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NURS 5315 / NURS5315 Module 5 CARDIOVASCULAR GRADED A+ Objectives with Advanced Organizer
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NURS 5315 / NURS5315 Module 5 CARDIOVASCULAR GRADED A+ Objectives with Advanced Organizer
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N5315 Advanced PathophysiologyCardiovascular
Core Knowledge Objectives with Advanced Organizers
Vascular Disease
1. Assess the etiology, clinical manifestations, and the pathophysiology of the diseases which
affect the blood vessels and describe the impact this knowledge has on the care you provide as
a nurse practitioner.
Disease Etiology Clinical Pathophysiology Clinical
Manifestations Implications
Hypertension Primary- thought Early stages only HTN is caused by Dx of HTN
Primary to be from combo. elevated HTN. increases in cardiac requires
· Secondary of genetic and Lack of output (heart rate or measurement
· Malignant environmental symptoms stroke volume) of B/P on two
factors. means pt is /total peripheral different
Secondary- unlikely to seek resistance occasions
Altered tx, so it’s a (increased blood averaging two
hemodynamics lathanic (silent) viscosity or readings at
associated with disease. vasoconstriction). least 2 minutes
an underlying Manifestations Genetic apart, with the
primary disease tend to be vulnerabilities with pt seated, the
(renal, endocrine, specific to environmental risks arm supported
pregnancy, organs or tissues cause at the heart
vascular, neuro, affected, such as neurohumoral level, after 5
acute stress from Heart Disease, dysfunction minutes rest
surgery, burns, renal (Sympathetic with no
sickle cell crisis, insufficiency, nervous system, smoking or
ETOH withdrawal, CNS dysfunction, RAAS, adducin, caffeine intake
pancreatitis, impaired vision natriuretic within the past
increased and mobility, hormones) and 30 mins.
intravascular vascular promote Evaluate
volume) and occlusion, or inflammation and complete
drugs such as edema. insulin resistance. medical hx and
corticosteroids, Ins. Resistance and assess lifestyle,
antihistamines, neurohumoral as well as
licorice, MAO Dysfunction cause possible
inhibitors, oral sustained systemic secondary
contraceptives vasoconstriction causes.
Malignant- rapidly and increased Physical exam-
progressive HTN peripheral optic fundi,
in which diastolic resistance. BMI, auscultate
pressure is Inflammation for carotid, abd,
greater than 140, contributes to renal and femoral
and can cause dysfunction, which bruits, examine
encephalopathy combines with heart & lungs,
due to high neurohum pulses and
arterial pressure alterations, causing edema.
rendering the renal salt and water Labs:U/A, hct,
cerebral arterioles retention and glucose, K+,
, incapable of increased blood Ca+,
regulating blood volume. Creatinine, Hdl,
flow to cerebral cholesterol. Tx:
capillary beds. reduce risk
Capillary factors, restrict
permeability is NA to 2.4 g a
increased, and day, increase
can cause K+, low fat diet
cerebral edema. Stage 1: (Sys
b/p 140-159,
dias 90-99)
thiazide
diuretics, may
consider ACE,
ARB, beta
blocker, CCB,
or combo
Stage 2: (Sys
BP 160 or
above, diastolic
100 or above)
two drug
combo,
typically
thiazide diuretic
and ACE, or
ARB, BB, or
CCB
Atherosclerosis Accumulation of S/S of Inflammatory disease Exam may
lipid-laden inadequate from elevated plasmareveal
macrophages tissue perfusion. cholesterol levels. decrease blood
within arterial Transient Lesions progress flow to tissues
walls, forms ischemic events from endothelial and arterial
plaques. from exercise or injury and bruits. Labs:
Pathologic stress. Lesion dysfunction to fatty lipids, blood
process that affect may cause tissue streak to plaque to glucose, CRP.
vascular system infarction. CAD complicated lesion. Use of x-rays,
throughout the from Endothelial injury U/S, nuclear
body, causes atherosclerosis from smoking, HTN, scanning, CT,
CAD and major cause of diabetes, increased MRI, and
cerebrovascular MI and stroke. LDL and decreased angiograph
disease. HDL, autoimmunity, identify affected
increased CRP. vessels, esp
Injured endothelial coronary. Drugs
cells become to reduce LDL
inflamed and can’t cholesterol by
make normal diet or meds,
amounts of smoking
antithromotic and cessation, HTN
, vasodilating and diabetes
cytokines. TNF, IL-1, control
interferongamma,
CRP, and heat shock
proteins released.
Macrophages adhere
to injured
endothelium by
adhesion molecules,
and then release
enzymes and toxic
oxygen radicals that
cause oxidative
stress, oxidize LDL,
and further injury
vessel wall. Growth
factors also released,
angiotensin II,
fibroblast growth
factor, TGF-Beta,
and platelet derived
growth factor, which
stimulate smooth
muscle cell
proliferation in
vessel.
Peripheral Atherosclerotic Pain with Causes lower Check for
Arterial disease of arteries ambulation extremity Bruits, ankle
Disease that perfuse the (intermittent ischemia, from nbrachial
limbs, esp lower claudication). If arterial obstruction index,
extremities. thrombus forms noninvasive
over the Doppler
atherosclerotic measurement
lesion, of blood flow.
perfusion Tx includes risk
ceases acutely, factor
causing severe reduction,
pain, loss of antiplatelet
pulses, and therapy.
skin color Symptomatic
changes of PAD managed
affected with
extremity. vasodialators in
combo with
antiplatelet or
antithrombin
meds (ASA,
cilostazol,
ticlopidine, or
, clopidogrel),
cholesterol
lowering meds,
exercise rehab.
Coronary Artery Disease and Acute Coronary Syndrome
2. Examine the risk factors, etiology, clinical manifestations, pathophysiology and
consequences of coronary artery disease and acute coronary syndrome.
a. Explain how modifiable risk factors contribute to the development of coronary artery disease:
Risk Factor Effects
Dyslipidemia Abnormal concentrations of serum lipoproteins from genetics and dietary
factors. Increased serum of LDL is coronary risk. LDL oxidation, migration
into the vessel wall, and phagocytosis by macrophages cause
atherosclerosis. LDL also plays role in endothelial injury, inflammation, and
immune response. Low HDL also a risk. HDL can remove excess cholesterol
from arterial wall by mediating the efflux of cholesterol from lipid-laden
macrophages through activation of ATP-binding cassette transporter
proteins. HDL also assists in endothelial repair and decreases thrombosis.
Triglycerides also a risk
Hypertension Contributes to endothelial injury, and causes myocardial hypertrophy, which
increases myocardial demand for coronary flow. Overactivity of SNS and
RAAS causes start of CAD.
Cigarette Increases atherosclerosis. Nicotine stimulates the release of catecholamines
Smoking (epi and norepinephrine) which increases HR and causes peripheral
vascular constriction. B/P increases, as well as cardiac workload and oxygen
demand. Increases LDL and decreases HDL, contributes to vessel
inflammation and thrombosis.
Diabetes Insulin resistance, hyperinsulinemia, and hyperglycemia affect
Mellitus cardiovascular system. Includes endothelial damage, thickening of the
vessel wall, increased inflammation and leukocyte adhesion, increased
thrombosis, glycation of vascular proteins, and decreased production of
endothelial derived vasodilators like nitric oxide. Causes dyslipidemia
because it alters hepatic lipoprotein synthesis and increases triglycerides
and in LDL oxidation.
Obesity and Metabolic syndrome (obesity, dyslipidemia, and HTN). Abdominal obesity
Sedentary has strongest risk for CAD and is related to insulin resistance, decreased
Lifestyle HDL, increased B/P, small artery changes, and inflammation. Also
associated with changes in adipokines that affect cardiovascular risk and
increased activity of SNS and RAAS. Sedentary lifestyle increases risk for
obesity and CAD risk.
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