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A functional Disorder caused by
intense vasospasm of the arteries
and arterioles in the fingers and
less often in the toes.
Raynaud's Phenomenon
Vasodilation occurs by
withdrawal of sympathetic
stimulation
Can be result of cooling of head, neck and trunk
Can also be caused by emotional stress, anxiety
It is associated with other disease states that cause
vasospasm
Can be associated with previous vessel injury like:
frostbite
Cause of Raynaud's
occupational trauma (heavy vibrating tools)
Phenomenon
collagen diseases
neurologic disorders
chronic arterial occlusive disorders
Exposure to alternating hot and cold temperatures
It is often the first symptom of collagen diseases like
scleroderma and systemic lupus erythematosus (SLE)
, All fingers usually affected symmetrically but can affect
only 1-2 digits or only part of a digit
Ischemia due to vasospasm causes change in skin color
Progresses from pallor to cyanosis
A sensation of cold
Raynaud's Phenomenon Changes in sensory perception (Numbness and
Manifestations Tingling)
Followed by period of hyperemia
Nails may become brittle
Skin over tips of fingers may thicken
Nutritional impairment may give rise to arthritis
Can cause ulceration and gangrene
Eliminate factors that cause vasospasm
Protect digits from trauma during ischemic episode
Abstinence from smoking
Avoid vasoconstrictor medications (Decongestants)
Raynaud's Phenomenon
Use vasodilator drugs to avoid thrombosis and
Treatment
gangrene (calcium channel blockers, alpha adrenergic
blocker)
Sympathectomy-surgical interruption of sympathetic
nerve pathways
Hypercholesterolemia
Increasing age
Family history of premature Coronary Heart Disease
Male Sex
Strong Family History of heart disease/stroke
Risk increases for women after menopause (estrogens
no longer protectant)
Cigarette smoking (Worsens endothelial damage)
Atherosclerosis Risk Factors Obesity
Visceral fat
Hypertension
Diabetes Mellitus
C-Reactive Protein (CRP)-serum marker for systemic
inflammation
Serum Homocysteine
Serum Lipoprotein
Infectious Agents (Chlamydia, herpes, cytomegalovirus)
, Formation of fibrofatty lesions in
the intimal lining of the large and
medium sized arteries
Clinical manifestations can take
20-40 years
Atherosclerosis Step 1-Endothelial Cell Injury
Pathophysiology Step 2-Migration of Inflammatory
Cells
Step 3-Lipid Accumulation and
Smooth Muscle Cell Proliferation
Step 4-Plaque Structure (Usually
by 3rd decade of life)
1. Fatty Streak (thin, flat, yellow,
progressively enlarge by
becoming thicker and elevated.
-Present in children in 1st year of
life
-Increase in number throughout
life until age 20
2. Fibrous Atheromatous Plaque
3 Types of Atherosclerosis
(Gray, pearly white, accumulation
Lesions
of intracellular and extracellular
lipids
-Proliferation of vascular smooth
muscle cells
-Formation of scar tissue
3. Complicated Lesion (contains
hemorrhage, ulcerations, scar
tissue deposits)
"Thrombophlebitis"
The presence of a thrombus
(Clot) in a vein and the
accompanying inflammatory
Venous Thrombosis
response in the vessel wall.
2 TYPES:
1. Superficial Venous Thrombosis
2. Deep Venous Thrombosis
, Venous Thrombosis
Pathophysiology
Combined:
Virchow's Triad 1. Stasis of Blood
2. Increased Blood Coagulability
(Hypercoagulability)
3. Vessel Wall Injury
Stasis:
Bed rest
immobility
spinal cord injury
acute myocardial infarction
Congestive Heart Failure
Shock
Venous Obstruction
Hypercoagulability:
Genetic (Factor V Leiden)
Stress and Trauma
Venous Thrombosis Risk Pregnancy
Factors Childbirth
Oral Contraceptives/Hormones
Dehydration
Cancer
Antiphospholipid syndrome
Hyperhomocystinemia
Vascular Trauma:
Indwelling Venous Catheters
Surgery
Massive Trauma or infection
Fractured hip
Orthopedic Surgery
An abnormal decrease in blood
pressure on assumption of the
upright position
Orthostatic Hypotension
Lower pressure + Increased
vascular compliance = decreased
vascular resistance