Ch 10, 11, 12 Pathology

Chapter 10

Blood and Circulatory System Disorders

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.

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

Blood Vessels (Cont.)

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

Composition of Blood Plasma

Plasma proteins Cellular component

Erythrocytes Leukocytes Thrombocytes (platelets)

Components of Blood and Their Functions

Hematopoiesis

Normal Red Blood Cells

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.

Normal Blood Cells

Breakdown of Hemoglobin

Blood Clotting—Hemostasis Three steps:

Vasoconstriction or vascular spasm after injury Platelet clot Coagulation mechanism

Plasmin will eventually break down the blood clot.

Hemostasis and Anticoagulant Drugs

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

ABO Blood Groups

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

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

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.

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.

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

Blood Dyscrasias

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

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).

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

Iron Deficiency Anemia—Blood Smear

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

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

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

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

Development of Pernicious Anemia

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.

Vitamin B12 Deficiency

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

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

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!

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

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.

Sickle Cell Anemia (Cont.)

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.

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

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

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

Comparison of Selected Anemias

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

Polycythemia: Signs and Symptoms

Distended blood vessels, sluggish blood flow Increased blood pressure Hypertrophied heart Hepatomegaly Splenomegaly Dyspnea Headaches Visual disturbances Thromboses and infarctions

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

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

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

Petechiae

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

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

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

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

Disseminated Intravascular Coagulation (Cont.)

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.

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

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

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

Acute Lymphocytic Leukemia

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

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

Complications of Leukemia Opportunistic infections, including pneumonia Sepsis Congestive heart failure Hemorrhage Liver failure Renal failure CNS depression and coma

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

Multiple Myeloma of the Skull

Chapter 11

Lymphatic System Disorders

Review of the Lymphatic System

Structures Lymphatic vessels Lymphoid tissue Lymphatic nodules Tonsils Lymph nodes Spleen Thymus gland Red bone marrow

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

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

Lymph Clear, watery, isotonic fluid Circulates in lymphatic vessels Resembles blood plasma, with a lower

protein content Returned to the cardiovascular system

Lymphatic Disorders

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

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

Reed-Sternberg Cell

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

Hodgkin’s Lymphoma (Cont.)

Hodgkin’s Lymphoma (Cont.) Staging and prognosis dependent on:

Number of nodes involved Location of nodes involved

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

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

Multiple Myeloma of the Skull

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

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

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

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

Review of the Normal Cardiovascular System

Path of Erythrocyte in the Circulation

Circulatory System The circulatory system is composed of:

Vessels Fluid Pump

Blood flows from systemic to pulmonary to systemic circulation

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

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

Heart: Conduction System (Cont.)

Electrocardiogram (ECG) P wave

• Depolarization of atria QRS wave

• Depolarization of ventricles T wave

• Repolarization of ventricles

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)

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

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

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.

Major Coronary Arteries

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

Cardiac Cycle (Cont.)

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

ECG Strip Chart Recordings

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

Cardiac Output

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.

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)

Blood Pressure (Cont.)

Heart Disorders

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

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

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

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

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

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

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

Selected Cardiovascular Drugs

Coronary Artery Disease (CAD) or Ischemic Heart Disease (IHD) or

Acute Coronary Syndrome

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

Normal (top) Versus Atherosclerotic Aorta (bottom)

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

Possible Consequences of Atherosclerosis

Development of an Atheroma

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

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

Coronary Artery Bypass Grafting

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

Angina: Imbalance of Oxygen Supply and Demand

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

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

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.

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

Myocardial Infarction (MI)

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

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)

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.

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.

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

Conduction System in the Heart

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.

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

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

Cardiac Dysrhythmias

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.

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

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.

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

Effects of Congestive Heart Failure

Left-sided congestive heart failure

Effects of Congestive Heart Failure (Cont.)

Right-sided congestive heart failure

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

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.

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

Congestive Heart Failure (CHF)

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

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

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

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

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

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

Effects of Heart Valve Defects

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

Congenital Heart Defects

Inflammation and Infection in the Heart

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

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

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

Development of Rheumatic Fever and Rheumatic Heart Disease

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

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

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

Effects of Pericardial Effusion

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

Vascular Disorders

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

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

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.

Development of Hypertension

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

Effects of Uncontrolled Hypertension

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

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.

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

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.

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

Types of Aortic Aneurysms

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.

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

Venous Disorders

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

Varicose Veins (Cont.)

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

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

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

Types of Shock

Shock: Early Manifestations Anxiety Tachycardia Pallor Light-headedness Syncope Sweating Oliguria

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

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

Manifestations of Shock

General Effects of Circulatory Shock

Ch 10, 11, 12 Pathology

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