Card Set Information
High sodium intake
excessive calorie intake
coarctation of aorta-narrowing
are more muscular-tunica intima and media
dilate more easily-dependent on skeletal muscle for blood return.
Stage 2 hypertension?
formation of plaque within the arteries
: Damage to the vessel wall.
: Vessel becomes inflamed.
Step 3: Fatty streak appears.
Step 4: Plaque develops.
Step 5: Fibrous lesion becomes calcified, hemorrhagic, ulcerated, or thrombosed.
risk factors for atherosclerosis
Age greater than 60 years old
Family history of HTN
Excessive calorie consumption
Excessive alcohol intake
High salt & caffeine intake
Decreased intake of K+, Ca++, Mg++
S-D normal is 30-40mmhg
Deep, usually between toes, blackish intermittent claudication
ulcers created due to a lack of 02 and nutriets. Atherosclerosis predisposes pt. to this.
Venous ulcers aka stasis leg ulcer
Shallow-weeping wounds that are poor to heal-poor venous return of blood flow.
Types of PVD
venous stasis ulcers
prolonged periods of inactivity
surgery to a limbg
◦Prolonged venous hypertension◦
Waste products build up in tissues
Results in different types of diseases-thrombosis, varicose veins, ulcers, stasis dermatitis
Diabetic peripheral disease
Loss of sensation
reduced blood flow
Uncontrolled blood sugar
sedentary life style
S&S-neuropathy-inability to recognize objects by feel, injury without pain, paresthesia
PVD for pediatrics
Same risk factors as adult PVD primary and secondary. and same lifestyle changes to treat PVD
75% occur in children
Acute systemic vasculitis
hydrocephalus, liver damage, renal damage
Unknown, but higher incidence due to ASA use in pediatrics. Pediatrics should not receive ASA along with teenagers.
Main treatment is prevention of MI/CAD. Primary treatment is Intravenous Immunoglobulin
secondary is corticosteroids
ASA may be considered, but will be placed under close observation for reyes