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Pathophysiology > Class 1 chapter 18 > Flashcards

Class 1 chapter 18 Flashcards

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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
Complications of peripheral artery disease
Ulceration | Gangrene
26
Peripheral artery disease diagnosis
``` Blood pressure changes in leg Pulse changes Doppler Ultrasound MRI Ateriography/Spiral CT arteriography Contrast angiography ```
27
Raynaud phenomenon
Intense episodic vasospastic disorder of arteries and arterioles (usually fingers, less often toes) Usually young women Precipitated by cold, strong emotions
28
Primary raynaud phenomenon
Symmetrical
29
Secondary raynaud phenomenon
Non symmetrical Associated with pre-existing PAD Frostbite, occupational trauma (vibrating tools, hot/cold environment)
30
Raynaud phenomenon manifestations
Tingling/numbness/aching/throbbing pain | Pallor to cyanosis
31
Aneurysms
Abnormal localized dilation of blood vessel | Types (true and false)
32
True aneurysms
Berry (happens at branch of artery - bifurcation) Saccular (sac on one side of artery) Fusiform (all the way around – like innertube around artery)
33
False aneurysms
Dissecting (seperation of anterior wall – get bulge – artery is dissectiong – layers of wall separate – blood leaking in it)
34
Aortic aneurysms
Often discovered during routine xray (ECG, ultrasound, MRI, CT)
35
Aortic aneurysm risk factors
Atherosclerosis | Age+
36
Aortic aneurysm manifestations
Dependent on size, location, stage
37
Thoracic aneurysm
``` Substernal, back, neck pain Pressure on: Trachea = stridor, cough, dyspnea Laryngeal nerve = hoarsness Esophagus = difficulty swallowing Superior vena cava = facial/neck edema ```
38
Abdominal aortic aneurysm
``` "Triple A" Most common Asymptomatic Pulsating mass if >4cm often first sign Mild to severe abdominal and back pain ```
39
Aneurysm complications
Thrombi Compression (vasculature is vessels, nerves) Rupture
40
Dissecting aortic aneurysm
Often occurs without atherosclerotic changes
41
Dissecting aortic aneurysm risk factors
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
Dissecting aortic aneurysm manifestations
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
Determinants of BP
Short term regulation (neural mechanisms, hum oral mechanisms) Long term regulation (kidneys retain or excrete water and sodium to regulate vascular volume)
44
Neural mechanisms ANS
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
Reflexes of neural mechanisms
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
Humoral mechanisms
Renin-Angiotension-Aldosterone System (released in response to SNS activity, decreased volumes, converts angiotensin I to angiotension II) Vasopressin (ADH) Epinephrine
47
Primary/essential hypertension
Chronic/ Without evidence of other disease processes
48
Primary/essential hypertension risk factors
Family history Race Older age Lifestyle factors (High salt/caloric/fat intake, chronic excessive alcohol consumption, smoking, stress)
49
Secondary hypertension
Results from another disorder
50
Secondary hypertension risk factors
Numerous | Diabetes, liver disease, kidney disease
51
Target organ damage
Hypertension is asymptomatic until long-term effects are seen in organs Heart, brain, kidney, liver, lungs, eye
52
Hypertensive crisis
Elevated BP with impending target-organ damage 1. Severe (SBP >180 mmHg & DBP >110 mmHg) 2. Emergency (DBP >120 mmHg)
53
Orthostatic hypotension
Sustained drop in BP d/t a change in body position (usually standing)
54
Orthostatic hypotension causes
Reduced blood volume Pharmaceuticals Aging Bedrest/immobility
55
Orthostatic hypotension manifestations
Visual changes, dizziness, syncope (temporary loss of consciousness) Drop in systole BP of 20 mmHg and diastolic BP of 10 mmHg
56
Orthostatic hypotension diagnosis
``` Lying/standing blood pressure with 2-3 minute wait Tilt table (people upside down and test BP) ```
57
Disorders of venous circulation
``` Skin Subcutaneous tissues Superficial veins Deep veins Heart ```
58
Varicose veins
Dilated tortuous veins Aching/edema 25-30% of women; 10-20% of men
59
Varicose veins risk factors
Obesity (increased abdominal pressure) | >50 years old
60
Types of varicose veins
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
Chronic venous insufficiency causes/manifestations
``` 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
Deep vein thrombosis
Thrombus and inflammation Superficial or deep veins Virchows triad (stasis, hypercoagulability, vessel wall injury)
63
Deep vein thrombosis risk factors
``` 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
Deep vein thrombosis manifestations
``` Often asymptomatic (50%) – vein not totally occluded Pain Swelling Deep muscle tenderness Signs of inflammation ```
65
Deep vein thrombosis complications
Pulmonary/cerebral embolus
66
Deep vein thrombosis treatment
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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