Cardiovascular 20

Basic anatomy and physiology of the heart

● Cardiovascular Function:​ Transport of nutrients, oxygen, and hormones to cells throughout the body and
removal of metabolic wastes (carbon dioxide, nitrogenous wastes), Protection of the body by white blood
cells, antibodies, and complement proteins that circulate in the blood and defend the body against foreign
microbes and toxins, and Regulation of body temperature, fluid pH, and water content of cells.

Atherosclerosis: risk factors, pathophysiology

● Form of arteriosclerosis
● Thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall
● Plaque development
● Progression: Inflammation of endothelium, Cellular proliferation, Macrophage migration and adherence,
LDL oxidation (foam cell formation), Fatty streak, Fibrous plaque, Complicated plaque
● Risk factors include diabetes, smoking, hyperlipidemia/dysliPidemia, hypertension
● Results in—inadequate perfusion, ischemia, necrosis
● Lipid metabolism
○ Dyslipidemia ​is a general term referring to abnormally high or low lipid levels in the blood.
○ Hyperlipidemia​ is the most common form of dyslipidemia, which is defined as an elevated level
of blood lipids.
○ Hypercholesterolemia ​(high blood cholesterol levels)
○ Hypertriglyceridemia ​(high blood triglyceride levels)
● Lipoproteins
○ Low-density lipoproteins (LDLs) a​ re the primary carriers of cholesterol. Elevated levels of LDL
promote atherosclerosis because LDL deposits cholesterol on arterial walls. (LDL can also be
considered a mnemonic for "less desirable lipoproteins.")
○ High-density lipoproteins (HDLs) help to clear cholesterol from the arteries, transporting it to the
liver for excretion. (HDL can also be considered a mnemonic for "highly desirable lipoproteins.")
 ○ Triglycerides​ are an important risk factor for cardiovascular disease. Triglycerides contain three
fatty acids bound to glycerol and are used for fat storage and energy use by the body. Almost all
triglycerides are transported to adipose tissue for storage by very-low-density lipoproteins
(VLDL). Through a series of steps, the VLDLs are transformed into LDL molecules after the
triglycerides have been transported to adipose tissue.
● Atherosclerosis begins when endothelial cells are damaged.
○ The region of plaque, called an ​atheroma,​ consists of calcium, macrophages, lipids, and fibrous
connective tissue. Depending on various factors such as the presence of associated risk factors,
especially hyperlipidemia, the atheroma may grow slowly or rapidly.
○ The presence of T cells, monocytes, and macrophages at the site of plaque formation creates a
chronic inflammatory response​. As a consequence of chronic inflammation, growth factors are
released from platelets, macrophages, and endothelial cells that stimulate the proliferation of
smooth muscle cells.
○ The smooth muscle cells secrete ​extracellular matrix,​ which tends to ​stabilize the plaque​.
○ Over many years, the continued inflammation and proliferation enlarge the ​atheroma​, which may
eventually​ intrude on the vessels lumen and impair circulation​. In addition to growing larger,
and impair circulation. in addition to growing larger, atheromas commonly undergo calcification
overtime.

Hypertension: Types; control of blood pressure; treatment

Types of Blood Pressure Systolic Diastolic

Normal 120 mmHg 80 mmHg

Prehypertensive 121–139 mmHg 81–89 mmHg

Stage 1 hypertension 140–159 mmHg 90–99 mmHg

 Stage 2 hypertension 160 mmHg 100 mmHg

● Hypertension
○ Consistent elevation of systemic arterial blood pressure
■ Sustained systolic blood pressure of 140 mm Hg or greater or a diastolic pressure of 90
mm Hg or greater
○ Causes: Hypertension creates excess pressure on arterial walls, Arteriosclerosis thickens arterial
wall, Categories of blood pressure
○ Factors affecting blood pressure: Hormones (Renin-angiotensin-aldosterone system (RAAS)),
Nervous
○ Primary hypertension
■ No known cause
■ Essential or idiopathic hypertension
■ Genetic and environmental factors
■ Affects 92% to 95% of individuals with hypertension
■ Risk factors: High sodium intake, Natriuretic peptide abnormalities, Inflammation,
Obesity, Lack of exercise, Insulin resistance, Smoking and alcohol consumption, Race,
Age, Genetics, Increased stress, Endothelial dysfunction, Sympathetic nervous system
(SNS)
○ Secondary hypertension
■ Identifiable cause
■ Caused by a systemic disease process that raises peripheral vascular resistance or cardiac
output
● Renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary
tumors, and drugs
○ Complicated hypertension
■ Chronic hypertensive damage to blood vessels and tissues leading to target organ damage
in the heart, kidney, brain, and eyes
■ Myocardial hypertrophy
○ Malignant hypertension
■ Rapidly progressive hypertension
■ Diastolic pressure is usually >140 mm Hg
■ Life-threatening organ damage
○ Orthostatic (postural) hypotension
■ Decrease in both systolic and diastolic blood pressure upon standing
■ Lack of normal blood pressure compensation in response to gravitational changes on the
circulation
■ Acute orthostatic hypotension
■ Chronic orthostatic hypotension
● Clinical manifestations
○ Long-term consequences
■ Stroke, Heart failure, MI, Chronic kidney disease, Vision loss, Erectile dysfunction
○ Hypertensive emergency (HTN-E)
○ Hypertensive urgency
○ Chest pain and dyspnea
● Diagnosis
○ Measurement of blood pressure
 ● Nonpharmacologic treatment
○ Restrict sodium consumption, Limit alcohol consumption, Stop smoking, Maintain an optimal
weight, Reduce saturated fat, cholesterol; increase fruits, vegetables, Increase physical activity,
Reduce stress levels
● Pharmacologic treatment
○ First-line antihypertensives: Angiotensin-converting enzyme (ACE) inhibitors, Angiotensin
receptor blockers (ARBs), Calcium channel blockers (CCBs), Thiazide diuretics
○ Second-line antihypertensives: Adrenergic blockers, Centrally acting drugs, Direct-acting
vasodilators, Direct renin inhibitors

Shock: types
● Shock: a clinical syndrome characterized by acute circulatory failure with inadequate or inappropriately
distributed tissue perfusion resulting in generalized cellular hypoxia and end-organ dysfunction.) ​Leads to
impaired cellular metabolism (Impaired oxygen use , Impaired glucose use)
○ Manifestations vary based on stage but often include hypotension, tachycardia, increased
respiratory rate
○ ↓ Blood pressure, Extensive vasodilator (Increase permeability = Edema)
● Types of shock
○ Shock caused by obstruction of blood flow is ​obstructive shock.​
○ Failure of the heart to pump is ​cardiogenic shock​.
○ Abnormal redistribution of blood is ​distributive shock
○ Low blood volume is ​hypovolemic shock
○ Shock due to inflammatory vascular response to infection is ​septic shock or anaphylactic shock
○ Categories of shock
 ○ Hypovolemic shock (hemorrhagic shock)
■ Rapid blood or other ECF fluid loss
○ Cardiogenic shock
■ Heart unable to maintain adequate cardiac output due to myocardial damage
○ Distributive shock
■ Abnormal redistribution of blood
■ Results from extensive vasodilation and loss of vascular tone
○ Obstructive shock
■ Obstruction of blood flow
○ Anaphylactic shock
■ Acute, life-threatening, IgE-mediated allergic reaction
■ Occurs on re-exposure in in those persons sensitive to an allergen or antigen

Hypovolemic Shock ● Hypovolemic shock, which is also called hemorrhagic shock, is a

life-threatening condition that occurs when a patient ​loses more than 15%
of the body's fluids​.
● Hypovolemic shock occurs when there is rapid or excessive loss of
significant amount of whole blood as in trauma, internal bleeding from a
ruptured ectopic pregnancy or gastrointestinal lesions, or loss of other
body fluids (from diarrhea, vomiting, diaphoresis, severe burns, or diuresis
as occurs in diabetes mellitus and diabetes insipidus), edema, or severe
dehydration.

Cardiogenic Shock ● Myocardial damage can result in the heart's being ​unable to contract
effectively or in restricted filling of the ventricles such that output is
significantly reduced.
● When the heart is unable to circulate an adequate amount of blood,
hypoxic damage to the organs can result.
● Cardiogenic shock is a sudden onset of ​decreased cardiac output ​and
tissue hypoxia without evidence of intravascular fluid loss associated with
a large myocardial infarction and ​heart failure.
● Cardiogenic shock is due to failure of the cardiac pump related to loss of
myocardial function and contractility resulting in elevations of diastolic
filling pressures and volumes.

Distributive Shock ● Distributive shock results in impaired ​distribution of blood flow due to
extensive vasodilation and loss of vascular tone.

Anaphylactic Shock ● Anaphylaxis is an acute, life-threatening, IgE-mediated allergic reaction

that occurs on reexposure in individuals who are sensitive to an allergen or
antigen. Anaphylactic shock occurs when the antibody IgE produced by
plasma cells binds to membrane receptors on the mast cells and basophils.
Subsequent exposure to the antigen results in the binding of the antigen to
the antibody on the mast cells, leading to the release of histamine and
other substances of anaphylaxis (leukotrienes and bradykinin).

Septic Shock ● is defined as​ life threatening organ dysfunction caused by a dysregulated
host response to infection.
Neurogenic Shock ● Neurogenic shock is caused by ​blockage of the sympathetic nervous
system outflow to the intrathoracic sympathetic chain. It can be caused
by any factor/condition that increases parasympathetic stimulation.

Obstructive Shock ● Obstructive shock is a life-threatening condition caused by an ​obstruction

of blood flow to the body's organs.​ Obstructive shock is diagnosed when
acute circulatory failure occurs as a result of obstruction of blood supply
to central vessels of systems or pulmonary circulation, causing the clinical
symptoms of shock.

Heart failure: RHF and LHF

● Heart Failure: General term used to describe several types of cardiac dysfunction that result in inadequate
perfusion of tissues with blood-borne nutrients
● Left heart failure (congestive heart failure)
○ Systolic heart failure
■ inability of the heart to generate adequate cardiac output to perfuse tissues
■ Ventricular remodeling
■ Causes include myocardial infarction, myocarditis, cardiomyopathy
○ Diastolic heart failure
■ Pulmonary congestion despite normal stroke volume and cardiac output
■ Causes include myocardial hypertrophy and ischemia, diabetes, valvular and pericardial
disease
● Manifestations of left heart failure:
○ Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation
○ Include dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema
○ Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural
effusions), hypotension or hypertension, an S3 gallop, and evidence of underlying CAD or
hypertension
● Right heart failure
○ Most commonly caused by a diffuse hypoxic pulmonary disease
○ Can result from an increase in left ventricular filling pressure that is reflected back into the
pulmonary circulation
● High-output failure
○ Inability of the heart to supply the body with blood-borne nutrients despite adequate blood volume
and normal or elevated myocardial contractility .
○ Causes include anemia, hyperthyroidism, septicemia, and beriberi
Infectious endocarditis
● Inflammation of the endocardium
● Agents: Bacteria, Viruses, Fungi, Rickettsiae, Parasites
● Pathogenesis
 ○ Damaged (prepared) endocardium
○ Blood-borne microorganism adherence
○ Proliferation of the microorganism (vegetations)
● Manifestations:
○ Classic findings
■ Fever , New or changed cardiac murmur, Petechial lesions of the skin, conjunctiva, and
oral mucosa
○ Characteristic physical findings:
■ Osier nodes (painful erythematous nodules on the pads of the fingers and toes)
■ Janeway lesions (nonpainful hemorrhagic lesions on the palms and soles)
○ Other: weight loss, back pain, night sweats, and heart failure
Raynaud’s phenomenon
● Raynaud phenomenon
○ Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes
○ Primary
■ Vasospastic disorder of unknown origin
● Secondary Raynaud phenomenon
○ Secondary to other systemic diseases or conditions:
■ Collagen vascular disease, Smoking, Pulmonary hypertension, Myxedema, Cold
environment
○ Manifestations include pallor, cyanosis, cold, pain
Varicose vein and arterial aneurysm
● Varicose veins
○ A vein in which blood has pooled
○ Distended, tortuous, and palpable veins
○ Caused by trauma or gradual venous distention
○ Risk factors:
■ Age, Female gender, Family history, Obesity, Pregnancy, Deep vein thrombosis, Prior
leg injury
● Aneurysm
○ Local dilation or outpouching of a vessel wall or cardiac chamber
○ True aneurysms
■ Fusiform aneurysms, Circumferential aneurysms, Saccular aneurysms
○ False aneurysms
■ atravascular hernatoma that communicates with the intravascular space
○ Aorta most susceptible, especially abdominal
■ Causes include atherosclerosis, hypertension
■ Can lead to aortic dissection or rupture
Cardiac ischemia and ECG changes
● Ischemia is the occlusion of the coronary artery leading to perfusion abnormalities. Myocardial: restriction
of blood supply to the heart muscles tissues, causing a shortage of O2 and nutrients needed for cellular
function and survival.
● The ECG is key in diagnosing both acute and chronic coronary syndromes. ECG abnormalities depend on
the time of ischemia, including whether it is an acute process or a developing chronic process; the extent of
the ischemia, such as its size and transmural location; and whether there are any other underlying
abnormalities, such as dysrhythmias. The early and consistent ECG abnormality that occurs in acute
ischemic processes is deviation of the ST segment from the isoelectric line. Under normal conditions, the
ST segment is isoelectric as a result of the plateau phase of the ventricular action potential as the
transmembrane voltage stays at approximately the same potential in all cardiomyocytes. However, the
process of ischemia reduces the resting membrane potential, which shortens the action potential and
decreases the amplitude of the action potential plateau phase. The resulting voltage gradient between the
normal cells and ischemic cells causes an injury current between the normal zone and ischemic zones on
the myocardium, reflected by deviation of the ST segment. Subendocardial injury involves the inner layer,
not the full thickness, of the affected ventricle and causes ST-segment depression. Transmural (epicardial)
injury affects the outer ventricular layer as it extends from the subendocardium to the epicardium and
causes ST elevation with the presence of ST-segment depression in other leads. Eventually, if the ischemia
is severe and perfusion of blood flow is not restored, cardiomyocytes distal to the occluded coronary artery
are irreversibly injured and die, and the tissue is considered necrotic, or infarcted.
Myocardial infarction
● Cellular injury
● Cellular death
● Structural and functional changes:
○ Myocardial stunning
○ Hibernating myocardium
○ Myocardial remodeling
● Repair
● Manifestations:
○ Sudden severe chest pain; may radiate; Nausea, vomiting; Diaphoresis; Dyspnea
● Complications: Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability
● Area of tissue death, or necrosis, related to obstructed blood flow to the myocardium occurs. Commonly
caused by atherosclerosis leading to a thromboembolism.

Hematology 30
A&P of blood
Disorders of RBC
Anemia: Types and characteristics - sickle cell disease, pernicious, hemolytic, aplastic, Thalassemia
● Hemolytic Anemias
○ Hemolysis of red blood cells (RBCs)
■ Physical trauma and stress to RBC
■ Disruption in hemoglobin formation
■ Immune-mediated process
○ Major causes of hemolytic anemia are genetic
○ Signs and symptoms similar to other forms of anemia but includes jaundice
● Sickle Cell Disease
○ Cluster of autosomal recessive disorders
 ■ Hemoglobin sickle or crescent in shape
■ Genetic mutation
○ Pathogenesis
■ Hemoglobin cannot bind oxygen effectively
■ RBC collapses into sickle shape when oxygen released
■ RBC clump together and obstruct blood flow
■ RBC lifespan 10–20 days (as compared to 120 days)
■ Chronic inflammation
○ Clinical manifestations
■ Hypoxia, Tissue ischemia
○ Treatment
■ Prevention, screening, Supportive care, Disease-modifying strategies, Curative
procedures, Genetic analysis, prenatal counseling
● Thalassemia
○ Group of autosomal recessive diseases that affect production of hemoglobin
■ Increased incidence in individuals from Mediterranean and Asia
○ Cause: Defect in production of one or more globin chains
○ Clinical manifestations
■ Defects at birth
● Growth retardation and cognitive deficits
■ Jaundice
● Aplastic Anemia
○ Decrease in all cell populations produced by bone marrow
■ Erythrocytes, leukocytes, platelets
○ Body stops producing enough new blood cells
○ Causes
■ Genetic, Viral exposure, Drugs or toxins, Immune-mediated attack on bone marrow
○ Diagnosis
■ Decreased:
● White blood cells, Platelets, RBCs, Reduced hemoglobin
■ Normocytic, normochromic
● Treatment of Hemolytic Anemias
○ Determination of severity
○ Hematocrit and hemoglobin levels monitored
○ Blood transfusion
○ Considerations for sickle cell disease
■ Hydroxyurea may be given to infants
■ Blood transfusion
■ Stem cell transplantation
● Pernicious anemia (PA),​ the most common type of macrocytic anemia, is caused by vitamin B12
deficiency, which is often associated with the end stage of type A chronic atrophic (autoimmune) gastritis.4
Pernicious means highly injurious or destructive and reflects the fact that this condition was once fatal. It
most commonly affects individuals older than age 30 who are of Northern European descent; however, it
has now been recognized in all populations and ethnic groups.
Blood group & transfusion
● Blood groups
○ The surface of the red blood cell contains molecules called antigens and in the plasma there are
molecules called antibodies. The antibodies are specific to certain antigens. When an antibody
combines with the specific antigen on the red blood cell, they form a link to connect other red
blood cells to it. As a result, clumping or agglutination of the red blood cells occurs.
○ The antigens on the red blood cells have been categorised into blood groups. Although numerous
blood groups have been identified, ABO (Figure 8.7) and rhesus (Rh) blood groups are the most
important in blood transfusion.
 ○ Type A blood group has type A antigen on its surface and anti-B antibody in the plasma; type B
blood group has type B antigen on its surface and anti-A antibody in the plasma; type AB blood
group has both antigens A and B on its surface but does not contain either antibodies in the
plasma; and type 0 blood group has neither antigens A nor B on its surface but contains both
anti-A and anti-B antibodies in the plasma. About 45% of the population in the UK is blood group
O and 55% of the population is either blood group A, B or AB (Waugh and Grant, 2010). People
with blood group O are known as universal donors as their red blood cells do not have either A or
B antigens on their surface. Conversely, people with blood group AB are known as universal
recipients as their red blood cells contain A and B antigens on their surface (Table 8.2).
● Transfusion
● Before you receive a transfusion, compatibility testing is performed between the donated blood
and a patient's blood sample.
● When a transfusion is given, it is preferable for patients to receive blood of the same ABO and
RhD group. However, in an emergency or special circumstance, if the same blood group isn’t
readily available, a patient may be given another group that their immune system will not react to.
Blood transfusions do not need to be matched to gender or race.
Polycythemia and implications
● Bone marrow disorder
○ Too many red blood cells produced
○ Increased viscosity prevents blood from flowing efficiently, leading to end organ ischemia
● Primary
○ Abnormality of stem cells in the bone marrow
○ Polycythemia vera (PV)
● Secondary polycythemia
○ Increase in erythropoietin as a normal response to chronic hypoxia or an inappropriate response to
erythropoietin-secreting tumors
● Clinical manifestations
○ Increased blood viscosity and volume, Headache, dizziness, blurred vision, Hypertension,
Thrombi
● Diagnosis
○ Hematocrit over 70, Increased platelets and white blood cells, Decreased iron count
● Treatment
○ Anticoagulation, Therapeutic erythropheresis, Chemotherapeutic approaches
Classical signs of bleeding

Disorders of Coagulation (Hemostasis​)

Thrombocytopenia; clotting disorder & bleeding
● Primary Disorders of Hemostasis
● Decrease in number of circulating blood platelets
● Most common cause of abnormal bleeding
● Causes: Artifact, Deficient production, Increased destruction, consumption, or both, Abnormal distribution
or pooling
● Types
○ Pseudothrombocytopenia
■ Artifact, Platelet clumping due to ethylenediaminetetraacetic acid
○ Deficient platelet production
■ Marrow aplasia, Type 1 heparin-induced thrombocytopenia (HIT), Type 2 HIT
○ Increased destruction and/or consumption of platelets
■ Immune thrombocytopenic purpura (ITP), Thrombotic thrombocytopenic purpura (TTP)
○ Abnormal distribution or pooling of platelets
■ Reversible pooling of up to 90% of total body platelets, Chronic liver disease with portal
hypertension, Congestive splenomegaly
● Clinical manifestations: Purpura, Ecchymoses, Epistaxis, Serious hemorrhages
● Clinical manifestations of TTP (pentad of TTP): Microangiopathic hemolytic anemia, Thrombocytopenia,
Renal insufficiency, Fever, Mental status changes that can wax and wane
● Treatment
○ Cases of significant blood loss: Plasmapheresis (emergent care), TTP therapy
○ Infusion of fresh frozen plasma
Hemophilia A; Von Willebrand disease;
● ​Hemophilia A
○ Secondary disorders of hemostasis
○ Deficiency in factor VIII
○ X-linked – only males exhibit the disease
○ Mild or moderate – bleeding only with local lesion or trauma
○ Severe – bleeding occurs in childhood (circumcision) and is spontaneous and severe
○ Bleeding in soft tissue, GI tract, joints (starts when child begins walking)
○ Can cause joint fibrosis, contractures
○ Potential for life-threatening intracranial hemorrhage
○ Treatment: replacement therapy, DDAVP
● Von Willebrand disease
○ There are two treatment options for spontaneous bleeding episodes: desmopressin (DDAVP) and
transfusion with plasma-derived vWF products.
○ Diagnosed in adulthood
○ Most common hereditary bleeding disorder
○ Deficiency or defect in vWF, a carrier protein for factor VIII
○ Reduced levels of factor VIII (because of missing vWF) results in defective clot formation
○ Bruising; excessive menstrual flow; bleeding from nose, mouth, and GI tract
○ Treatment: in severe cases – replace deficient clotting factors, DDAVP

Disorders of WBC
Leukemia: types & characteristics
● Acute leukemia: Presence of undifferentiated or immature cells, usually blast cells
○ Acute lymphocytic leukemia (ALL)
■ Too many lymphoblasts
■ Mostly occurs in children
○ Acute myelogenous leukemia (AML)
■ Too many myeloblasts
■ Most common adult leukemia
● Chronic leukemia: Predominant cell is mature but does not function normally
○ Chronic myelogenous leukemia (CML)
■ Too many blood cells made in bone marrow
○ Chronic lymphocytic leukemia (CLL)
■ Too many immature lymphocytes
■ Most common adult leukemia in western world
○ Slow progression
○ Lymphadenopathy
Lymphoma: types & characteristics
Infectious mononucleosis
● Acute, self-limiting infection of B lymphocytes transmitted by saliva through personal contact
● Commonly caused by the Epstein-Barr virus (EBV)-85%
○ B cells have an EBV receptor site
○ Others viral agents resembling IM:
■ Cytomegalovirus (CMV)
■ Hepatitis
■ Influenza
■ HIV
● Symptoms:
○ Fever
○ Sore throat
○ Swollen cervical lymph nodes
○ Increased lymphocyte count
○ Atypical (activated) lymphocytes
● Serious complications are rare
○ Splenic rupture is the most common cause of death
● >50% lymphocytes and at least 10% atypical lymphocytes
● Diagnostic test
○ Monospot qualitative test for heterophilic antibodies
● Treatment: symptomatic
WBC types and function: A&P
Type of Description
Lymphocyte

T cells ● Mature in the thymus

● Responsible for acquired immunity
● CD4 surface protein= T-helper cell; produces cytokines
● CD8 surface protein= cytotoxic T cell; recognizes specific antigens and kills
them

B cells ● Mature in the bone marrow

● Responsible for acquired immunity
● Produce large amounts of antibodies in response to specific antigens

Natural killer cells ● Form in the bone marrow

● Part of the innate immune system
● Activated by cytokines released by the T cells
● Can kill tumor cells and cells infected by viruses without prior exposure to the
antigen
● Contain perforin and granzyme, which activate cell apoptosis

Type of Description
Granulocytes

Neutrophils ● Most common type of WBC; 60-70%

● Typically the first responders to an infection or injury
● Major component of pus related to acute inflammation
● Phagocytose bacteria and generate oxygen (hydrogen peroxide) and nitric oxide
to kill pathogens
● Immature cells (band cells) released during severe acute infection

Eosinophils ● 4% of all leukocytes

● Defends against parasitic infections
● Responds to allergic reactions

Basophils and Mast ● Make up 1% of all leukocytes

Cells ● Release histamine and other vasoactive amines in response to infection, injury,
or allergic reaction
● Involved in wound healing and chronic inflammation
● Basophils circulate in blood vessels
● Mast cells found in connective tissue near blood vessels

Type of Monocytes Description

 Monocytes ● Develop from bone marrow stem cells
● Immature macrophages or dendritic cells
● 6% of circulating leukocytes with macrophages
● Irregularly shaped and target bacteria, viruses, and debris

Macrophages ● Develop from bone marrow stem cells

● Large and irregularly shaped with large bean-shaped nucleus
● Cell surface covered with receptor proteins, allowing them to locate
antigens coated by antibodies

Dendritic Cells ● Antigen-presenting cells

● Found in tissue that has contact with the external environment
● Processes antigen material and presents it on the cell surface to the T
cells, helping to shape the adaptive immune response.

The different growth factors that affect blood cells

White blood cell growth factors are proteins that help the body produce white blood cells. They are also called
hematopoietic, meaning blood-forming, colony-stimulating factors (CSFs). White blood cells help fight infection
and can be destroyed during some types of cancer treatment.

Having low numbers of white blood cells is called neutropenia. People with neutropenia are more likely to develop
infections. Some people with neutropenia develop a fever, called febrile neutropenia, and some do not. Febrile
neutropenia may be a sign of an infection. A person with febrile neutropenia may need antibiotics and to stay in the
hospital until the infection is gone.

CSFs are supportive medications. This means that they do not treat the cancer, but prevent patients from developing
side effects of cancer treatment, such as infections. CSFs are given as shots, usually 24 hours after a chemotherapy
treatment, and include filgrastim (Neupogen, Zarxio), sargramostim (Leukine), and pegfilgrastim (Neulasta). These
medications are made in the laboratory and are similar to those naturally produced by the body.

Immunity/HIV-AIDS 25
Clinical manifestations Aging and immune response;
● Aging is responsible for changes in immune responsiveness that affect both cell-mediated and humoral
immune responses. Older adults are more susceptible to infection and have a higher incidence for cancer.
● The immune response is often diminished in older adults, owing to changes in the immune system that
occur with age. This diminished responsiveness is called energy, and it an result in a negative TB skin test,
even when the patient has active disease.
● The immune system becomes less able to distinguish self from nonself (that is, to identify foreign antigens).
As a result, autoimmune disorders become more common.
● Macrophages (which ingest bacteria and other foreign cells) destroy bacteria, cancer cells, and other
antigens more slowly. This slowdown may be one reason that cancer is more common among older people.
● T cells (which remember antigens they have previously encountered) respond less quickly to the antigens.
● There are fewer white blood cells capable of responding to new antigens. Thus, when older people
encounter a new antigen, the body is less able to remember and defend against it.
● Older people have smaller amounts of complement proteins and do not produce as many of these proteins
as younger people do in response to bacterial infections.
● Although the amount of antibody produced in response to an antigen remains about the same overall, the
antibodies become less able to attach to the antigen. This change may partly explain why pneumonia,
 influenza, infective endocarditis, and tetanus are more common among older people and result in death
more often. These changes may also partly explain why vaccines are less effective in older people and thus
why it is important for older people to get booster shots (which are available for some vaccines).
Autoimmunity - Lupus;
● Etiology and Pathogenesis
o Systemic lupus erythematosus (SLE)
▪ Known as lupus
▪ Chronic autoimmune disease that causes generalized inflammation
o Etiology and pathogenesis
▪ Multifactoral but not fully known
▪ More common in women than in men and manifests most often between the ages of 15
and 44 years
▪ Affects African Americans and people of Asian descent more than individuals of other
races and ethnicities
▪ Drug-induced SLE is caused by the body’s overreaction in response to certain
medications
▪ Clinical manifestations of SLE are mediated both directly and indirectly by antibody
formation and the creation of immune complexes (IC)
● Clinical Manifestations and Diagnosis
o Constitutional symptoms
▪ Fatigue, fever, myalgia, and weight change
▪ Hallmark symptom is acute cutaneous lupus erythema, commonly referred to as a
butterfly rash
o Diagnosis
▪ Clinical judgment after alternative diagnoses have been excluded
▪ Serologic data
● Anti–double-stranded DNA and anti-Smith antibodies
● Treatment
o Focuses on ensuring long-term survival, achieving the lowest possible disease activity, preventing
organ damage, minimizing drug toxicity, improving quality of life, and educating patients about
their role in disease management
o Nonpharmacologic measures
▪ Protection from sunlight, maintaining adequate nutritional intake, getting enough
exercise, stopping smoking, and receiving appropriate immunizations
o Pharmacologic therapy
▪ Depends on the predominant symptoms, organ involvement, response to previous
therapies, and disease activity and severity
▪ All individuals diagnosed with SLE are treated with hydroxychloroquine to provide relief
of constitutional manifestation and symptoms associated with the musculoskeletal and
mucocutaneous systems
Aging and immune response;
● Affecting Innate Immunity in the Elderly
o Normal numbers of cells of innate immunity but possible diminished function (e.g., decreased
phagocytic activity, decreased antibody production, and altered cytokine synthesis)
o Increased incidence of chronic inflammation, possibly related to increased production of
proinflammatory mediators
o At risk for impaired healing and infection associated with chronic illness (e.g., diabetes mellitus,
peripheral vascular disease, or cardiovascular disease) and decreased phagocytosis.
o Use of medications interfering with healing (e.g., anti-inflammatory steroids)
o Loss of subcutaneous fat, diminishing layers of protection against injury
o Atrophied epidermis, including underlying capillaries, which decreases perfusion and increases
risk of hypoxia in wound bed
o Aging of the immune system, diminishing the effectiveness of vaccines
 ● Affecting Mechanisms of Self-Defense in the Elderly
o Immune function decreases with age; diminished T-cell function and reduced antibody responses
to antigenic challenge occur with age.
o The thymus reaches maximum size at sexual maturity and then undergoes involution until it is a
vestigial remnant by middle age; by 45 to 50 years of age, the thymus is only 15% of its maximum
size.
o With age there is a decrease in thymic hormone production and the organ's ability to mediate
T-cell differentiation.

Definitions – allergy, autoimmunity,

● Allergy: T ​ ype I reactions often occur within minutes of an antigen challenge. These reactions are referred
to as allergic reactions. In the context of an allergic response, the antigens are often referred to as allergens.
Allergens that are associated with this type of response include the protein in pollen, house dust mites,
animal dander, foods, and chemicals like the antibiotic penicillin. Not naturally found in individuals
● Autoimmunity: A ​ utoimmune diseases are caused by a breakdown in the ability of the immune system to
differentiate between self-and nonself-antigens. These diseases can affect any cell or tissue in the body.
Autoimmune disorders include Hashimoto thyroiditis, which is tissue specific, and SLE, which can affect
multiple organs and systems.
Types of immune response; Innate and Adaptive;
● Innate immunity
o Nonspecific immunity present at birth
▪ 1​st​ line of defense in immune response
● Provides protection from exposure to antigen until adaptive immune response
▪ Causes redness, swelling, heat, and pain
▪ Components
● Physical barriers​: skin, mucous membranes, mucus
● Enzymes​ in epithelial and phagocytic cells
● Inflammation-related proteins​, like C-reactive protein (CRP)
● Toll-like receptors​ that help to sense pathogens and signal response
● Cell that release inflammatory mediators​, like cytokines
● Antimicrobial peptides
● Phagocytes
● Acquired immunity
o Also known as adaptive immunity
o Continually refined throughout the life of the individual
o Highly specific to a pathogen
▪ Once exposed, individual has long-lasting protection against that particular pathogen
o Basis of vaccination
o Lymphocytes (B and T cells) important to this type of immunity
▪ B cells produce antibodies that attach to a specific antigen, allowing immune cells to
destroy the antigen
▪ T cells directly attack the antigen and help control the immune response

Characteristics Characteristics Acquired Immunity

Line of defense First line of defense Second line of defense

Timing of defense Immediate response Delay between exposure to antigen and
response. Can take days to weeks. Once
acquired immunity to a specific antigen has
developed, response is immediate.
Specificity Broad Specific response to specific antigen
 Memory No memory involved Memory involved

Cells involved Mast cells, granulocytes (neutrophils, T and B lymphocytes, macrophages,

eosinophils, basophils), monocytes, dendritic cells
macrophages, natural killer cells, platelets,
endothelial cells
Immunizations and acquired immunity;
● Immunity: 3rd line of defense; long-term protection against specific infections
● Memory cells - remember the infections that showed up in the body before.
● Active
o Actively producing antibodies (Igs)
o Memory cells – long lasting – slow response
o Go through stages of producing antibodies
▪ Natural
● Antibodies + memory cells
● Actively involved b/c they naturally have it in their body
● Ex. Flu (body can fight off infection normally)
▪ Artificial
● Antibodies + memory cells
● Must be given the vaccination → activate the antibodies so they can help the
immune system
● Ex. Flu shot
● Passive
o Performed antibodies of T cells are administered to you
o Must get antibodies from somewhere else
o No memory cells – short lasting – fast response
▪ Natural
● Not actively producing antibodies to help themselves
● Ex. breast milk/placenta (mother → child)
▪ Artificial
● Fast reaction → need it immediately
● Protective short lasting
● Ex. Serum shot → given to a man who was bit by a snake
Examples of immune response; clinical manifestations;

Ways to test for adaptive immunity example, Skin test

Different immunoglobulins and their functions & clinical applications

IgG ● Major serum immunoglobulin (80% of antibodies in serum (plasma).

● Responsible for immunological defense of newborns; only class of Ig's that crosses the placenta
(providing the fetus with passive immunity).
● Produced mainly in secondary immune response (serves as body's memory to specific antigens).
● Smallest immunoglobulin (monomer)
● provides long term protection because it persists for months and years after the presence of the
antigen that has triggered their production
● They can leave the blood cells and move to areas of inflammation
● Protect against bacteria, viruses, neutralise bacterial toxins, trigger complement protein systems and
bind antigens to enhance the effectiveness of phagocytosis (Major antibacterial and antiviral
antibody)
 ● It appears in all body fluids
● Classic antibody reactions, including precipitation, agglutination, neutralization, and complement
fixation
● IgG Most prevalent antibody; major antibody of the tissues; produced after IgM; only
antibody to cross placenta; antitoxin; antiviral
IgM ● Accounts for 6% of total serum Immunoglobulin.
● Predominant Immunoglobulin involved in the body's primary or initial immune response to an
antigen.
● Can bind up to 10 antigens, even in the absence of prior immunization.
● Largest immunoglobulin (so do not leave the blood vessels) (pentamer)
● Involved in the ABO blood group antigens on the surface of RBCs
● Effective in aggregating antigens because it has ten binding sites
● Involved in complement
● Enhance ingestions of cells by phagocytosis
● Usually found only in the vascular system
● Classic antibody reactions, including precipitation, agglutination, neutralization, and complement
fixation
● IgM First to respond; activates the complement system; stimulates ingestion by macrophage;
principal antibody of the blood
IgE ● Found only in trace amounts on surface of mast cells.
● Immunoglobulin E (IgE) is the antibody involved in immediate hypersensitivity reactions, or
allergic reactions that develop within minutes of exposure to an antigen. Such as Hay fever, asthma,
hives.
● Monomer
● Bind to mast cells and basophils which participate in the immune response
● When an antigen such as pollen binds to ths antibody, the mast cell or basophil releases histamine
● It attract complement and phagocytic cells.
● Involved in release of vasoactive amines stored in basophils and tissue mast
cell granules that cause the allergic effects
● IgE stimulates the release of mast cell granules, which contain histamine and heparin.
● IgE For allergic reactions
IgA ● Predominant Ig found in body secretions; saliva, tears, breast milk, vaginal fluid, bronchial mucus,
colostrum, nasal fluids, and respiratory, GI .
● First line of defense against local infections, especially at the surfaces of mucous membranes. 13%
of serum Igs.
● Polymeric, normally Dimer (consists of two monomers joined together)
● Main function is to bind antigens on microbes before they invade tissues.
● It aggregates the antigens and keeps them in the secretions so when the secretion is expelled, so is
the antigen
● Important role in preventing antigenic agents from attaching to epithelial surfaces
● IgA Principal antibody of the GI tract; found in tears, saliva, sweat, breast milk; protects
epithelial lining
IgD ● Function is unclear compared to other Igs.
● Found on surface of B lymphocytes membranes and involved in antigen recognition. 1% serum.
● Minute amounts found in serum (monomer)
● Primarily an antigen receptor
● Possible function in controlling lymphocyte activation or suppression
● is present in plasma and is easily broken down.
● IgD Only in minute concentrations; function unknown
Hypersensitivity Reactions: Different types with examples
● Hypersensitivity Reaction: inappropriate activation of the immune system
Type I ● IgE – mediated reaction (histamine released)
Immediate/Anaphylaxis ● Allergic reaction
Reaction ● Antibody + IgE → allergic response immediately
● Anaphylactic Reactions
o Anaphylaxis is a systemic life-threatening Type I hypersensitivity
reaction
▪ Results from the presence of an antigen introduced by
injection, insect sting, or absorption through the epithelial
surface of the skin or gastrointestinal mucosa
● Atopic (Local) Reactions
○ Often occur when an antigen is confined to a particular site of
exposure
■ Most common: urticaria, allergic rhinitis (hay fever), atopic
dermatitis, food allergies, and some forms of asthma
● Allergic Rhinitis
○ Characterized by symptoms of sneezing, itching, and
rhinoconjunctivitis (watery discharge from the nose and eyes)
■ Typical allergens include pollens from ragweed, grasses,
trees, and weeds; fungal spores; house dust mites; animal
dander; and feathers
● Food Allergy
○ Any food can cause an allergic reaction
■ Foods most commonly associated with a Type I
hypersensitivity reaction in children
● Milk, eggs, peanuts, soy, tree nuts (e.g., walnuts,
almonds, pecans, cashews, hazelnuts), fish, and
shellfish
■ In adults, foods commonly attributed to allergy
● Peanuts, shellfish, and fish
Type II ● Tissue-specific reaction
Antibody-Mediate/ ● Mediated by IgG or IgM antibodies directed against target antigens on cell
Cytotoxic Reaction surfaces or in connective tissues
● Attacks the cells that are affect, but goes overboard by killing good tissues as
well
● Three different types of antibody-mediated mechanisms:
1. Complement- and antibody receptor–mediated phagocytosis
a. mismatch blood transfusions, hemolytic disease of newborn
due to ABO or Rh incompatibility, or certain drug reaction
2. Complement- and antibody receptor–mediated inflammation
a. Inflammation occurs when antibodies are deposited in
extracellular tissues
3. Antibody-mediated cellular dysfunction
a. Graves disease, Myasthenia gravis
Type III ● Auto-immune complex (the body begins to attack itself)
Immune Complex-Mediated ● IgG + IgM (classical complement system)
Reaction ● Systemic Lupus, Rheumatoid Arthritis, Kidney damage, serum sickness, arthus
reaction
Type IV ● Mediated by T cells → NO ANTIBODIES INVOLVED
Cell-Mediated Reaction / ● Two types of Type IV hypersensitivity reactions:
Delayed ○ Direct cell-mediated cytotoxicity
■ Killing of a target cell by an effector cell (natural killer cells
or cytotoxic T lymphocytes)
○ Delayed-type hypersensitivity
■ Often takes 24-72 hours to develop
■ Cell mediated (T cells and macrophages), not
antibody-mediated
■ Antigen is engulfed by macrophages and monocytes and is
processed and sent to a T cell that has a specific receptor for
that processed antigen
● Liver transplant (organ rejection), TB skin test reaction, Allergic contact
dermatitis by poison ivy, latex in gloves

Characteristics of HIV virus & stages of replication;

Means of HIV transmission;

Life cycle of HIV and the T lymphocyte;

● HIV Lifecycle-Receptors, Attachment, Fusion, and Entry
○ HIV infects cells that express the CD4 receptor on their surface
○ Interaction between CD4 and major histocompatibility complex (MHC) class II molecules is
necessary for T cells to recognize antigens
○ CD4+ cells that are susceptible to HIV infection include the helper subset of T lymphocytes,
monocytes/macrophages, dendritic, and brain microglial cells
○ HIV uses chemokine receptors as co-receptors to gain entry into target cells
■ CXCR4 mediates infection by T tropic viral isolates
■ CCR5 mediates infection by M tropic viral isolates
○ Viral attachment involves two binding events
■ Involves binding of the CD4+ molecule and chemokines
○ Following fusion, the virus sheds its core protein coat and releases the core contents into the target
cell cytoplasm
● HIV Lifecycle-Transcription and Translation
○ Reverse transcriptase is a viral polymerase that generates two copies of DNA using the viral RNA
as a template
■ DNA strand is partially transcribed at one end of the RNA template and then jumps to the
other end of the template
■ Continues transcription in the opposite direction until a complete strand has been
transcribed
○ DNA copies are flanked at each end by structures called long terminal repeats (LTRs)
■ Contain binding sites for viral proteins that regulate replication
○ Viral DNA and the enzyme integrase migrate to the cell nucleus through nuclear pores
■ Links the LTRs into the host DNA in a random fashion
■ Integrated viral DNA is known as the provirus
■ Viral genes are now part of the host’s chromosomes and will replicate each time the
infected cell replicates
 ●T Lymphocytes
○ Category 1: CD4+ cell count greater than or equal to 500
○ Category 2: CD4+ cell count 200 to 499
○ Category 3: CD4+ cell count less than 200
HAART for HIV and clinical categories;
● HIV Pharmacologic Treatment
○ Antiretroviral therapy (ART)
■ Usually combines a minimum of three medications that diminish viral replication;
cornerstone of treatment
○ Highly active antiretroviral therapy (HAART)
■ Use of a combination of antiretroviral therapies to help decrease viral resistance
○ Six classes of antiretroviral drugs
■ Nucleoside reverse transcriptase inhibitors (NRTIs): First class approved for use in the
United States; block reverse transcriptase to inhibit HIV replication
■ Nonnucleoside reverse transcriptase inhibitors (NNRTIs): Bind to reverse transcriptase
and inhibits its activity, inhibiting HIV replication
■ Protease inhibitors: Act in the late stage of the viral lifecycle; binds and blocks protease,
preventing immature HIV to become mature HIV
■ Fusion inhibitors: Prevent fusion of the viral and host cell membranes
■ Entry inhibitors: Inhibit HIV’s ability to bind to chemokine molecules on the target cell’s
surface, blocking HIV invasion to the cell
■ Integrase strand transfer inhibitors (INSTIs): Block the enzyme integrase, which is
necessary for HIV to accomplish viral replication
● HIV-Approaches to Pharmacotherapy
○ Current recommendation is offering HAART to all individuals infected with HIV
 ○ Early-stage HIV
■ Primary goal is suppression of plasma HIV RNA to undetectable levels
○ Interruption of antiretroviral therapy typically is not recommended
■ May result in viral rebound, leading to even more pronounced immunosuppression and
worsening of the individual’s overall health status
○ Benefits for early HAART therapy:
■ Preservation of immune function
■ Prolongation of clinical latency
■ Possible reduced risk of transmission
○ Risks for early HAART therapy:
■ Drug toxicity
■ Increased risk for developing drug-resistant disease
● Clinical Categories
○ Category A​ (conditions present in patients with documented HIV infection):
■ asymptomatic HIV infection persistent, generalized lymph node enlargement or acute
(primary) HIV infection with accompanying illness or history of acute HIV infection
○ Category B​ (conditions present in patients with symptomatic HIV infection):
■ bacillary angiomatosis, oropharyngeal or persistent vulvo-vaginal candidiasis, fever or
diarrhea lasting over 1 month, idiopathic thrombocytopenic purpura, pelvic inflammatory
disease (especially with a tubo-ovarian abscess), and peripheral neuropathy
○ Category C​ (conditions present in patients with acquired immunodeficiency syndrome):
■ candidiasis of the bronchi, trachea, lungs, or esophagus; invasive cervical cancer;
disseminated or extrapulmonary coccidioidomycosis; extrapulmonary cryptococcosis;
chronic intestinal cryptosporidiosis; cytomegalovirus (CMV) disease affecting organs
other than the liver, spleen, or lymph nodes; CMV retinitis with vision loss;
encephalopathy related to HIV; herpes simplex involving chronic ulcers or herpetic
bronchitis, pneumonitis, or esophagitis; disseminated or extrapulmonary histoplasmosis;
chronic, intestinal isosporiasis; Kaposi's sarcoma; Burkitt's lymphoma or its equivalent;
immunoblastic lymphoma or its equivalent; primary brain lymphoma; disseminated or
extrapulmonary Mycobacterium avium complex or M. kansasii; pulmonary or
extrapulmonary M. tuberculosis; any other species of Mycobacterium (disseminated or
extrapulmonary); Pneumocystis carinii pneumonia; recurrent pneumonia; progressive
multifocal leukoencephalopathy; recurrent Salmonella septicemia; toxoplasmosis of the
brain; wasting syndrome caused by HIV.
Course of infection including window period;
● Window period:​ Time after infection and before seroconversion; A persons HIV antibody test will result in
negative
● Latent phase: ​Person has no signs or symptoms of the illness. The median time lasts about 10 years.
During this time CD4+ cells count fall gradually from normal range or 800-1000 to 200 or lower. Some
people experience swollen lymph nodes at this time
Diagnosis and treatment; Mother-fetal infection;

Clinical stages (CDC classification) of HIV infection leading to AIDS;

● The Centers for Disease Control and Prevention (CDC) system of classifying the severity of HIV infection
○ Based on age-specific CD4+ T-lymphocyte count or CD4+ T-lymphocyte percentage of total
lymphocytes
● Stages of HIV infection
○ Range from 0 to 3
○ Based on the individual’s CD4+ T-lymphocyte count

Age at Time of C D4 T-lymphocyte Test

< 1 Year 1–5 Years Greater than or equal to​ 6

Years

Stage Cells/µL % Cells/µL % Cells/µL %

 1 Greater than Greater than Greater than Greater than Greater than Greater than
or equal to or equal to 34 or equal to or equal to 30 or equal to or equal to 26
1500 1000 500

2 750–1499 26–33 500–999 22–29 200–499 14–25

3 < 750 < 26 < 500 < 22 < 200 < 14

Precautions to decrease infection;

Opportunistic infections;
● Opportunistic infection
○ An infection that occurs with increased frequency or greater severity as a result of the host’s
weakened or compromised immune response
○ In healthy individuals, the causative agent for these infections generally do not cause illness
● Among individuals with HIV, the most common opportunistic infections are cytomegalovirus diseases and
tuberculosis
● Cytomegalovirus (CMV)
○ Double-stranded DNA virus carried by 60% of the U.S. population
○ Ec immunity inhibits CMV replication
○ With severe immunosuppression, active viral replication can occur with dissemination to target
tissues such as the retina, gut, lungs, and central nervous system
● Tuberculosis
○ Acid-fast bacillus transmitted through aerosolized droplets
○ Once inhaled, the bacilli are transported to the pulmonary alveoli, where they are ingested and
walled off in granulomas by alveolar macrophages
■ Granuloma is a mass of fused macrophages that isolates persistent infectious agents and
prevents their activation and dissemination
HLA compatibility;

Cardiovascular 20
1. Mitral valve insufficiency results in blood regurgitation from the: Left ventricle back into the left atrium
2. Target- organ damage that occurs as the results of long-term uncontrolled hypertension is associated with:
Atherosclerosis
3. Atherosclerosis of coronary arteries: Narrowed coronary artery and decreased blood flow
4. Modifiable Risk factors for atherosclerosis: Obesity, LDL levels, lifestyle changes
5. Atherosclerosis: Build of fats, cholesterol, and other substances in and out of the artery wall
6. Major​ modifiable risk factors​ for atherosclerosis includes all of the following except:- Female more than 55
years of age
7. The earliest visible pathologic change apparent in the coronary blood vessel in the development of coronary
atherosclerosis is:Fatty streaks in the intima
8. Obese white 49yr, diagnosed with hypercholesterolemia, physician prescribed a low-fat, low calorie and
low cholesterol diet to promote weight loss and lower blood lipid level, what are other risk factors for
coronary artery disease that the nurse should assess for: A history of Diabetes Mellitus
9. DWhen teaching about primary hyperlipidemia, it's important to encourage the client to continue with an
exercise program because it: Elevates High-Density Lipoprotein (HDL)
10. The nurse is teaching a client newly diagnosed with high cholesterol. Which type of fatty acid will the
nurse teach the client to avoid? Saturated fatty acids
11. Dietary factors that increase serum cholesterol and its lipoprotein fractions are:Complex carbohydrates,
saturated fats, cholesterol
12. LDL is bad HDL is good
13. Saturated fats are bad
14. Difference between unsaturated vs saturated: Saturated fats are solid at room temperature, while
unsaturated fats are liquid.
15. modifiable risk factors for high cholesterol: Diet, obesity, physical activity/ exercise
16. Which is preferable, saturated, unsaturated, etc: unsaturated
17. Which one of the following total serum cholesterol levels is considered desirable? A total serum
cholesterol: less than 200 mg/dL
18. Causes of secondary hyperlipoproteinemia include: diabetes mellitus and obesity
19. Dietary factors that increase serum cholesterol and its lipoprotein fraction are: excess calories, saturated
fats, cholesterol
20. According to the American Heart Association, major risk factors for atherosclerosis that can be changed
include: hypertension, cigarette smoking, blood cholesterol levels
21. Which statement by a patient about lipid levels does the nurse need to clarify? "High levels of high-density
lipoproteins are desirable for a healthy heart."
22. Hypertension from renal disease: Secondary hypertension
23. The doctor was examining a 70 year old woman Ms jones to have peripheral edema and elevated blood
pressure. Further urine lab tests showed the presence of protein in the urine. What is the diagnosis of Ms.
Jones condition: Hypertension secondary to renal disease
24. When counseling a patient, the nurse explains that according to the 2017 American Heart Association
guidelines his blood pressure of 135/85 is a diagnosis of: stage 1 hypertension.
25. Your client with chronic renal failure asks you why she has developed hypertension (HTN). What is the
basis of your response? HTN is caused by alteration in renin-angiotensin levels
26. That the RAAS system regulates BP: Aldosterone helps the body to retain sodium, which increases blood
volume and raises blood pressure. This is known as the renin-angiotensin-aldosterone system (RAAS).
27. RAAS causes sodium (salt) and water retention
28. A patient with hypertension develops renal disease. The kidneys assist in the control of BP by: Activation
of the renin-angiotensin-aldosterone system
29. Condition that will stimulate the juxtaglomerular cells to increase renin production: Decrease in the serum
sodium concentration
30. Septic shock: Widespread infection; Significant drop in blood pressure that can cause heart failure, stroke
and other organ failure
31. Anaphylactic shock: Allergic reaction to an antigen to which the body has becomes hypersensitive
32. 4 months old ulcer with odor and pale skin: Circulatory shock
33. Mr. B had an open ulcer on his left leg for 4 months. Today, he is brought to the ER because… BP was
90/45, temp 98.6, HR 120 bpm. What is a possible diagnosis for Mr. B?Septic shock
34. Mrs. J was given a shot of penicillin at the ER. Shortly after that, she complained of difficulty breathing.
What type of shock does this reaction represent? Anaphylactic
35. In response to heart failure, certain compensatory mechanisms are invoked. Which of the following
represents one of these mechanism? Ventricular Hypertrophy
36. Definition of congestive heart failure: Chronic progressive condition that affects the pumping power of
your heart muscles
37. Congestive heart failure can best be described as follows:Inability of the heart to pump blood to meet the
metabolic needs of the body
38. Left sided heart failure:Dyspnea
39. The most common cause of pulmonary edema is: Left sided heart failure
40. The best description of cor pulmonale is: hypertrophy of the right ventricle caused by lung disease.
41. The nurse, assessing a patient with endocarditis, notes small red painful growths on the fingers and toe
pads. The nurse documents these findings as: Osler nodes.
42. Effects of cigarette smoking on vessel walls: Smoking has a direct effect on blood vessels, increasing the
risk for Raynaud disease.
43. Raynaud’s phenomenon is characterized by _____________, while thromboangitis obliterans (Buerger’s
disease) is characterized by ____________ of the arterial vessels in the hands and/or feet. Vasospasm;
inflammation
44. Client recovering from a surgical repair of dissecting aortic aneurysm. Nurse should evaluate the client for
signs and bleeding and recurring dissection. These signs include: Hypotension and Tachycardia
45. Because of its arterial location, often the first sign of an abdominal aneurysm is: a pulsating abdominal
mass
46. Compression of the lumbar nerve roots causing low back and leg pain may be caused by which vascular
disease? Abdominal aortic aneurysm
47. Cardiac conduction: Ischemia disrupts the cardiac conduction system
48. The signs and symptoms of myocardial infarction include:Pain in the left arms that occurs on arising and is
accompanied by….
49. Cor pulmonale: alteration in structure and function of right ventricle (Pulmonary Hypertension)
50. Renin, an enzyme secreted from the juxtaglomerular apparatus causes: the activation of angiotensin I
51. Venous thrombosis = immobility
52. A patient having a heart rate of 100 a systolic blood pressure of 200, and a stroke volume of 40 ml would
have an average cardiac output of: none of the above (0.5, 4, 8000)
53. Myocardial oxygen demand is increased by all of the following except: bradycardia
54. Cardiologist prescribed diltiazem hydrochloride (cardizem) 20 mg as an IV bolus over 2 minutes for a
patient diagnosed with atrial fibrillation the pharmacy dispenses a 5 mg/ml vial. How many ml should the
nurse administers: 4ml
55. Patient has a systolic pressure of 146 mmhg and a diastolic pressure of 82 mmhg. The nurse knows that
these readings equal a pulse pressure of which of the following: 64 (systolic-diastolic=pulse pressure)
56. Client with angina pectoris must learn how to manage acute angina episodes and reduce risk factors that
exacerbate this condition. When developing the clients care plan, the nurse should include which expected
outcome? Client will verbalize an understanding to stop smoking
57. A serious complication of varicose vein is: thrombophlebitis
58. A vital part of non-pharmacological management of hypertension would include: stress management
59. The most characteristic sign of varicose veins is: dilated tortuous veins of the legs
60. Person with congestive heart failure would be on, diuretic therapy for the therapeutic purpose of:
decreasing the ECF volume
61. Depolarization of cardiac muscle cells occurs because of: the cells interior becoming less negatively
charged
 62. Blood vessel disorder characterized by lipid deposition on the initial layer of an artery is called:
Atherosclerosis
63. Client reports of chest pain that begins after sporadic activity accompanied by fatigue. He also complained
of ankle Edema that's worse at the end of the day. Nurse suspect cardiovascular disorder, What are other
symptoms: shortness of breath
64. Nurse is assisting the client to manage the cardiovascular risk factors of hyperlipidemia and hypertension.
Client asked what kind of diet would be best. The nurse is correct response is which of the following: A
diet low in sodium, fat, cholesterol
65. Client admitted for treatment of prinzmetal's angina. When developing the care plan, the nurse keep in
mind that this type of angina is triggered by coronary vasospasms
66. Left ventricle her failure would be manifested as an: increase in pulmonary capillary wedge pressure
67. Client has just been told that he has an infection of the inner surface of the heart. He's also told that the
bacteria has invaded his heart. He's also told that the bacteria has invaded his heart valves: infection
endocarditis
68. SA,AV,his, purkinje
69. Group of medications for hypertension ask by decreasing angiotensin II and it's multiple effects on blood
pressure: ace-inhibitors
70. The most common complication of early myocardial infarction is: dysrhythmias

Hematology 30
1. Life span for normal platelets: 3-4 months (90-120) 8-9 days
2. Not a cause of blood disorders such as anemia: Rhinovirus Infection
3. Following conditions is a client with multiple myeloma (MM) monitored: Hypercalcemia
4. Bence Jones Proteinuria is a diagnostic finding found in: Multiple Myeloma
5. Factors that may precipitate sickle cell crisis include: Dehydration Infection
6. And sickle cell anemia, the predominant type of abnormal hemoglobin is: Hemoglobin S
7. Most common symptom in patients who are in sickle cell in crisis is: Pain
8. Statement concerning the sickle cell that is false? The abnormal gene is inherited from both parent
(homozygous)
9. The nurse is counseling a couple who would like to start a family. The man has sickle cell disease and the
woman does not have sickle cell disease or the sickle cell trait. Which statement by the man indicates an
understanding of the transmission of the disease? "All our children will have the sickle cell trait."
10. Which type of anemia has defective secretion of the Intrinsic factor? Pernicious
11. Pathologic Findings in aplastic anemia include: Leukopenia Thrombocytopenia
12. which of the following diagnostic findings are most likely for a client with aplastic anemia: Decreased
levels of white blood cells, red blood cells and platelets
13. Patient is transfused with a unit of unmatched packed RBC which of the following is true regarding
transfusion? Patient with O type blood have neither A nor B Antigens
14. 18 yr old Woman has to donate blood at a blood clinic. While the clinician is testing her blood type, women
ask why it’s important for blood types to match between donor and recipient. What factors would underlie
the clinicians explanation? If blood types do not match, cell lysis occurs on a large scale
15. Client with a gunshot won’t requires an emergency blood transfusion. His blood type is a B negative.
Which blood type would be the safest for him to receive? A Rh negative
16. Which type of ABO antibodies would a person with type O blood have? AB
17. Client with Polycythemia Vera is at risk for thrombosis from which condition: Increased Blood Viscosity
18. Why are 28/24 hrs of oxygen reduce polycythemia and improve ventilation
19. Which one of the following would differentiate acute from chronic hypoxia? Polycythemia (“Difference
between acute and chronic renal failure: I put polycythemia”)
20. Symptoms classic for thrombocytopenia: Bruising and Petechiae
21. Disorder resulting from a deficiency of factor VIII: Hemophilia A
22. Food client with leukemia should avoid: Carrot sticks
23. Adult client is being test for leukemia. Lab work shows the presence of Philadelphia chromosomes. Based
on the result, which type of leukemia does the nurse knows the patient has: Chronic Myelogenous
Leukemia (CML)
24. 12-year-old client is admitted to the unit for a diagnostic workshop. Child has been complaining of
headache and nausea and vomiting. Blood work shows high levels of immature precursor B and T
lymphocytes. A physical assessment indicated lymphadenopathy, splenomegaly and hepatomegaly. What
does the nurse suspect: Acute Lymphocytic Leukemia (ALL)
25. When reviewing the medical record of a patient with Hodgkin lymphoma, the oncology nurse would expect
to note the presence of: Reed-Sternberg cells.
26. client is diagnosed with infectious mononucleosis. Which organism is associated with the disorder? Epstein
- BARR virus
27. Which white blood cell is the first to arrive at the site of inflammation? Neutrophils
28. The lifespan of the neutrophil in the tissues is approximately: 1 to 3 days
29. Neutropenia refers to: a decrease in neutrophils
30. Which granulocyte functions in antibody-mediated defense against parasites? Eosinophils
31. A client is in renal failure. The physician has ordered parental erythropoietin for this client. The nurse gives
this medication with confidence, knowing the client has which of the following anemia: Chronic Disease
Anemia (CDA)
32. A patient with multiple myeloma will most likely exhibit signs and symptoms of which type of anemia?
Normochromic
33. Which laboratory assessment data indicates to the nurse that a patient has anemia? Reduced erythrocytes
34. The plan of care for a patient with anemia due to alcoholism should include administration of which
vitamin? B vitamins
35. ALL are considered major modifiable risk factors for coronary artery disease (CAD) in a patient except:
male gender, age 48
36. Raynaud's syndrome is a pathologic condition of the arteries and arterioles due to: An exaggerated
vasoconstrictor response
37. A client is in renal failure. The physician has ordered parental erythropoietin for this client. The nurse gives
this medication with confidence, knowing the client has which of the following anemia: Chronic disease
anemia
38. Red blood cell production is stimulated by which of the following hormones: Erythropoietin
39. Young African-American woman with a history of sickle cell disease is complaining of severe abdominal
pain. Which of the following nursing interventions should the nurse NOT plan for this client? Forcing oral
fluid intake
40. Patient has been diagnosed with hemolytic anemia. This type of anemia results from: increased destruction
of RBC’s
41. Philadelphia gene, exposures to radiation= CML
42. Megaly/micro of rbc hallmark of cobalamin deficiency (B12)
43. Precursor: stem cell: organ of all blood cells
44. Injection: increase in WBC
45. Hematopoiesis: formation of RBC, WBC
46. ALL= children
 47. CML= Adults
48. Pancytopenia: anemia, infection, bleeding
49. CLL: severity is less, timing is more
50. Pathologic feature in all forms of leukemia is: uncontrolled proliferation of leukocytes

Immunity
1. Food excluded from dietary approaches to stop hypersensitivity (DASH): Steak
2. A Client most at risk for systemic Lupus erythematosus (SLE): 25 yr old woman
3. Breast Fed infants start life with positive immunity, which they acquire from their mother as which
Immunoglobulins: IgG, IgA
4. Identified as having a utero infection. The infant is receiving antibody and phototherapy and mother is
breastfeeding: IgG, IgA, IgM
5. Autoimmune disease mean that: Antibodies attack the bodies normal tissue
6. Autoimmune disease is most common in: women
7. The nurse is educating a client about the functions of the immune system. Which statements will the nurse
include in the teaching materials? "The immune system protects against invading microorganisms.", "The
immune system prevents cancer cell proliferation.", "The immune system mediates the healing of damaged
tissue."
8. The nurse is caring for a newborn baby. What is the nurse's understanding of this client's immunity?
Maternal IgA is transferred to breastfed infants.
9. The nurse is caring for a client with an allergic reaction. What is the nurse's understanding of this type of
hypersensitivity reaction? It is a Type I reaction, an IgE mediated disorder.
10. The nurse is caring for a client diagnosed with systemic lupus erythematosus (SLE). What does the nurse
understand about the etiology and pathogenesis of this condition? Clinical manifestations are mediated by
antibody formation and the creation of immune complexes (IC).; Lupus can be drug-induced by the body's
overreaction to medications such as isoniazid, hydralazine, and procainamide.; The rate ICs are cleared in
the liver and spleen are believed to be impaired in SLE.
11. The nurse is caring for a client who began experiencing symptoms of systemic lupus erythematosus (SLE)
about one year ago. What does the nurse understand to be potential causes of this condition? Heredity,
Trigger microorganisms, Environment, Self-antigen from a tissue in the body
12. The nurse is performing a skin assessment on a client diagnosed with systemic lupus erythematosus (SLE).
Which assessment findings does the nurse anticipate? Facial butterfly rash, Discoid lesions, Alopecia
13. The nurse is providing education for a client diagnosed with systemic lupus erythematosus (SLE). Which
statement by the client indicates an understanding of the teaching? "I will use high sun protection factor
(SPF) sunscreen when I spend time outdoors."
14. Goodpasture: Antibody attack
15. The nurse is educating an older adult client about age-related changes in immunity. Which statements will
the nurse include in the education? Select all that apply. "There is a higher incidence of cancer with
advanced age.""Older adults are more susceptible to infection.""Both types of immune responses are
affected with advanced age."
16. The nurse is caring for an older adult client with active tuberculosis (TB) who has a negative TB skin test.
The nurse understands that this phenomenon is due to: a diminished immune response due to changes in
immunity occurring with age.
17. Type I - Anaphylaxis
18. Type II- Antibody mediated
19. Type III- immune complex
 20. Type IV- cell mediated
21. Individual has come to the clinic several times in the past six months with a middle ear infection(Otis
media); one possible X explanation may be a deficiency in: humoral immunity
22. IgG- crosses placenta long term immunity
23. IGA- found in body fluids breastmilk, blood, saliva
24. IGM- largest found in the vascular system, first to arrive to immune system, Neonate life
25. IGD- binds to b cells
26. IGE- allergy part of the type one hypersensitivity release of histamine

HIV/AIDS
1. Role of reverse transcriptase in HIV infection: Converts RNA into double stranded DNA
2. Patient suffering from AIDS has a defect in cellular immunity namely: T cell suppression
3. How should a nurse respond when a patient with human immunodeficiency virus (HIV) asks about the
course of the disease? "The disease has a variable progression, so it's hard to know right now."
4. The school nurse is talking with a high school class about sexual transmission of HIV. Which of the
following would the nurse advise the students? "Penile-vaginal and penile-anal intercourse most efficiently
transmit the virus."
5. When taking a health history from a patient during the period of chronic HIV, the nurse would expect to
find: no clinical manifestations of HIV infection.
6. Which patient statement indicates to the nurse that more teaching regarding early highly active
antiretroviral therapy (HAART) is needed? "Early HAART reduces the potential for developing
drug-resistant strains."
7. In response to an HIV-infected patient asking about tuberculosis (TB), the nurse should explain that: TB is
the leading cause of death in HIV-infected people.
8. In the initial stages of distal symmetric polyneuropathy (DSP) in an HIV-infected patient, the nurse would
expect to find on physical assessment: a diminished ankle reflex.
9. The nurse is teaching an HIV-infected patient about highly active antiretroviral therapy (HAART). The
nurse should consider the teaching effective if the patient says: "HAART with a minimum of three
antiretroviral medications reduces the chance of developing viral resistance."
10. An HIV-infected patient has cytomegalovirus (CMV) retinitis and a CD4+ lymphocyte count of 150
cells/mm3. How should the nurse interpret this data? The patient has AIDS.
11. The “window phase” of HIV infection refers to the period of time: between infection and detectable
antibody levels
12. Opportunistic infections are: infections involving usually harmless microorganisms that develop in persons
with compromised immune function
13. When counseling about HIV transmission, which patients does the nurse recognize as being at greatest risk
for being newly diagnosed with HIV? Black men who have sex with men
14. In response to an HIV-infected patient asking about tuberculosis (TB), the nurse should explain that: TB is
the leading cause of death in HIV-infected people.
15. Laboratory results indicate that the viral load of a newly diagnosed, untreated HIV-infected client has
stabilized. The nurse explains to the patient that: he has reached the viral set point.
16. The nurse is caring for a client who is five months pregnant and HIV positive. What is the nurse's
understanding of the neonate's HIV status? The neonate may or may not be infected with HIV.
17. Client with aids: Prakashan when performing mouth care, put on mask, gloves, and gown
18. Nurse stuck himself with a needle. best tie for in employer immediately then again in six weeks
19. Misconception about HIV infection: person recently exposed to HIV test negative for a virus two months
later he or she is not infected
20. Body substance most easily transmitted human immunodeficiency virus: blood semen
21. Factors make it difficult to develop a vaccine for HIV: HIV mutates easily
22. Seroconversion occurs how many weeks after exposure to HIV: 6-12 weeks
23. Deficient and people with infections caused by viruses, fungi: T cells
24. During which eight steps of HIV replication does the virus enter the CD4 T cells: fusion
25. Nurse respond when a patient with human immunodeficiency ask about the course of the disease? The
disease has a variable progression, so it is hard to know right now
26. clot lysis: cell burst