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NUR 376 Exam 1 Blueprint / Study Guide
Intro to Pathophysiology (Davis College)
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NUR 376 Exam #1 Blueprint
Test is on 10/12 at 0900 for PDX. If you have lab during this time, you will take the
exam on Monday at 0900. For MN-please follow the schedule in your announcements.
You will have 1.5 minutes per question. This exam will cover modules 1-3b. The test
will have multiple choice, select all that apply, matching, and sequence questions. See
below for an explanation of the aptitude level of each question.
Remember to tear up your paper before the last question.
We wish you luck!
MOutcome
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1 Distinguish between the three phases of inflammatory reaction.
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Vascular Permeability
● During the vascular phase at a site of inflammation, inflammatory mediators
such as histamine and bradykinin cause the blood vessels to dilate and become
more permeable.
● This permits fluids, WBCs, and platelets to travel to the site of injury or
infection.
● The increased fluid in the tissues dilutes the toxin and lowers the pH of the
surrounding fluids so they are not conducive to microbial growth.
Leukocytosis (Chemotaxis)
● During the cellular phase of inflammation, a chemical signal from microbial
agents, endothelial cells, and WBCs attracts platelets and other WBCs to the
site of injury.
● This is referred to as chemotaxis. During this phase, an increased number of
leukocytes (WBCs) are released from the bone marrow into the bloodstream, a
process known as leukocytosis.
● During inflammation, the WBC count in the blood commonly increases from a
normal baseline of 4,000 to 10,000 cells/mL to 15,000 to 20,000 cells/mL.
● The clinician can use the number of WBCs to determine the severity of the
infectious process that the patient is experiencing.
● Types of WBCs include neutrophils, eosinophils, basophils, lymphocytes, and
monocytes, which turn into macrophages.
Systemic Responses
● Persons enduring acute inflammation experience symptoms throughout the
whole body, such as fever, pain, lymphadenopathy (swollen lymph nodes),
anorexia, sleepiness, lethargy, anemia, and weight loss. These are known as
systemic responses. Inflammatory mediators such as prostaglandins (PGs),
TNF-alpha, and ILs are responsible for many of these systemic effects.
Tumor necrosis factor-alpha ( from Macrophages) Symptom - Fever, lack of appetite,
raises metabolism to cause cachexia, hypotension
Interleukins (from Macrophages) Symptoms - Fever, stimulates platelet production,
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fatigue, anemia, headache
1 Identify key lab values in inflammatory and infectious diseases.
An antibody titer:
● is the level of antibodies against the pathogen in the bloodstream.
(The normal values of an antibody titer depend on the type of antibody. If the
testing is done to detect autoantibodies, the normal value should essentially be
zero or negative) Positive means you have been exposed through infection or
vaccine.
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E. coli
● E. coli are gram-negative, rod-shaped bacteria that inhabit the human intestine. o e
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There are multiple different strains. Although most strains of E. coli are
harmless, the organisms can cause cholecystitis, bacteremia, cholangitis, UTI, i b
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traveler’s diarrhea, neonatal meningitis, and pneumonia.
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● bacteria are acquired by the fecal-oral route, usually in food or contaminated
water. The bacteria live in the intestines of healthy cattle.
● Eating infected meat that is rare or undercooked is the most common way of
acquiring the infection.
● Infection can also occur after consuming fecal-contaminated vegetation or
unpasteurized milk, juice, or cider.
● In addition, person-to-person transmission can occur. Infants and elderly adults
are most susceptible to illness caused by E. coli
1 Recognize portals of entry and modes of transmission of infectious diseases.
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1
Differentiate between immunocompetence and
immunosuppression.
● Immunocompetence: the ability to protect oneself from infectious agents
because of a strong immune system
● Immunosuppression: impaired ability to provide an immune response
1 Compare and contrast innate and acquired immunity responses, including
acquired and passive immunity (B Lymphocytes and T Lymphocytes)
Active acquired adaptive immunity:
● is obtained through exposure to an antigen (which commonly causes an
illness) or through a vaccination that provides immunization.
● For example, after a child contracts measles infection (rubeola), the child
develops active acquired adaptive immunity
● In both forms of active acquired immunity, the body recognizes an antigen,
develops immune cells specifically against the antigen, attacks and neutralizes
the antigen, remembers the antigen, and develops long-lasting immunity.
Passive acquired adaptive immunity.
● To gain this form of immunity, an individual is given pre-made, fully formed
antibodies against an antigen.
● The patient is a passive recipient of the antibodies, and his or her body does
not have to perform the actions needed to develop immunity.
● This provides immediate immunity, but short term, not long lasting. An
example involves hepatitis B immunoglobulin (called HBIg)
The immune system has two basic parts:
1. Innate immunity:
● Innate immunity refers to natural mechanisms that ward off invaders as a first
line of defense. Comes to the body’s defense first and immediately.
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● It is composed of the body’s natural anatomic
barriers, normal flora, white blood cells (WBCs), and protective enzymes and
chemicals.
Natural anatomical barriers include skin and mucous membranes, whereas
normal flora includes bacteria that live on the skin and within the
gastrointestinal (GI) tract.
WBCs are macrophages that phagocytose foreign debris and antigens.
Interferon, cytokines, and hydrochloric acid are some of the protective
enzymes and chemicals that protect the body from bacteria and viruses.
If the innate defense mechanisms prove inadequate to deal with a foreign
invader, the second line of defense, the adaptive immune system, is activated
2. Adaptive immunity
The adaptive immune system allows the body to recognize an antigen, target the
specific antigen, limit its response to that antigen, and develop memory for the
antigen for future reference.
The adaptive immune system’s ability to recognize and remember specific antigens is
called specificity.
The ability to respond again and again to specific antigens is caused by a memory
response, which develops after a second exposure to an antigen.
The adaptive immune system allows the body to distinguish between antigens that
belong to the host versus antigens that are from an invader. MHCs & HCLs)
The two major categories of adaptive immunity are:
1. B lymphocyte immunity, also known as humoral immunity
● After exposure to antigens, B lymphocytes are transformed into plasma cells
that release antigen-attacking Igs.
● Also called plasma or B cells. They mature within the bone marrow, spleen,
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and lymph nodes.
B cells are naïve or immature until they encounter antigens
After exposure to an antigen, B cells are stimulated to further mature into
plasma cells
As plasma cells, they have the ability to produce specific proteins called
immunoglobulins (Igs), also called antibodies, which attack the antigen or
pathogen.
Upon first exposure to the antigen, the process of B-cell maturation into
plasma cells that synthesize immunoglobulins takes days to initiate
2. T lymphocyte immunity, also known as cell-mediated immunity
● After exposure to antigen, T lymphocytes attack antigens themselves.
● T lymphocytes, also called T cells, mature within the thymus gland, a small
gland located in the mid-chest.
● The thymus gland degenerates with age, contributing to decreased
immunocompetence in old age
● After maturation in the thymus, mature T cells are found in the bloodstream
and T-cell zones of lymph nodes.
● The most common T cells that take part in cell-mediated immunity are called
CD4 cells, also called T helper cells, and CD8 cells, also called cytotoxic T
cells.
● The CD4 cell influences all other cells of the immune system, including other
T cells, B lymphocytes, macrophages, and NK cells
● The CD8 cell directly attacks an antigen
● HIV targets CD4 cells. By targeting CD4 cells, HIV defeats both cell-mediated
and antibody-mediated immune responses, the human body’s strongest two
defense mechanisms.
● The adaptive immune system allows the body to distinguish between antigens
that belong to the host versus antigens that are from an invader.
● T cells cannot be activated by antigen alone; APCs process the antigen first
and induce cell-mediated immunity
● APCs capture and attach to antigen and process it before the antigen is
attacked.
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● APCs include dendritic cells and macrophages.
● Dendritic cells, which are named for their numerous fine dendritic cytoplasmic
projections, attach to the broadest range of antigens.
● They are located within the epidermis and mucous membranes, where antigens
enter the body.
● When dendritic cells come in contact with bacteria or viruses, they release
cytokines that stimulate cells of the innate and adaptive immune systems to
respond.
Immunity that is present before exposure and effective from birth. Responds to a
broad range of pathogens.
Adaptive immunity: immunity or resistance to a specific pathogen; slower to
respond, has memory component acted out by B and T cells
1 Identify four types of hypersensitivity reactions
Type I Immediate hypersensitivity
● which is an allergic or atopic reaction
Within minutes after exposure, itching, urticaria, and skin erythema appear, followed
by bronchoconstriction. Laryngeal edema, tongue swelling, and angioedema, a
swelling of the facial regions—particularly the lips, mouth, and periorbital regions—
can occur.
Type II is a cytotoxic reaction
● Such as a transfusion reaction. For example, if type A blood from a donor is
administered to a type B recipient, the anti-A Igs of the recipient will attack
and destroy the type A red blood cells, causing a massive hemolytic reaction.
● Because of widespread vasodilation, blood pressure drops and can induce
vascular shock, at which point the disorder is anaphylactic shock. The patient
may lose consciousness and require cardiac monitoring.
● This is a medical emergency and requires rapid response from emergency
medical personnel
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● IV or intramuscular (IM) antihistamines, glucocorticoids, and epinephrine are
required immediately.
● The patient needs cardiac monitoring and periodic blood pressure
measurement until recovery.
● Patients should be aware of the allergen that triggered the reaction and wear a
medical alert bracelet or necklace.
● Also, for prophylaxis, the patient should carry an EpiPenR (pre-drawn syringe
of epinephrine) at all times.
Type III occurs by immune complex deposition,
● as in Rheumatoid Arthritis & Systemic lupus erythematosus (SLE)
Type IV is delayed hypersensitivity,
● such as the body’s delayed reaction to the Mantoux TB test which develops
after 48 hours,
● A good example is type IV delayed hypersensitivity occurs in transplant
rejection. This usually takes a few days to become apparent
1 Understand the etiology, pathophysiology and clinical manifestations of common S A 1
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autoimmune disorders.
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Systemic Lupus Erythematosus (SLE)
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Etiology
● SLE, commonly called lupus, is a multisystem autoimmune disease
characterized by autoantibodies, particularly antinuclear antibodies (ANAs).
● SLE is a chronic disease that can have an acute or insidious onset.
● It is characterized by remissions and exacerbations with fever; skin rash; joint
inflammation; and damage to the kidney, lungs, and serosal membranes.
● The cause of SLE is unknown. Risk factors include genetic predisposition and
environmental, hormonal, and immunological elements
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● The presence of Epstein-Barr virus (EBV) antibodies
significantly increases the risk of SLE. The risk is noted to be more intense in
African Americans, as EBV increases risk five- to six-fold in this racial group
● Drugs such as hydralazine, procainamide, quinidine, phenytoin, isoniazid, and
penicillamine can also induce SLE-like reactions.
● Exposure to ultraviolet (UV) light exacerbates the disease.
● The hormone most often linked to SLE is estrogen, with exacerbations of
disease often occurring in women during menses or pregnancy
Pathophysiology
● The pathological process of SLE involves formation of autoantibodies,
particularly ANAs
● Some patients have an increased risk of arterial and venous thromboembolism
● Practically every organ system can be affected by SLE due to destruction of
the microvasculature within the organs.
● Antibodies form immune complexes that are deposited in organs and tissues
such as the skin, heart, joint synovial membranes, glomeruli of the kidney, and
lungs.
● The deposition of immune complexes triggers an inflammation reaction that
damages small blood vessels and various organ membranes.
● The kidneys are particularly susceptible to inflammation in SLE, termed as
Lupus nephritis.
● The lungs also commonly succumb to inflammatory changes such as
pneumonitis, pleuritic, and pulmonary hypertension.
● Cardiac involvement in individuals with SLE can cause pericarditis,
endocarditis, and coronary artery disease.
Clinical Presentation
● Rash, Fever, Weight loss, joint inflammation, Myositis, Splenic enlargement,
Pneumonitis. Pleural effusion, Vasculitis, Pericarditis, Anemia,
Thrombocytopenia, Cardiac valve deformities and renal dysfunction are
common, Renal inflammation is common; lupus nephritis.
Diagnostic/Labs/Tests
● Antibodies to double-stranded DNA and the Smith (Sm) antigen.
● Antiribosomal, antineuronal, anti-Ro, anti-La, and antiphospholipid antibodies.
Complement levels in blood are decreased.
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● Elevated ESR, CRP. Elevated CPK possible if
myositis.
● Liver enzymes necessary.
● Serum creatinine may be elevated in lupus nephritis.
● Urinalysis may show hematuria and proteinuria.
● Biopsy of rash can diagnose SLE.
● Chest x-ray may show pleuritis or pneumonitis.
Treatment
● Hydroxychloroquine or chloroquine (antimalarial drugs),
● NSAIDS,
● short-term corticosteroids.
● Other immunosuppressive agents that may be used include (azathioprine,
rituximab, methotrexate, cyclophosphamide, or mycophenolate)
1 Understand etiology and pathophysiology of HIV/AIDS
Etiology & Pathophysiology
● HIV is contracted via blood, sexual activity, transplacental route, or
breastfeeding.
● CD4 cells are necessary components for a fully functioning immune system,
and their depletion leads to immunodeficiency. Attacking CD4 cells allows the
virus to destroy both immune mechanisms of the body.
● HIV replicates mainly within the CD4 cells and kills them.
● As virus increases in the blood, CD4 cell count decreases, which diminishes
both humoral and cell-mediated immunity, leaving the patient susceptible to
opportunistic infections.
1 Understand the etiology, pathophysiology, prevention and treatment of common
viruses and bacterial infections
Streptococcal
● A number of streptococcal organisms cause human disease. Group A beta
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hemolytic streptococcus (GABHS), also called
Streptococcus pyogenes, is a bacterium that causes many different infections.
● Rheumatic fever, streptococcal pharyngitis (strep throat), scarlet fever,
glomerulonephritis, skin infections, pneumonia, necrotizing fasciitis, and toxic
shock syndrome are among the many possible diseases caused by GABHS
● In persons suffering from sore throat, a throat culture is the only method that
can accurately diagnose or rule out GABHS pharyngitis.
Influenza Virus
● The three major types of influenza virus, A, B, and C, are among the most
common causes of upper and lower respiratory tract infection
● Transmission of influenza occurs through droplet infection and aerosols
generated by coughs and sneezes of individuals. Fomites and hand-to-hand
contact also can spread the virus. Initially the virus enters the upper respiratory
tract and then invades the lower respiratory tract mucous gland cells, alveolar
cells, and macrophages.
● The infection usually presents as an abrupt onset of fever, chills, headache,
myalgias, arthralgias, cough, and sore throat. Uncomplicated influenza
generally resolves over a 1-week period, although cough may persist for 2
weeks or longer.
● Influenza in older adults also increases susceptibility to pneumonia.
● Test: Influenza virus can be isolated from throat culture, nasopharyngeal
secretions, or sputum.
● Treatment consists of antipyretic medications, hydration, and rest. Amantadine,
rimantadine, zanamivir, and oseltamivir are antiviral medications that can be
used to shorten the disease’s course.
● Influenza vaccine is recommended annually for all persons older than age 6
months, but it is particularly important for older adults and people with chronic
illnesses and health workers.
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Module 1 Total Questions
2 Describe basic cellular adaptations and injury.
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Cell Injury & death
● Cells are vulnerable to many kinds of injurious agents that can cause
adaptations, maladaptive changes, and reversible or irreversible damage.
● Physical trauma, temperature extremes, electrical injury, radiation, free
radicals, high circulating glucose in diabetes, and high blood pressure can all
damage the plasma membrane and leave cellular organelles vulnerable to
injury.
● Apoptosis and necrosis are the two major forms of cell death. In apoptosis,
cells degenerate at a specific time with no adverse effects on the body. Cellular
necrosis, however, is cell death caused by injury.
Metaplasia: The replacement of one cell type by another
Atrophy: Atrophy is the diminished size and growth of tissue
Apoptosis: is the cell’s genetically programmed degeneration
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2 Identify the various body compartments and mechanisms for fluid movement
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Cellular Fluid Compartment
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● The extracellular compartment is within the bloodstream ECF (blood,
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electrolytes,O2, glucose, etc)
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● intracellular compartment is within each cell ICF (K+)
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● the interstitial compartment is in the tissue between the cells and bloodstream , p
ISF (Na+)
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Osmotic pressure
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● pressure exerted by the solutes in solution
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● A solution with a greater number of particles has a higher osmotic pressure
● High osmotic pressure in the bloodstream favors fluid movement from the ICF o
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and ISF into the bloodstream.
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● Conversely, when the osmotic pressure is reduced, fluid moves out of the
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bloodstream and into interstitial and intracellular spaces
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Oncotic pressure, also called colloidal osmotic pressure
● is a type of osmotic pressure exerted specifically by albumin in the
bloodstream. Oncotic pressure and osmotic pressure exert the same type of
pulling force from ICF to ECF.
● Albumin attracts water and helps keep it inside the blood vessel.
● Albumin is the main colloidal protein in the bloodstream and is essential for
maintaining the oncotic pressure in the vascular system.
● Total albumin in the bloodstream is indicative of the body’s protein nutritional
status.
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● The normal serum albumin level is 3.1 to 4.3 g/dL.
● Changes in this albumin level alter oncotic pressure.
● For example, in hypoalbuminemia (lack of sufficient albumin in the
bloodstream), oncotic pressure is reduced.
● Hypoalbuminemia causes an imbalance in the oncotic pressure versus
hydrostatic pressure forces.
● With reduced albumin, the oncotic pressure is low and the force exerted by
hydrostatic pressure overwhelms the oncotic pressure.
● This causes water in the bloodstream to push outward from the capillary pores
toward the ISF and ICF
Hydrostatic pressure
● the pushing force exerted by water in the bloodstream.
● The heart’s pulsatile pumping action is the source of hydrostatic pressure,
which exerts an outward force that pushes water through the capillary
membrane pores into the ISF and ICF compartments
Dehydration
● Lack of body water in intracellular and extracellular fluid.
● Causes: Bleeding, Breastfeeding, Burns, Fever, Gastrointestinal (GI) fluid loss,
Hypotension, Nephrolithiasis, Polyuria, Surgical drains, Sweating, Tachypnea
● Signs & Symptoms/manifestation: Thirst, Dry mucous membranes, Weakness,
Low urine output, Dark urine, Poor skin turgor, Dry mucous membranes,
Hypotension, In infants depressed fontanelle.
● Diagnosis/Labs: High blood urea nitrogen (BUN), Oliguria, Hypernatremia
caused by low water in blood.
● Treatment: Oral fluids, IV 0.45% NaCl
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excess secretion of ADH
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● Causes excess water reabsorption, which results in hypervolemia and
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dilutional hyponatremia
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Aldosterone
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● Its secretion increases sodium and water reabsorption into the bloodstream and
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excretes potassium into the urine.
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Explain how the RAAS affects fluid balance
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● The RAAS is a compensatory mechanism of the body that will raise blood
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volume and stimulate arterial vasoconstriction, leading to an increase in blood
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● Hypovolemia, hypotension, or low perfusion of the kidney stimulates the
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RAAS
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● RAAS involves ADH & Aldosterone
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Describe the relationship between protein, ADH,
aldosterone and fluid balance.
2 Compare and contrast isotonic and hyper/hypotonic IV solutions, including the
effect on fluid shift
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Isotonic solution:
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● This has the same tonicity as blood; when infused as an IV solution, it does not r y
cause fluid shifts or alter body cell size
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● It has a concentration of particles and fluid that is similar to blood and body
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fluids.
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● A standard isotonic IV solution is 0.9% NaCl solution, also called normal
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saline.
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● It is used frequently as a bloodstream volume expander.
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● Often an isotonic solution is used to keep an open connection to the IV route
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for medication administration or a blood transfusion.
Hypotonic solution:
● This has fewer particles and more water than blood and body fluids.
● When a hypotonic solution is infused, water is added to the bloodstream and
causes a fluid shift from ECF to ICF to deliver water to the body, as in
dehydration treatment.
● A standard hypotonic solution is 0.45% NaCl and is also referred to as half
normal saline.
Hypertonic solution:
● This contains more particles and less water than blood and body fluids.
● When a hypertonic solution is infused into the bloodstream, solutes are added
to the bloodstream and cause fluids to shift from ICF to ECF, causing body
cells to shrink.
● A commonly used hypertonic IV solution is mannitol. It can be used to
diminish cell swelling, particularly in cerebral edema.
● Another hypertonic solution that is used less often is 3.0% NaCl.
2 Differentiate and evaluate common electrolyte imbalances including, and
clinical manifestations.
Magnesium Imbalance
● Magnesium (Mg++) is largely stored in bone and, like calcium, is protein
bound within the bloodstream.
● About 60% of the body’s magnesium is found in the bones.
● It is required for many cellular metabolic processes, such as functioning of
nerve conduction, replication and transcription of DNA, translation of RNA,
intracellular enzyme reactions, and all processes that require ATP.
● The cardiovascular system requires magnesium for vasodilation and normal
functioning.
● Magnesium also affects sodium and potassium levels both inside and outside
the cell membrane.
● In addition, magnesium can compete with and exert effects on calciummediated processes because of its effect on the parathyroid gland.
Hypomagnesemia
● Serum magnesium level less than 1.5 mg/dL.
● Causes: Can be caused by malnutrition/malabsorption, excessive loss of GI
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fluids, alcoholism/cirrhosis, diuretic therapy,
hyperparathyroidism, hyperaldosteronism, diabetic ketoacidosis, thyroid
malfunction, pancreatitis, NG suction, fistulas, renal diseases, proton pump
inhibitors (PPIs), and certain antibiotic, immunosuppressive, and
chemotherapeutic agents.
● Signs & Symptoms/manifestation: Muscle cramps, Personality change,
Uncontrollable movements, Positive Chvostek’s and Trousseau’s sign,
Nystagmus, Positive Babinski’s sign, Hypertension.
● Diagnosis/labs: Serum magnesium level less than 1.5 mg/dL, ECG:
tachycardia, arrhythmias.
● Treatment: Replacement Mg++ therapy
Hypermagnesemia
● Serum magnesium level greater than 2.5 mg/dL.
● Causes: Can be caused by excessive use of Mg-containing antacids and
laxatives, untreated diabetic ketoacidosis, excessive Mg infusion as in
treatment of eclampsia of pregnancy, renal failure
● Signs/symptoms/manifestations: Lethargy, Confusion, Weakness, Decreased
reflexes (hyporeflexia), Hypotension, Weak muscles.
● Diagnosis/labs: Serum magnesium level greater than 2.5 mg/dL., ECG:
Arrhythmias, Cardiac arrest possible.
● Treatment: IV calcium or dialysis.
Hypernatremia
● Serum sodium greater than 145 mEq/L.
● Causes: Commonly caused by loss of water, fluid restriction, hypertonic IV
fluids, diaphoresis with more water loss than sodium, tube feedings without
adequate free water, Cushing’s syndrome, diabetes insipidus.
● Signs/symptoms/manifestations: Decreased salivation. Thirst, Headache,
Agitation, Seizures, Decreased skin turgor if low water volume, Decreased
reflexes, Tachycardia, Weak, thready pulse, Hypertension or hypotension
depending on water volume.
● Diagnosis/labs: Na+ >145
● Treatment: If caused by inadequate water: Replace with IV fluid 0.45% NaCl,
If excess water is present, diuretic therapy may be necessary
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Distinguish between the four types of acid/base disturbances
Respiratory Acidosis
● Lungs are not ventilating; retaining too much CO2, creating too much H+.
Commonly due to COPD, severe asthma, or any cause of reduced ventilation.
Respiratory Alkalosis
● Lungs are hyperventilating; losing too much CO2 creates too little H+ in the
blood. Commonly due to hyperventilation secondary to anxiety or shallow
respirations in asthma
Metabolic Acidosis
● Excessive acid in the bloodstream (e.g., ketoacids or lactic
acid) or excessive loss of HCO3− (e.g., GI tract loss).
Commonly due to DKA, lactic acidosis, drug toxicity, or GI loss
of excessive HCO3− as in diarrheal illness.
Metabolic Alkalosis
● Excessive base in the bloodstream (such as toxic ingestion) or lack of
sufficient acid in the bloodstream caused by high loss of H+ (such as loss of
HCl with excessive vomiting)
Describe respiratory and renal compensations in relation to acid/base
disturbance.
● In metabolic acidosis, the high H+ ion levels stimulate chemoreceptors, which
in turn stimulate the respiratory center to increase the respiratory rate.
● Deep, rapid breathing due to metabolic acidosis is referred to as Kussmaul’s
breathing. Kussmaul’s breathing is particularly common in DKA.
● In addition, to compensate for metabolic acidosis, the kidneys,
if healthy, reabsorb HCO3− and excrete H+.
● In compensated metabolic acidosis, pH is normal or rising toward normal.h
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Uncompensated metabolic acidosis
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● An excess of acid or a loss of HCO3− in
the blood causes metabolic acidosis. In uncompensated
metabolic acidosis, HCO3− will be lower than 22 mEq/L and
the pH will be lower than 7.35
Uncompensated metabolic alkalosis
● Metabolic alkalosis is caused by excessive loss of acids, shift of H+ ions into
the intracellular space, or increase in bicarbonate in the bloodstream. In
uncompensated forms, the blood pH will be greater than 7.45 and the
bicarbonate concentration greater than 26 mEq/L.
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Module 2 Total Questions
3 Describe the pathophysiology of arterial disorders including epithelial damage.
a
Pathophysiology of Arterial Disorders
● CVD begins in the body’s arteries.
● Arteriosclerosis and atherosclerosis are the fundamental changes in the body
that initiate widespread CVD.
● Many agents can injure the endothelial lining of arteries, and this damage is
the inciting event for arteriosclerosis, which may lead to atherosclerosis.
● Many conditions, such as HTN, hyperlipidemia, and diabetes mellitus, may
predispose patients to arteriosclerotic and atherosclerotic damage.
Atherosclerosis
● Widespread arterial wall plaque composed of lipid, platelets, fibroblasts, and
WBCs, which protrudes into arterial lumen.
● The arteriosclerotic plaque hardens over time and calcifies.
● It then can rupture into pieces that travel as emboli and can lodge in smallerdiameter arteries to cause ischemia in tissue.
● Symptom; none
● Clinical manifestations: Retinal blood vessel changes in some affected persons
—copper-silver wiring, cotton wool spots. Carotid, aortic, or renal artery bruits
are found in some affected persons.
● Diagnosis/lab: Elevated hs-CRP, Total cholesterol greater than 200 mg/dL,
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LDL greater than 130 mg/dL in most affected
persons, HDL less than 40 mg/dL in most affected persons, Elevated blood
homocysteine level.
● Treatment: Diet low in fat, low in salt to diminish formation of cholesterol and
decrease BP, Antilipidemic medications, Folic acid to lower homocysteine,
Anticoagulants such as aspirin. Keep BP low & Exercise daily.
3 Define and identify risk factors, pathophysiology, clinical presentation,
a diagnosis, and treatment of hypertension.
Hypertension & its Management
● Elevated BP, which causes endothelial injury and increases susceptibility to
atherosclerosis.
● HTN directly targets the small arteries of the retina, glomerulus, and brain, as
well as peripheral arteries throughout the body.
● High pressure in cerebral arteries can cause strokes.
● It targets the heart by causing high aortic resistance against the left ventricle,
which causes LVH. LVH is a risk factor for MI.
● Risk Factors: Age, African American ethnicity, Family history,
Obesity (body mass index [BMI] >30), Diabetes mellitus
(fasting blood glucose ≥126 mg/dL on multiple office visits or
A1c ≥6.5%), Sedentary behavior, tobacco use, Excess sodium
in diet (<1,500 mg sodium = low-salt diet), Insufficient
potassium in diet (approx. 4,700 mg K+ needed/day,
insufficient vitamin D in diet (approx. 400 to 800 units vitamin
D needed/day, Excess alcohol (>1 alcohol drink/day women or
>2 alcohol drinks/day men), Stress
● Symptoms: None
● Manifestations: Headache in some affected persons, BP greater
than 130/80 mm Hg, HTN in adults older than age 60 years is
≥150/90, S4 heart sound, Retinal blood vessel changes in
some affected persons—arteriovenous nicking, flame
hemorrhages caused by retinal artery rupture.
● Diagnosis/labs: Increased renin levels in some affected persons, which in turn
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will cause constant cycling of the RAAS, ECG shows
LVH in some affected persons, urinalysis, complete blood count (CBC), blood
glucose, serum potassium, serum creatinine, and serum calcium.
● Treatment: Low-salt, low-fat diet, Daily exercise will lower BP over the long
term, Antihypertensive agents such as beta blockers decrease HR and inhibit
vasoconstriction, Diuretics decrease the water content of blood, Calcium
antagonists inhibit vasoconstriction, ACE inhibitors, renin inhibitors, or ARBs
are used.
Primary HTN
● Cause is unknown
● Primary HTN commonly has no signs or symptoms.
● The disease may be quite advanced before it is detected or diagnosed and may
have already caused target organ damage.
● Rarely, persons with HTN complain of headache, nosebleeds, blurred vision,
or palpitations.
Secondary HTN
● Secondary HTN is a side effect of another systemic disorder such as Cushing’s
disease, cardiovascular, endocrine, neurogenics, drugs and toxins,
hypercalcemia, sleeping apnea, pregnancy induced, pheochromocytoma,
kidney disease, or hyperaldosteronism,
● Treating the systemic disorder will lower BP in secondary HTN.
Hypertension Stages
● Normal: Less than 120/80 mm Hg
● Elevated: Systolic between 120 and 129 and diastolic less than 80
● Stage 1 HTN: Systolic between 130 and 139 or diastolic between 80 and 89
● Stage 2 HTN: Systolic at least 140 or diastolic at least 90 mm Hg
● Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients
needing prompt changes in medication if there are no other indications of
problems, or immediate hospitalization if there are signs of organ damage
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● According to the JNC-8 BP guidelines, the BP goal
for individuals older than age 60 years is <150/90.
HTN Target organs:
● The target organs of HTN include the retina, kidney, heart, brain, and
peripheral arteries of the extremities.
3 Describe the concept of cardiac output and key symptoms found with
a dysfunction.
Intermittent claudication
● a cramping leg pain that occurs with exertion and is usually relieved by rest.
● Its Peripheral arterial disease (PAD) of lower extremities.
● Reduced arterial blood flow (reduced oxygen to organs) leads to tissue
ischemia, which presents as intermittent claudication
● Intermittent claudication is similar to angina, an episodic pain that occurs
because of ischemia. However, the pain in PAD is caused by episodes of
ischemia in the leg rather than in the chest.
● The pain or numbness associated with PAD in the lower extremities is
intermittent, associated with exertion, and relieved by rest
● Persons with PAD can often predict how much exercise of the leg will trigger
pain.
Myocardial Infarction(MI)
● Myocardial Infarction is an acute coronary syndrome (ACS) that occurs when
myocardial ischemia is prolonged and death of tissue (infarction) occurs.
● Can be a STEMI if it is a transmural MI or an NSTEMI if it is a
subendocardial MI.
● Causes: MI occurs because of a disparity between the oxygen needs of the
myocardium and the oxygen available to it. The influences on the heart that
increase myocardial oxygen demand include the following: Increased heart
rate, Increased muscle mass & Increased systemic BP
● The most common cause of MI is coronary artery atherosclerosis. MI usually
develops due to coronary artery obstruction, which causes ischemia
● Signs & symptoms: Diaphoresis, Dyspnea, xtreme anxiety, Levine’s sign (fist
to chest), Pallor, Retrosternal crushing chest pain that radiates to shoulder,
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arm, jaw, or back, Weak pulses, Commonly occurs
with exertion, Patient may lose consciousness.
● Clinical manifestation: Vital signs show increased respiratory rate, slowed
heart rate, and low blood pressure, Levine’s sign, Decreased level of
consciousness (LOC) possible, Pallor, Diaphoresis, Respiratory distress,
Diminished peripheral pulses.
● Diagnosis & labs: Elevated cTnI and cTn T, Elevated CPK-MB fraction, ECG
shows ST elevation or ST depression, as well as inverted T waves, Cardiac
catheterization with angiography shows coronary artery obstruction,
Radionuclide angiogram, Cardiac CT scan, Calcium CT scan,
Echocardiogram.
● Treatment: IV nitrates, Morphine, Aspirin, Oxygen, Heparin or another
anticoagulant, Antiplatelet therapy. Beta blockers if stable. Ca++ antagonists,
Thrombolytic agent to dissolve the clot for some eligible persons, PCI which
includes PTCA with stent placement or CABG, Cardiac rehabilitation.
3 Describe the presentation of patients with conditions impacting cardiac
a perfusion supply and demand
Differentiate between Peripheral Artery Disease and Coronary Artery Disease
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Differentiate between acute coronary syndrome and stable coronary syndrome
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Unstable Angina Pectoris
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● Chest pain caused by myocardial ischemia is part of ACS.
s d
● There is inadequate coronary artery blood flow to the heart muscle.
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● Ischemia develops, which causes myocardial cell hypoxia, triggering anaerobic a
metabolism.
b
● Anaerobic metabolism yields 2 ATP and lactic acid. Lactic acid is noxious to
l
muscle cells, and 2 ATP is inadequate energy for the needs of the myocardial
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tissue.
● Signs & Symptoms: An episode of retrosternal crushing, squeezing chest pain a
with radiation to the left arm, jaw, epigastric area, or back with a duration of 1 n
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to 15 minutes.
● Physical assessment: Vital signs show increased respiratory rate, slowed heart i
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rate, and low BP,
● Patient often brings fist to chest (Levine’s sign), indicating the crushing feeling a
on the chest.
● Pallor, dyspnea, and diaphoresis are apparent.
● Pulses are weak.
● Chest pain most commonly occurs with exertion and is accompanied by
dyspnea, diaphoresis, and pallor.
● Diagnosis/labs:
● ECG shows ST depression or ST elevation or T-wave inversions.
● Cardiac catheterization with coronary angiogram will show areas of coronary
artery occlusion caused by arteriosclerosis.
● Cardiac CT scan.
● Total cholesterol, HDL, LDL, hs-CRP, homocysteine, fibrinogen, lipoprotein
(a). Calcium CT scan.
● Graded exercise stress test.
● ECG.
● Cardiac enzymes are used to rule out MI.
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● The cTn is used to rule out MI.
● Treatment: Low-fat diet, Daily exercise, Oxygen, Nitrates (NTG sublingual or
nasal spray), One aspirin/day, Anticoagulants, Dual antiplatelet therapy, Ca++
antagonists, Beta-adrenergic blockers, Ranolazine, Possible PCI procedures
include PCTA with stent placement in the affected coronary artery and CABG
Stable angina:
● Episodes of myocardial ischemia that are predictable and have the same pain
pattern. Patient self-medicates with NTG.
3 Differentiate between Peripheral Artery Disease and Coronary Artery Disease
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3 Identify how select dysrhythmias affect perfusion
a
Ventricular Fibrillation
● Onset of VF is rapidly followed by loss of consciousness and, if untreated,
death.
● Most patients whose VF is treated successfully within the first 48 hours of the
onset of acute MI have a good long-term prognosis with a low rate of
recurrence or cardiac death.
● Cardiopulmonary resuscitation and defibrillation are the treatments for VF.
● Patients can also have cardioverters/defibrillators surgically implanted, which
promptly recognize and terminate life-threatening ventricular arrhythmias.
● VT predisposes to VF, which is considered cardiac arrest and requires
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defibrillation.
Atrial Fibrillation
● When ventricular rate increases to tachycardic levels, AF can cause
decompensation of the ventricle in the form of myocardial ischemia or heart
failure.
● AF can also increase the risk of embolic stroke.
● The non contracting, quivering atria in AF allow for stasis of blood and
subsequent clot formation.
● A clot can form in the left atrium, travel into the left ventricle, then move into
the aorta and up the subclavian artery to the internal carotid and middle
cerebral artery of the brain.
● The rate of ischemic stroke in the presence of AF is two to seven times the rate
of stroke in patients without AF.
ALERT! AF can cause thrombus formation and embolism to the brain. It is a frequent
cause of ischemic stroke
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Endocarditis
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● A noncontagious infection of the cardiac endothelium that most commonly
c y
affects the heart valves.
a z
● It is mainly caused by the bacteria S. aureus.
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● Damaged valves are prone to infection and provoke aggregation of platelets to d
form a thrombus.
i
● Intracardiac devices such as prosthetic valves, pacemakers, cardiac
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defibrillators, or intravascular lines can incite the same conditions.
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● IV drug use is also a common cause of endocarditis.
s
● Signs & Symptoms
/
● Nonspecific symptoms, including fever, chills, anorexia, weight loss, myalgias, M
and arthralgias.
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● Fever may be blunted or absent in elderly or severely debilitated persons.
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● Assessment:
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● Fever may be present.
a
● New heart murmur or changed pre-existent heart murmur.
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a Describe inflammatory processes and complications that can affect the heart.
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● Septic emboli form and can be manifested as
infarction in organs such as the brain, which causes signs of stroke, such as
neurological deficits.
● Clinical signs caused by septic emboli include petechiae, splinter hemorrhages,
Janeway lesions, Osler’s nodes, and Roth spots.
● Diagnosis/labs:
● At least three blood cultures are performed at three different times of the day.
See Duke Major and Minor criteria.
● Transthoracic echocardiogram or transesophageal echocardiogram is used to
visualize heart valves.
● Laboratory tests are necessary, including CBC, electrolytes, serum creatinine,
blood urea nitrogen, blood glucose, ESR, CRP, coagulation panel, and
urinalysis.
● Leukocytosis is observed in acute endocarditis.
● ESR, although not specific, is elevated in more than 90% of cases.
● Glomerulonephritis, which elevates serum creatinine and causes proteinuria
and microscopic hematuria, is present in approximately 50% of cases.
● Treatment:
● Treatment consists mainly of parenteral antibiotics for 6 weeks or a more
prolonged course.
● Surgical removal of prosthetic valve, pacemaker, cardiac defibrillator, or
intravascular line necessary.
● Patient needs antibiotics prophylactically any time there is an invasive
procedure that can cause bacteremia
Myocarditis
● Myocarditis is inflammation of the muscle layer of the heart’s wall. It can
occur by direct invasion of a pathogen or a toxin that is liberated by a
pathogen.
● It can also occur as an immunological mechanism initiated by an infectious
agent or chest radiation. Myocarditis is also the major cause of cardiac
transplant rejection
● Signs & symptoms
● Chest pain, chills, fever, and dyspnea.
● Patients may report a flu like syndrome of fever, myalgia, arthralgia,
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pharyngitis, tonsillitis, and upper respiratory
●
●
●
●
●
●
●
●
●
●
●
●
●
●
●
●
●
●
infection.
Symptoms of palpitations or syncope can occur.
Sudden cardiac death can develop because of ventricular arrhythmias or AV
block.
Adults can develop heart failure signs and symptoms, including ankle edema,
ascites, and dyspnea with exertion
Patients may be asymptomatic.
Assessment:
On physical examination, cardiac auscultation may reveal an S3 gallop rhythm
indicative of heart failure.
A pericardial friction rub and other signs such as lymphadenopathy and rash
can be present, depending on etiology.
Diagnosis/labs
CBC, which demonstrates leukocytosis; elevated ESR and CRP, which
indicate inflammation; and cTn and cardiac enzymes, which are elevated with
myocardial injury.
Various viral antibody titers are drawn. Presence of a viral genome within a
biopsy of endomyocardium is confirmatory.
Echocardiograms can reveal heart function and degree of heart failure, if
present.
Antimyosin scintigraphy can identify myocardial inflammation.
Cardiac MRI.
Gadolinium MRI.
Treatment:
Decrease myocardial workload, including activity restrictions.
Treatment measures for heart failure such as diuretics, nitrates, ACE inhibitors,
and inotropic agents are often necessary. Antiarrhythmic agents.
Pacemaker insertion may be needed. In severe cases of heart failure, cardiac
transplantation is considered.
3 Understand pathophysiology, etiology, and clinical manifestations of venous
a disorders.
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Deep Vein Thromboembolism
● Inflammation and thrombus formation in the vein.
● Thrombus becomes an embolism that can travel up into the IVC and into the
right side of the heart and pulmonary artery to cause a pulmonary embolism.
● Signs & Symptoms:
● Tenderness, warmth, redness, swelling, and ropiness over a vein in the leg.
● Assessment:
● May have positive Homan’s sign (only in 10% of cases).
● Unilateral leg edema, tenderness, ropiness, warmth, and erythema over a vein.
● Diagnosis/labs:
● Wells criteria can be used to assess probability of PE.
● Multidetector CT pulmonary angiography is the major diagnostic test for PE.
● Duplex ultrasonography demonstrates reduced venous flow.
● Radiopaque venography and impedance plethysmography identify the location
of the clot.
● D-dimer blood test is positive (high amount of fibrinogen in blood).
● Follow clotting/bleeding time with either PT/aPTT or INR.
● Treatment:
● Antiplatelet drugs, low-molecular-weight heparin, or unfractionated heparin
used, followed by warfarin.
● Monitor anticoagulant effects and levels.
● Monitor for signs of embolism—pulmonary, myocardial, or cerebral.
● Advise bedrest initially.
● Educate patients on risk reduction and wearing of support hose.
● Teach patients not to stand for prolonged periods, to avoid constricting
garments, to elevate legs periodically during the day, and to ambulate or do leg
exercises that will promote blood flow and reduce venous stasis.
Chronic Venous Insufficiency
● Veins are unable to keep blood moving in unidirectional flow up to the heart.
● Incompetent veins allow venous stasis and risk for thrombus formation.
● Signs & Symptoms:
● Heaviness of the legs.
● Sensation of fullness of the legs.
● Fatigue
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● Assessment:
● Edema and dusky, tan discoloration (hyperpigmentation) with distended veins.
●
●
●
●
●
Diagnosis/labs:
Doppler ultrasonography demonstrates reduced blood flow in veins.
Photoplethysmography and venography are used to identify location of clot.
Treatment:
Graduated compression over the lower legs via support hosiery or pneumatic
compression device.
● Low-molecular-weight heparin.
● Educate patients on risk reduction and wearing of support hose.
● Teach patients not to stand for prolonged periods, to avoid constricting
garments, to elevate legs periodically during the day, and to ambulate or
perform leg exercises that will promote blood flow and reduce venous stasis.
Cardiac 3a Total Questions
1
4
3 Differentiate the pathophysiologic mechanisms of left and right heart failure.
b
Left Ventricle Failure LVF (backward effects)
● Weak left ventricle causes a backup of hydrostatic pressure in the left atrium,
pulmonary veins, and pulmonary capillaries.
● Hydrostatic pressure increases in lungs.
● Fluid builds in pulmonary interstitium, often to the point of pulmonary edema
● Signs & Symptoms:
● Cough (cough with pink, frothy sputum equals pulmonary edema).
● Dyspnea.
● Orthopnea.
● PND
● Assessment:
● Pulmonary bibasilar crackles (widespread pulmonary coarse, loud crackles
equals pulmonary edema).
● Cyanosis.
● S3 or S4 audible through a stethoscope
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●
●
●
●
● Diagnosis/labs:
.Pulmonary congestion on chest x-ray (Kerley A and B lines) caused by
pulmonary interstitial fluid.
Cardiomegaly on chest x-ray caused by enlarged, dilated ventricles.
Elevated BNP caused by elevated water volume in the bloodstream.
Elevated PCWP caused by backup of hydrostatic pressure
● Treatment:
● Fowler’s position to ease breathing.
● oxygen for hypoxia caused by pulmonary edema.
● Low-sodium diet (<1,500 mg/day) to decrease water retention.
● Fluid restriction.
● Daily weight measurement to monitor water weight gain.
● Diuretics.
● Aldosterone antagonists.
● Beta-1-adrenergic blockers.
● Ivabradine.
● ACE inhibitors.
● Angiotensin II receptor blockers.
● Neprilysin inhibitor/ARD combination drug.
● Nitrates.
● Isosorbide dinitrate/hydralazine.
● Digitalis or another inotropic drug.
Left Ventricle Forward LVF (forward effects)
● Weak left ventricle forward pumping of blood into the aorta, peripheral, and
cerebral arteries. Kidneys sense low circulation caused by the weak forward
pump of the heart.
● Kidneys release renin. RAAS is triggered. Blood volume increases, blood
pressure increases.
● Peripheral vasoconstriction occurs.
● The SNS is triggered by baroreceptors in the arterial walls caused by decreased
blood pressure. SNS causes increased HR and vasoconstriction of peripheral
arteries.
● These compensatory mechanisms worsen LVF.
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● Signs & Symptoms:
● Cool, pale extremities.
● Confusion, disorientation.
● Edema.
● Nocturia.
● Assessment:
● Decreased peripheral pulses.
● Cool, pale extremities.
● Confusion, disorientation.
● S3 or S4 audible through a stethoscope.
● Diagnosis/labs:
● Decreased LVEF.
● HR may be high.
● Pulses are weak.
● Treatment:
● Fowler’s position.
● Oxygen.
● Diuretics.
● Low-sodium diet (<1,500 mg/day).
● Fluid restriction.
● Daily weight.
● ACE inhibitors or ARBs.
● Nitrates.
● Inotropic agents.
● Beta-adrenergic blockers.
Right Ventricle Failure RVF (backward effects)
● Weak right ventricle causes backup of hydrostatic pressure into the right
atrium, superior vena cava, and jugular veins, then into inferior vena cava,
causing venous congestion in gastrointestinal, peritoneal, hepatic, and splenic
veins.
● Signs & Symptoms:
● Jugular neck vein distension.
● Swelling (rings, shoes may feel tight).
● Anorexia, indigestion.
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● Abdominal swelling.
●
●
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●
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●
●
●
●
●
●
●
●
●
●
●
●
●
Assessment:
JVD.
Weight gain.
Ascites.
Hepatojugular reflux.
Hepatomegaly.
Splenomegaly.
Ankle or sacral edema.
Ascites; shifting dullness on abdominal exam.
S3 or S4.
Diagnosis/lab
Elevated jugular venous pressure.
Elevated central venous pressure.
Dilutional hyponatremia.
Hypokalemia.
Treatment:
Daily weight measurement.
Low-sodium diet.
Fluid restriction.
Inotropic agents.
● Diuretics.
● Nitrates.
● ACE inhibitors and ARBs.
3 Compare/contrast and provide rationales for the clinical manifestations of left
b and right sided heart failure.
Explain pulmonary dysfunction in heart failure.
Chronic Pulmonary Disease
● Chronic pulmonary disease is the leading cause of RVF.
● When pulmonary disease is the etiology of RVF, the condition is referred to as
cor pulmonale.
● In cor pulmonale, the initiating event of heart failure is a lung disease that
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causes chronic hypoxia.
● The heart starts out in good health until a lung disease exerts detrimental
effects on the right ventricle.
Pulmonary Embolism
● A pulmonary embolism can cause acute RVF. An embolus lodged in the
pulmonary artery suddenly raises pressure within the pulmonary artery.
● This acute rise in pulmonary artery pressure places an overwhelming amount
of resistance against the right ventricle.
● This can rapidly and severely weaken the right ventricular muscle, causing
acute RVF.
Sleep apnea
● Sleep apnea can cause hypoxia and increases the risk of rhythm disturbances.
● Chronic hypoxia can lead to pulmonary artery vasoconstriction, which leads to
pulmonary HTN.
● Pulmonary HTN increases the risk of RVF. Rhythm disturbances can weaken
the heart muscle contractility.
Pulmonary Edema.
● In LVF, as the forward ventricular pump is weakened, backward pressure
builds within the left atrium, resulting in high hydrostatic pressure in the
pulmonary veins.
● This high hydrostatic pressure is transmitted further backward into the
pulmonary capillary bed.
● At the pulmonary capillaries, high hydrostatic pressure causes fluid
extravasation into the interstitial spaces, leading to pulmonary edema.
● Edematous fluid builds within the pulmonary interstitial spaces and
intracellular fluid compartments and hinders oxygen diffusion from the alveoli
into the pulmonary capillaries (see Fig. 17-21).
● As the alveoli attempt to open and close against the accumulated fluid,
crackles can be heard through a stethoscope.
● The patient experiences dyspnea and cough as fluid accumulates between the
alveoli and capillary membranes.
Left Ventricle Failure mainly causes pulmonary symptomatology: dyspnea on
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exertion, cough, orthopnea, PND, cyanosis, and crackles on
auscultation.
LVF can cause pulmonary edema, which can be exhibited by pink, frothy sputum and
loud, coarse crackles.
3 Differentiate between two major types of valvular dysfunction.
b Aortic Stenosis
● Narrowed aortic valve opening; blood flow hindered from fully ejecting into
aorta from left ventricle; coronary arteries suffer lack of sufficient blood flow.
A
● Aortic blood flow is low and may diminish blood flow to cerebral arteries.
● Left ventricle can also fail because of the high resistance of the aortic opening.
● Aortic sclerosis, which is calcification of the valve due to aging, commonly
causes aortic stenosis.
● Signs & Symptoms:
● Chest pain (angina pectoris), fatigue, exertional dyspnea, exertional syncope
(fainting caused by lack of cerebral blood flow).
● Assessment:
● Systolic ejection murmur, second intercostal space, right sternal border,
opening snap, crescendo, low-pitched murmur after S1 before S2, split S2 (P2
A2)
● Diagnosis/labs:
● Echocardiogram showing narrowed aortic valve, left ventricular enlargement,
left ventricular hypertrophy caused by excess resistance of aorta against left
ventricle.
● BNP level for heart failure and measurement of LVEF necessary.
● Cardiac catheterization to measure hemodynamic pressures in heart chambers.
● Treatment:
● Treatment according to symptoms of angina or heart failure.
● Anticoagulation to prevent clot formation on valve deformity or left
ventricular failure.
● Bisphosphonates can decrease calcification of the aortic valve.
● Surgical valve replacement, percutaneous valvotomy, or transcatheter
replacement.
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Mitral Insufficiency
Incompetent mitral valve leaflets that cannot close; during systolic contraction
of left ventricle, blood regurgitates up into the left atrium.
Left ventricular ejection is decreased, and backup of blood into the left atrium,
pulmonary veins, and pulmonary capillaries occurs, which causes pulmonary
edema.
Aortic blood volume is diminished, as is blood volume entering coronary
arteries.
Myocardial ischemia results.
Mitral insufficiency is the most common heart valve disorder that occurs with
MI; papillary muscle rupture causes loosened valve leaflets.
Signs & Symptoms:
Dyspnea, cough, fatigue, orthopnea, PND.
Chest pain (angina).
Assessment
Holosystolic murmur, fifth intercostal space, left sternal border, radiating into
the axilla. S3 may be heard.
If severe, bibasilar pulmonary crackles are heard.
Pallor, diaphoresis, respiratory distress, fatigue, and exercise intolerance.
Left atrial enlargement can lead to atrial fibrillation; irregular pulse.
Diagnosis/labs:
Echocardiogram showing regurgitant mitral valve leaflets; may show left atrial
and ventricular enlargement. LVEF and cardiac output (CO) can be reduced
with subsequent heart failure.
ECG may show atrial fibrillation.
Treatment
Oxygen.
Anticoagulation to prevent clot formation in the left atrium.
Heart failure medications such as diuretics, ACE inhibitors, digitalis, and beta
blockers.
Coronary artery disease medications such as oxygen, morphine, and nitrates if
myocardial ischemia.
Surgical valve replacement; open heart, percutaneous route or transcatheter
valve replacement.
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● Mitral clip: noninvasive catheter insertion if surgery
is not an option.
3 Explain the pathophysiology of valvular dysfunction including the
b manifestations and consequences.
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Total Module 3b Questions:
4
*Heart failure is to be well-studied as it transcends all modules.
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