Chapter 11-13 Hematopoietic

● Hematopoiesis = formation and development of blood cells

○ From bone marrow
○ Necessary substances - protein, vitamin B12, folic acid (another V B), iron
● Disorders of red blood cells
○ Polycythemia = excessive RBCs
○ Anemia = decrease in O2 carrying capacity of RBCs
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● Anemia
● Etiology
○ Reduction in RBCs or subnormal level of hemoglobin
■ Due to iron, V B12, or folic acid deficiency
○ Inability to deliver adequate RBCs into circulation
■ Due to marrow damage (aplastic anemia), infected BM, little production
○ Excessive loss of RBCs
■ Due to external blood loss (hemorrhage), hereditary hemolytic anemia (defective RBCs),
accelerated destruction
● Classification based on RBC appearance
○ Normocytic anemia = normal size and appearance
○ Macrocytic anemia = cells larger than normal
■ Folic acid or V B12 deficiency
○ Microcytic anemia = cells smaller than normal

○ Hypochromic anemia = reduced hemoglobin content

○ Normochromic anemia = normal hemoglobin content
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● Clinical Man.
○ Weakness, palor, tachycardia, tachypnea
○ Cardiac arrhythmias = heart sensitive to O2 changes, thus, heart is working harder
● Compensatory mechanisms
○ Arteriole dilation - Increase B flow
○ Increased cardiac output - Increase B flow
○ Anaerobic metabolism - use less O2
○ Release of erythropoietin
● Diagnostic tests
○ RBC count, MCV, MCHC, reticulocyte counts (check rate of EPO)
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● Types of Anemia
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● (1) Iron deficiency anemia
○ Most common cause of anemia
○ Iron - 75% contain in hemoglobin; stored in liver, BM, and spleen as ferritin
● Pathogenesis
○ Low intake, chronic blood loss (GI bleeding), excessive period, blood donation, surgery
● Diagnostic tests
○ High in Platelet count, normal WBCs, other tests are low
● Small erythrocytes (microcytic) and low hemoglobin (hypochromic)
● Treatment - more iron intake, learn the cause
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● (2) B12 and Folate deficiency
○ B12 - meat, liver, animal protein
○ Folic acid - green leafy veggies and animal protein
○ Both required for hematopoiesis and normal maturation
○ Stored in liver (3 yrs), BM and other tissues
● Absence or low in B12 and folic acid
○ Abnormal maturation
○ Megaloblastic erythropoiesis → megaloblasts
○ Macrocytic anemia
○ B12 → neurologic disturbances
● Pernicious anemia = lack of intrinsic factor; cannot absorb B12
○ Gastric mucosal atrophy
● Clinical Man.
○ Signs of anemia, central/peripheral neuropathies
● D Test
○ RBCs are microcytic → BM enlarged → megalsts → megaloblastic anemia
● Treatment - B12 intake, IM injection for pernicious anemia
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● (3) Anemia from conditions that suppress bone marrow (BM) function
○ Anemia of chronic disease → Normocytic normochromic anemia
○ Marrow infiltrative → Leukemia and metastatic carcinoma
○ Aplastic anemia → damage BM stem cells
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● (4) Hemorrhagic anemia
○ Acute blood loss → Normocytic anemia
○ Chronic blood loss → Microcytic anemia
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● (5) Hemolytic anemia
○ Premature destruction of RBCs
○ Clinical Man. - jaundice, gallstones, hepatomegaly, lethargy, high bilirubin
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● (6) Autoimmune hemolytic anemia
○ Antibodies attack normal RBCs
○ Due to tumors, infection, inflammation, therapeutic drugs, idiopathic
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● (7) Sickle cell anemia
○ SCA is a chronic, autosomal, recessive disease, and most serious
○ Presence of abnormal hemoglobin (HbS) within RBCs
○ HbS reacts to dehydration and deoxygenation → sickle appearance
● Pathogenesis
○ Clump and obstruction of blood flow
○ Damage to heart, kidney, spleen
○ Increase in BM from EPO
● Clinical Man.
○ Hemolytic anemia
● D Test - DNA analysis, neonatal screening
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 ● Polycythemia

● (1) Primary polycythemia vera

○ BM hyperplasia from neoplastic BM
● Clinical Man.
○ Increased viscosity → CO, blood flow, hypertension
● Complication - clot formation

● (2) Secondary polycythemia vera

○ When blood O2 levels are low
○ Increased EPO and RBC production
● Etiology
○ Emphysema, pulmonary fibrosis, congenital heart disease, BM tumor, high altitude
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● Disorders of Platelets

● (1) Immune thrombocytopenic purpura (ITP)

○ Idiopathic
○ Common autoimmune disorder
○ Associated with platelet antibodies
■ Produce platelets and destroy rapidly
○ Acute in children (from post-viral infection, chickenpox, vaccine)
○ Chronic in adults (from HIV)
● Pathogenesis
○ Circulating immunoglobulins (antibodies) react with platelets by phagocytosis
● Clinical Man.
○ Petechiae (pinpoint hemorrhages)
○ Purpura (epidermis hemorrhage)
● D Test - platelet counts, size and shape
● Treatment
○ Corticosteroids to suppress immune system
○ Splenectomy - antibody site destruction

● (2) Secondary thrombocytopenic purpura

○ Results from underlying bone marrow disease
○ Due to drugs and chemicals
○ BM infiltrated by leukemia or metastatic carcinoma
Ch17-20 Cardio A

● Blood volume, vessel size, and blood viscosity are main factors that produce blood pressure
● BP adjusted by kidney and nervous system
○ Sympathetic NS - arterial constriction (increase peripheral resistance)
○ Parasympathetic NS - vasodilation; decrease peripheral resistance
○ Kidneys - control blood volume and secretes renin
■ Renin increases BP
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● Hypertension
○ = long-term force of blood against artery walls
● Types of hypertension
○ Essential (or Primary, or Idiopathic) hypertension
■ Due to obesity, no exercise, salt intake, alcohol, and genetic
■ Most common, 90-05%
○ Secondary hypertension
■ Due to peripheral vascular resistance of cardiac output
■ From chronic renal disease, endocrine diseases, or diabetes, etc.
○ Malignant hypertension
■ A severe form that may arise from either type
● Pathogenesis
○ Increase cardiac output, HR, stroke volume, p. Resistance, b. Viscosity, vasoconstriction
● Complications
○ Renal failure - narrowed renal arterioles
○ Hypertensive heart disease - long-standing hypertension
■ Increased p. Resistance
■ Increased afterload (= the force the heart must pump against in order to eject blood)
■ Enlarged left ventricle
○ Vascular effects - injuries to arteries
○ Aneurysm = bulge in arterial wall caused by weakened vessel
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● Atherosclerosis
○ Most common vascular disease
○ Affects large arteries
○ Formation of atheroma or atheromatous plaque
○ Lipid deposits
● Atheroma or atheromatous plaque - mushy debris on lumen
● Stable plaque - surrounded by fibrous tissue
● Endothelial damage - an initiating factor of development

● Pathogenesis
○ Endothelial injury → monocytes adhere to intima → macrophages
○ Cholesterol and LDL in cytoplasm (unstable plaques) of macrophages (foam cells)
○ Foam cells accumulate and form plaque

○ Cholesterol crystals → hardening of arteries

● Sequela
○ Predisposes to thrombus formation, reduced BF, hemorrhage
● D Test
 ○ Lipid profile
○ C reactive protein
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● Peripheral coronary arterial disease
○ = Plaque obstructs blood flow to lower extremity
○ Femoral artery is common
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● Ischemic heart disease or coronary artery disease (CAD)
○ Decreased blood supply to heart muscle
○ From narrowing or obstruction of coronary arteries (myocardial ischemia)
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● Angina pectoris
○ Chest pain from reduced blood flow to cardiac muscles despite increased oxygen demand
○ Stable angina = chronic chest pain, patient has felt before
○ Unstable angina = first time feeling
○ → necrosis (infarct)
○ Lactic acid accumulates → low pH → acidosis
○ Clinical Man.
■ Asymptomatic, radiating pain, cool extremities
○ Treatment - to prevent MI
■ Oxygen therapy, nitrates (vasodilators), aspirin (decrease clot formation)
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● Myocardial Infarction (Note that infarct = a dead of tissue from no blood)
○ = Prolonged myocardial ischemia with irreversible damages
○ Complete obstruction of coronary artery
○ → necrosis of heart muscle
● Transmural infarct - when endocardium to epicardium become thick; from clot
● Subendocardial infarct - when only a part of wall undergoes necrosis
● Changes in ST segment

● Lab Findings
○ CPK-MB cardiac enzymes
● Complications
○ Pulmonary edema (blood accumulation within left side
○ Intracardiac thrombus - thrombus (blood clot) forms on ventricular wall
○ Pericarditis = inflammation of the pericardial membrane
○ Cardiac rupture = rupture in ventricular septum or papillary muscle
○ Papillary muscle dysfunction = infarcted papillary muscle
○ Ventricular aneurysm = outward bulging of healing infarct during ventricular contraction (systole)
● Arrhythmias
○ = from conduction disturbance (heart block)
○ Fibrillation (rapid irregular contraction of heart muscle)
○ Heart block → 24 hrs → ventricular tachycardia and fibrillation
○ Anterior wall infarction - prolonged PR interval, fail SA node, bradycardia (60 bpm)
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● Conduction disturbances
○ AV heart block = a delay or complete stop from atria to ventricles
○ Mild AV block = a delay from atria to ventricles; prolonged PR interval
○ Incomplete heart block = not all SA node conduction to AV bundle
 ○ Complete heart block = no conduction to AV bundle at all
● Treatment - pacemaker
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● Atrial fibrillation = absence of coordinated rhythmic atrial contraction
○ Multiple irregular P waves
○ From stasis of blood in chamber predisposes to clot formation
● Premature ventricular contraction
○ Most common occurrence with MI
○ Ventricles contract without SA or AV nodes conduction
○ No P or T wave; weird QRS wave
● Ventricular tachycardia
○ Widened QRS wave; no P or T
● Ventricular fibrillation (quivering)
○ Ventricles shaking (quivering) rather that contracting
○ → death, loss of consciousness
○ Treatment - defibrillation, pulmonary resuscitation
● Cardiac Arrest
○ = prolonged or severe myocardial ischemia
○ Asystole = no contraction

Ch17-20 Cardio B

● Cardiac Inflammation and Infections

● Endocarditis = non contagious infection of the cardiac endothelium

○ Affects heart valves
○ From fibrin deposits along with microbes = vegetations
● Myocarditis = inflammation of the heart muscle
○ Virus is the most common cause; coxsackievirus
● Pericarditis = inflammation of the epicardium and pericardium
○ Virus is most common
○ Occurs ager MI
○ Due to permeable pericardial membranes → fibrin rich exudate edema
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● Heart Failure
○ Weakened ventricular muscle unable to pump blood
○ 4 major causes
■ Volume overload, impaired ventricular filling, ventricular muscle problem, decreased
vent. contraction
○ Etiology
■ Ischemic heart disease (most common)
■ Chronic hypertension (leading cause of LVF)
■ Chronic pulmonary disease
● Cor pulmonale = a condition of RVF caused by pulmonary disease
■ Dilated cardiomyopathy = enlargement of the heart / its chambers
■ Hypertrophic cardiomyopathy - hypertrophy of heart muscle
● Categories of HF
○ Acute HF = sudden from ventricular muscle injury
 ○ Chronic HF = gradual weakening of myocardium
○ Systolic dysfunction = weakened ventricle cannot contract
○ Diastolic dysfunction = ventricles cannot relax
● Right-sided disease = a buildup of blood flowing into the right side of the heart; enlargement of veins
● Left-sided disease = a buildup of fluid in lungs or pulmonary edema

● Left sided
○ LVF Backward effects
■ Backup of hydrostatic pressure in left atrium, pulmonary veins, and p capillaries
○ LVF Forward effects
■ Pump into aorta and arteries
● Right sided
○ RVF Backward effects
■ Backup of hydrostatic pressure in right atrium, superior/inferior vena cava, veins
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● Valvular diseases
○ Mitral valve prolapse = MV prolapse during L atrium contraction → backflow into R atrium
○ Aortic stenosis = narrowed valve opening → reduced blood flow from L ventricle
○ Pulmonic stenosis = narrowed pulmonic valve → backflow to R ventricle
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● Disorders of Veins
○ Varicose veins = abnormal dilated superficial vein
■ Due to incompetent valves
○ Deep venous thromboembolism = thrombus in deep leg vein and inflammation
■ → pulmonary embolism (blood clot in lung arteries)