Q

Complications of peripheral artery disease

A

Ulceration

Gangrene

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26
Q

Peripheral artery disease diagnosis

A 
Blood pressure changes in leg
Pulse changes
Doppler Ultrasound 
MRI Ateriography/Spiral CT arteriography
Contrast angiography
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27
Q

Raynaud phenomenon

A

Intense episodic vasospastic disorder of arteries and arterioles (usually fingers, less often toes)
Usually young women
Precipitated by cold, strong emotions

28
Q

Primary raynaud phenomenon

A

Symmetrical

29
Q

Secondary raynaud phenomenon

A

Non symmetrical
Associated with pre-existing PAD
Frostbite, occupational trauma (vibrating tools, hot/cold environment)

30
Q

Raynaud phenomenon manifestations

A

Tingling/numbness/aching/throbbing pain

Pallor to cyanosis

31
Q

Aneurysms

A

Abnormal localized dilation of blood vessel

Types (true and false)

32
Q

True aneurysms

A

Berry (happens at branch of artery - bifurcation)
Saccular (sac on one side of artery)
Fusiform (all the way around – like innertube around artery)

33
Q

False aneurysms

A

Dissecting (seperation of anterior wall – get bulge – artery is dissectiong – layers of wall separate – blood leaking in it)

34
Q

Aortic aneurysms

A

Often discovered during routine xray (ECG, ultrasound, MRI, CT)

35
Q

Aortic aneurysm risk factors

A

Atherosclerosis

Age+

36
Q

Aortic aneurysm manifestations

A

Dependent on size, location, stage

37
Q

Thoracic aneurysm

A 
Substernal, back, neck pain
Pressure on:
Trachea = stridor, cough, dyspnea
Laryngeal nerve = hoarsness
Esophagus = difficulty swallowing
Superior vena cava = facial/neck edema
38
Q

Abdominal aortic aneurysm

A 
"Triple A"
Most common
Asymptomatic
Pulsating mass if >4cm often first sign
Mild to severe abdominal and back pain
39
Q

Aneurysm complications

A

Thrombi
Compression (vasculature is vessels, nerves)
Rupture

40
Q

Dissecting aortic aneurysm

A

Often occurs without atherosclerotic changes

41
Q

Dissecting aortic aneurysm risk factors

A

Hypertension (increased pressure)
40-60 year old men
Marfan’s syndrome (connective tissue disorder – everything is stretched – lessens strength of aortic walls)
Pregnancy
Congenital defects of aortic valve
Aortic coarctation (like elastic band around aorta – interferes with good blood flow – increases pressure in aorta)
Blunt trauma

42
Q

Dissecting aortic aneurysm manifestations

A

Excruciating pain anterior chest and back
Blood pressure (initially high, later unobtainable in one or both arms)
Syncope
Lower extremity hemiplegia/paralysis
Heart failure if aortic valve involvement

43
Q

Determinants of BP

A

Short term regulation (neural mechanisms, hum oral mechanisms)
Long term regulation (kidneys retain or excrete water and sodium to regulate vascular volume)

44
Q

Neural mechanisms ANS

A

Medulla and lower pons (CV center)
Parasympathetic impulses via vagus nerve to heart = slows HR
Sympathetic impulses via spinal cord & peripheral sympathetic nerves to heart and blood vessels = increased HR and vasocontriction (increase PVR)

45
Q

Reflexes of neural mechanisms

A
  1. Intrinsic
    Baroreceptors/stretch receptors (carotid and aortic walls, heart)
    Chemoreceptors (carotid and aortic bifurcation)
  2. Extrinsic
    Diffuse reactions d/t pain, cold via hypothalamus/SNS pathways
46
Q

Humoral mechanisms

A

Renin-Angiotension-Aldosterone System (released in response to SNS activity, decreased volumes, converts angiotensin I to angiotension II)
Vasopressin (ADH)
Epinephrine

47
Q

Primary/essential hypertension

A

Chronic/ Without evidence of other disease processes

48
Q

Primary/essential hypertension risk factors

A

Family history
Race
Older age
Lifestyle factors (High salt/caloric/fat intake, chronic excessive alcohol consumption, smoking, stress)

49
Q

Secondary hypertension

A

Results from another disorder

50
Q

Secondary hypertension risk factors

A

Numerous

Diabetes, liver disease, kidney disease

51
Q

Target organ damage

A

Hypertension is asymptomatic until long-term effects are seen in organs
Heart, brain, kidney, liver, lungs, eye

52
Q

Hypertensive crisis

A

Elevated BP with impending target-organ damage

  1. Severe (SBP >180 mmHg & DBP >110 mmHg)
  2. Emergency (DBP >120 mmHg)
53
Q

Orthostatic hypotension

A

Sustained drop in BP d/t a change in body position (usually standing)

54
Q

Orthostatic hypotension causes

A

Reduced blood volume
Pharmaceuticals
Aging
Bedrest/immobility

55
Q

Orthostatic hypotension manifestations

A

Visual changes, dizziness, syncope (temporary loss of consciousness)
Drop in systole BP of 20 mmHg and diastolic BP of 10 mmHg

56
Q

Orthostatic hypotension diagnosis

A 
Lying/standing blood pressure with 2-3 minute wait
Tilt table (people upside down and test BP)
57
Q

Disorders of venous circulation

A 
Skin
Subcutaneous tissues
Superficial veins
Deep veins
Heart
58
Q

Varicose veins

A

Dilated tortuous veins
Aching/edema
25-30% of women; 10-20% of men

59
Q

Varicose veins risk factors

A

Obesity (increased abdominal pressure)

>50 years old

60
Q

Types of varicose veins

A
  1. Primary
    Originate in superficial saphenous veins
    Caused by prolonged standing, pregnancy, abdominal pressure, prolonged heavy lifting
    Stick out and you can see on legs
  2. Secondary
    Impaired flow in deep veins d/t other disease
    Caused by arteriovenous fistulas (abnormal opening/tunnel), venous malformations, tumor, pregnancy.
61
Q

Chronic venous insufficiency causes/manifestations

A 
Venous hypertension (dilation and stretching of vessel wall)
Impaired blood flow results in (edema, impaired tissue nutrition, schema, necrosis, brown pigmentation - hemosiderin deposits, stasis dermatitis - inflammation of the skin in lower legs caused by chronic venous insufficiency, venous ulcers
62
Q

Deep vein thrombosis

A

Thrombus and inflammation
Superficial or deep veins
Virchows triad (stasis, hypercoagulability, vessel wall injury)

63
Q

Deep vein thrombosis risk factors

A 
1. Venous stasis
Bedrest/immobility 
Spinal cord injury
AMI/CHF/Shock (acute MI, chronic heart failure)
Venous obstruction
2. Vascular trauma 
Venous catheters
Surgery, especially orthopedic
Trauma/infection
Fractured hip (huge bone breaking – can send off fat globules)
3. Hypercoagulability
Genetics 
Stress/trauma
Pregnancy/Childbirth
Oral contraceptives/hormone replacement
Dehydration
Cancer
64
Q

Deep vein thrombosis manifestations

A 
Often asymptomatic (50%) – vein not totally occluded
Pain
Swelling
Deep muscle tenderness
Signs of inflammation
65
Q

Deep vein thrombosis complications

A

Pulmonary/cerebral embolus

66
Q

Deep vein thrombosis treatment

A

Prevention
Anticoagulation (med to stop more from happening)
Elevate limb (good blood flow back to heart)
Bedrest
Gradual ambulation with elastic support
Heat (only do when ordered)

Pathophysiology (13 decks)

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