Pathophysiology: Cardiovascular System

Cardiac tamponade

"Cardiac compression" Impeding the mechanical activity of the heart, decreases cardiac input, therefore output as well.

Pathophysiology associated with renal failure. Approach to treating it?

"renal anemia" One approach to treating this type of anemia is a drug form of erythropoietin, works very effectively.

What is the standard initial therapy for MI

-Continuous EKG monitoring for arrhythmias -Control pain (morphine sulfate or nitroglycerin) -Supplemental nasal O2 to maintain partial oxygen -Aspirin or heparin (blood thinners) -Acute repercussion (angioplasty or thrombolytic therapy, tPA)

Five stages of atherosclerosis plaque to myocardial infarction

1. Damaged endothelium (smoking, HTN, bacteria, etc.) 2. Fatty streak (yellow): lipid macrophages bind to endothelium 3. Fibrous plaque (white): smooth muscle cells proliferate in lesion and deposit collagen creating firm, rigid mass. LDL oxidized, vascular lesion reversible with diet modification 4. Complicated lesion: progressive and relentless of stages 1-3 and rupture of endothelium. Thrombus forms and can instantly occlude lumen.

Difference between 1, 2, 3 heart blocks

1st: increase in P-R interval 2nd: increase in P-R ratio 3rd: "compete" block, AV node doesn't conduct action potentials into ventricles. Atria and ventricles beat independently. Need artificial pacemaker.

ALL (Acute lymphocytic leukemia)

2-4 years of age Accumulation of leukemic lymphoblasts in bone marrow and blood Malignant cells: alterations in number and/or structure of chromosomes (hyperdiploidy >50 chromosomes, translocation of genetic material) Chemotherapy: 90% of children able to achieve complete remission and approx. 2/3 can be considered cured.

AML (acute myelogenous leukemia)

2-4 years of age Malignant cells have alterations in number and/or structure of chromosomes (absence or deletion and/or translocation of genetic material. Fast-growing and aggressive Chemotherapy: 60% of patients achieve remission. Only 15-30% remain free from disease for 5 years. CAR-T therapy Bone marrow transplant: first remission 50-60% cure rates.

What the responses in the myocardium following myocardial infarction after 24 hours, 2 weeks, and 6 weeks?

24 hrs: leukocyte infiltration to the area, proteolytic enzymes degrade necrotic tissue. 2 weeks: increased insulin release, weak collagen matrix forms that is mushy and vulernable. 6 weeks: strong scar tissue develops, scar tissue is non-contractile or conductive.

The average MCHC

34g/100mL

Mean corpuscular diameter

7-8 um

Describe pericardial effusion

Accumulation of fluid between the pericardial cavity (normally 10-30 cc)

Pathophysiology associated with acute and chronic hemorrhagic anemia

Acute: large quantity loss of blood in short amount of time Chronic: small quantity loss of blood over long period of time

Compare and contrast general characteristics of acute and chronic forms of leukemia

Acute: usually "younger" people. Abrupt onset, more severe symptoms. Immature cell forms. Chronic: usually "older" people. Gradual onset, symptoms are less severe. Differentiated cell forms

Explain why chronic forms of leukemia are less responsive to chemotherapy compared to rapidly dividing cells associated with acute forms of leukemia

After blast crisis, all forms of treatment are basically ineffective.

What is afterload?

Amount of pressure heart needs to exert to eject blood during contraction of the ventricles

Identify three diseases associated with causing restrictive cardiomyopathy

Amyloid (multiple myeloma), hemochromatosis, and glycogen storage disease. Excessive iron or glycogen deposit in tissue of organs and can trigger inflammation and destruction, leading to collagen fibrosis, scar tissue. amyloid: plasma cells overproduce antibodies and cancer will trigger scar tissue- stiffness and rigidity.

How to diagnose heart failure

B-type natriuretic peptide (BNP) (Nat: sodium!!)

Treatment of hypertrophic cardiomyopathy

Beta blockers and calcium channel blockers (they help increase cardiac output). Surgical resection removes excess heart tissue Ethanol- controlled heart attack, 100% ethanol kills heart tissue

Describe Gleevac

Binds to and inhibits the activity of protein that is only expressed in cancer cells, and no other cell in the body. Near total elimination of cancer cells, no side effects of chemotherapy. BUT you need to take it every single day or cancer will come back.

Pathophysiology associated with aplastic anemia

Bone marrow failure

How does coronary artery bypass graft surgery work?

Bypassing the coronary artery and directing the bloodstream elsewhere.

Rheumatic Heart Disease

Cardiac involvement coming from group A beta hemolytic streptococcus infection (rheumatic fever). Heart, muscle, brain, and synovial joints bind bacterial antigens.

Cardiac iso-enzymes and other bio markers that diagnosis myocardial infarction

Cardiac iso-enzymes present in plasma serve as biomarkers of myocardial infarction because if the heart muscle cells died, the iso-enzymes are released into the bloodstream. Isoenzymes have no physiological function in the blood, they are supposed to be inside living heart muscle cells. These biomarkers indicate the heart muscle cells have died.

What is shock?

Cardiovascular system fails to perfume tissues adequately, causing widespread impairment of cellular metabolism. Progresses to organ failure and death. Untreated shock overwhelms body's mechanisms through positive feedback loops, initiating a downward physiologic spiral.

cardiogenic shock

Caused by heart failure, myocardial infarction, coronary artery disease

Ventricular fibrillation

Chaotic ventricular depolarization, very active heart muscle- rate can be 300 bpm. Muscle cells quiver, not synchronized- cardiac output decreases.

What is angina pectoris? Symptoms?

Chest pain, severe and sudden onset upon exertion. Pain will stop when exertion stops.

Leukocytosis

Common reaction in many acute inflammatory stress leukocyte count is greater than 10,000/uL.

Possible treatments for heart failure

Decrease workload on heart by: -Correcting valvular dysfunction (surgery) -Vasodilators to decrease blood flow resistance -Diuretics to decrease blood volume -Inotropic drugs increase force of myocardial contractility

The major pathology that distinguishes iron deficiency anemia

Decreased RBC count. Cells are microcytic, smaller than normal. Cells contain less Hgb than normal, transport less oxygen than usual.

Dilated cardiomyopathy pathophysiology

Decreased cardiac contractility, systolic performance, stroke volume. Increased EDV. The ventricular chambers are enlarged, the pressure is directed outward and so the walls of the heart become thinner and weak. Muscle cells die, and cardiac output decreases and there can be no CO and you die.

neurogenic (vasogenic) shock

Decreased vasomotor tone, resistance, BP

How to rapidly treat ventricular fibrillation

Defibrillation

Pathophysiology of atherosclerosis

Deposition of fat and fibrin in the wall of arteries, tends to harden over time. Decreases compliance of vessels. Reduces blood flow causing ischemia (brain, myocardial, and peripheral)

In aortic valvular insufficiency, why diastolic pressure decreases accounting for a widening of pulse pressure.

Diastolic pressure decreases in aortic valvular insufficiency because of Starling's Law of the Heart.

How do diuretics, beta blockers, vasodilators work to decrease workload of the heart?

Diuretics: lower blood volume. Beta-blockers: drugs decrease HR and myocardial contractility. Calcium channel blockers: vasodilate, decrease resistance to blood flow. Decrease arterial smooth muscle cells tension.

Complications of myocardial infarction

Dysrhythmias, Heart Failure, rupture of heart structures, rupture of wall of infarcted ventricle, systemic thromboembolism, and sudden death.

What is secondary hypertension?

Elevated BP with a specific cause that raises peripheral vascular resistance. Accounts for 10 % of HTN cases

Purpose of clot-busting drug, like tPA

Enzymatically dissolve any clots that form in coronary arteries.

Outline the process of erythropoiesis and describe the role of vitamin B12, folic acid, and EPO

Erythropoiesis is the formation of red blood cells; it occurs within the bone marrow. The process starts with uncommitted stem cells that differentiate into proerythroblasts. These become basophilic erythroblasts then normoblast. The nucleus leaves the normoblast and the cell becomes reticulocyte which is released from the bone marrow. After 24 hours in circulation, this round cell becomes the biconcave shape of an erythrocyte. The role of vitamin B12, folic acid, and erythropoietin is to help with the formation of nucleotides of DNA.

What is primary hypertension?

Essential or idiopathic, accounts for 90% of HTN cases. Initiated by increased blood volume and C.O. Blood vessels irreversibly adapt to new level of BP

What does mean corpuscular hemoglobin measure

Estimates the average amount (weight) of hemoglobin in each RBC. Amt of Hgb in JUST RBCs

Major symptoms of anemia

Fatigue, weakness, pallor, dyspnea

Avg normal values for males and females hematocrit

Female: 42% Male: 47%

How does fluid accumulate in alveoli causing an increased wedge-pressure and difficulty breathing.

Fluid accumulates in alveoli by because the decreased cardiac output leads to increased blood volume and pressure backs up into pulmonary circulation.

Sickle cell treatment

Gene therapy, treating mutation in amino acid sequence.

What is gradual vs rapid accumulation?

Gradual can accommodate 1000 cc of fluid of serous fluid. Rapid: 50-100cc usually blood

Normocytic normochromic anemia.

HCT & Hgb decreased MCV & MCHC normal The few that are made are normal but there are WAY TOO FEW (like all on the sidewalk and not in the body) so that's why it's a problem. Aplastic anemia and acute hemorrhagic anemia.

Microcytic hypochromic anemia

HCT & Hgb decreased MCV decreased MCHC decreased (Smaller & less pigment) Problem making Hgb and fewer RBCs Iron deficiency anemia and thalassemia

Macrocytic normochromic anemia

HCT & Hgb decreased MCV increased MCHC normal Not a problem of Hgb, problem of making RBCs -Pernicious anemia (vitamin B12 deficiency) -Folic acid deficiency

Treatment of a third degree heart block

HR= 30 bpm, not enough oxygen going to the brain- fainting, passing out, falling. The atria and ventricles contract independently, junctional rhythm. Pharmacologic until pacemaker is inserted.

Several risk factors associated with development of CAD

HTN, diabetes mellitus, obesity, sedentary lifestyle, alc., gender, personality.

In multiple myeloma describe how hypercalemia arises

Hypercalcemia arise in multiple myeloma because malignant cells localize to bone.

anaphylactic shock

Hypersensitivity rxns and allergies

What are four endocrine disorders that could be the causative factor of a a diagnosis of secondary hypertension?

Hyperthyroidism: increase of TH, makes heart work harder. Hypercortisolism: cortisol increases HR & peripheral resistance. Hyperaldosteronism: High aldosterone in blood vessels and increased sodium absorption and expansion of ECF. Pheochromocytoma: Synthesize excessive adrenaline.

Describe hypertrophic cardiomyopathy

Hypertrophy of inter-ventricular septum, it becomes so large not enough blood can come in and go out. Myocardium becomes non-compliant. Treatment: beta-blockers, calcium channel blockers, surgical resection.

Aortic semilunar valve regurgitation

Hypertrophy of left ventricle, decreased stroke volume and cardiac output- decreased tissue perfusion. Narrowed pulse pressure

Differentiate between the four stages of lymphoma and indicate which stages are most responsive to chemotherapy and therefore have the best prognosis.

I: malignant cells confined to single node. II: two or more lymph nodes affected confined to one side of diaphragm. III: involves lymph nodes above and below the diaphragm IV: multiples or disseminated foci of involvement

Causes of cardiomyopathies

Idiopathic, alcoholism, post-partum, following previous infection

In valvular regurgitation how does fluid accumulate in alveoli

In aortic valvular insufficiency valve leaflets fail to shut completely. Blood flows backwards because of the increased blood volume and therefore workload in the chamber leading to hypertrophy. Retrograde flow of blood into the left ventricle. The left ventricle deals with a higher volume, stretching more, the higher volume In, the increase in stroke volume.

Pathophysiology associated with aortic valvular insufficiency

In aortic valvular insufficiency valve leaflets fail to shut completely. Blood flows backwards because of the increased blood volume and therefore workload in the chamber leading to hypertrophy. Retrograde flow of blood into the left ventricle. The left ventricle deals with a higher volume, stretching more, the higher volume In, the increase in stroke volume.

Pathophysiology of myocardial ischemia (changes in cellular function, ventricular function, stroke volume, and EDV)

Increase in anaerobic metabolism, increased production of lactic acid. Impaired left ventricular function, lack of oxygen and lactic acid accumulation. Stroke volume decreases, EDV increases

How do the levels of biomarkers C-reactive protein and cholesterol serve as an index for rel. risk of a future heart attack?

Increased cholesterol and CRP increases risk for future coronary events.

Why does diastolic pressure increase in aortic valvular stenosis

Increased diastolic because baroreceptor reflex increased vasoconstriction (increased sympathetic nervous system).

Left sided heart failure

Increased pulmonary hydrostatic pressure leads to pulmonary edema. Alveoli fill with fluid, orthopnea, suspense, impaired gas diffusion, suffocation

Right sided heart failure outline events

Increased pulmonary vascular resistance, caused by primary pulmonary pathology or come secondary to left heart failure. Increased central venous pressure Increased systemic capillary hydrostatic pressure Peripheral edema

Three consequences of chronic, unmanaged high blood pressure on the human body

Increased risk of heart failure, shortened life span expectancy significantly, and reduced quality of life.

Describe how common manifestations of leukemia (infections, bleeding, and anemia) arise.

Infections: opportunistic bacteria and decreased protection, immune deficiency. Plus, chemotherapy and/or corticosteroids. Bleeding: Reduction of megakaryocytes leads to thrombocytopenia. Anemia: Decreased stem cell input and/or ineffective erythropoiesis.

How do ACE inhibitors work?

Inhibit angiotensin converting enzyme to decrease angiotensin II. Angiotensin II causes vasoconstriction which increases BP.

How does balloon angioplasty work?

Inserted into artery via catheter, inflates to open artery back up

Myocardial infarction characteristics

Irreversible hypoxic injury to cells and cell death and tissue necrosis.

Major difference between myocardial ischemia and myocardial infarction is

Ischemia is transient/reversible myocardial tissue damage. Infarction is permanent tissue damage.

Pathophysiology of first degree heart block

It is the least serious of the three types. Ventricles are contracting and pumping normally, blood is just being held a little longer. Sometimes it is due to scar tissue and/or pathologies that affect the AV node, heart attacks, cardiomyopathies, etc. The pathophysiology is local hypoxia, scarring of intra-atrial conduction pathways, electrolyte imbalances, and increased atrial preload.

Valvular regurgitation

Leaky, not closing. Left ventricle dealing with higher volume, stretching more.

Left atrioventricular valve stenosis (mitral valve)

Left atrial hypertrophy, decreased cardiac output, pulmonary congestion, leads to right sided heart failure.

Aortic Semilunar valve stenosis pathophysiology

Left ventricular hypertrophy, decreased stroke volume & cardiac output, and narrowed pulse pressure (from 40-20 mmHg). Narrowed path, increases resistance, decreases SV & CO. Left ventricle has to work harder, compensatory Hypertrophy. Cells tend to start dying, becoming weaker and weaker leads to heart failure. More volume, more pressure in capillaries, keeps backing up, can get into alveoli.

Why the lower systolic pressure in aortic valvular stenosis?

Lower volume, lower pressure. Decreased systolic because decreased stroke volume.

Describe conditions which characterize as a cells as a macrocyte or microcyte

Macrocyte: greater than 95 fL Microcyte: less than 80 fL

Avg normal values for males and females hemoglobin

Male: 16 g/100mL Female: 14 g/100mL

Avg normal values for males and females RBC count.

Male: 5.4 mil/uL Female: 4.8 mil/uL

What does mean corpuscular volume (MCV) measure?

Measures the size of the red blood cell

Describe the characteristics of Hodgkin's disease and indicate the significance of the pre scene of the Reed-Sternberg cell

More common in males. enlarged, non-painful single group of axial lymph nodes (cervical, axillary, inguinal, and retroperitoneal). The most common appearance of the affected lymph node is nodular sclerosis. If the Reed-Sternberg cell is present in the biopsy of a lymph node it is Hodgkin's lymphoma. 90% cure rate with radiation/chemotherapy. Stem cell transplant, immunotherapy.

Define the term polycythemia.

Myeloproliferative RBC disorder. Higher number of RBC volume--> increase in blood viscosity --> hypercoagulability of blood.

Restrictive cardiomyopathy

Myocardium becomes non-compliant, stiff and rigid. Doesn't expand as much or increase in volume or contract and decrease in volume.

Hypertrophic cardiomyopathy

Myocardium becomes non-compliant- the wall of interventricular septum becomes a lot thicker, so much so that the volume of the chambers are so low that such a low amount of blood going in and coming out of the heart, you can faint.

CLL (chronic lymphocytic leukemia)

Neoplastic disorder of B lymphocytes. Leukemic lymphocytes differentiated, small mature looking lymphocytes accumulate in blood and bone-marrow. Long-live, unable to to differentiate into plasma cells. Hypogammaglobulinemia, increased susceptibility to bacterial infections Over-expression of bcl-12 gene immortalizes CLL cells trisomy 12 most common abnormal finding Radiation and chemotherapy long term control. Corticosteroid reduce abnormal high lymphocyte count. CAR T therapy (eliminated 7 lbs)

How does nitroglycerine relieve with angina pectoris?

Nitroglycerine is a vasodilator. Nitroglycerin converts to nitric oxide, and NO promotes relaxation of vascular smooth muscle. Veins are dilated and so the workload on the heart is quickly decreased. Myocardium doesn't have to generate as much force during systole, afterload. The heart isn't working as hard, and so the oxygen demand in the myocardial cells is lessened.

Differentiate between nodular (follicular) and diffuse pattern of spread of malignant cells in lymph nodes and indicate which pattern is associated with a more favorable prognosis.

Nodular: Clusters of identifiable nodules surrounded by fibrotic collagen bands. Diffuse: Cells spread diffusely throughout node with an absence of fibrotic collagen bands. Nodular is better prognosis

What are non-modifiable risk factors and modifiable risk factors for atherosclerosis?

Non-modifiable: age, gender, family history, race Modifiable: smoking, LDLs, HDLs, HTN, C Reactive Protein (CRP)

What are the values of avg normal BP? Elevated? Stage 1 hypertension? Stage 2 hypertension?

Normal: <120/80 mmHg Elevated: 120-129 / <80 mmHg Stage 1 HTN: 130-139/ 80-89 mmHg Stage 2 HTN: >140/90 mmHg

Describe conditions that characterize as a cell as being normochromic or hypochromic

Normochromic: 29 pg. Hypochromic less than 25 pg.

How atherosclerosis affects normal anatomy and physiology of a coronary artery and increases workload of the heart

Occludes arterial lumens: increases peripheral resistance to blood flow, increases workload on the heart.

Sickle cell anemia treatment

One approach to treating this type of anemia is gene therapy, treating the mutation in the amino acid sequence. It is currently being tested, but it has cured some cases of sickle cell anemia.

Diagnostic Criteria of second degree heart block

PR ratio is increased, the R wave may be every other beat, heart "skips" a beat.

Define hematocrit, avg normal value

Percentage of packed RBCs: 47% Male 42% Female

List components of a sample of whole blood. Give relative percentages of plasma, RBCs, WBCs, and platelets

Plasma 55%, RBC 45%, Buffy coat 1%

Give the average normal value for platelet and describe the evolution and function of platelets

Platelets are derived from megakaryocytes. The function of platelets is coagulation, preventing hemorrhaging. The average normal value for platelets is 150,000-350,000 per microliter of blood.

What is pre-load?

Preload is the amount of blood sitting in the heart right before it contracts

what does a cold spot on Thallium 201 imaging indicate?

Presence of a cold spot indicates dead tissue. With a normal heart, radiation will visually show heat and living. You can localize where the infarction is and the size.

How do blood thinners work?

Prevent thrombus formation, they do not thin the blood, they prevent blood from clotting "thickening".

What is ejection fraction?

Proportion of end diastolic volume ejected from left ventricle during systole. Normal values: 56-78%

Theory behind stents?

Provide more support to keep lumen open, stays in once balloon has left so that it is 100% open.

How does left atrioventricular valve stenosis lead to right sided heart failure?

Pulmonary HTN --> Pulmonary edema --> right sided heart failure

Septic shock

Reaction to disseminated infection, response to bacterial endotoxins. Often called "warm shock" due to accompanying fever from infection.

Treatment for dilated cardiomyopathy

Reducing blood volume, increasing contractility, and reversing underlying disease if possible. Heart transplant in severe cases.

Four health benefits of reducing high blood pressure

Reduction of incidence of kidney disease, heart failure, stroke, and heart disease.

Left AV Valve regurgitation

Retrograde flow into left atrium causes dilation and hypertrophy Left ventricle hypertrophied for compensation, eventually fails pulmonary hypertension and right ventricular failure

Describe connection between rheumatic fever and rheumatic heart disease

Rheumatic fever is an inflammatory disease, and it can cause scarring and deformity of cardiac structures, that can lead to rheumatic heart disease. 10% of Rheumatic fever leads to rheumatic heart disease.

Average normal SV, EDV?

SV: 70 mL EDV: 120 mL

Describe function of adrenaline and arginine vasopressin for treating circulatory shock

Shocks the system with energy, to restart function. Vasopressin increases organ perfusion

Function and location of stem cells, myeloid cells, and lymphoid cells.

Stem cells: bone marrow Myeloid: develop in bone marrow- basophils, eosinophils, neutrophils, monocytes, platelets, RBCs Lymphoid: develop in lymphoid organs (lymph nodes and spleen)- B cells, NK cells, T cells

Difference between valvular stenosis vs insufficiency

Stenosis: valve opening is constricted, blocking forward flow of blood and increasing workload of the heart. Insufficiency: valve leaflets fail to shut completely and continue even when valve is supposed to be closed. Blood leaks back into the chamber. Chamber dilates and workload leads to hypertrophy.

What is the difference between subendocardial ischemia and transmural ischemia?

Subendocardial is just below the endocardium, transmural is through the whole wall of the heart

Symptoms associated with myocardial infarction

Sudden and severe chest pain (not relieved by nitrates), initial drop in BP, sympathetic NS activation, abnormal heart sounds, release of iso-enzymes from damaged myocardial cells.

Procedure to remove fluid in pericardial space.

Surgical thoracoscopy, incision into the 5th intercostal space. Pericardial synthesis, withdrawing fluid with a syringe.

Provide symptoms and treatments for polycythemia

Symptoms: blood shot eyes, plethoric, headache, blurred vision, HTN, increase blood clots Treatment: phlebotomy (drain excess blood, frequent blood draws). Drugs suppress bone marrow, myelosuppressive drugs, produce anemia.

In aortic valvular insufficient why systolic pressure increases

Systolic pressure increases in aortic valvular insufficiency because of the increase in volume.

Describe the lesion referred to as multiple myeloma including the malignant cell type and typical findings upon analysis of the serum

The changes in the skeleton in multiple myeloma are rounded "punched out" lesions, appear as lucent areas, abnormal plasma cells of multiple myeloma fill the bone marrow. There are increased levels of immunoglobulins in blood and Bence-Jones protein (light chain immunoglobulins) in the urine.

Describe the characteristics of Non-Hodgkin's lymphoma and compare the general features that differentiate Hodgkin's disease from Non-Hodgkin's lymphoma

The characteristics of non-Hodgkin's lymphoma are no Reed-Sternberg cell, multicentric, spreads widely. Most cases are B cell in origin impaired results in decreased antibody production. The general features that differentiate Hodgkin's disease from Non-Hodgkin's lymphoma are Hodgkin's disease is usually localized to a single group of nodes whereas Non-Hodgkin's lymphoma involved multiple peripheral nodes.

Thrombocytopenia and differentiate between thrombocytopenia conditions caused by pathologies of bone marrow vs. decreased platelet survival

The clinical lab value of a platelet count for diagnosing thrombocytopenia is less than 100,000 platelets/microliter of blood. Aplastic anemia, cancer (leukemia), side effect of chemotherapy. Decreased platelet survival causes are idiopathic thrombocytopenia purpura, drugs, viral infections, and/or pregnancy.

Describe where EPO is made. What conditions regulate its formation and its effect upon release.

The organ that makes the hormone erythropoietin is the kidney and liver. The conditions that regulate its formation are arterial oxygen levels. Decreased arterial oxygen levels result in decreased tissue oxygen that stimulate kidney to increase production of erythropoietin. The effect upon release is regulation of erythropoiesis, increased release of red blood cells in circulation, correcting hypoxia in the tissues.

Describe Pathophysiology of mitral valvular insufficiency, how does fluid accumulate in alveoli

The pathophysiology associated with mitral valvular insufficiency is left ventricle hypertrophy because the heart struggles to push more forward, it eventually fails. Pulmonary hypertension occurs. Blood flows into left atrium causing dilation and hypertrophy. The right ventricle fails.

Define thrombocytosis and distinguish between transient and chronic types of thrombocytosis

Thrombocytosis is platelet count is above 400,000 per microliter of blood. Transient thrombocytosis is stress, infection, trauma, exercise, and ovulation. Chronic thrombocytosis is accelerated platelet production in bone marrow. A risk associated with thrombocytosis is too much blood clotting.

The consequences the myocardium may suffer with chronic, untreated HTN

Transient, reversible lack of oxygen and damage.

What do EKG changes look like with transmural and subendocardial myocardial infarctions?

Transmural: elevated ST segment, indicates entire wall is dead- very severe heart attack. Subendocardial: very large Q wave, will remain as long as they live.

CML (chronic myelogenous leukemia)

Usually dramatic increase of leukocytes, ranging from 100,000 to 500,000 cells/uL. Malignant transformation of pluripotent stem cells with leukemic granulocytic precursors constituting the dominant cell line. More common in older adults. Slow progression, without treatment 3 yrs survival rate. Chemotherapy and radiation do not significantly alter 3-4 yr. survival. Bone marrow is the only cure. After blast crisis, all forms are basically ineffective. Etiology: Philadelphia chromosome - reciprocal translocation of long arms of 9 & 22 Gleevac works! Inhibits protein only expressed in cancer cells, and no other cell in the body. Near total elimination of cancer cells, but it must be taken every day or it will come back.

Normal flow of blood through the heart- but backwards.

Whiteboard it or write it out

What is "wedge pressure"

a catheter is thread through capillaries until it gets to a capillary lumen that is much smaller, it needs to be wedged into it. Wedge pressure is increased pulmonary capillary hydrostatic pressure. The worse the problem, the worse the wedge pressure is.

Treatment of hereditary spherocytosis

a splenectomy. It allows the red blood cells to survive longer by removing the organ, the spleen, that removes them

CML age group with the highest incidence, cellular characteristics of malignant cell, typical progression of disease, and responsiveness to therapy.

age group with the highest incidence, cellular characteristics of malignant cell, typical progression of disease, and responsiveness to therapy.

Several normal characteristics about RBCs (erythrocytes)

anuculeated, 7-8 um diameter, 120 day life span

What are the leading causes of myocardial infarctions?

atherosclerotic plaque formation in coronary vessels, hemorrhage into a plaque, embolism, spasm of coronary arteries

What is tissue perfusion?

blood flow through capillaries to body tissues. 5 liters/min

What does mean corpuscular hemoglobin concentration measure

concentration of hemoglobin in 100 mL whole blood

What is anemia?

decrease in total number of red blood cells, decreased hemoglobin, and/or decrease in quality of RBCs.

List several causes of anemia

decreased erythropoiesis, blood loss (hemorrhage), increased destruction, and/or deficiency of hemoglobin.

Hypovolemic shock

decreased intravascular volume Hemorrhage Burns

Folic Acid and Vitamin B12 Deficiency Anemia

decreased red blood cell count. Cells are macrocytic, larger than normal because of decreased RBC production and maturation.

What is pulse-pressure?

difference between systolic and diastolic pressure

Heart blocks

dysfunction of the intrinsic conduction system

Leukopenia

fewer circulating white blood cells; white blood cell count is between 500-1000/uL.

Describe diagnostic criteria of first degree heart block

first-degree AV node conduction heart block the P-R interval is a little longer P-R interval is longer than 200 milliseconds.

In multiple myeloma, describe the Bence-Jones protein.

free immunoglobulin light chains in plasma that are toxic to renal tubular cells leading to renal insufficiency and renal failure. Myelomas can be detected by a spike of Bence-Jones proteins in the urine.

Mitral valve prolapse

improper closure of the mitral valve

What is acute pericarditis?

inflammation of the pericardium, mostly caused by infections. Produces

Thalassemia

inherited defect in ability to produce hemoglobin, leading to hypochromia

Hereditary spherocytosis

inherited disorder caused by defects in the membrane skeleton of RBCs that causes RBCs to be spherical, less deformable, and vulnerable to destruction. Anemia, jaundice, and splenomegaly occur.

Pathophysiology with second degree heart block

local hypoxia, coronary artery disease, myocardial infarction, increased preload, valvular surgery, diabetes, hypokalemia, and faulty cell metabolism in AV node.

Define lymphoma

malignant neoplasm characterized by proliferation of lymphoid tissue cells.

Leukemia

malignant neoplasms of hematopoietic cells in bone marrow.

List the major classic symptoms associated with thrombocytopenia

minor bleeding problems that occur over several days and progress to major hemorrhage in mucosal sites. Wright loss, fever, and headache are symptoms.

Describe the genetic defect and basic pathophysiology of sickle cell anemia

mutation in the beta globin chain, a glutamic acid changed to valine. This single amino acid change causes a sickle shape, instead of a biconcave shape. The sickle cell shape causes the cells to stick together- increased blood clots potentially leading to prolonged ischemia in the capillaries, everywhere in the body (painful).

Define heart failure

pathophysiologic condition that the heart is unable to generate an adequate cardiac output that is adequate to perfuse tissue.

Third degree heart block

still beating, still ventricular activity. Abnormal rhythm. Regular atrial activity, reflected on the P wave. R waves being generated at a regular rate much slower than a P waves.

Treatment for iron deficiency anemia

supplemental iron and/or finding the cause for a loss of blood such as excessive menstrual flow.

Possible clinical uses for EPO

treat anemia that is caused by chronic renal failure. If an induvial take recombinant human erythropoietin, it increases the blood reticulocyte count, increasing levels of erythrocytes.