Chapter 18: Disorders of Blood Flow and Blood Pressure Flashcards
Discuss the possible causes of hyperlipidemia and describe the different types of lipoproteins that affect lipid blood levels.
Causes
- Nutrition
- High calorie diet increases production of VLDL & it’s conversion to LDL
- Genetics
- Comorbid conditions/disease
- Medication
- Tobacco use
Types of Lipoproteins
LDL (Low-density) - main carrier of cholesterol but leaves some behind for uptake in arterial wall
-60% is transported to liver, 40% is left to tissue
HDL (high-density) - carries cholesterol but removes it from tissues and takes to liver for disposal
Chylomicrons
- largest
- transfer their triglycerides to the cells of adipose and skeletal tissue. Remant chylomicron particles, contains cholesterols are taken up by the liver.
VLDL (very low)
-carry their triglycerides to fat and muscle cells
IDL (intermediate)
List the risk factors for atherosclerosis
NON-MODIFIABLE Age Male Post-menopausal women Family history of premature CAD Genetically determined alterations in lipoprotein and cholesterol metabolism
MODIFIABLE Smoking Obesity Hypertension Hyperlipidemia Diabetes mellitus C-reactive protein Hyperhomocystinemia Increased serum lipoprotein (a
List the vessels most commonly affected by atherosclerosis and describe the types of atherosclerotic lesions that can occur
MOST COMMON: ARTERIES
- Abdominal aorta
- Proximal coronary
- Thoracic aorta
- Femoral & popliteal
- Iliac
- Internal carotid
- Vertebral, basilar, middle cerebral
TYPES
Fatty Streak
-thin, flat, yellow
-Found in all ages/geographic areas/race/lifestyle, etc
Fibrous Atheromatous Plaque
Lipids, smooth muscle, scar tissue
Predispose to thrombus formation
Complicated Lesion
Describe the pathological process involved in the development of atherosclerosis
Endothelial Cell Injury
-agents such as smoking. LDL, stress causes injury with adhesion of monocytes and platelets
Migration of Inflammatory Cells
- binding of monocytes and other inflammatory cells that initiate lesions
- Macrophages engulfs LDL
Lipid Accumulation and Smooth Muscle Cell Proliferation
-Activated macrophages releases toxic oxygen that oxidize LDL, then macrophages injests oxidized LDL in which forms foam cells, which are primary component of atherosclerotic lesions.
Plaque Structure
-plaque consists of smooth muscle cells, macrophages, and leukocytes; ECM and intracellular and extracellular lipids.
Describe the role of inflammation in the development of atherosclerosis and how it can be assessed clinically
-agents causes damages in lining in which attracts the inflammatory cells to initiate lesions
- CRP is an acute-phase reactant synthesized in the liver that is a marker for systemic inflammation
- A number of population-based studies have demonstrated that baseline CRP levels can predict future cardiovascular events among apparently healthy individuals.
- High-sensitivity CRP (hs-CRP) may be a better predictor of cardiovascular risk than lipid measurement alone.
- Because CRP is an acute inflammatory phase reactant, major infections, trauma, or acute hospitalization can elevate CRP levels (usually 100-fold or more). Thus, CRP levels to determine cardiovascular risk should be performed when the person is clinically stable
Compare the risk factors, manifestations, and possible treatments associated with peripheral arterial disease and Raynaud phenomenon.
PERIPHERAL ARTERIAL DISEASE RISK FACTOR -Male ->60 years old -Smokers -Diabetes Melitus
MANIFESTATION
- Intermittent claudication
- Thinning of skin & s/c tissue
- Gradual atrophy os muscles
- Decreases blood supply, leads to:
- Weak/absent pulses
- Cool extremities
- Brittle toenails, hair loss
- Pallor
- Dependent rubor
TREATMENT
- Walking to the point of claudication
- Avoiding surface injury as slow to heal
- Address the causes
- Antiplatelet therapy (ASA, clopidogrel)
- Statins
- Invasive procedures such as femoral popliteal bypass grafting
- Percutaneous transluminal angioplasty and stenting
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 -Precipitated by cold, strong emotions
MANIFESTATION
- Tingling & numbness/aching/throbbing -pain
- Pallor to cyanosis
TREATMENT Avoidance of triggers Avoidance of vasocontrictive medications Vasodilatory medications Sympathectomy
Distinguish between the possible aneurysms types based on appearance and location.
Abnormal localized dilation of blood vessel
True
- bounded by a complete vessel wall.
- Berry (small pouch)
- Saccular (small sac to one side)
- Fusiform (small sack around whole)
False
- localized dissection or tear in the inner wall of the artery with formation of an extravascular hematoma that causes vessel enlargement.
- dissecting
Distinguish between the pathology, manifestations, and complications of aortic and thoracic aneurysms.
AORTIC ANEURYSMS -associated with severe atherosclerosis ->50 age -smoking and genetics MANIFESTATION -depends on size, location and stage -Pulsating mass if >4cm often first sign -Mild to severe abdominal and back pain
Dissecting Aortic Aneurysm Often occurs without atherosclerotic changes Risk Factors Hypertension 40-60 year old men Marfan's syndrome Pregnancy Congenital defects of aortic valve Aortic coarctation Blunt trauma
Excruciating pain anterior chest & back Blood pressure changes -Initially high -Later unobtainable in one or both arms Syncope Lower extremity hemiplegia/paralysis Heart failure if aortic valve involvement
THORACIC
-may involve one or more aortic segments.
MANIFESTATION
- asymptomatic
- when symptoms occur, depends on size, and position
- Substernal, back, neck pain
Pressure on: Trachea = stridor, cough, dyspnea Laryngeal nerve = hoarseness Esophagus = difficulty swallowing Superior vena cava = facial/neck edema
COMPLICATIONS: Thrombi Compression -Vasculature -Nerves
Define the terms arterial blood pressure, systolic blood pressure, diastolic blood pressure, pulse pressure, and mean arterial blood pressure
Arterial Blood Pressure - the rhythmic ejection of blood from the left ventricle into the aorta
Systolic Blood Pressure - the highest pressure
Diastolic Pressure - the lowest pressure
Pulse Pressure - the difference between the systolic and diastolic pressure
Mean Arterial Pressure - average pressure in the arterial system during ventricular contraction and relaxation
MAP = diastolic pressure + pulse pressure divided by 3
Explain how changes in cardiac output and peripheral vascular resistance interact in determining systolic and diastolic blood pressure.
The arterioles are referred to as the resistance vessels because they can selectively constrict or relax to control the resistance to outflow of blood into the capillaries
The body maintains blood pressure by adjusting the cardiac output to compensate for changes in PVR, and its changes the PVR to compensate for changes in cardiac output
Discuss the short-term and long-term determinants of blood pressure
SHORT TERM:
Neural Mechanism
-Medulla and lower pons (CV center)
- Parasympathetic impulses via vagus nerve to heart = slow HR
- Sympathetic impulses via spinal cord & peripheral sympathetic nerves to heart and blood vessels – increase HR and vasoconstriction (increase PVR)
INTRINSIC REFLEXES:
Baroreceptors
Carotid & aortic walls, heart
Chemoreceptors
Carotid and aortic bifurcation
EXTRINSIC REFLEXES:
diffuse reactions d/t pain, cold via hypothalamus/SNS pathways
HUMORAL MECHANISM
Renin-Angiotension-Aldosterone System
Released in response to SNS activity, decreased volumes
Converts angiotensin I to angiotensin II
Vasopressin (ADH)
Epinephrine
LONG TERM
Long-Term Regulation
Kidneys retain or excrete water and sodium to regulate vascular volume (ECV)
Cite the definition of hypertension and Differentiate between primary and secondary forms of hypertension
Defined as high blood pressure, is categorized as primary and secondary
Primary is defined as an elevation of blood pressure without evidence of other disease conditions
Risk Factors Family history Race Older age Lifestyle factors High salt/caloric/fat intake Chronic excessive alcohol consumption Smoking stress
Secondary is an elevation of blood pressure resulting from some other disorder, such as kidney disease
Risk Factors Kidney disease Adrenal cortical disorders Pheochromocytoma Coarctation of the aorta Pharmaceuticals Obstructive sleep apnea
Explain the term “target organ damage” as it pertains to hypertension and its effect on body organs and tissues
Target organ damage is the long-term effects of hypertension on other organ systems such as the kidneys, heart, eyes, brain, liver, lungs and blood vessels
Define the term orthostatic hypotension
Sustained drop in BP d/t a change in body position (usually standing)
Explain how fluid deficit, medications, aging, disorders of the ANS, and bed rest contribute to the development of orthostatic hypotension
Fluid Deficit
-when blood volume is decreased, the vascular compartment is only partially filled; although cardiac output may be adequate when a person is in the recumbent position
Medication
-because hypertensive drugs are used to lower blood pressure, therefore the chances of orthostatic hypotension is increased.
Aging
- diminished ability to produce an adequate increase in HR, ventricular stroke volume, or peripheral vascular resistance
- decreased function of the skeletal muscle pumps and decreased blood volume
Bed rest
-prolonged bed rest promotes a reduction in plasma volume, a decrease in venous tone, failure of peripheral vasoconstriction, and weakness of the skeletal muscle that support the veins and assist in returning blood to the heart
