Blueprint Exam 2 PDF

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Pathophysiology Exam 2 Blueprint

Chapter 10 1. Define the terms describing abnormalities in the blood. This is a general objective that simply means the term definitions in the beginning of the chapter are key to understanding the chapter content.   

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Hematocrit—percent by volume of cellular elements in blood—essentially erythrocytes Hemoglobin—amount of hemoglobin per unit volume of blood o Mean corpuscular volume (MCV)—indicates oxygen carrying capacity of blood Hematopoiesis—development of blood cells from a single stem cell o Erythropoiesis—production of RBCs o Leukopoiesis—production of WBCs o Thrombopoiesis—production of platelets Erythropoietin (EPO)—hormone that originates from the kidneys which stimulates RBC production in the red bone marrow in response to tissue hypoxia Hemostasis—process of stopping bleeding o Intrinsic (activated by endothelial injury IN blood vessel) and extrinsic pathways (activated by tissue and platelet injury) Pancytopenia—decrease in RBCs, WBCs, and platelets in the blood Leukopenia—a decrease in WBCs Leukocytosis—an increase in WBCs Dyspnea—increased effort to breathe Pallor—pale face Microcytic—blood cells are smaller o Occurs in iron-deficient anemia and thalassemia Macrocytic—blood cells are large o Occurs in pernicious anemia Petechiae—flat, red, pinpoint hemorrhages on the skin

2. Describe and compare the pathophysiology, etiology, manifestations, diagnostic tests, and treatment for each of the selected anemias: iron-deficiency, pernicious, aplastic, sickle cell, and thalassemia. The key is to be able to differentiate between these anemia Iron deficiency anemia 

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Pathophysiology o Insufficient iron impairs hemoglobin synthesis (iron sits on hemoglobin to change its structure) o Microcytic, hypochromic RBCs—result of low hemoglobin concentration in cells Etiology (cause)

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o Dietary intake, chronic blood loss, duodenal absorption, severe liver disease, infections and cancers Signs and symptoms o Pallor of the skin, fatigue, lethargy, irritability, degenerative changes (brittle hair and ridged nails) o Stomatitis and glossitis, inflammation in the mucosa and tongue o Delayed healing and tachycardia, heart palpitations, dyspnea (shortness of breath), possible fainting as the anemia becomes more severe Diagnostic tests and treatment o Lab tests demonstrate low values for hemoglobin and hematocrit. On microscopic examination the erythrocytes appear hypochromic and microcytic o Underlying cause must be identified and resolved if possible, treatment and prognosis depend on cause. o Iron rich foods/supplements may be administered

Pernicious anemia—Vitamin B12 Deficiency 

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Pathophysiology o Lack of absorption of vitamin B12 due to lack of intrinsic factor secreted by gastric mucosa o Parietal cells can no longer produce hydrochloric acid which occurs with the atrophy of the mucosa, resulting in a low level/absence of acid in gastric secretions—achlorhydria o Deficit of B12 absorption leads to impaired maturation of erythrocytes owing to interference with DNA synthesis Etiology o Most common cause of vitamin B12 deficiency is malabsorption  Surgical procedures as gastrectomy also result as an outcome o Dietary insufficiency is rare as the source of B12 is animal foods  Vegans/vegetarians need to include a B12 fortified food in daily intake Signs and symptoms o Tongue enlarged, red, sore and shiny o Digestive discomfort o Paresthesia in the extremities or loss of coordination and ataxia Diagnostic tests o Megaloblastic on microscopic examination, marrow is hyperactive, vitamin B12 level and the presence of hypochlorhydria or achlorhydria Treatment o Oral supplements, injections and replacement therapy

Aplastic anemia 

Pathophysiology

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o Results from impairment/failure of bone marrow which leads to loss of stem cells and pancytopenia—decreased numbers of erythrocytes, leukocytes and platelets in the blood Etiology o May be temporary or permanent depending on the cause o Often idiopathic but possible causes include  Myelotoxins—radiation (cancer patients), industrial chemicals, drugs  Viruses—particularly hepatitis C  Genetic abnormalities—myelodysplastic syndrome and Fanconi’s anemia Signs and symptoms o Onset is insidious and because the entire bone marrow is affected manifestations include anemia, leukopenia (recurrent infections), thrombocytopenia (petechiae— flat, red, pinpoint hemorrhages on the skin and a tendency to bleed excessively, particularly in the mouth) Diagnostic tests and treatment o Blood counts indicate pancytopenia, a bone marrow biopsy may be required to confirm the cause as erythrocytes are usually normal in appearance o Prompt treatment of cause and removal of any bone marrow suppressants are essential to recovery of the bone marrow. Bone marrow transplant may also be helpful

Sickle cell anemia 

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Pathophysiology o An inherited characteristic that leads to the formation of abnormal hemoglobin, hemoglobin S (HbS). Altered hemoglobin becomes deoxygenated (is unstable and changes shape in hypoxemia) and crystallizes, changing from a disc to a crescent/sickle shape Etiology o Genetic condition—autosomal, incomplete dominance  Anemia occurs in homozygous recessive (HbS) o Crisis occurs whenever oxygen levels are lowered Signs and symptoms o The proportion of HbS in the erythrocytes determines the severity of the condition o Severe cases cause pallor, weakness and dyspnea (shortness of breath), splenomegaly, vascular occlusions and infarctions—which damage organs and tissues; congestive heart failure may develop as the body attempts to improve oxygen supply o Infections are common as the spleen has lowered defenses Diagnostic tests and treatment o Blood test can determine if one carries the defective gene

o Hydroxyurea reduces frequency of crises and prolonged the life span for many, dietary supplementation with folic acid is recommended, gene therapy, bone marrow transplant Thalassemia 

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Pathophysiology o Results from a genetic defect and interferes with the production of the amount of hemoglobin synthesized and the number of RBCs is reduced o Thalassemia alpha  Decrease or lack of alpha chains o Thalassemia beta (autosomal dominant inheritance)  Decrease or lack of beta chains Etiology o most common genetic disorder in the world o beta form affects those of Mediterranean countries and is the more common form Signs and symptoms o Usual signs of anemia and increased hemolysis Diagnostic tests and treatment o RBCs are microcytic and hypochromic (low hemoglobin) and an increase in erythropoietin levels and prenatal diagnosis can be done at 12 weeks o Blood transfusions are only treatment

3. Differentiate between primary and secondary polycythemia and describe the effects on the blood and circulation. The key is to be able to differentiate between primary and secondary Primary polycythemia—polycythemia vera   

Increased production of erythrocytes and other cells in the bone marrow Neoplastic disorder of unknown origin Serum erythropoietin levels are low

Secondary polycythemia—erythrocytosis  

Increase in RBCs in response to prolonged hypoxia Erythrocytosis

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Increased erythropoietin secretion Compensation mechanism to provide increased oxygen transport

Signs and symptoms    

Client appears plethoric and cyanotic Hepatomegaly and splenomegaly Pruritus (itching) Headaches and hypertension

4. Describe hemophilia A: its pathophysiology, signs, and treatment. Pathophysiology is definitely a must know as well as the signs of any bleeding disease 

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Pathophysiology o Classic hemophilia—deficit or abnormality of clotting factor 8 o Most common inherited clotting disorder  X-linked recessive trait  Manifested in men, carried by women o Varying degrees of severity o Spontaneous bleeding/excessive bleeding following minor tissue trauma  Persistent bleeding from gums/repeated nosebleeds and bruising, petechiae, feeling faint/anxious, low BP Signs and symptoms o Prolonged or severe hemorrhage occurs following minor tissue trauma o Spontaneous bleeding into joints o Possible hematuria or blood in feces Diagnostic tests o Bleeding time and PT (prothrombin time) normal o PTT, activated PTT (aPTT), coagulation time prolonged and serum levels of factor 8 are low

Hemophilia B (Christmas disease) 

Similar to A but involves deficit of factor 9

Hemophilia C (Rosenthal’s) 

Milder form and involves decrease in factor 11

5. Discuss the disorder disseminated intravascular coagulation: its pathophysiology, etiology, manifestations, and treatment. Contributing factors and clinical manifestation are the most important at this point in your training  

Involves both excessive bleeding and clotting Excessive clotting in circulation—thrombi and infarcts occur

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Clotting factors are reduced to dangerous level and widespread, uncontrollable hemorrhage results Poor prognosis with high death rate and complication of many primary problems o OB complications (abruptio placentae), infections, carcinomas and major trauma Clinical manifestations—depend on the underlying cause o Low plasma fibrinogen level is present o Thrombocytopenia occurs (low platelet count) o Multiple bleeding sites common o Petechiae may be present on skin or mucosa

6. Discuss the myelodysplastic syndrome and its relationship to other blood disorders. This is just nice to know but don’t spend much time on it   

Diseases that involve inadequate production of cells by the bone marrow Signs and symptoms o Anemia—dependent on type of deficiencies that occur May be idiopathic or occur after chemo or radiation therapy

7. Compare acute and chronic leukemia: the incidence, onset and course, pathophysiology, signs, diagnostic tests, and treatment. Acute and chronic is the focus 

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Signs and symptoms o Usual signs at onset  Frequent or uncontrolled infections, petechiae and purpura and signs of anemia o Severe and steady bone pain o Weight loss, fatigue, possible fever o Enlarged lymph nodes, spleen and liver o Headache, visual disturbances, drowsiness and vomiting Complications of leukemia o Opportunistic infections (pneumonia), sepsis, congestive heart failure, hemorrhage, liver and renal failure and CNS depression and coma

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High proportion of immature nonfunctioning cells in bone marrow and peripheral circulation Onset is usually abrupt, marked signs of complications Acute lymphocytic leukemia (ALL) o Malignant B cells o Primarily affects young children Acute myelocytic leukemia (AML) o Malignant granulocytic stem sells o Primarily affects adults

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Higher proportion of mature cells Insidious onset, mild signs and better prognosis than acute Chronic lymphocytic leukemia (CLL) o Malignant B cells o Affects adults greater than 50 Chromic myelocytic leukemia (CML) o Malignant granulocytic stem cells o Affects adults 30-50

Chapter 11 Very general questions directly from the power points

Chapter 12 1. Describe the common diagnostic tests for cardiovascular function. Yes, the power point slide is important 

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Electrocardiography (EKG) o Noninvasive procedure that can illustrate the conduction activity of the heart along with effects of systemic abnormalities—sternum electrolyte imbalance Auscultation—heart sounds “lub-dub” o Can detect murmurs Echocardiography o Ultrasound is used to record the image of the heart and valve movements Exercise stress tests o Running on a treadmill but can also be done chemically Chest X-ray films o Used to show shape and size of heart Angiography

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o Blood flow in coronary arteries can be visualized Doppler studies o Blood flow in peripheral vessels can be assessed Blood tests o Dead cells release enzymes, inflammatory response can increase WBC count Arterial blood gas determination o Tells pH, CO2, and oxygen levels Teaching—diet exercise and smoking

2. Describe the dietary and lifestyle changes, and the common drug groups used, in the treatment of cardiovascular disease. Remember this is not pharmacology but the factor one can change as opposed to the ones you can’t are important to know 

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Dietary modifications o Reducing total fat intake and intake of saturated (animal) fat as well as trans fats o Weight reduction may be recommended o Salt intake is decreased to reduce BP Regular exercise o Suggested to improve overall cardiovascular function and circulation to all areas of the body o Lowers serum lipid levels, increasing high-density lipoprotein (HDL) levels and reducing stress levels—lessening peripheral resistance and BP Drug therapy o Vasodilators o Beta blockers o Calcium channel blockers o Diuretics o Antihypertensive drugs  ACE (angiotensin-converting enzyme) inhibitors, digoxin, arbs o Anticoagulants o Cholesterol lowering drugs

3. Explain the role of cholesterol and lipoproteins in the development of atheroma’s. The pictorial explanation on the power points as well as text is very simple and easy to understand

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Atheroma—plaques consisting of lipids, cells, fibrin and cell debris often with attached thrombi, which form inside the walls of large arteries Lipids or fats, including cholesterol and triglycerides are essential elements in the body and are synthesized in the liver Because of their fat-like properties, they are not able to easily circulate in the bloodstream. In order for cholesterol and triglycerides to travel in the blood, they are often carried by proteins that make the cholesterol and triglycerides more soluble in blood.

4. Explain the significance of metabolic syndrome in the development of cardiovascular disease. Nice to know but don’t spend much time on this 

Obesity is the primary indicator of metabolic syndrome, which is directly linked with the development of coronary artery disease in adulthood

5. State the factors predisposing to atherosclerosis. Just got to know this 

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Nonmodifiable o Age and gender o Genetic or familial factors Modifiable o Obesity, diabetes mellitus and cigarette smoking o Sedentary lifestyle o Poorly controlled hypertension o Combination of oral contraceptives and smoking

6. Compare angina and myocardial infarction. Know the difference between ischemia and infarct  7. Describe the common arrhythmias and cardiac arrest. Remember these are ventricular rhythms  8. Discuss the causes of congestive heart failure and the effects of left-sided and right-sided failure Very important to understand the conceptual physiology behind this instead of just memorizing the charts or diagrams. YOU ARE BSN STUDENTS 

 9. Explain the changes in blood flow and their effects in common congenital heart defects. Don’t spend much time on this  10. Discuss the development of rheumatic fever and rheumatic heart disease. Understand this in general as well as some of the signs and symptoms  11. Describe the etiology and pathophysiology of infectious endocarditis and pericarditis. What is this doing to the function of the heart as well as cardiac output  12. Explain the development and possible effects of essential hypertension. Clue, CHF end organ disease and failure, what organs?  13. Compare the arterial peripheral vascular diseases atherosclerosis and aneurysms. In general  14. Describe the development and effects of the venous disorders varicose veins, phlebothrombosis, and thrombophlebitis. Why, Why, Why, signs symptoms and treatment.  15. Discuss the types of shock and the initial and progressive effects of shock on the body. If you don’t understand the physiology behind each of these you will not be qualified to treat them....