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N5315 Advanced Pathophysiology-Cardiovascular-Core Concepts and Objectives with Advanced Organizers-
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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 elevated HTN. increases in requires
· Secondary combo. of Lack of cardiac output measurement of
· Malignant genetic and symptoms (heart rate or B/P on two
environmental means pt is stroke volume) different
factors. unlikely to seek /total peripheral occasions
Secondary- tx, so it’s a resistance averaging two
Altered lathanic (silent) (increased blood readings at least
hemodynamics disease. viscosity or 2 minutes apart,
associated with Manifestations vasoconstriction). with the pt
an underlying tend to be Genetic seated, the arm
primary disease specific to organs vulnerabilities with supported at the
(renal, endocrine, or tissues environmental heart level, after
pregnancy, affected, such as risks cause 5 minutes rest
vascular, neuro, Heart Disease, neurohumoral with no smoking
acute stress from renal dysfunction or caffeine intake
surgery, burns, insufficiency, (Sympathetic within the past
sickle cell crisis, CNS dysfunction, nervous system, 30 mins.
ETOH impaired vision RAAS, adducin, Evaluate
withdrawal, and mobility, natriuretic complete
pancreatitis, vascular hormones) and medical hx and
increased occlusion, or promote assess lifestyle,
intravascular edema. inflammation and as well as
volume) and insulin resistance. possible
drugs such as Ins. Resistance secondary
corticosteroids, and neurohumoral causes. Physical
antihistamines, Dysfunction cause exam-optic fundi,
licorice, MAO sustained systemic BMI, auscultate
inhibitors, oral vasoconstriction for carotid, abd,
contraceptives and increased and femoral
Malignant- peripheral bruits, examine
rapidly resistance. heart & lungs,
progressive HTN Inflammation pulses and
in which diastolic contributes to renal edema.
pressure is dysfunction, which Labs:U/A, hct,
greater than 140, combines with glucose, K+,
and can cause neurohum Ca+, Creatinine,
encephalopathy alterations, Hdl, cholesterol.
due to high causing renal salt Tx: reduce risk
, arterial pressure and water factors, restrict
rendering the retention and NA to 2.4 g a
cerebral increased blood day, increase
arterioles volume. K+, low fat diet
incapable of Stage 1: (Sys b/p
regulating blood 140-159, dias
flow to cerebral 90-99) thiazide
capillary beds. diuretics, may
Capillary consider ACE,
permeability is ARB, beta
increased, and blocker, CCB, or
can cause combo
cerebral edema. 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 Exam may reveal
lipid-laden inadequate disease from decrease blood
macrophages tissue perfusion. elevated plasma flow to tissues
within arterial Transient cholesterol levels. and arterial
walls, forms ischemic events Lesions progress bruits. Labs:
plaques. from exercise or from endothelial lipids, blood
Pathologic stress. Lesion injury and glucose, CRP.
process that may cause tissue dysfunction to fatty Use of x-rays,
affect vascular infarction. CAD streak to plaque to U/S, nuclear
system from complicated lesion. scanning, CT,
throughout the atherosclerosis Endothelial injury MRI, and
body, causes major cause of from smoking, HTN, angiograph
CAD and MI and stroke. diabetes, increased identify affected
cerebrovascular LDL and decreased vessels, esp
disease. HDL, autoimmunity, coronary. Drugs
increased CRP. to reduce LDL
Injured endothelial cholesterol by
cells become diet or meds,
inflamed and can’t smoking
make normal cessation, HTN
amounts of and diabetes
antithromotic and control
vasodilating
cytokines. TNF, IL-
1, 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 index,
limbs, esp lower claudication). If arterial noninvasive
extremities. thrombus forms obstruction Doppler
over the measurement of
atherosclerotic blood flow. Tx
lesion, includes risk
perfusion factor reduction,
ceases acutely, antiplatelet
causing severe therapy.
pain, loss of Symptomatic
pulses, and skin PAD managed
color changes with
of affected vasodialators in
extremity. 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.
b. Describe the function of VLDL, LDL, HDL, triglycerides, and cholesterol, and the impact this
has on the diagnosis and treatment of patients with hyperlipidemia.
Lipoprotein Function Clinical Implications
VLDLs Very low-density lipoprotein-
LDLs Low density lipoproteins- mostly LDL oxidation, migration into the
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