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Patho Exam #2
Terms in this set (88)
On the second or third day after an acute myocardial infarction, the area of necrosis is
soft and yellow
In older adults, sudden death from an acute myocardial infarction is usually caused by
acute ventricular arrhythmia
Dilated cardiomyopathy with left ventricular dysfunction is characterized by increased wall
Endocarditis and rheumatic heart disease (carditis) are both cardiac complications of under-treated systemic infections. Characteristics include a new or changed heart murmur caused by
vegetative valve destruction
Chronic stable angina, associated with inadequate blood flow to meet the metabolic demands of the myocardium, is caused by
fixed coronary obstruction
Atherosclerotic plaque is most likely to be unstable and vulnerable to rupture when the plaque has a thin fibrous cap over a
large lipid core
Congenital heart defects can cause a right heart to left heart shunting of blood that results in increased
unoxygenated blood flow
Cardiac tamponade and pericardial effusion can be life-threatening when the pericardial sac _______ and ______ the heart.
fills rapidly; compresses
Patients with ischemic coronary vessel disease and acute coronary syndrome (ACS) are classified as low or high risk for acute myocardial infarction based on characteristics that include significant
In aortic regurgitation, failure of aortic valve closure during diastole causes an abnormal drop in diastolic pressure. The pressure change causes decreased
Pericarditis / Pericardial effusion
*Inflammation of the pericardium causes pain & exudate.
*Serous exudate filling the pericardial cavity (pericardial)
*Cardiac tamponade which is the rapid accumulation of exudate which compresses the heart
*Fibrous scar tissue making the pericardium stick to the
*ECG changes occur
Coronary Heart Disease
Atherosclerosis blocks coronary arteries.
Ischemia may cause:
Chronic Ischemic Heart Disease
Imbalance in blood supply and the heart's demands for
Higher oxygen demand
Kinds of Angina
º Pain when heart's oxygen demand increases
º Pain when coronary arteries spasm
Silent myocardial ischemia
º Myocardial ischemia without pain
Acute Coronary Syndromes
Spectrum of acute ischemic heart diseases ranging from unstable ischemia to acute MI.
Classified on presence or absence of ST-segment elevation on the ECG.
Presence of serum cardiac markers from necrotic heart cells (Myoglobin, creatine, kinase, troponin).
Inflammation of the heart usually caused by viral infections. Can be fungal or bacterial infections as well.
Gradual, abrupt or fulminant heart failure.
Positive serum cardiac biomarkers
Infection of the endocardial surface of the heart
Often called bacterial endocartitis
Can cause valve destruction
Rheumatic Heart Disease
Valve damage following rheumatic fever associated
with streptococcal throat infections
Most likely to occur in young children (5-15)yrs old)
Immune-mediated inflammatory disease
Effects may be seen years later as chronic valvular
Valvular Disorders & Heart Defects
The endocardial )structures lining the heart can cause
If the AV valves leading into the ventricles do not
work (mitral or tricuspid problems)
If the semilunar valves leading out of the ventricles do
not work (aortic or pulmonary problems)
Stenosis: valve will not open all the way; it is harder to force blood through it
Regurgitation: valve will not close all the way; it leaks when it should be closed
Patent ductus arteriousus
Duct remains open beyond the 3 months in a full-term infant.
high-pressure blood of the aorta is shunted back to the pulmonary artery.
Blood shunts from left to right.
Atrial septal defects
Opening in atrial septum as a result of improper septal formation
May be single or multiple
Blood shunts left to right
At risk for pulmonary vascular disease
Ventricular septal defects
opening in the ventricular septum that results from an incomplete separation of the ventricles during early fetal development.
May be single or multiple
Blood shunts left to right
Most children asymptomatic
Endocardial cushion defects
Defect may be partial or complete
Blood flows between chambers of the heart
Failure to thrive
Signs of CHF
Obstruction of blood flow from right ventricle to pulmonary circulation.
Isolated valvular lesions
Combination of stenoses in multiple areas
Right to left atrial shunting
Right ventricular hypotensions
Infant shows signs of cyanosis
Tetralogy of Fallot
Ventricular septal defect
Dextroposition of the aorta
Right ventricular outflow obstruction
Right ventricular hypertrophy
Transposition of the Great Vessels
The pulmonary artery is attached to the left side of the heart and the aorta to the right side.
Coarctation of the Aorta
Localized narrowing of the aorta.
Disparity in pulsations and blood pressure in the arms and legs (BP in legs lower).
Untreated results in
Complications of AMI
Rupture of the heart
Treatment of AMI
Oxygen (increase oxygenation of hemoglobin)
Beta blockers (damp autonomic signals to heart)
Reperfusion therapy with thrombolytic drugs)(clot)
Insertion of a guide catheter with a collapsed balloon-expandable stent mount over a guide wire into a coronary artery.
Advancement of guide wire across coronary lesion
Positioning of the balloon-expandable stent across the lesion.
Balloon inflation with expansion of the stent. Once stent is expanded, the balloon system is removed.
Acute febrile disease of young children
Can produce aneurysmal disease of the coronary arteries
Probably immunologic in origin
Begins with high fever (acute)phase)
Progresses to desquamation (skin peeling)of fingers and
toes, possibly other areas (subacute phase)
Anaphylactic shock is directly associated with
type I hypersensitivity response
One of the principle mechanisms by which the heart compensates for increased workload is
Severe shock can be followed by acute respiratory distress syndrome (ARDS), characterized by
hyperinflated alveolar sacs
Hypovolemic shock occurs as a result of
acute intravascular volume loss
A common symptom of the ischemic gastrointestinal redistribution of blood flow is
The most common causes of left-sided heart failure include
acute myocardial infarction
The pathophysiology of heart failure involves an interaction between decreased pumping ability and the ________ to maintain cardiac output.
In shock, one of the best indicators of blood flow to vital organs is
Cardiac output is the ________ each minute.
In right-sided heart failure, the peripheral edema accumulation is evidenced by
Because cholesterol is insoluble in plasma, it is mainly carried by the lipoprotein
By definition, primary (essential) or secondary hypertension is systolic blood pressure of ____ or higher and diastolic blood pressure of ____ or higher.
Small vessel vasculitides, a group of vascular disorders that cause vasculitis, are mainly mediated by
A major cause of secondary hyperlipoproteinemia is _______, which increases the production of VLDL and conversion to LDL.
a high-calorie diet
Because of its location, the presence of an abdominal aortic aneurysm may first be noticed as
a pulsating mass
A serum marker for systemic inflammation, _____, is now considered a major risk factor marker for atherosclerosis and vascular disease.
Atherosclerotic peripheral vascular disease is symptomatic with at least 50% occlusion. The primary peripheral symptom, due to ischemia, is
Although both are characterized by ischemia, Raynaud disease is caused by _______, and thromboangiitis obliterans is caused by __________.
The patient is immobilized after a hip injury. He has lower leg discoloration with edema, pain, tenderness, and increased warmth in the mid-calf area. He has many of the manifestations of
deep vein thrombosis
The most important complication of atherosclerosis is ______, which may cause occlusion of small heart vessels.
Develops because scavenger cells encounter the fatty
deposits (LDL's) in the artery lining and
Try to destroy the fats by oxidizing them
º Oxidized fats injure the endothelium
º Clots form and release growth factors
º Smooth muscle grows over the fatty core
Try to remove the fats by eating them
Become "foam cells" in the core of the
Have thick fibrous caps
Partially block vessels
Do not tend to form clots or emboli
Have thin fibrous caps
Plaque can rupture and cause a clot to form
May completely block the artery
The clot may break free and become an embolus
Atherosclerotic occlusive disease
usually lower leg and foot. Produce ischemia, pain, impaired function, and in some cases infarction and tissue necrosis.
Thromboangiitis obliterans (Buergers disease)
distal arterial ischemia, primarily feet and digits.
vasospasm of the arteries and arterioles in the
fingers and sometimes toes
Wall of artery weakens and stretches
Risk of rupture and hemorrhage
Risk of clot formation
Short term blood pressure controls:
renin-angiotensin-aldosterone (RAA) system
Baroreceptor feedback to cardiovascular centers in the
Autonomic Nervous System
Long term blood pressure controls:
Mediated by the kidneys
Fluid balance shifts
Essential (Primary, Idiopathic) Hypertension Risk factors
Race (African Americans much higher incidence and
severity than whites)
Insulin resistance (prediabetes, diabetes, obesity)
High sodium intake
Hypertension secondary to another disease condition
Common in acute kidney diseases
Cancer of adrenal medulla
Produces excess epinephrine
Coarctation (narrowing) of the Aorta
More common in the elderly
Weakness or dizziness on standing
Fainting occurs in extreme cases
Chronic Venous Insufficiency
Can be caused by deep vein thrombosis (DVT) or valvular incompetence
Leads to tissue congestion, edema, and eventual impairment of tissue nutrition
Necrosis of subcutaneous fat deposits occurs, followed by skin atrophy
Impaired tissue nutrition causes stasis dermatitis and the development of stasis or venous ulcers
Also known as thrombophlebitis
Formation of thrombi in the veins
Caused by static blood flow (venous stasis)
Treatment: exercise and/or support stockings and other leg compression devices
List signs & symptoms for hypertension
Headache in back of head or neck (present upon waking and subsides throughout day).
Alcohol and tobacco use
irregular, tortuous veins with incompetent valves. Usually affect lower extremities (long & short saphenous veins)
Abnormally high level of blood lipids and lipoproteins.
Life-threatening emergency caused by a tear in the intima of the aorta with hemmorhage into the media.
Sudden excruciating pain
BP rapidly falls
Absent peripheral pulses
Responds to renal perfusion
Drop in renal perfusion stimulate renin release
Renin converts angiotensin to angiotensin I
Converts to angiotensin II in the lungs by ACE
promotes sodium and water constriction
Adrenal medulla releases aldosterone
SVR & CO increase, raising BP
loading of the heart with blood at the end of diastole
• Dependent on venous return to the heart
the force the heart must generate to expel blood from the filled heart
• Dependent on peripheral resistance and ventricular
• Mechanical performance of the heart contractile units
• Increased by sympathetic (autonomic) stimulation
The greater the stretch of cardiac muscle fibers, the greater the force of contraction. Increases CO and myocardial O2 demands.
Sympathetic Nervous System
Increases heart rate and contractility
• Increase sodium and water excretion and cause
• Antagonists of the renin-angiotensin-aldosterone
• Potent vasoconstrictors
• May be involved in pulmonary hypertension following
existing cardiac muscle cells enlarge, increasing their contractile elements and force of contraction.
Left-sided Heart Failure
Systolic: LV does not pump enough blood to body
Diastolic: LV does not accept enough blood from lungs
Body lacks blood
Lungs fill with fluid
Decreased tissue perfusion
Impaired gas exchange
Right-sided Heart Failure
Systolic: RV does not pump enough blood to lungs
Diastolic: RV does not accept enough blood from body
Body fills with blood
Lungs do not oxygenate enough blood
Congestion of peripheral tissues
GI tract congestion
Anorexia, GI distress, weight loss
• Capillary fluid moves into alveoli
• Lung becomes stiffer
• Harder to inhale
• Less gas exchange in alveoli
• Frothy pink sputum
• Hemoglobin not completely oxygenated
• Heart fails to pump blood adequately
• Decreased cardiac output lowers BP
• Sympathetic system responds
• Vasoconstriction increases resistance to blood flow
• Increased workload on heart worsens heart failure
Treatment of Cardiogenic Shock
•Dilate peripheral vessels
•Intra-aortic balloon pump
Types of Shock
Complications of Shock
• Acute respiratory distress syndrome
• Acute renal failure
• Gastrointestinal complications
• Disseminated intravascular coagulation
• Multiple organ dysfunction syndrome
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