``` Cholesterol & triglycerides (dietary lipids) are insoluble in plasma as encapsulated by lipoproteins 5 types of lipoproteins Chylomicrons VLDL LDL IDL HDL ``` - LDL is the main carrier of cholesterol but leaves some behind for uptake in arterial wall - HDL also carry cholesterol but remove it from tissues and take to liver for disposal. - Genetic defect of these proteins may accelerate atherosclerosis

- Increases blood lipid levels - Damages endothelium - Enhances thrombosis formation - Increases blood viscosity - Increases circulating catecholamines.

Intense episodic vasospastic disorder of arteries and arterioles - Usually fingers, less often toes Primary: symmetrical - Secondary: non-symmetrical - Associated with pre-existing PAD - Frostbite, occupational trauma (vibrating tools, hot/cold environment) - Usually young women

Abnormal localized dilation of blood vessel 1. True - Berry (happens at a branch of an artery) - Saccular (pouches out) - Fusiform (all the way around the artery) 2. False - Dissecting (layers of the wall separate b/c there is blood leaking)

Often discovered during routine Xray - ECG, Ultrasound, MRI, CT Risk Factors - Atherosclerosis - Age+ Manifestations - Dependent on size, location, stage

Disorders of blood flow and blood pressure Flashcards by Fiona Orr

hyperlipidemia

Cholesterol &amp; triglycerides (dietary lipids) are insoluble in plasma as encapsulated by lipoproteins
5 types of lipoproteins
Chylomicrons
VLDL 
LDL 
IDL 
HDL

LDL is the main carrier of cholesterol but leaves some behind for uptake in arterial wall
HDL also carry cholesterol but remove it from tissues and take to liver for disposal.
Genetic defect of these proteins may accelerate atherosclerosis

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hyperlipidemia causes/risks

Lipid blood levels raised by
Nutrition
- High-calorie diet increases production of VLDL &amp; it’s conversion to LDL
Genetics
Comorbid conditions/diseases
Medication

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Atherosclerosis Risk Factors: non-modifiable

Risk Factors: non-modifiable

Age
Gender
Post-menopausal women
Family hx of premature CAD
Genetically determined alteration in lipoprotein and cholesterol metabolism.

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Atherosclerosis Risk Factors: modifiable

Risk Factors: modifiable

Cigarette smoking
Obesity
Hypertension
Hyperlipidemia
Diabetes mellitus

C-reactive protein
Hyperhomocystinemia
Increased serum lipoprotein

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Tobacco use

Increases blood lipid levels
Damages endothelium
Enhances thrombosis formation
Increases blood viscosity
Increases circulating catecholamines.

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Arteriosclerosis, Arteriolosclerosis, & Atherosclerosis

Arteriosclerosis
Hardening of medium to large arteries

Arteriolosclerosis
Hardening of small arterioles

Atherosclerosis
Hardening d/t atheromatous plaque

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Atherosclerosis plaques

Stable plaques

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

Unstable plaques

Thin fibrous caps
May rupture causing clot formation
May completely block artery
Clot may break free

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Sites of Atherosclerosis: Arteries

Abdominal aorta
Proximal coronary
Thoracic aorta
Femoral & popliteal
tend to form at branches*

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Types of Atherosclerotic Lesions

Fatty Streak
- Found in all ages/geographic areas/race/lifestyle, etc.
Fibrous Atheromatous Plaque
- Lipids, smooth muscle, scar tissue
- Predispose to thrombus formation
Complicated Lesion- clots & lesions forming

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Peripheral Artery Disease & Risk Factors

Atherosclerosis distal to the
aortic arch

Risk Factors

Male
> 60 years old
Smokers
Diabetes Mellitus

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Peripheral Artery Disease Manifestations

Intermittent claudication (pain in the legs when moving)
Thinning of skin & tissue
Gradual atrophy of muscles
Decreases blood supply, leads to: weak/absent pulses, cool extremities, brittle toenails, hair loss, pallor, dependent rubor.

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Peripheral Artery Disease Complications

-Ulceration, gangrene

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Peripheral Artery Disease Diagnosis

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

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Raynaud Phenomenon

Intense episodic vasospastic disorder of arteries and arterioles
- Usually fingers, less often toes

Primary: symmetrical

Secondary: non-symmetrical
Associated with pre-existing PAD
Frostbite, occupational trauma (vibrating tools, hot/cold environment)
Usually young women

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Raynaud Phenomenon Manifestations

Precipitated by cold, strong emotions

Manifestations
Tingling/numbness/aching/throbbing pain
Pallor to cyanosis

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Aneurysms

Abnormal localized dilation of blood vessel

True
- Berry (happens at a branch of an artery)
- Saccular (pouches out)
- Fusiform (all the way around the artery)
False
- Dissecting (layers of the wall separate b/c there is blood leaking)

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Aortic Aneurysm

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Often discovered during routine Xray
- ECG, Ultrasound, MRI, CT

Risk Factors

Atherosclerosis
Age+

Manifestations
- Dependent on size, location, stage

Aneurysm: Thoracic

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Substernal, back, neck pain

Pressure on:
Trachea = cough, stridor, dyspnea 
Laryngeal nerve = hoarseness
Esophagus = difficulty swallowing
Superior vena cava = facial/neck edema

Aneurysm: Abdominal Aortic

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“Triple A” – Most Common

Asymptomatic
Pulsating mass if >4cm often first sign
Mild to severe abdominal and back pain.

Aneurysm: Complications

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Thrombi

Compression

Vasculature
Nerves

Rupture

Risk Factors for Aortic Aneurysm

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Often occurs without atherosclerotic changes

Risk Factors

Hypertension
40-60 year old men
Marfan’s syndrome
Pregnancy
Congenital defects of aortic valve
Aortic coarctation (band around the aorta which decreases bloodflow)
Blunt trauma.

Dissecting AA Manifestations

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> Excruciating pain anterior chest & back

> Blood pressure

Initially high
Later unobtainable in one or both arms

> Syncope
Lower extremity hemiplegia/paralysis
Heart failure if aortic valve involvement

Determinants of Blood Pressure (review!)

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Short-Term Regulation
Neural Mechanisms
Humoral Mechanisms

Long-Term Regulation
Kidneys retain or excrete water and sodium to regulate vascular volume (ECV)

Neural Mechanisms: ANS

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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 & vasoconstriction (incr PVR)

Neural Mechanisms con't

Intrinsic reflexes Baroreceptors/stretch receptors - Carotid & aortic walls, heart Chemoreceptors - Carotid and aortic bifurcation Extrinsic reflexes: diffuse reactions d/t pain, cold via hypothalamus/SNS pathways.

Humoral Mechanisms

> Renin-Angiotension-Aldosterone System (renin released by JG cells in smooth muscle increases BP) - Released in response to SNS activity, decreased volumes - Converts angiotensin I to angiotension II > Vasopressin (ADH) > Epinephrine

Primary/Essential Hypertension (Risk Factors)

- Chronic/ Without evidence of other disease processes Risk Factors - Family history - Race - Older age - Lifestyle factors: high salt/caloric/fat intake, chronic excessive alcohol consumption, smoking, stress

Secondary Hypertension

- Results from another disorder | - Numerous risk factors

Target Organ Damage

Hypertension is asymptomatic until long-term effects are seen in organs ``` Heart Brain Kidney Liver Lungs Eye ```

Hypertensive Crisis

Elevated BP with impending target-organ damage Severe: SBP >180 mmHg & DBP >110 mmHg Emergency: DBP >120 mmHg Vascular damage! Symptoms!

Orthostatic Hypotension

Sustained drop in BP d/t a change in body position (usually standing) ``` Causes Reduced blood volume Pharmaceuticals Aging Bedrest/immobility ```

Orthostatic Hypotension (cont) manifestations & diagnosis

Manifestations - Visual changes, dizziness, syncope - Drop in systole BP of 20 mmHg and --diastolic BP of 10 mmHg Diagnosis - Lying/Standing Blood Pressure with 2-3 minute wait - Tilt Table

Disorders of Venous Circulation

- Skin - Subcutaneous tissues - Superficial veins - Deep veins - Heart -Low Pressure System

Varicose Veins

Dilated tortuous veins Aching/edema (slower blood movement --> increased pressure) 25-30% of women; 10-20% of men Risk Factors Obesity >50 years old.

Varicose Veins: Primary & Secondary

1. Primary - Originate in superficial saphenous veins - Caused by prolonged standing, pregnancy, abdominal pressure, prolonged heavy lifting 2. Secondary - Impaired flow in deep veins d/t other disease - Caused by arteriovenous fistulas, venous malformations, tumor, pregnancy.

Chronic Venous Insufficiency: Causes/Manifestations

``` Causes/Manifestations -Venous hypertension -Dilation & stretching of vessel wall -Impaired blood flow results in: Edema, impaired issue nutrition Ischemia, necrosis Brown pigmentation Stasis dermatitis Venous ulcers ```

Deep Vein Thrombosis

Thrombus & Inflammation Superficial or Deep Veins Virchow’s Triad: - Venous stasis - Vascular trauma

Risk Factors for DVT

1. Venous stasis - Bedrest/immobility - SC injury - AMI/CHF/Shock - Venous obstruction 2. Vascular trauma - Venous catheters - Surgery, especially orthopedic - Trauma/infection - # hip

Risk Factors for DVT con't

``` Hypercoagulability Genetics Stress/trauma Pregnancy/Childbirth Oral contraceptives/hormone replacement Dehydration Cancer ```

DVT manifestations

``` Often asymptomatic (50%) Pain Swelling Deep muscle tenderness Signs of inflammation ```

DVT complications and treatment

``` > Complication -Pulmonary/cerebral embolus > Treatment -Prevention -Anticoagulation -Elevate limb -Bedrest -Gradual ambulation with elastic support -Heat ```

Disorders of blood flow and blood pressure Flashcards

(41 cards)