Pathology of Endocrine Disease Adrenal glands Dr. Arrigo Capitanio Department of Pathology 05-11.
Ch 10, 11, 12 Pathology
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Transcript of Ch 10, 11, 12 Pathology
Chapter 10
Blood and Circulatory System Disorders
•2•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc.
Review of the Circulatory System The circulatory system consists of the
cardiovascular system and lymphatic system This chapter will cover the blood vessels, the
blood, and associated disorders.
•3•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc.
Blood Vessels Arteries—arterioles
Transport blood away from heart Veins—venules
Return blood back to the heart Capillaries
Microcirculation within tissues Systemic circulation
Exchange of gases, nutrients, and wastes in tissues
Pulmonary circulation Gas exchange in lungs
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Blood Vessels (Cont.)
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Histology of Arteries and Veins Tunica intima—endothelium (simple
squamous epithelium) Tunica media—middle layer, mostly smooth
muscle Tunica adventitia (externa)—connective
tissue with fibrocytes, collagen (type I), and elastic fibers
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Blood
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Composition of Blood Plasma
Plasma proteins Cellular component
Erythrocytes Leukocytes Thrombocytes (platelets)
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Components of Blood and Their Functions
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Hematopoiesis
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Normal Red Blood Cells
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Erythrocytes (Red Blood Cells) Biconcave flexible discs No nucleus in mature state Contains hemoglobin
Globin portion Heme group
Life span—120 days Erythropoietin produced in the kidney
stimulates erythrocyte production.
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Normal Blood Cells
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Breakdown of Hemoglobin
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Blood Clotting—Hemostasis Three steps:
Vasoconstriction or vascular spasm after injury Platelet clot Coagulation mechanism
Plasmin will eventually break down the blood clot.
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Hemostasis and Anticoagulant Drugs
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Blood Typing
Blood typing is based on antigens in the plasma membrane of the erythrocytes.
ABO system Based on the presence or absence of specific
antigens Antibodies in the blood plasma
Rh system Antigen D in plasma membrane: Rh+ Absence of antigen D: Rh
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ABO Blood Groups
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Diagnostic Tests Complete blood count (CBC)
Includes total red blood cells (RBCs), white blood cells (WBCs), and platelets
Leukocytosis (increased WBCs)• Associated with inflammation or infection
Leukopenia (decreased WBCs)• Associated with some viral infections, radiation,
chemotherapy Increased eosinophils
• Common in allergic responses Differential count for WBCs
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Diagnostic Tests (Cont.) Morphology
Observed with blood smears Shows size, shape, uniformity, maturity of cells
• Different types of anemia can be distinguished. Hematocrit
Percent by volume of cellular elements in blood Hemoglobin
Amount of hemoglobin per unit volume of blood Mean corpuscular volume (MCV)
• Indicates the oxygen-carrying capacity of blood
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Diagnostic Tests (Cont.) Reticulocyte count
Assessment of bone marrow function Chemical analysis
Determines serum levels of components, such as iron, vitamin B12, folic acid, cholesterol, urea, glucose
Bleeding time Measures platelet function
Prothrombin time (PT) and partial thromboplastin time (PTT) Measure function of various factors in coagulation process International normalized ratio (INR) is a standardized
version.
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Blood Therapies Whole blood, packed red blood cells, packed
platelets For severe anemia or thrombocytopenia
Plasma or colloid volume-expanding solutions To maintain blood volume
Artificial blood products Compatible with all blood types None of them can perform all the complex
functions of normal whole blood.
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Blood Therapies (Cont.) Epoetin alfa
Artificial form of erythropoietin • Before certain surgical procedures• Anemia related to cancer• Chronic renal failure
Bone marrow or stem cell transplantation Close tissue match necessary
• Treatment of some cancers• Severe immunodeficiency• Severe blood cell diseases
Drug treatment Aids in the clotting process
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Blood Dyscrasias
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The Anemias Anemia causes a reduction in oxygen
transport. Basic problem is hemoglobin deficit Oxygen deficit leads to:
Less energy production in all cells• Cell metabolism and reproduction diminished
Compensation mechanisms• Tachycardia and peripheral vasoconstriction
General signs of anemia• Fatigue, pallor (pale face), dyspnea, tachycardia
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The Anemias (Cont.) Oxygen deficit leads to:
Decreased regeneration of epithelial cells• Digestive tract becomes inflamed and ulcerated, leading
to stomatitis• Inflamed and cracked lips• Dysphasia• Hair and skin may show degenerative changes.
Severe anemia may lead to angina or congestive heart failure (CHF).
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Iron Deficiency Anemia Insufficient iron impairs hemoglobin
synthesis. Microcytic, hypochromic RBCs
• Result of low hemoglobin concentration in cells Very common
Ranges from mild to severe Occurs in all age groups, but more common in
women of childbearing age Estimated that one in five women is affected
• Proportion increases for pregnant women Frequently sign of an underlying problem
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Iron Deficiency Anemia—Blood Smear
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Iron Deficiency Anemia: Causes Dietary intake of iron below minimum
requirement Chronic blood loss
As from bleeding, ulcer, hemorrhoids, cancer Impaired duodenal absorption of iron
In many disorders, malabsorption syndromes Severe liver disease
May affect iron absorption as well as storage
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Iron Deficiency Anemia: Signs and Symptoms
Pallor of skin and mucous membranes Fatigue, lethargy, cold intolerance Irritability Degenerative changes Stomatitis and glossitis Menstrual irregularities Delayed healing Tachycardia, heart palpitations, dyspnea,
syncope
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Pernicious Anemia: Vitamin B12 Deficiency
Basic problem is lack of absorption of vitamin B12 because of lack of intrinsic factor Intrinsic factor secreted by gastric mucosa Required for intestinal absorption of vitamin B12
Characterized by very large, immature, nucleated erythrocytes Carry less hemoglobin Shorter life span
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Pernicious Anemia: Vitamin B12 Deficiency (Cont.)
Dietary insufficiency is very rarely a cause. Genetic factors have been implicated.
More common in light-skinned women of northern European ancestry
Often accompanies chronic gastritis May also be an outcome of gastric surgery
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Development of Pernicious Anemia
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Vitamin B12 and Nerve Cells
Vitamin B12 is needed for the function and maintenance of neurons.
Significant deficit of the vitamin will cause symptoms in the peripheral nerves.
These may be reversible.
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Vitamin B12 Deficiency
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Pernicious Anemia: Vitamin B12 Deficiency (Cont.)
Manifestations in addition to those typical for anemias Tongue is typically enlarged, red, sore, and shiny. Digestive discomfort, often with nausea and
diarrhea Feeling of pins and needles, tingling in limbs
Diagnostic tests Microscopic examination (erythrocytes) Bone marrow examination (hyperactive) Vitamin B12 serum levels below normal Presence of hypochlorhydria or achlorhydria
• Presence of gastric atrophy
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Aplastic Anemia Impairment or failure of bone marrow May be temporary or permanent Often idiopathic but possible causes include:
Myelotoxins • Radiation, industrial chemicals, drugs
Viruses• Particularly hepatitis C
Genetic abnormalities• Myelodysplastic syndrome• Fanconi’s anemia
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Aplastic Anemia (Cont.) Blood counts indicate pancytopenia.
Anemia, leukopenia, thrombocytopenia Bone marrow biopsy may be required. Erythrocytes often appear normal.
Identification of cause and prompt treatment needed for bone marrow recovery Removal of any bone marrow suppressants Failure to identify cause and treat effectively is life-threatening!
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Hemolytic Anemia Results from excessive destruction of RBCs Causes
Genetic defects Immune reactions Changes in blood chemistry Infections such as malaria Toxins in the blood Antigen-antibody reactions
• Incompatible blood transfusion• Erythroblastosis fetalis
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Sickle Cell Anemia Genetic condition
Autosomal Incomplete dominance Anemia occurs in homozygous recessive. Diagnostic testing is available. More common in individuals of African ancestry
• Heterozygous condition is somewhat protective against malaria.
• One in ten African Americans is heterozygous for the trait.
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Sickle Cell Anemia (Cont.)
•41•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc.
Sickle Cell Anemia (Cont.) Abnormal hemoglobin (HbS) Sickle cell crisis occurs whenever oxygen
levels are lowered. Altered hemoglobin is unstable and changes
shape in hypoxemia. Sickle-shaped cells are too large to pass
through the microcirculation. Obstruction leads to multiple infarctions and
areas of necrosis.
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Sickle Cell Anemia (Cont.)
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Sickle Cell Anemia (Cont.)
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Sickle Cell Anemia (Cont.) Multiple infarctions affect brain, bones,
organs In addition to basic anemia:
Hyperbilirubinemia, jaundice, gallstones• Caused by high rate of hemolysis
Clinical signs Do not usually appear until the child is about 12
months old
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Sickle Cell Anemia: Signs and Symptoms
Severe pain because of ischemia of tissues and infarction
Pallor, weakness, tachycardia, dyspnea Hyperbilirubinemia—jaundice Splenomegaly Vascular occlusions and infarctions
In lungs• Acute chest syndrome
Smaller blood vessels• Hand-foot syndrome
Delay of growth and development Congestive heart failure
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Sickle Cell Anemia (Cont.) Diagnostic tests
Blood test• Hemoglobin electrophoresis
Prenatal DNA analysis Treatment
Hydroxyurea has reduced the frequency of this crisis.
Dietary supplementation with folic acid Bone marrow transplantation Immunization in children
• Against pneumonia, influenza, meningitis
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Comparison of Selected Anemias
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Polycythemia Primary polycythemia—polycythemia vera
Increased production of erythrocytes and other cells in the bone marrow
Neoplastic disorder Serum erythropoietin levels are low.
Secondary polycythemia—erythrocytosis Increase in RBCs in response to prolonged
hypoxia Increased erythropoietin secretion Compensation mechanism to provide increased
oxygen transport
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Polycythemia: Signs and Symptoms
Distended blood vessels, sluggish blood flow Increased blood pressure Hypertrophied heart Hepatomegaly Splenomegaly Dyspnea Headaches Visual disturbances Thromboses and infarctions
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Polycythemia (Cont.) Diagnostic tests
Increased cell counts Increased hemoglobin and hematocrit values Hypercellular bone marrow Hyperuricemia
Treatment Identify cause Drugs or radiation
• Suppression of bone marrow activity Periodic phlebotomy
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Indications of Blood-Clotting Disorders
Persistent bleeding from gums Repeated epistaxis Petechiae
Pinpoint, flat, red spots on skin and mucous membrane
Frequent purpura and ecchymosis More than normal bleeding in trauma Bleeding into joint—hemarthroses
Swollen, red, painful Hemoptysis
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Blood-Clotting Disorders Hematemesis
Coarse brown particles (coffee ground emesis) Blood in feces
Black or occult Anemia Feeling faint and anxious Low blood pressure Rapid pulse
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Petechiae
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Hemophilia A Classic hemophilia
Deficit or abnormality of factor VIII Most common inherited clotting disorder
X-linked recessive trait Manifested in men, carried by women
Varying degrees of severity Prolonged bleeding after minor tissue trauma Spontaneous bleeding into joints Possible hematuria or blood in feces
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Hemophilia A (Cont.) Diagnostic tests
Bleeding time and PT normal PTT, activated PTT (aPTT), coagulation time
prolonged Serum levels of factor VIII are low.
Treatment Desmopressin (DDAVP) Replacement therapy for factor VIII
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Von Willebrand’s Disease Most common hereditary clotting disorder Three major types Signs and symptoms include:
Skin rashes Frequent nosebleeds Easy bruising Bleeding of gums Abnormal menstrual bleeding
Treatment based on type and severity
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Disseminated Intravascular Coagulation
Involves both excessive bleeding and clotting Excessive clotting in circulation
Thrombi and infarcts occur. Clotting factors are reduced to a dangerous level. Widespread, uncontrollable hemorrhage results. Very poor prognosis, with high fatality rate Complication of many primary problems
Obstetrical complications, such as abruptio placentae Infections Carcinomas Major trauma
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Disseminated Intravascular Coagulation (Cont.)
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Thrombophilia Group of inherited or acquired disorders Risk of abnormal clots in veins or arteries Blood testing for clotting factor levels and
abnormal antibody levels Causative condition should be treated.
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Myelodysplastic Syndromes Diseases that involve inadequate production
of cells by the bone marrow Signs and symptoms include anemia;
dependent on type of deficiencies that occur May be idiopathic or occur after
chemotherapy or radiation treatment Treatment measures depend on deficiency
type. Transfusion replacement Chelation therapy to reduce iron overload Bone marrow transplantation
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The Leukemias Group of neoplastic disorders involving white blood
cells Uncontrolled WBC production in bone or lymph
nodes Other hemopoietic tissues are reduced. One or more types of leukocytes are undifferentiated,
immature, and nonfunctional. Large numbers released into general circulation Infiltrate lymph nodes, spleen, liver, brain, other
organs
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The Leukemias (Cont.) Acute leukemias (ALL and AML)
High proportion of immature nonfunctional cells in bone marrow and peripheral circulation
Onset usually abrupt , marked signs of complications
• Occurs primarily in children and younger adults Chronic leukemias (CLL and CML)
Higher proportion of mature cells Insidious onset Mild signs and better prognosis
• Common in older adults
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Acute Lymphocytic Leukemia
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Signs and Symptoms of Acute Leukemia
Usual signs at onset Frequent or uncontrolled infections Petechiae and purpura Signs of anemia
Severe and steady bone pain Weight loss, fatigue, possible fever Enlarged lymph nodes, spleen, liver Headache, visual disturbances, drowsiness,
vomiting
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The Leukemias (Cont.) Diagnostic tests
Peripheral blood smears• Immature leukocytes and altered numbers of WBCs• Numbers of RBCs and platelets decreased• Bone marrow biopsy for confirmation
Treatment Chemotherapy ALL in young children responds well to drugs Biological therapy (interferon)
• May be used to stimulate the immune system
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Complications of Leukemia Opportunistic infections, including pneumonia Sepsis Congestive heart failure Hemorrhage Liver failure Renal failure CNS depression and coma
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Multiple Myeloma Neoplastic disease that involves increased
production of plasma cells in bone marrow Unknown cause Occurs in older adults Production of other blood cells is impaired Multiple tumors in bone
Loss of bone Severe bone pain
Prognosis poor, with short life expectancy
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Multiple Myeloma of the Skull
Chapter 11
Lymphatic System Disorders
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Review of the Lymphatic System
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Structures Lymphatic vessels Lymphoid tissue Lymphatic nodules Tonsils Lymph nodes Spleen Thymus gland Red bone marrow
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Function Return of excess interstitial fluid to the
cardiovascular system Vessels empty into the subclavian veins.
Filter and destroy foreign material Initiate the immune response
Absorb lipids from the GI tract
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Lymphatic Vessels Originate as capillaries in contact with blood
capillary bed in tissues Lymph collected by lymphatic trunks Lymphatic trunks empty into ducts Ducts empty into the subclavian veins
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Lymph Clear, watery, isotonic fluid Circulates in lymphatic vessels Resembles blood plasma, with a lower
protein content Returned to the cardiovascular system
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Lymphatic Disorders
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Lymphomas Malignant neoplasms involving lymphocyte
proliferation in lymph nodes Specific causes not identified
Higher risk in adults who received radiation during childhood
Two main disorders Hodgkin’s lymphoma Non-Hodgkin’s lymphoma
• Distinguished by multiple node involvement • Nonorganized, with widespread metastases
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Hodgkin’s Lymphoma Initially involves a single lymph node Cancer spreads to adjacent nodes
To organs via lymphatics T lymphocytes seem to be defective; lymphocyte
count decreased Presence of Reed-Sternberg cells
• Giant cells present in lymph node Four subtypes
• Based on cell found at biopsy
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Reed-Sternberg Cell
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Hodgkin’s Lymphoma (Cont.) Symptoms
First indicator—usually a painless enlarged lymph node
Later—splenomegaly and enlarged lymph nodes General signs of cancer
• Weight loss, anemia, low-grade fever, night sweats; fatigue may develop.
Treatment Radiation, chemotherapy, surgery
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Hodgkin’s Lymphoma (Cont.)
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Hodgkin’s Lymphoma (Cont.) Staging and prognosis dependent on:
Number of nodes involved Location of nodes involved
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Non-Hodgkin’s Lymphoma Increasing in incidence
Partially caused by HIV infection Similar to Hodgkin’s lymphoma
Clinical signs and symptoms are similar. More difficult to treat when tumors are not
localized Initial manifestation—enlarged, painless
lymph node
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Multiple Myeloma Neoplastic disease that involves increased
production of plasma cells in bone marrow Unknown cause Occurs in older adults Production of other blood cells is impaired Multiple tumors in bone
Loss of bone Severe bone pain
Prognosis poor, with short life expectancy
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Multiple Myeloma of the Skull
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Signs and Symptoms of Multiple Myeloma
Onset usually insidious Malignancy well advanced before diagnosis Pain caused by bone involvement Anemia and bleeding tendency Impaired kidney function and eventually
failure Chemotherapy to encourage remission
Median survival, 3 years
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Lymphedema Obstruction of lymphatic vessels Most common form is congenital Extremities swell because of lymph
accumulation Treatment:
Diuretics Bed rest Massage of affected area Elevation of affected extremity
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Elephantiasis Lymphedema
Caused by blockage because of parasitic infection Significant swelling of affected extremity
Extreme swelling of legs, breast, and/or genitalia Thickening of subcutaneous tissue Frequent infections Skin ulcerations Fever
Treatment—medication regimen to kill parasite
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Castleman’s Disease Rare illness
Involves overgrowth of lymphoid tissue Two types
Unicentric form• Affects a single lymph node
Multicentric form• Affects multiple lymph nodes and tissue—may have
severe effects on the immune system Signs, symptoms, and treatment depend on
the type of the disease
Chapter 12
Cardiovascular System Disorders
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Review of the Normal Cardiovascular System
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Path of Erythrocyte in the Circulation
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Circulatory System The circulatory system is composed of:
Vessels Fluid Pump
Blood flows from systemic to pulmonary to systemic circulation
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Heart: Anatomy Located in the mediastinum Located in the pericardial sac
Parietal pericardium Epicardium (visceral pericardium) Pericardial cavity Myocardium Endocardium
Heart valves Atrioventricular valves Semilunar valves
Septum
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Heart: Conduction System Conduction pathway
Sinoatrial (SA) node• Pacemaker• Sinus rhythm
Atrioventricular (AV) node Located in floor of the right atrium
AV bundle (bundle of His) Right and left branches
Purkinje fibers Terminal fibers
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Heart: Conduction System (Cont.)
Electrocardiogram (ECG) P wave
• Depolarization of atria QRS wave
• Depolarization of ventricles T wave
• Repolarization of ventricles
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Control of the Heart Cardiac control center in medulla oblongata
Controls rate and force of contraction Located in the medulla
Baroreceptors Detect changes in blood pressure Located in the aorta and internal carotid arteries
Sympathetic stimulation (cardiac accelerator nerve) Increases heart rate (tachycardia)
Parasympathetic stimulation (cranial nerve [CN] X; vagus nerve) Decreases heart rate (bradycardia)
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Factors that Increase Heart Rate Increased thyroid hormones or epinephrine Elevated body temperature, infection
Example: Fever Increased environmental temperature
Especially in high humidity Exertion or exercise Smoking Stress response Pregnancy Pain
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Coronary Circulation Right and left coronary arteries
Branch of aorta immediately distal to the aortic valve
Part of the systemic circulation Left coronary artery divides into:
Left anterior descending or interventricular artery Left circumflex artery
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Coronary Circulation (Cont.) Right coronary artery branches
Right marginal artery Posterior interventricular artery
Many small branches extend from these arteries to supply the myocardium and endocardium.
Collateral circulation is extremely limited.
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Major Coronary Arteries
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Cardiac Cycle Diastole
Relaxation of myocardium required for filling chambers Systole
Contraction of myocardium provides increase in pressure to eject blood
Cycle begins with Atria relaxed, filling with blood AV valves open blood
flows into ventricles atria contract, remaining blood forced into ventricles atria relax ventricles contract AV valves close semilunar valves open blood into aorta and pulmonary artery ventricles relax
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Cardiac Cycle (Cont.)
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Heart Sounds “Lubb-dub”
“Lubb”—closure of AV valves “Dub”—closure of semilunar valves
Murmurs Caused by incompetent valves
Pulse Indicates heart rate
Pulse deficit Difference in rate between apical and radial pulses
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ECG Strip Chart Recordings
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Cardiac Function Cardiac output (CO)
Blood ejected by a ventricle in 1 minute CO = SV HR (heart rate)
Stroke volume (SV) Volume of blood pumped out of ventricle—
contraction Preload
Amount of blood delivered to heart by venous return
Afterload Force required to eject blood from ventricles
• Determined by peripheral resistance in arteries
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Cardiac Output
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Blood Pressure Systolic pressure
Exerted when blood is ejected from ventricles (high)
Diastolic pressure Sustained pressure when ventricles relax (lower) Blood pressure (BP) is altered by cardiac output,
blood volume, and peripheral resistance to blood flow.
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Blood Pressure (Cont.) Changes in blood pressure
Sympathetic branch of ANS • Increased output → vasoconstriction and increased BP• Decreased output → vasodilation and decreased BP
BP is directly proportional to blood volume. Hormones
• Antidiuretic hormone (↑ BP); aldosterone (↑ blood volume, ↑ BP); renin-angiotensin-aldosterone (vasoconstriction; ↑ BP)
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Blood Pressure (Cont.)
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Heart Disorders
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Diagnostic Tests for Cardiovascular Function
Electrocardiography Useful in the initial diagnosis and monitoring of
dysrhythmias, myocardial infarction, infection, pericarditis Auscultation
Determination of valvular abnormalities or abnormal shunts of blood that cause murmurs
Detected by listening through a stethoscope Echocardiography
Used to record heart valve movements, blood flow, and cardiac output
Exercise stress tests Used to assess general cardiovascular function
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Diagnostic Tests for Cardiovascular Function (Cont.)
Chest x-ray films Used to show shape and size of the heart
• Nuclear imaging• Tomographic studies
Cardiac catheterization Measures pressure and assesses valve and heart
function• Determines central venous pressure and pulmonary
capillary wedge pressure Angiography
Visualization of blood flow in the coronary arteries
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Diagnostic Tests for Cardiovascular Function (Cont.)
Doppler studies Assess blood flow in peripheral vessels Record sounds of blood flow or obstruction
Blood tests Assess levels of serum triglycerides, cholesterol,
sodium, potassium, calcium, other electrolytes Arterial blood gas determination
Checks the current oxygen level and acid-base balance
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General Treatment Measures for Cardiac Disorders
Dietary modifications To decrease total fat intake General weight reduction Reduce salt intake
Regular exercise program Increases high-density lipoprotein levels Lowers serum lipid levels Reduces stress levels
Cessation of smoking Decreases risk of coronary disease
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General Treatment Measures for Cardiac Disorders: Drug Therapy Vasodilators
Reduction of peripheral resistance Beta blockers
Treatment of hypertension and dysrhythmias Reduction of angina attacks
Calcium channel blockers Decrease cardiac contractility Antihypertensives and vasodilators Prophylactic against angina
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General Treatment Measures for Cardiac Disorders: Drug Therapy
(Cont.) Digoxin
Treatment for heart failure Antidysrhythmic drug for atrial dysrhythmias
Antihypertensive drugs Used to lower blood pressure
Adrenergic blocking drugs Act on SNS centrally or on the periphery
Angiotensin-converting enzyme (ACE) inhibitors Block conversion of angiotensin I to angiotensin II
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General Treatment Measures for Cardiac Disorders: Drug Therapy
(Cont.) Diuretics
Remove excess sodium and/or water. Treat high BP and congestive heart failure.
Anticoagulants Reduce risk of blood clot formation
Cholesterol-lowering drugs Reduce low-density lipoprotein and cholesterol
levels
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Selected Cardiovascular Drugs
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Coronary Artery Disease (CAD) or Ischemic Heart Disease (IHD) or
Acute Coronary Syndrome
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Arteriosclerosis and Atherosclerosis
Arteriosclerosis General term for all types of arterial changes
• Degenerative changes in small arteries and arterioles• Loss of elasticity• Lumen gradually narrows and may become obstructed• Cause of increased BP
Atherosclerosis Presence of atheromas in large arteries
• Plaques consisting of lipids, calcium, and possible clots• Related to diet, exercise, and stress
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Normal (top) Versus Atherosclerotic Aorta (bottom)
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Lipid Transport Lipids are transported in combination with
proteins. Low-density lipoprotein (LDL)
Transports cholesterol from liver to cells Major factor contributing to atheroma formation
High-density lipoprotein (HDL) Transports cholesterol away from the peripheral
cells to liver—“good” lipoprotein Catabolism in liver and excretion
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Possible Consequences of Atherosclerosis
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Development of an Atheroma
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Risk Factors for Atherosclerosis Nonmodifiable
Age Gender Genetic or familial factors
Modifiable Obesity Sedentary lifestyle Cigarette smoking Diabetes mellitus Poorly controlled hypertension Combination of oral contraceptives and smoking
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Atherosclerosis Diagnostic tests
Serum lipid levels Treatment
Weight loss Increase exercise. Lower total serum cholesterol and LDL levels by dietary
modification. Reduce sodium intake. Control hypertension. Cessation of smoking Antilipidemic drugs Surgical intervention, such as coronary artery bypass
grafting
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Coronary Artery Bypass Grafting
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Angina Pectoris Occurs when there is a deficit of oxygen to
meet myocardial needs Chest pain may occur in different patterns.
Classic or exertional angina Variant angina
• Vasospasm occurs at rest. Unstable angina
• Prolonged pain at rest—may precede myocardial infarction
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Angina: Imbalance of Oxygen Supply and Demand
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Angina Pectoris (Cont.) Recurrent, intermittent brief episodes of
substernal chest pain Triggered by physical or emotional stress Attacks vary in severity and duration but
become more frequent and longer as disease progresses.
Relieved by rest and administration of coronary vasodilators Example: nitroglycerin
• Primarily acts by reducing systemic resistance, decreasing the demand for oxygen
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Emergency Treatment for Angina Rest, stop activity Patient seated in upright position Administration of nitroglycerin—sublingual Check pulse and respiration. Administer oxygen, if necessary. Patient known to have angina
Second dose of nitroglycerin Patient without history of angina
Emergency medical aid
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Myocardial Infarction Occurs when coronary artery is totally
obstructed Atherosclerosis is most common cause Thrombus from atheroma may obstruct artery Vasospasm is cause in a small percentage. Size and location of the infarct determine the
damage.
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Warning Signs of Heart Attack Feeling of pressure, heaviness, or burning in
chest—especially with increased activity Sudden shortness of breath, weakness,
fatigue Nausea, indigestion Anxiety and fear Pain may occur and, if present, is usually
Substernal Crushing Radiating
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Myocardial Infarction (MI)
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Myocardial Infarction (Cont.) Diagnostic tests
Changes in ECG Serum enzyme and isoenzyme levels Serum levels of myosin and cardiac troponin are
elevated. Leukocytosis, elevated CRP and ESR common Arterial blood gas measurements may be altered
in severe cases. Pulmonary artery pressure measurements helpful
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Myocardial Infarction: Complications
Sudden death Cardiogenic shock Congestive heart failure Rupture of necrotic heart tissue/cardiac
tamponade Thromboembolism causing cerebrovascular
accident (CVA; with left ventricular MI)
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Myocardial Infarction: Treatment Reduce cardiac demand. Oxygen therapy Analgesics Anticoagulants Thrombolytic agents may be used. Tissue plasminogen activator Medication to treat:
Dysrhythmias, hypertension, congestive heart failure
Cardiac rehabilitation begins immediately.
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Cardiac Dysrhythmias (Arrhythmias)
Deviations from normal cardiac rate or rhythm Caused by electrolyte abnormalities, fever,
hypoxia, stress, infection, drug toxicity Electrocardiography—for monitoring the
conduction system• Detects abnormalities
Reduction of the efficiency of the heart’s pumping cycle Many types of abnormal conduction patterns exist.
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Sinus Node Abnormalities SA node
Pacemaker of the heart; rate can be altered. Bradycardia
Regular but slow heart rate Tachycardia
Regular rapid heart rate Sick sinus syndrome
Marked by altering bradycardia and tachycardia• Often requires mechanical pacemaker
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Conduction System in the Heart
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Atrial Conduction Abnormalities Premature atrial contractions or beats (PACs,
PABs) Extra contraction or ectopic beats
• Irritable atrial muscle cells outside conduction pathway Atrial flutter
Atrial heart rate of 160 to 350 beats/min• AV node delays conduction—ventricular rate slower
Atrial fibrillation Rate over 350 beats/min
• Causes pooling of blood in the atria• Thrombus formation is a risk.
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Atrioventricular Node Abnormalities
Heart blocks Conduction excessively delayed or stopped at AV
node or bundle of His First-degree block
Conduction delay between atrial and ventricular contractions
Second-degree block Every second to third atrial beat dropped at AV
node Third-degree block
No transmission from atria to ventricles
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Ventricular Conduction Abnormalities
Bundle branch block Interference with conduction in one of the bundle branches
Ventricular tachycardia Likely to reduce cardiac output as reduced diastole occurs
Ventricular fibrillation Muscle fibers contract independently and rapidly Cardiac standstill occurs if not treated immediately!
Premature ventricular contractions (PVCs) Additional beats from ventricular muscle cell or ectopic
pacemaker; may lead to ventricular fibrillation
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Cardiac Dysrhythmias
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Treatment of Cardiac Dysrhythmias
Cause needs to be determined and treated. Antidysrhythmic drugs are effective in many
cases. SA nodal problems or total heart block
require pacemaker Defibrillator may be implanted for conversion
of ventricular fibrillation.
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Cardiac Arrest Cessation of all heart activity
No conduction of impulses Flat ECG
Many reasons Excessive vagal nerve stimulation Potassium imbalance Cardiogenic shock Drug toxicity Insufficient oxygen Respiratory arrest Blow to heart
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Congestive Heart Failure Heart is unable to pump out sufficient blood
to meet metabolic demands of the body. Usually a complication of another
cardiopulmonary condition May involve a combination of factors Various compensation mechanisms maintain
cardiac output. Some of these often aggravate the condition.
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Congestive Heart Failure (Cont.) When heart cannot maintain pumping
capability Cardiac output or stroke volume decreases.
• Less blood reaches the various organs.• Decreased cell function• Fatigue and lethargy• Mild acidosis develops.
Backup and congestion develop as coronary demands for oxygen and glucose are not met.
• Output from ventricle is less than the inflow of blood.• Congestion in venous circulation draining into the
affected side of the heart
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Effects of Congestive Heart Failure
Left-sided congestive heart failure
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Effects of Congestive Heart Failure (Cont.)
Right-sided congestive heart failure
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Signs and Symptoms of Congestive Heart Failure
Forward effects (similar with failure on either side) Decreased blood supply to tissues, general
hypoxia Fatigue and weakness Dyspnea and shortness of breath
Compensation mechanisms Tachycardia Cutaneous and visceral vasoconstriction Daytime oliguria
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Signs and Symptoms of Congestive Heart Failure (Cont.)
Backup effects of left-sided failure Related to pulmonary congestion Dyspnea and orthopnea
• Develop as fluid accumulates in the lungs Cough
• Associated with fluid irritating the respiratory passages Paroxysmal nocturnal dyspnea
• Indicates the presence of acute pulmonary edema• Usually develops during sleep• Excess fluid in lungs frequently leads to infections such
as pneumonia.
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Signs and Symptoms of Congestive Heart Failure (Cont.)
Signs of right-sided failure and systemic backup Dependent edema in feet, legs, or buttocks Increased pressure in jugular veins leads to
distention. Hepatomegaly and splenomegaly
• Digestive disturbances Ascites
• Complication when fluid accumulates in peritoneal cavity• Marked abdominal distention
Acute right-sided failure • Flushed face, distended neck veins, headache, visual
disturbances
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Congestive Heart Failure (CHF)
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Young Children with CHF Often secondary to congenital heart disease Feeding difficulties often first sign
Failure to gain weight or meet developmental guidelines
Short sleep periods Tripod position to play Cough, rapid grunting respirations, flared
nostrils, wheezing Radiographs show cardiomegaly. Arterial blood gases used to measure hypoxia
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Congenital Heart Defects Cardiac anomalies
Structural defects in the heart that develop during the first 8 weeks of embryonic life
Congenital heart disease Valvular defects Septal defects Detected by the presence of heart murmurs If untreated, child may develop heart failure.
May be cyanotic or acyanotic, depending on direction of shunting
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Congenital Heart Defects (Cont.) Signs and symptoms of large defects
Pallor Tachycardia
• Occurs with very rapid sleeping pulse and frequent pulse deficit
Dyspnea on exertion Squatting position—toddlers and older children
• Appears to modify blood flow, more comfortable Clubbed fingers Intolerance for exercise and exposure to cold
weather Delayed growth and development
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Congenital Heart Defects (Cont.) Severe defects are often diagnosed at birth. Others may not be detected for some time. Examination techniques
Radiography Diagnostic imaging Cardiac catheterization Echocardiography Electrocardiography
Surgical repair
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Ventricular Septal Defect VSD is the most common congenital heart
defect. Opening in the interventricular septum
May vary in size and location Untreated VSD
Pressure usually higher in left ventricle. Shunt from left → right Acyanotic condition unless respiratory condition
increases pressure in right ventricle
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Valvular Defects Usually affect aortic and pulmonary valves May be classified as stenosis or valvular
incompetence Failure of valve to close completely Blood regurgitates or leaks backward
Mitral valve prolapse Abnormally enlarged and floppy valve leaflets
Surgical replacement Mechanical or animal (porcine) tissue
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Effects of Heart Valve Defects
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Tetralogy of Fallot Most common cyanotic (R → L shunt) congenital
heart condition Cyanosis occurs because shunt bypasses the
pulmonary circulation. Alters pressures in heart and alters blood flow Includes four abnormalities
Involves heart as well as joints VSD Dextroposition of the aorta Right ventricular hypertrophy
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Congenital Heart Defects
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Congenital Heart Defects
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Inflammation and Infection in the Heart
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Rheumatic Fever and Rheumatic Heart Disease
Rheumatic fever Acute systemic inflammatory condition
• May result from an abnormal immune reaction• Can occur a few weeks after an untreated infection
(usually group A -hemolytic Streptococcus) Involves heart as well as joints Usually occurs in children ages 5 to 15 years Long-term effects
• Rheumatic heart disease• May be complicated by infective endocarditis and heart
failure in older adults
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Rheumatic Fever and Rheumatic Heart Disease (Cont.)
Acute stage—inflammation of the heart Pericarditis Myocarditis Endocarditis and incompetent heart valves
Other sites of inflammation Large joints Erythema marginatum Nontender subcutaneous nodules Involuntary jerky movement of the face, arms, legs
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Rheumatic Fever and Rheumatic Heart Disease (Cont.)
Signs and symptoms Low-grade fever, leukocytosis, malaise, anorexia,
fatigue, tachycardia Diagnostic tests
Heart function test Electrocardiography ASO titer
Treatment Prophylactic antibacterial agents Anti-inflammatory agents
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Development of Rheumatic Fever and Rheumatic Heart Disease
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Infective Endocarditis Subacute
Streptococcus viridans Acute
Staphylococcus aureus Basic effects
Same regardless of organism Factors that predispose to infection
Presence of abnormal valves in heart Bacteremia Reduced host defenses
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Infective Endocarditis (Cont.) Low-grade fever or fatigue Anorexia, splenomegaly, congestive heart
failure in severe cases Acute endocarditis
Sudden, marked onset—spiking fever, chills, drowsiness
Subacute endocarditis Insidious onset—increasing fatigue, anorexia,
cough, and dyspnea Blood culture to identify causative agent
Antimicrobial drugs for several weeks, often IV
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Pericarditis Usually secondary to another condition Classified by cause or type of exudate Acute pericarditis
May involve simple inflammation of the pericardium
May be secondary to:• Open heart surgery, myocardial infarction, rheumatic
fever, systemic lupus erythematosus, cancer, renal failure, trauma, viral infection
Effusion may develop.• Large volume of fluid accumulates in pericardial sac• Leads to distended neck veins, faint heart sounds,
pulsus paradoxus
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Effects of Pericardial Effusion
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Pericarditis (Cont.) Chronic pericarditis
Results in formation of adhesions between the pericardial membranes
Fibrous tissue often results from tuberculosis or radiation to the mediastinum.
Limiting movement of the heart during diastole and systole → reduced cardiac output
Inflammation or infection may develop from adjacent structures.
Causes fatigue, weakness, abdominal discomfort• Caused by systemic venous congestion
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Vascular Disorders
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Arterial Diseases—Hypertension High blood pressure
Common May occur in any age group More common in individuals of African ancestry
Sometimes classified as systolic or diastolic
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Arterial Diseases—Hypertension (Cont.)
Primary Essential hypertension Blood pressure consistently above 140/90 mm Hg
• May be adjusted for age Increase in arteriolar vasoconstriction Over long period of time—damage to arterial walls
• Blood supply to involved area is reduced. • Ischemia and necrosis of tissues, with loss of function
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Arterial Diseases—Hypertension (Cont.)
Secondary hypertension Results from renal or endocrine disease,
pheochromocytoma (benign tumor of the adrenal medulla)
Underlying problem must be treated to reduce blood pressure.
Malignant or resistant hypertension Uncontrollable, severe, and rapidly progressive
form with many complications Diastolic pressure is extremely high.
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Development of Hypertension
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Arterial Diseases—Hypertension (Cont.)
Areas most frequently damaged by hypertension Kidneys Heart Brain Retina
Predisposing factors Incidence increases with age. Men affected more frequently and more severely Incidence in women increases after middle age. Genetic factors Sodium intake, excessive alcohol intake, obesity, smoking,
prolonged or recurrent stress
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Effects of Uncontrolled Hypertension
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Arterial Diseases—Hypertension (Cont.)
Frequently asymptomatic in early stages Initial signs vague and nonspecific
• Fatigue, malaise, sometimes morning occipital headache Essential hypertension treated in steps
Lifestyle changes Reduction of sodium intake Weight reduction Reduction of stress Drugs
• Diuretics, ACE inhibitors, drug combinations
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Peripheral Vascular Disease: Atherosclerosis
Disease in arteries outside the heart Increased incidence with diabetes Most common sites
Abdominal aorta Carotid arteries Femoral and iliac arteries
Diagnostic tests Blood flow assessed by Doppler studies and
arteriography Plethysmography measures the size of limbs and
blood volume in organs or tissues.
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Peripheral Vascular Disease: Atherosclerosis (Cont.)
Signs and symptoms Increasing fatigue and weakness in the legs Intermittent claudication (leg pain)
• Associated with exercise caused by muscle ischemia Sensory impairment
• Tingling, burning, numbness Peripheral pulses distal to occlusion become
weak. Appearance of the skin of the feet and legs
changes.• Marked pallor or cyanosis• Skin dry and hairless• Toenails thick and hard
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Peripheral Vascular Disease: Atherosclerosis (Cont.)
Treatment Maintain control of blood glucose level. Reduce body mass index. Reduce serum cholesterol level. Platelet inhibitors or anticoagulant medication Cessation of smoking Increase activity and exercise Maintain dependent position for legs—improves
arterial perfusion Peripheral vasodilators Observe skin for breakdown and treat promptly. If gangrene develops, amputation is required.
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Aortic Aneurysm Localized dilation and weakening of arterial
wall Develops from a defect in the medial layer Different shapes
Saccular• Bulging wall on the side
Fusiform• Circumferential dilation along a section of artery
Dissecting aneurysm• Develops when there is a tear in the intima of the wall
and blood continues to dissect or separate tissues
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Types of Aortic Aneurysms
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Aortic Aneurysm (Cont.) Causes
Atherosclerosis Trauma Syphilis and other infections Congenital defects
Signs and symptoms Bruit may be heard on auscultation. Pulse may be felt on palpation of abdomen. Frequently asymptomatic until they become large
or rupture• Rupture may lead to moderate bleeding but usually
causes severe hemorrhage and death.
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Aortic Aneurysm (Cont.) Diagnostic tests
Radiography Ultrasound CT scanning MRI
Treatment Maintain blood pressure at normal level. Prevent sudden elevations caused by exertion. Prevent stress, coughing, constipation Surgical repair
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Venous Disorders
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Varicose Veins Irregular, dilated, tortuous areas of superficial
veins Familial tendency Increased body mass index, parity, and
weight lifting are risks. In the legs
May develop from defect or weakness in vein walls or valves
Appear as irregular, purplish, bulging structures Treatment
Keep legs elevated, support stockings Restricted clothing, crossing legs to be avoided
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Varicose Veins (Cont.)
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Thrombophlebitis and Phlebothrombosis
Thrombophlebitis Thrombus development in inflamed vein (e.g., IV
site) Phlebothrombosis
Thrombus forms spontaneously without prior inflammation; attached loosely
Factors for thrombus development Stasis of blood or sluggish blood flow Endothelial injury Increased blood coagulability
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Thrombophlebitis and Phlebothrombosis (Cont.)
Signs and symptoms Often unnoticed Aching, burning, tenderness in affected legs Systemic signs—fever, malaise, leukocytosis
Complication—pulmonary embolism Treatment
Preventive measures• Exercise, elevating legs
Anticoagulant therapy Surgical intervention
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Shock Hypovolemic shock
Loss of circulating blood volume Cardiogenic shock
Inability of heart to maintain cardiac output to circulation
Distributive, vasogenic, neurogenic, septic, anaphylactic shock Changes in peripheral resistance leading to
pooling of blood in the periphery
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Types of Shock
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Shock: Early Manifestations Anxiety Tachycardia Pallor Light-headedness Syncope Sweating Oliguria
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Shock (Cont.) Compensation mechanisms
SNS and adrenal medulla stimulated—increase heart rate, force of contraction, systemic vasoconstriction
Renin secretion increases. Increased ADH secretion Secretion of glucocorticoids Acidosis stimulates increased respiration.
• With prolonged shock, cell metabolism is diminished, waste not removed—leads to lower pH
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Shock (Cont.) Complications of shock
Acute renal failure Shock lung, or adult respiratory distress syndrome Hepatic failure Paralytic ileus, stress or hemorrhagic ulcers Infection or septicemia Disseminated intravascular coagulation Depression of cardiac function
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Manifestations of Shock
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General Effects of Circulatory Shock