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Flashcards in Unit 2 Deck (33):

What are factors that cause atherosclerosis and that can lead to coronary artery disease?

•Fatty material accumulates
•Vasculature is damaged
•Plaquedecreases the lumen of the affected vessel
•Decreased flow
•Sluggish flow


What is ischemia?



Describe the difference between angina pectoris and an M.I.

Angina pectoris is a warning.

M.I. is prolonged ischemia that is severeenough to cause death of myocardial cells...usually occurs when atherosclerosis causes thrombus formation


What are the three zones (levels) of damage seen in an M.I.?

Zone of ischemia - myocardial ischemia causes ST sement depression with or without T wavwe inversion as result of altered repolarization.

Zone of injury - Myocardial injury causes ST segment elevation with or without loss of R wave.

Zone of infarction - Myocardial infarction causes deep Q waves as result of absence of depolarization current from dead tissue and receding currents from opposite side of heart.


Which part of the heart are infarctions likely to occur and why are they significant here?

Myocardial tissue. Insufficient blood supply.


How does the body try to compensate for coronary ischemia?

Phagocytosis of necrotic tissue
•Necrotic tissue is replaced with scartissue (fibrosis)
•Generates collateral circulation
•May not occur quickly enough
•May not be effective enough


What are signs, symptoms, and test findings for an M.I.?

Chest pain that may radiate:
•Arms, shoulders, neck, jaw, upper back, and abdomen
•Crushing, persistent pressure sensation
•Profuse diaphoresis
•Nausea & Vomiting
•Feeling of Impending Doom
-sudden onset of symptoms
In women:
-profound sense of fatiue
-flu-like discomfort
-feeling of indigestion, heartburn
-symptoms or a number of days.
•CRP (C-reactive protein)
•Cardiac enzymes


How is an M.I. initially treated and then how may it be treated after the patient has stabilized?

Cathlab to diagnose the severity of the blockage.


What types of arrhythmias are most common after an M.I. (recognize them on an EKG) and how are the treated?

PVC - Premature Ventricular Contraction
PVC is a wasted beat
• no effective output
• myocardium still consumes oxygen
Usually, bigger and wider than normal QRS
Treat? O2, Beta Blockers, Ca2+ channel blockers, ablation(?) anti-arrhythmic (?)

V-TACH - Ventricular Tachycardia
3 or more consecutive PVC’s... Or may be continuous!
Treat? O2, anti-arrhythmic (Lidocaine, Procainamide, Amiodorone)
• Patient will often lose consciousness:
• No effective output!
• CPR and defibrillation

V-FIB - Ventricular Fibrillation
• Multiple, irritable foci in the ventricles
• Results in chaotic electrical activity
• Ventricle “quivers”, does NOT contract
• No effective cardiac output!
• Form of Cardiac Arrest
• CPR and rapid defibrillation


How does CHF develop after an M.I.?

Post- M.I., the cardiovascular system tries to maintain adequate blood flow by:
• Increase in heart rate
• Increase in systemic vascular resistance
• Fluid retention (done by the kidney)
• This is the problem!


What are the symptoms, signs, and test findings seen in CHF?

• VentricularHypertrophy
• Edema
• Systemic
• Swollen feet & ankles
• Pulmonary
• Wet lung sounds
• Gurgling
• SOB w/exertion or at rest
• Hypoxia & Cyanosis
• Hypernatremia & Hypokalemia


How is CHF treated?

• Oxygen
• NPPV for respiratory distress
• Diuretics
• ACEinhibitor
• Beta-blocker
• Inotropicdrugs
• LifestyleΔ’s


What is cardiogenic shock and what are its manifestations?

Is the worst complication of an M.I.
The heart can NOT maintain cardiac output adequate for tissue perfusion
• Severely low BP
• Severe SOB, rapid breathing
• Sudden tachypnea
• Weak pulse
• Sweating
• Cold hands and/or feet
• Urinating less than normal or not at all
• Loss of Consciousness


What can a Swan-Ganz measure and how is it used in the diagnosis and treatment of an M.I.?

• Pulmonary artery pressure (PAP)
• Pulmonary capillary wedge pressure (PCWP)
• Saturation mixed venous O2 (SvO2)
• Cardiac Output (C.O.)
Having an M.I.?
• Pressures and C.O are higher
• Mixed venous O2 lower


Describe the pathology and treatment for the following: ASD

Atrial Septal Defect
Cause - Embryonic anomaly
Lesion - Hole in the septum between right and left atria
Manifestations - murmur, heart failure


Describe the pathology and treatment for the following: VSD

Ventricular Septal Defect
cause - embryonic anomoly
lesion - hole in the septum between right and left ventricles
Manifestations - murmur, heart failure


Describe the pathology and treatment for the following: PDA

Patent ductus arterioles.
• Didn’t close at birth?
• Blood flows from aorta to lungs
• PA is overloaded
• Can lead to heart failure
• Treat:
• O2
• Anti-inflammatories
• Abx’s
• Surgery?

Higher blood pressure in aorta
Lower blood pressure in pulmonary artery - blood flows backward into pulmonary artery


Describe the pathology and treatment for the following: Tetralogy of Fallot

cause - embryonic anomaly
lesions - overriding aorta, pulmonary stenosis, ventricular septal defect, right ventricular hypertrophy
manifestations - murmurs, cyanosis, retarded body, growth, heart failure


Describe the pathology and treatment for the following: Coarctation of the Aorta

cause - embryonic anomaly
lesion - stenosis of descending thoracic aorta
manifestations - decreased femoral pulse, hypertension in upper extremity, murmur, heart failure (late)


What are the causative organisms in rheumatic heart disease and infectious endocarditis?

Etiology: complication of strep infection
Pathology: antibodies that develop against streptococci attack
host tissue (heart & joints)
Vegetations form on valves!! (mitral #1)
Inflammation of the inner lining of the heart
Organisms live on the heart valves & produce an inflammatory reaction!
Microbial infection (typically bacteria)
• Strep=sub-acute infection...gradual destruction
• Staph=acute infection...rapiddestruction!!!


Describe which heart valves are commonly affected and how their function is affected in rheumatic hea disease and infectious endocarditis.

Leads to vegetations forming on valves (mitral or aortic)
• Vegetations -> stenosis, insufficiency, but may also break off!
• Emboli -> carried to other organs -> multiple abscesses, lodging in vessels, death!!


How are infectious endocarditis and rheumatic heart disease treated?

• Immediate & extensive antimicrobial treatment
• Extensive damage?
• Surgical intervention


What are the two general types of anemia? Give examples of each.

Decreased RBC Production - Pernicious Anemia and iron-deficiency anemia

Increased RBC Production - hemolytic anemia


What are the general signs and symptoms of anemia?

Eyes - yellowing
Skin - paleness, coldness, yellowing
Respiratory - shortness of breath
Muscular - weakness
Intestinal - changed stool color
central - fatigue, dizziness, fainting
blood vessels - low blood pressure
heart - palpitations, rapid heart rate, chest pain, angina, heart attack
spleen - enlargement


Describe the pathology of pernicious anemia and its treatment.

• Dietary B12 must combine w/protein (intrinsic factor) and be carried to small intestine BEFORE it can be absorbed
(SO: if low intrinsic factor, then there is low absorption of B12)
• Membranes of RBC’s rupture easily
• Occurs mostly in persons older than 60
• Strict Vegetarians
• Chronic Bowel Disorders
• Individuals w/ stomach or bowel partially/fully removed

• B12 supplements • Injection


What are causes of iron deficiency anemia?

• Loss of iron or inadequate intake of iron
• Chronic, low-grade blood loss in adults
• Poor dietary intake, pregnancy, and rapid growth spurts in young children


List examples of hemolytic anemias.

• Hereditary Defects
• Infectious agents
• Medications/Drug Rxn
• Immune Disorders
• Exposure to toxins
• Cytotoxic hypersensitivity (Erythroblastosis Fetalis)


List signs and symptoms associated with hemolytic anemias.

• SOB, easily fatigued • Pallor
• Enlarged spleen
• elevated bilirubin levels
• ?? Jaundice
• elevated reticulocytes
• Organ dysfunction
• Neurologic dysfunction


What is the difference between primary polycythemia and secondary polycythemia and how is each treated?

Primary Polycythemia
• Unknown: causes an increase in number of RBC’s (WBC’s and platelets also increase)
• Blood becomes very thick (increase viscosity) and clots easily • Heart has to work harder to pump
• 45-60 y.o. males
• Neurologic: dizziness, headaches, visual problems
• Htn
• Itching and pain in fingers, toes
• Prone to thrombosis & organ infarction
• Enlarged spleen
Aimed at decreasing the viscosity of the blood!
• Phlebotomy
• Chemotherapeutic agents • Analgesics
• Antihistamines

Secondary Polycythemia
• Increased production of erythropoietin
• Hypoxia from:
• chronic lung disease
• living at high altitude
• Rare neoplasms Manifestations
• The cause of chronic hypoxia
• NO phlebotomy


What is the primary abnormality in (a) hemophilia and (b) Thrombocytopenia Purpura? Describe manifestations and treatment for each.

Poor blood clotting
Continuous bleeding
• X-linked recessive disorder
• Transmitted from mother to son
• Causes absence of clotting factor VIII
• Mild to severe disorder
• Mild-severe bleeding
• GI tract
• Joints
• Hip,knee,elbow,ankle
• Under the skin...deep! Inflammation: pain & swelling
Intracranial hemorrhage Platelets usually OK
• Administer missing clotting factor
• Chronic replacement of factor VIII
• Additional doses during acute bleeding
• Synthetic hormone • desmopressin

Thrombocytopenia Purpura
An abnormally small number of circulating platelets
• Normalplateletcount: 150,000 - 400,000 platelets per mcL
• Purpura appears when platelet count is less than 60,000
• Purple/redbruises
• Markedly depressed platelet count is associated with spontaneous bleeding from small vessels- petechiae
• Small,flat,redspots

• CAchemo&radiation
• Malignantbonemarrow disease
• Shiftinplateletdistribution • Hypersplenism
• Increased destruction of platelets • Idiopathic
• Auto-immune
• Coagulation disorders

• Petechiae
• Prolonged bleeding from
minor & major trauma
• Spontaneous bleeding from mucous membrane of mouth & internal organs
• Excessive menstrual bleeding
• Excessive bleeding during dental procedures
• No joint or deep tissue bleeding!
Depends on the age of the patient and severity of the illness
• Corticosteroids: decrease destruction
• Splenectomy
• Packed RBC’s with platelets: if bleeding is life-threatening


Describe the pathologies for leukemia.

Bone marrow taken over by malignant cells
• Increase production of useless WBC’s
• Decrease production of RBC’s and platelets Reduced immune function
• Severe and refractory infections Organ enlargement
• Lymph nodes, spleen, bones (usually cranial) CNS dysfunction
• Increased intracranial pressure
Death (usually due to complications of pathology)
• Sepsis, bleeding, anemia, organ dysfunction from metastasis


How is leukemia treated?

• Initially:
• Chemotherapy and
• Bone marrow transplant


What is the name for the abnormal cell seen in Hodgkin’s lymphoma and how is Hodgkin’s treated?

Reed-Sternberg cell

• Radiation and / or
• Chemotherapy