Chap 18 Disordes of Bld Flow & BP Flashcards
*Atherosclerosis
a progressive disease characterized by the formation of fibrofatty plaques in the intima of large and medium-sized vessels, including aorta, coronary arteries, and cerebral vessels, that protrude into and can eventually obstruct blood flow.
Atheros- paste
sclerosis- hardening
The major risk factors for atherosclerosis are?
Hypercholesterolemia and inflammation
*Hyperlipidemia
involves abnormally elevated levels of any or all lipids and/or lipoproteins in the blood
-cholesterol & triglycerides (dietary lipids) are insoluable in plasma as encapsulated by lipoproteins
*Name different types of lipoproteins:
Chylomicrons
VLDL-very low density lipo=
55-65% triglycerides
10% cholesterol
5-10% protein
LDL- low density lipo
10% triglyceride
50% cholesterol
25% protein
IDL- intermediate density lipo
HDL- high density lipo (good one)
5% triglyceride
20% cholesterol
50% protein
lipoproteins are named based on their?
protein content, which is measured by their density. Fats are less dense than protein
Possible causes of hyperlipidemia
Lipid blood levels raised by:
- nutrition
- genetics
- comorbid conditions
- meds
2 areas of lipoprotein synthesis
liver and small intestine
*Risk factors of atherosclerosis
nonmodifiable:
potentially modifiable:
additional nontraditional:
Nonmodifiable
- hypercholesteremia
- increasing age
- gender, male
- family hx
- premature coronary artery disease that cannot be changed
Potentially modifiable
- smoking
- obesity
- HTN
- Hyperlipidemia
- DM
Additional nontraditional
- inflammation marked by elevated C-reactive protein
- increased lipoprotein
*Sites of atherosclerosis: arteries
these form at branches!!
1- Adb aorta and iliac arteries
2-Proximal coronary arteries
3-Thoracic aorta, femoral ad popliteal arteries
4-interna carotid arteries
5- Vertebral, basilar and middle cerebral arteries
Describe the types of lesions that can occur from atherosclerosis
1- the fatty streak
2-the fibrous atheromatous plaque
3- complicated lesions
*The fatty streak
the complicated lesion. Thin, flat, yellow intimal discolorations that progressively enlarge by becoming thicker and slightly elevated as they grow in length.
- in childrens 1st year of life.
- found in all ages/geographic areas/race/lifestyle/ect.
*Fibrous atheromatous plaque
accumulation of lipids, smooth muscle cells and scar tissue. Eventually may occlude artery and may predispose to thrombus (!!!most important complication!!!)
*The complicated lesion
-most advanced atherosclerotic lesions may contain hemorrhage, ulceration and scar tissue deposits.
The development of atherosclerotic lesions is a progressive process involving:
1- Endothelial cell injury
2- Migration of inflammatory cells
3- Lipid accumulation and smooth muscle cell proliferation
4- Plaque structure
Endothelial Cell Injury
The vascular endothelium is single layer cell-to-cell protection of subendothelial layer that separates blood cells and other blood components.
- agents that are the cause the endothelial injury cause adhesion of monocytes and platelets.
Migration of inflammatory cells
Early in develop athero lesions, endo cells begin to express selective adhesion molecules that bind monocytes and other inflam cells that initiate atherosclerotic lesions.
-after monocytes adhere endothelium, they migrate between the endo cells to localize in the intima, transform into macrophages, and angulf lipoproteins> largely LDL.
Lipid accumulation and smooth muscle cell proliferation
Although The adhesion of monocytes to remove LDL protects, it is also the contribution of athero.
- the activated macrophages release toxic O2 species that oxidize LDL
- the oxidized LDL is then ingested by macrophages through scavenger receptor, resulting in formation of foam cells, which are the primary component of athero lesions
- activated macrophages also produce growth factors that contribute to the migration and proliferation of smooth muscle cells (SMC) and the elaboration of the extracellular matrix (ECM).
Plaque structure
Athero plaque consists of aggregation of SMCs, macrophages, and other leukocytes, ECM-with collagen and elastic fibers, intra and extra cellular lipids.
- Fibrous cap consists of SMCs and dense ECM.
- beneath SMCs, and around cap consists of macrophages, and lymphocytes.
- Below that is central core of lipid laden foam cells and fatty debris.
- Rupture , ulceration or erosion of cap may lead to hemorrhage into the plaque or thrombotic occlusion of the vessel lumen.
*LDL is the main carrier of ________ but leaves some behind for uptake in arterial wall
cholesterol
*HDL also carry _________ but remove it from tissues and take to ______ for disposal.
cholesterol
Liver
*Lipid blood levels raised by
Nutrition
- -High-calorie diet increases production of VLDL & it’s conversion to LDL
- -Genetics
- -Comorbid conditions/diseases
- -Medication
*Tobacco Use
Increases blood lipid levels Damages endothelium Enhances thrombosis formation Increases blood viscosity Increases circulating catecholamines
*Arteriosclerosis
hardening of walls of artery
*Arteriolosclerosis
sclerosis and thickening of the walls of arterioles
*Atherosclerosis
a disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls
*What happens during atherosclerosis?
Inflam is key factor to athero.
- wht bld cells LDL accumulates in the arterial wall, it undergoes chemical changes and signals to endothelial cells to latch onto wht bld cells circulating in the bld. These immune cells penetrate into the intima and trigger an inflame response, devouring LDLs, to become fat-laden “foam cells” and
- form a fatty streak, the earliest stage of atherosclerotic plaque.
- the 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 bld flow and trigger a heart attack.
*Stable plaques
- thick fibrous caps
- partially blocks vessels
- doesn’t tens to form clots/thrombus
*Unstable plaques
- thin fibrous caps
- may completely block arery
- may break free
*Peripheral Artery Disease:
and risk factors:
Atherosclerosis distal to the aortic arch Risk Factors: Male >60 years old Smokers Diabetes Mellitus
*Peripheral Artery Disease:
manifestations:
- Intermittent claudication (pain with walking). stops when you stop moving
- Thinning of skin & SC tissues of the lower leg
- Gradual atrophy of muscles
- Decreases blood supply, leads to:
- –weak absent pulses
- –cool extremities
- –brittle toenails, hair loss (men and women no hair on legs)
- – pallor
- – dependent rubor- when blood pools in the legs and arteries cant move the blood
*PAD complications:
ulceration and gangrene
*PAD diagnosis:
- Blood pressure changes in leg
- Pulse changes
- Doppler Ultrasound
- MRI Ateriography/Spiral CT arteriography
- Contrast angiography.
*PAD treatment:
- -Walking to the point of claudication, increases collateral circulation.
- -Avoiding surface injury as slow to heal
- -Address causes; like other cardiovascular risk factors (smoking, HTN, DM, hyperlipidemia)
- -Antiplatelet therapy (ASA, Clopidogrel)
- -Statins
- -Femoralpopliteal bypass grafting (if severe)
- -Percutaneous transluminal (through tube) angioplasty (balloon) and stenting (balloon area of stenosis)
*Raynaud Phenomenon
> Intense episodic vasospastic disorder of arteries and arterioles
-usually involves fingers and toes, less often toes
> Primary: occurs w/o cause: symmetrical
Secondary: non-symmetrical
-Associated with other disease states or known cause of vasospasm
-Frostbite, occupational trauma (vibrating tools, hot/cold environment)
Usually young _women
*Raynaud Phenomenon usually precipitated by:
-cold or strong emotions
*Raynaud Phenomenon
manifestations:
- change in skin color (pallor to cyanosis)
- sensation of cold
- changes in sensory perception (numb/tingle)
*Raynaud Phenomenon
treatment:
- Avoidance of triggers
- Avoidance of vasoconstrictive medications
- Vasodilatory medications
- Sympathectomy (cut sympathetic nerve).
*Aneurysms
Abnormal localized dilation of blood vessel
-most common in the aorta
*Types of aneurysms:
> True-bonded by complete vessel wall. The blood in true aneurysm remains in vascular compartment.
- -Berry-sml spherical dilation of vessel at a bifurcation
- -Saccular- part of circumference of vessel-saclike.
- -Fusiform- entire circumference of the vessel, characterized by gradual progression of dilation of vessel.
> False-localized dissection or tear in the inner wall of the artery with formation of an extravascular hematoma that causes vessel enlargement.
–Dissecting- false aneurysm. Resulting in tear in the intimal layer of the vessel that allows bld to enter vessel wall, dissecting layers to create bld-filled cavity.
*Aortic Aneurysm discovered during?
routine Xray
ECG, Ultrasound, MRI, CT
*Aortic Aneurysm
Risk factors:
Atherosclerosis
Age+
*Aortic Aneurysm
Manifestations:
Dependent on size, location, stage
Thoracic
Substernal, back, neck pain
>Pressure on:
–Trachea = dyspnea, stridor, brassy cough
–Laryngeal nerve = voice hoarseness
–Esophagus = difficulty swallowing
–Superior vena cava = distension of neck veins and edema of face and neck
Abdominal Aortic (most common) “Triple A”
>Asymptomatic
>Pulsating mass if >4cm often first sign
>Mild to severe abdominal and back pain.
*Aneurysm: Complications
>Thrombi >Compression --Vasculature --Nerves >Rupture
*Dissecting Aortic Aneurysm
Risk factors:
Often occurs without atherosclerotic changes
Risk Factors:
-Hypertension
-40-60 year old men
-Marfan’s syndrome- genetic disorder of CT. defects of heart valves and aorta. (Tall, long fingers and toes…)
-Pregnancy-bc increased thoracic pressure
-Congenital defects of aortic valve
-Aortic coarctation- like elastic band around aorta
-Blunt trauma.
*Dissecting AA Manifestations:
> Excruciating pain like tearing & ripping in anterior chest and back
Blood pressure
–Initially moderate
–Later unobtainable in one or both arms
Syncope
Lower extremity hemiplegia/paralysis
Heart failure if aortic valve involvement
*Mean Arterial Blood Pressure (MAP)
Systolic Blood Pressure
Diastolic Blood Pressure
Pulse Pressure
3
CO =
HR x SV (stroke vol)
BP =
CO x SVR systemic vascular resistance
Determinants of Blood Pressure (review!)
short term regulation:
Acting over minutes or hours. Intended to correct temp imbalances in BP. Ex exercise and in life threatening situations.
>Neural Mechanisms- transmit parasympathic impulses in brain= slowing of heart
>Humoral Mechanisms- renin-angiotensin kidneys
Determinants of Blood Pressure (review!)
long term regulation:
Kidneys retain or excrete water and sodium to regulate vascular volume (ECV)
Neural Mechanisms: ANS for regulating BP
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 = increase heart rate and vasoconstriction (increase PVR)
Neural Mechanisms (cont) ANS for regulating BP Intrinsic reflexes:
for rapid and short term regulation of BP
> Baroreceptors/stretch receptors- pressure sensitive in walls of heart. Carotid and aortic. Respond to changes in stretch of vessel wall by send impulse to cardiovas center in brain stem.
Chemoreceptors- Monitor O2, CO2 and H+ in bld. Located in carotid bodies of aorta. Regulate ventilation and communicate with cardiovas centers in brain stem.
Neural Mechanisms (cont) ANS for regulating BP Extrinsic reflexes:
diffuse reactions d/t pain, cold via hypothalamus/SNS pathways
Humoral Mechanisms for regulating BP
Renin-Angiotension-Aldosterone System
–Released in response to SNS activity, decreased volumes
–Converts angiotensin I to angiotension II (from enz in lungs)
Vasopressin (ADH)- released from post pit bc decrease in BP (vasoconstrictor)
Epinephrine- directly increases BP by increasing HR, cardiac contractility and vascular tone.
Hypertension is the leading cause of
CV disorders
stages of HTN:
180+ high stage 2 140-160 high stage 1 120-140 prehypertension 90-120 normal 40-90 low
Primary/Essential Hypertension-
risk factors:
Chronic/ Without evidence of other disease processes. No cause identified.
Risk Factors: >Family history >Race >Older age >Lifestyle factors- high Na intake/fat intake, chronic alcohol, stress (cortisol)
Secondary Hypertension-
risk factors:
Results from another disorder
Risk Factors:
>Kidney disease
>Adrenal cortical disorders
>Pheochromocytoma-sml vascular tumor of adrenal medulla, cause irreg secretion of epinephrine and norep
>Coarctation of the Aorta
>Pharmaceuticals
>Obstructive Sleep Apnea- messes up adrenal glad and cortisol levels
Target Organ Damage:
Hypertension is asymptomatic until long-term effects are seen in organs
Heart Brain Kidney Liver Lungs Eye
Hypertensive Crisis
Severe:
Elevated BP with impending target-organ damage
severe: SBP >180 mmHg &
DBP >110 mmHg
Hypertensive Crisis
Emergency:
Elevated BP with impending target-organ damage
DBP >120 mmHg
Orthostatic Hypotension
causes:
Sustained drop in BP d/t a change in body position (usually standing) acute and chronic conditions: -reduced bld vol -drug induced -altered vas respons from aging -bed rest -ANS dysfunction (unconscious actions)
Orthostatic Hypotension
manifestations:
> Visual changes, dizziness, syncope, nausea
>Drop in systole BP of 20 mmHg and diastolic BP of 10 mmHg
Orthostatic Hypotension
diagnosis:
> Lying/Standing Blood Pressure with 2-3 minute wait
>Tilt Table
Disorders of Venous Circulation. what areas of the body?
Skin Subcutaneous tissues Superficial veins Deep veins Heart
Low Pressure System!
Varicose Veins
> Dilated tortuous veins- lots of twists and turns
aching and edema
25-30% of women; 10-20% of men
Risk Factors:
>Obesity
>50 years old.
Varicose Veins (cont) Primary:
> Originate in superficial saphenous veins
>Caused by prolonged standing, pregnancy, abdominal pressure, prolonged heavy lifting
Varicose Veins (cont) secondary:
> Impaired flow in deep veins d/t other disease
>Caused by arteriovenous fistulas, venous malformations, tumor, pregnancy.
Chronic Venous Insufficiency
causes:
manifestations:
> Venous hypertension
–Dilation & stretching of vessel wall
> Impaired blood flow results in:
- -edema, impaired tissue nutrition
- -necrosis, ischemia
- -hemosiderin deposits (brown pigmentation)
- -ulceration (stasis dermatitis)
Deep Vein Thrombosis
Thrombus & Inflammation
Superficial or Deep Veins
Virchow’s Triad
Venous Stasis (no flow) + vascular trauma (vessel wall inj) + hypercoaguability = thrombosis
Risk Factors for DVT 1:
2:
- Venous stasis
- Bedrest/immobility
- SC injury
- AMI/CHF/Shock
- Venous obstruction - Vascular trauma
- Venous catheters
- Surgery, especially orthopedic
- Trauma/infection
- # hip
Risk Factors for DVT (cont) 3:
- Hypercoagulability
- Genetics
- Stress/trauma
- Pregnancy/Childbirth
- Oral contraceptives/hormone replacement
- Dehydration
- Cancer
DVT manifestations:
- -often asymptomatic (50%)- vein not totally occluded
- -pain
- -swelling
- -deep muscle tenderness
- signs of inflammation. you can feel the hot spot sometimes on leg or over area
DVT cont
Complications:
and Tx:
> Complication:
- Pulmonary/cerebral embolus
- often when you throw a clot, you will throw another
> Treatment
- Prevention
- Anticoagulation
- Elevate limb
- Bedrest
- Gradual ambulation with elastic support
- Heat
how do you test for atherosclerosis?
-C-reactive protein
-signs of inflammation
-hyperhomocystinemia
increased serum lipoprotein
