NURS 2090 Lecture Notes - Saturated Fat, Partial Thromboplastin Time, Nosebleed

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16 Apr 2013
Department
Course
Clinical Models for Altered Perfusion
Hypertension (HTN)
Pathophysiology
A progressive cardiovascular syndrome detected by an elevation in blood pressure and/or the
presence of organ damage due to persistent blood pressure elevations
Primary versus secondary
Risk factors:
Family history of hypertension
Aging
Diabetes mellitus
Obesity
Excessive dietary sodium intake
Smoking
Excessive alcohol intake
Sedentary lifestyle
Clinical Manifestations
Often asymptomatic
When advanced, causes CNS changes:
Headache
Fatigue
New-onset blurred vision
Weakness
Confusion
Vomiting
Mental status changes
Nausea
Diagnostic Criteria
History and physical examination
Serial blood pressure measurements
Laboratory studies
Classification:
Prehypertension
Stage 1
Stage 2
Treatment
Pharmacologic treatments
Lifestyle modifications
Weight reduction
Decreased alcohol, salt & saturated fat intake
Increased aerobic physical activity
Increased fruit and vegetable intake
Smoking cessation
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Shock
Pathophysiology
A condition of circulatory failure and impaired perfusion of vital organs
Sources of impaired perfusion:
Cardiogenic Shock: Ineffective cardiac pumping
Hypovolemic Shock: Decreased blood volume
Sources of impaired infusion (cont’d):
Massive systematic vasodilation:
Septic Shock
Neurogenic Shock
Anaphylactic Shock
Compensatory mechanisms
Clinical Manifestations
Tachycardia, tachypnea
Cool, clammy extremities with poor peripheral pulses
Decreased arterial blood pressure (a late sign indicative of decompensation)
Cyanosis and/or pallor
Restlessness, apprehension, decreased mental function
Poor urinary output
Diagnostic Criteria
No one test is completely specific or sensitive for shock
History and physical examination
Laboratory studies
Diagnostic testing
Treatment
Medical emergency: airway, breathing, circulation
Cardiogenic
Hypovolemic
Septic
Neurogenic
Anaphylactic
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