BIOL 205: Pathophysiology

Fall 2022
Midterm Study Guide

Introduction to Pathophysiology
 What is Pathophysiology?
o Patho:
 Study of disease
o Physiology:
 Study of bodily function
o Why is pathophysiology important?
 Helps to understand diseases, which can lead to better treatments
 Creates prevention methods to prevent a disease
 Gives us a foundational background
 Therapeutic & preventative
 Gives us an understanding of a disease
 Key Terms:
o Etiology:
 Cause of a disease
o Pathogenesis:
 Events that take place from coming in contact to the onset of the
symptoms
 Aka from infection phase to disease phase
o Morphology:
 Change of structures due to the impact of a disease
o Clinical Manifestations:
 How a disease prevents itself
o Diagnosis:
 Identifying what the causes of a disease is
o Clinical Course:
 The evolution of the disease process
 Ex  Acute, chronic, etc.
o Epidemiology:
 Study of a disease & how it spreads
o Risk Factors:
 Factors that make someone suspensible to a disease
 Modifiable factors:
 Can be controlled
 Teachable to aid with change
 Examples:
o Weight
o Relationship status
o Alcohol & drug use
 Non-modifiable factors:
 Can’t be controlled
  Examples:
o Pre-existing conditions
o Genetics
o Age
o Height
o Natural History:
 A study that follows a group of people overtime who have, or are at risk of
developing, a specific medical condition or disease
o Levels of Prevention:
 Primary Prevention:
 Preventing the disease from ever occurring
 Examples:
o Vaccines
o Immunizations
 Secondary Prevention:
 Detection in early stages
 Limit the effects that can’t be completely prevented
 Examples:
o Mammogram
o Colonoscopy
o Annual physical exam
o Blood pressure checks
 Tertiary Prevention:
 Treatment of disease
 Containing existing damage
 Disease has progressed beyond early stages
 Review of Cellular Function & Structure:
o Cells:
 Smallest functional unit of the
body
o Cell Membrane:
 Surrounds cell & separates it
from external environment
o Nucleus:
 Control center of cell
o Cytoplasm:
 Contains cell’s organelles,
ribosomes, lysosomes,
cytoskeleton, etc.
 Jelly-like fluid inside of cells
o Metabolism:
 Process of converting carbs,
fats, & proteins from foods into
energy for cellular functioning
 Review of Tissue Function & Structures:
o Organization of Body Cells:

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  Epithelial Tissue:
 Covers body surfaces
 Forms functional components of glandular structures
 Connective Tissue:
 Supports & connects body structures
 Muscle Tissue:
 Specifically designed for muscle contractility
 Types:
o Skeletal:
 Enables body to move & perform daily activities
 Plays an essential role in respiratory mechanics &
maintaining posture & balance
 Protects vital organs in body
o Smooth:
 Helps with contraction all over the body
 Helps with digestion & nutrient collection in the
stomach & intestines
 Helps rid the body of toxins & helps with
electrolyte balance in the urinary system
o Cardiac:
 Responsible for the contractility of the heart &
pumping action
 Nervous Tissue:
 Designed for communication purposes
 Cellular Responses:
o What will happen to a cell if it doesn’t adapt to the following?
 Stress:
 Cells can get injured without the ability to later structure &
function
 Injury:
 A new equilibrium with the cell’s environment can happen
 Aging:
 Cells become larger & are less able to divide & multiply

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 Cellular Adaptation:
o Atrophy:
 Cell degeneration
 Shrinking or shriveled
 What causes this?
 Lack of nutrients Smaller than
 Lack of oxygen before
 Not enough blood flow
 What is the good thing about this?
 More cells in other parts of Larger than
the body get more nutrients before
 “Use it or lose it” with relation to
cells
 If nutrients are needed
somewhere else in the body, More cells
the body will take from other than before
places within the body that
don’t need those nutrients
Weird
o Hypertrophy:
borders
 Cells are large
 Increased blood flow/swelling
Too many
 What causes this?
cells
 Exercising (Bigger muscle)
o Overusing the muscle
causes cells to
increase Irregular
 Why might this be a bad thing? borders
 Cells require more oxygen
now Too many
 Don’t want this to happen near the cells
heart
o Hyperplasia:
 Increased number of cells
 What causes this?
 Scarring due to injury
 Development of warts
 Normal during pregnancy
 Has more pattern to it
o Metaplasia:
 Pattern of cell growth
 Able to be reversed
 What causes this?
 Repetitive rubbing against an organ or body part
 May see this with:
 People with calluses on their hand
 People who smoke/drink

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  When is this bad?
 When alcohol is being overconsumed
o Dysplasia:
 Precursor to cancer
 Irregular borders & cell growth
 Intracellular Accumulations:
o Substances that may cause varying degrees of cell injury or be harmless
o Types:
 Normal body substances
 Ex  Lipids, proteins, pigments, etc.
 Abnormal endogenous substances
 Ex  Metabolic products, lipids, glycogen, etc.
 Abnormal exogenous substances
 Ex  Pigments
 Types of Cellular Injury:
o Physical:
 Trauma  Can cause damage to cells
 Heat/cold  Can kill due to vasocontraction/vasodilatation
 Electricity  Can shock cells
o Radiation:
 Ionizing  Can kill cells due to overdose
 Ultraviolet  Can burn skin, which kills cells
o Chemical:
 Can cause changes in DNA structure
 Ex  Drugs, lead, & mercury
o Biological:
 Can infect the host
 Ex  Bacteria, viruses, & parasites
o Nutritional:
 Lack of or too much of a certain nutrient
 Ex  Fats, vitamins, & minerals
 Mechanisms of Cellular Injury:
o Free Radicals:
 Extremely unstable & reactive
 Typically removed by antioxidants
 Antioxidants inhibit oxidation, which means a loss of electrons
o Hypoxia:
 Lack of oxygen
 Aerobic metabolism is stopped
 Aerobic metabolism produces energy with oxygen
 Anaerobic metabolism starts
 Anaerobic metabolism produces energy without oxygen
 Leads to cell death
o Impaired Calcium Homeostasis:
 Can cause abnormally high intracellular calcium levels
 Damages the cells

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 Outcomes of Cellular Injury:
o Reversible Cell Injury:
 Will return to
normal cell function
after the injury is
over
 Inflammation:
 Cells swell
& rupture
o Apoptosis:
 Also called
programmed cell
death (PCD) or cell
suicide
 Normal cell death
 Physiologic:
 Restructures tissues during development
 Replaces cells
 Immune function
o Cell Death:
 Why do we want this to happen?
 Cells can regenerate
Structure keeps
 Cells can replace old/infected cells changing
o Necrosis:
 The death of most or all of
the cells in an organ or tissue
due to disease, injury, or
failure of the blood supply Changed
 Unregulated death caused by Normal cell structure
injuries to cells
 No point of
return/nonreversible
 Liquefaction:
 Partial or complete Nucleus
dissolution of dead breaks apart
tissue & Cell breaks apart
transformation into a Old cell gets
liquid, viscous mass eaten by Apoptosis Diagram
 Coagulation: another cell
 Affected cells or tissues are converted into a dry, dull,
homogeneous eosinophilic mass without a nuclei
 Caseous necrosis:
 Causes tissues to become “cheese-like” in appearance
 Infarction:
 Obstruction of the blood supply to an organ or region of tissue,
typically by a thrombus or embolus

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  Causes local death of the tissue

Genetics, Genomics, & Disease

 Introduction:
o Genetics:
 Applies to a single gene
 Study of heredity
o Human Genome
 Made up of 25,000 genes
 Encoded by 3.2 billion base pairs (bp) of DNA
 All of the DNA of the human species
o Genomics:
 Applies to all genes in human genome
 Study of whole genomes (genes & function)
o Genes:
 Unit of heredity
 A linear polymer of DNA
 Can be formed by at least hundreds of bp
 Complex formation in sequences
 Chromatin (DNA & proteins) forms into chromosomes
 46 chromosomes (23 pairs) to each nucleated human cell
o DNA (deoxyribonucleic acid):
 Linear polymer of 4 different
monomeric units (nucleotides)
 2 chains with several thousand bps Breaks apart
 Foundation building blocks hydrogen bonds
 2 possible nucleotide pairings:
 A-T  Adenine & thymine
 C-G  Cytosine & guanine
 Arranged in groups of 3
codon/amino acids

DNA Strand

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 Protein Synthesis:

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 Transcription:
o Synthesis of an RNA molecule from a DNA template

Getting combined
together

 Translation:
o Process by which mRNA is decoded & a protein is produced

Will leave once it

places its code
down

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 Review of Cell Division:
o Mitosis:
 Division of body cells
 Connected to apoptosis
 Can occur multiple times
o Meiosis:
 Aka germ cells
 Division of sex cells
 Occurs once
 Creates sperm & eggs
 Gene Expression:
o Genes can “turn on” & “turn off”
o Induction:
 When a gene is enhanced or increased
o Repression:
 When a gene is suppressed or
decreased
o Transcription Factors:
 Proteins that are responsible for the
initiation of gene expression
 Genotype vs. Phenotype:
o Genotype:
 A person’s genetic material
 Determined by their location
 The smallest shift can have an
impact
o Phenotype:
 A person’s physical characteristics
 The way the genes are expressed
 What are some environmental factors that can influence phenotype:
 Physical location
 Weather such as sun exposure
 Diet
 If 2 people’s genotypes are different, will their phenotypes be different?
 Yes! You can have similar traits, but not the exact same.
 Key Genetic Terms:
o Expressivity:
 How a gene is expressed
o Penetrance:
 Ability of a gene to express its function
 Percent of individuals with a particular genotype
o Locus:
 The physical position of where the gene is on its chromosome
o Alleles:
 2 or more forms of a gene
 1 from each parent

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 o Monogenic/Mendelian:
 Single gene traits
o Polygenic:
 A trait controlled by 2 or more genes
o Pedigree:
 A diagram that shows occurrence of a genetic trait through generations
 The genetic history of a gene/trait/expression
 Inherited trait
o Homozygous:
 Identical alleles on a chromosome
o Heterozygous:
 2 or more different alleles on a chromosome
o Dominant:
 A trait that will be expressed no matter what
 Ex  Brown eyes
o Recessive:
 A trait that needs 2 copies in order to be shown Punnett Square
 Ex  Blue eyes
 Punnett Square:
o A chart that shows all the possible combinations of
alleles that can result from a genetic cross
 Gene Technology:
o Genetic Mapping:
 Assigning genets to specific chromosomes
in order to create a map of certain traits
o Haplotype Mapping:
 Clustering genes together to see how they
interact with each other
 Not used as often
 However, it can be used for figuring out disease transmission &
susceptibility
o Recombinant DNA Technology:
 Taking genes that aren’t naturally found with each other & putting them
together
 Helps produce different proteins that can be used to direct other cells
o Gene Therapy:
 Genetic engineering of genes
 Examples:
 Hybrid trees, fruits, & veggies
 Stem cell research
 Genes on Chromosomes:
o X or Y chromosomes are sex-linked
o Any other chromosome is autosomal
 Categories of Genetic Disorders:
o Chromosomal:
 Changes to structure of chromosome(s) or number of chromosomes

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 o Mendelian (monogenic):
 Autosomal dominant:
 A single mutant allele from a
parent is transmitted to
offspring regardless of sex
 Penetrance can impact actual
gene expression
 Occurrence rates:
o 50% chance of parent
transmitting disorder to each offspring Autosomal
o Unaffected offspring don’t transmit the disorder Dominant Pedigree
 Autosomal recessive:
Autosomal
 Manifests on when both Recessive
members of the gene pair are Pedigree
affected
 Both parents may be
unaffected, but are carriers of
affected gene
 Affects both sexes
 Occurrence rates:
o 25% in affected child
o 25% for carrier child
o 50% for unaffected/noncarrier child
 X-linked Anomalies:
 Pattern tends to be recessive, with heterozygous mother (Xx)
 Occurrence rates:
o Sons have 50% chance
of having disease
 Will not
transmit
disease to own
sons
o Daughters have 50%
chance of being
carriers
o Other chromosomal disorders:
 Down syndrome: X-Linked
 Occurs during replication (meiosis) of chromosome 21 Recessive Pedigree
o Individuals have an extra copy of chromosome 21
 Have older mothers since they are more at risk
 Have intellectual disabilities
 Turner Syndrome:
 Absence of all or part of a female’s X chromosomes
 Gene Mutations:
o Origin of variation & genetic diseases
o 2 types:

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 Large mutations:
 Deletion:
o A type of mutation
that involves the
loss of 1 or more
nucleotides from a
segment of DNA
 Insertion:
o A type of mutation
that involves the
addition of 1 or
more nucleotides
into a segment of
DNA
 Duplication:
o A type of mutation
in which 1 or more
copies of a DNA
segment are
produced
 Inversion:
o A special type of mutation in which a piece of
chromosomal DNA is flipped 180 degrees
 Expanding triplet:
o Occurs when the number of triplets present in a mutated
gene are greater than the number found in a normal gene
 Point mutations:
 Silent:
o When the change of a
single DNA nucleotide
within a protein-coding
portion of a gene
doesn’t affect the
sequence of amino
acids that make up the
gen’s protein
 Missense:
o A DNA change that
results in different
amino acids being
encoded at a particular
position in the
resulting protein
 Nonsense:
o A change in DNA that causes a protein to terminate or end
its translation earlier than expected

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  Teratogenic Agents:
o Agents that produce abnormalities during embryonic/fetal development
o Examples:
 Radiation:
 Can cause muscular deformities & birth defects
 Chemicals/Drugs:
 Can cause fetal alcohol syndrome
 What in our body helps protect against this?
o Blood brain barrier
o Placenta barrier
 Infectious Agents:
 Ex  Bacteria, viruses, etc
 Can affect development
 What in our body helps protect against this?
o Cerebral spinal fluid
o Placenta barrier
 Nutritional Deficiencies:
 Vitamin/iron deficiency
 What can new mothers do?
o Take prenatal vitamins & folic acid
 Screening Tools:
o Ultrasounds:
 Used to determine fetal structure, abnormalities, size, heart, etc.
o Amniocentesis:
 Looking at the amniotic fluid to determine any fetal abnormalities
o Umbilical Cord Sampling:
 Takes fetal blood directly from the umbilical cord
 Used to detect certain genetic disorders, blood conditions, & infections

Oncogenesis, Cancer-Related Manifestations, & Treatment  4 questions

 Neoplasia:
o Cancer/Neoplasia:
 A disorder of altered cell differentiation & growth
 Chronic disease
 If you had it once, you are at bigger risk of having it again
o Proliferation:
 To form new growth
 Cells that don’t stop growing can cause cancer
o Apoptosis:
 Cells commit suicide
 Cells perform this to keep the number of total cells constant
o Cell Differentiation:
 Cells develop to perform different functions around the body
 Cells often don’t measure normally to do the “job” the tissue is supposed
to do
o Benign Tumor:

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 An abnormal mass of cells that remains at its original site in the body
The good kind of cancer
Still proliferates
Well-differentiated
 Cells know what they are doing
 Can still cause damage
 Contains cells that look like normal tissue cells
 May perform the normal function of the tissue
o Ex  A “cell” that secretes hormones could eventually
oversecrete
 Grows very slowly
 Cells grow faster than they are dying
 Why are these tumors surrounded by a fibrous capsule?
 Prevents the tumor from entering the vasculature or lymph
 Doesn’t infiltrate, invade, or metastasize
 Can damage nearby organs by compressing them
o Malignant Tumor:
 Aka “neoplasms”
 A cancerous tumor that is invasive enough to impair the functions of one
or more organs
 The bad kind of cancer since it’s more harmful
 Less differentiated
 Still proliferates
 More at risk for traveling around the body
 Contains cells that don’t look like normal adult cells
 Doesn’t perform normal functions of the tissue
 In some situations, these “cells” can secrete signals, enzymes,
toxins, etc.
 Grows rapidly
 Lack capsules
 Sends “legs” into surrounding tissue
 Infiltrate, invade, & metastasize to distant sites
 Can compress &/or destroy the surrounding tissues
 Impairs functions of 1 or more organs
 Naming Tumors:
o Allows tumors to be described & identified
o Benign tumors  Tissue name + “-oma”
o Malignant tumors:
 Epithelial tissue  Tissue name + “-carcinoma”
 Glandular tissue  Tissue name + “-adenocarcinoma”
 Mesenchymal tissue  Tissue name + “-sarcoma”

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 Cell Cycle:
o Series of events that cells go through as Cell Cycle
they grow & divide
o Normally, the number of cells produced
equals the number of cells that die
o The total number of cells in the body
remains constant
o In cancer, growth factor increases &
doubling time decreases
o What happens if we don’t try & control
cancer cells?
 They could spread across the body
& will keep growing
 Tumor Growth:
o Cells divide only when they are told to do so by growth factors
 Growth factor:
 Cells divide only when they are told to do so
 Causes stable cells to enter the cell cycle in order to divide
o Multiplication
o Mechanical invasiveness
o Release of lytic enzymes
 Why do these enzymes get released by tumor cells?
 Tumors cells want to proliferate & destroy healthy tissues to get
more space for their new growth
o Diminished cell adhesion
o Increased cell motility
 Cell motility:
 Allows other cancer cells to shed into areas/tissues & metastasize
in other areas of the body
 Metastasis:
o Cells in primary tumor develop the ability to escape, travel, & survive in the
blood, exit the blood, & develop a secondary tumor
o Continuous extension
o Carcinomas tend to spread via lymphatics & sarcomas spread via vasculature
 Lymphatics:
 Transports interstitial fluid to the blood
 Vasculature:
 Network of blood vessels in a particular organ
o What are some way to see if a tumor has spread?
 Has same cell characteristics
 Will not be differentiated
 Other signs/symptoms that differentiate from original cancer cell
o Angiogenesis:
 Formation of new blood vessels
 Effects of Tumor Growth:
o Local Effects:

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  Compression of adjacent structures
 Hollow organs
 Blood vessels
o Could cause bleeding or hemorrhage
 Effusions:
o Escape of fluid into the body cavity
o Systemic Effects:
 Anemia
 Anorexia:
 Lack or loss of appetite for food
 Cachexia:
 Weakness & wasting of the body due to serve chronic illness
 Fatigue & sleep disturbances
 Ectopic hormones or factors secreted by tumor cells
 Ectopic hormones:
o Hormones produced by tumors derived from tissue that
isn’t typically associated with its production
 Paraneoplastic disorders:
o A group of rare disorders that are triggered by an abnormal
immune system response to a cancerous tumor known as a
“neoplasm”
 The Spread of Cancer:

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 What’s are the Causes of Cancer Spread?
o Oncogenesis:
 The process through which healthy cells become transformed into cancer
cells
o Disruption in balance between proto-oncogenes & anti-oncogenes
 Anti-oncogenes:
 Suppressor genes
o Familial predisposition
o Exposure to carcinogens
 Ex  Chemicals, radiation, & food
o Viruses
o Hormones
o Tumor antigens
 Associated Genes:
o Proto-oncogenes:
 Normal genes that can become cancer-causing agents if mutations occur
 Codes for normal cell division proteins:
 Growth factors
 Growth factor receptors
 Transcription factors
 Cell cycle proteins
 Apoptosis inhibitors
o Oncogenes:

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  Genes that can cause cancer by blocking the normal controls on cell
reproduction
 Proto-oncogenes can mutate to become these
 Insertion, deletions, & translocations are increased or activated
 Examples:
o Ras:
 Any of a family of genes that undergo mutation to
oncogenes & especially to some commonly linked
to human cancer
o Philadelphia chromosome:
 A piece of chromosome 9 & a piece of chromosome
22 breaks of & trade places
o HER-2/neu:
 A protein that helps breast cancer cells grow
quickly
o Tumor Suppressor Genes:
 Genes whose protein product inhibits cell division, which prevents
uncontrolled cell growth
 Doesn’t always work
 Everyone has them in their body
 Mutations get inhibited or decreased
 Diagnostics:
o Screenings:
 Looking for the cancer before symptoms appear
o Tumor Markers:
 Anything present in or produced by cancer cells or other cells of the body
in response to cancer or certain benign tumors
 Indicated from symptoms
 Ex  Bloodwork & prostate-specific antigen
o Cytologic Studies:
 The exam of a single cell type that is often found in fluid specimens
 Ex  Pap smear
o Tissue Biopsy:
 The removal of cells or tissues for examination by a pathologist
 Ex  Fine needle aspiration
o Immunohistochemistry:
 A laboratory method that uses antibodies to check for certain antigens
(markers) in a sample of tissue
 Ex  Estrogen receptor
o Microarray Technology:
 A laboratory tool used to analyze large numbers of genes or proteins at
one time
 Ex  Gene Chips
o Staging:
 Describes how for the cancer is/advanced
 Clinical, radiographic, surgical examination of extent & spread

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 Treatment & prognosis
TNM:
 T1-4  Tumor size
 N0-3  Lymph node involvement
 M0-1  Metastasis
 AJC:
 Stages 0-4  Size of primary lesion & presence of nodal spread &
metastasis
o Grading:
 Microscopic examination of differentiation & number of mitoses
 Stage 1 = Well-differentiated
 Stage 4 = Poorly differentiated
Cells are very
abnormal & are
poorly
differentiated

Cells differ slightly Cells are Cells are immature

from normal cells abnormal & & undifferentiated
that are well- moderately
differentiated differentiated Cells of origin is
difficult to determine
 Cancer Treatments:
o Primary Prevention:
 Limiting the things we know that can cause cancer
o Secondary Prevention:
 Early diagnosis
 Screenings
o Tertiary Prevention:
 Surgery:
 Removal depending on location
 Radiation:
 Shrinking of cells
 Can be used prior to any surgical prevention
 Chemotherapy:
 Use of drugs
 Stops replication of cells
 Can be used prior to any surgical prevention
 Hormone therapy:

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  Treatment of cancer with natural hormones or with chemicals that
produce hormone-like effects
o Biologic response modifiers (BRMs):
 Modifiers that alter or augments naturally occurring processes within the
body
 Types:
 Cytokines:
o Chemical released by the immune system that
communicate with the brain
 Monocolonal Antibodies (MoAbs):
o A specific antibody produced in vitro by a clone of B cells
hybridized with cancerous cells
 Tyrosine Kinase (TK) Inhibitors:
o A targeted therapy identifies & attacks specific types of
cancer cells while causing less damage to normal cells
 Vaccines:
o A biological preparation that provides active acquired
immunity to a particular infectious disease
 Gene Therapy:
o The insertion of working copies of a gene into the cells of a
person with a genetic disorder in an attempt to correct the
disorder

Hemostasis & Coagulopathies  2 questions

 Composition of Blood:
o Everything stems from the pluripotent stem cells
o Plasma:
 Liquid part of the blood
 Plasma proteins:
 Synthesized in the liver
 Circulates as inactive procoagulation factors
 Helps maintain osmotic pressure
 Can transport vitamins, lipids, hormones, & minerals
 Essential in the function of our immune response
o Blood cells:
 Erythrocytes:
 Red blood cells (RBCs)
 Biconcave
 Malleable to squeeze through small areas
 Reticulocytes:
o Slightly immature RBCs
 Hemoglobin:
o An oxygen-carrying proteins within each RBC

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 Thrombocytes:
 Aka platelets
 No nucleus
 Found in large numbers
throughout our blood
 Leukocytes:
 Responsible for immune
response,
identifying/destroying
cancer cells, & helping
with inflammatory
response & wound
healing
 Granulocytes:
o All have the
ability to engulf
microbes & other substances
o Types:
 Neutrophils:
 Responsible for maintaining normal host
defenses against invading bacteria, fungi,
cell debris, & etc
 Eosinophils:
 Important host defense roles in allergic
reactions, parasitic infections, & chronic
immune responses such as asthma
 Basophils:
 Involved in allergic & hypersensitivity
reactions
 Lymphocytes:
o Main functional cells of the immune system
o Makes antibodies to fight off infection
o B Lymphocytes:
 Formed in the bone marrow
 Differentiate to form antibody-producing plasma
cells
 Involved in humoral mediated immunity
o T Lymphocytes:
 Formed in the thymus
 Differentiate in the thymus to activate other cells in
the immune system
 Involved in cell-mediated immunity
 Macrophages:
o Found within the lymph nodes
o Help breaks down clots by engulfing larger & greater
quantities of foreign material

22
 o Become mobile in the blood during clotting
o Monocytes:
 What later turns in macrophages
 Able to migrate into tissues
 Platelets:
o Known as thrombocytes
o Always active
 Vital in preventing any sort of muscle spasm
o Can live 8-9 days in circulation
 Many are stored in the spleen
 Released when needed
o Megakaryocytes:
 Large fragments of this are in the
bone marrow
 Release packets of cytoplasm into
the circulating blood
o Thrombopoietin:
 A hormone that helps with the
production/formation of platelets
 Made in the liver, kidney, smooth
muscle, & bone marrow
 Hemostasis:
o What does it mean?
 Stoppage of bleeding
o Why is it important?
 Can prevent blood clots
o Has 5 main stages
o Components:
 Platelets
 Coagulation System:
 The system that forms blood
clot sin the body & facilitates
repairs to the vascular tree
 Endothelium
o Disorders:
 Hypercoagulability:
 An exaggerated form of
hemostasis that predisposes to
thrombosis & blood vessel
occlusion
 Increased ability of the blood to
coagulate
 Types:
o Conditions that created
increased platelet

23
 function cause what to happen?
 Increased platelet number
 Blood flow disturbances
 Endothelial damage
 Platelet aggregation
o Conditions that cause accelerated coagulation system
activity cause what to happen?
 Increased procoagulation factors
 Decreased anticoagulation factors
 Bleeding disorders:
 Thrombocytopenia:
o Decreased circulating platelet levels less than 150,000/uL2
o The greater the decrease in platelet count there is, the
greater the risk of bleeding is
o Etiology:
 Decreased platelet production
 Increased platelet destruction in spleen
 Platelets used up in forming clots
 Decreased platelet survival
o Types:
 Immune Thrombocytopenic Purpura:
 Results in platelet antibody formation &
excessive destruction of platelets
 Drug Induced Thrombocytopenia:
 When drugs induces an antigen-antibody
response & formation of immune complexes
that cause platelet destruction by
complement-mediated lysis
o Treatment:
 Based on platelet count & degree of bleeding
 Monitor platelet counts
 Treat underlying cause
 May transfuse platelets if:
 Severely thrombocytopenic  <10,000/mm3
 Symptomatic  bleeding
 Thrombocytopathia:
o Impaired platelet function
o Can result from inherited disorders of adhesion (von
Willebrane Disease) or acquired defects resulting from
drugs, disease, or surgery
 Coagulation Disorders:
o Can result from deficiencies or impaired function of 1 or
more of the clotting factors
o Von Willebrand Disease:
 A common hereditary bleeding disorder
 Deficiency of defect in vWF

24
 
Types:
 Type 1:
o Most common & most mild
o Reduced levels of vWF
 Type 2:
o Produces normal amounts of
abnormal vWF
o Defect in vWF
 Type 3:
o Most rare & most severe
o No measurable von Willebrand’s
factor or factor VIII
 Symptoms:
 Causes spontaneous bleeding from nose,
mouth, & gastrointestinal tract
 Excessive menstrual flow
 Prolonged bleeding
o Hemophilia A:
 An X-linked recessive disorder that primarily
affects males
 Causes bleeding in soft tissues, gastrointestinal
tract, & the hip, knee, elbow, & ankle joints
 Mediators of Hemostasis:
o Constricts blood vessels
o von Willebrand Factor:
 Aka vWF
 Helps platelets sticks together & adhere to the walls of blood vessels at the
site of the wound
o Degranulation of platelets:
 Adenosine diaphosphate (ADP) & Thromboxane A2 (TXA2) both increase
platelet aggregation
 Calcium plays a role in the tight regulation of coagulation cascade
 Cyclooxygenase Enzymes (COX):
o Arachidonic acid from membranes
 COX-1:
 Catalyzes production of thromboxane A2 (TXA2)
 Specifically for GI tract & kidneys
 Responsible for platelet functionality, cell-to-cell signaling, tissue
homeostasis, & cytoprotection
 COX-2:
 Catalyzes production of prostacyclin
 Responsible for mediating inflammation & growth factors
 Aspirin inhibit COX-1 & COX-2
 Why is aspirin used as a “blood thinner”?
o Can be used to prevent MIs
 Why is “blood thinner” not the best description?

25
 o Blood is not just clotting and not just getting thinner
 Coagulation Factors:
o Plasma Proteins:
 Circulates as inactive procoagulation factors
 Most are synthesized by the liver
 vonWillebrand factor made by megakaryocytes & endothelium
 Helps maintain the colloidal osmotic pressure at about 25 mmHg
o Calcium (factor 4)
 Coagulation Cascade:

 Hemostasis Stages:
o Step 1  Vessel Vasoconstriction:
 Injury to the blood vessel causes vascular
smooth muscle in the vessel wall to contract
 Causes reduced blood flow from the injury
 Both local nervous reflexes & local nervous Step 1
reflexes & local humoral factors contribute
to the vasoconstriction
 TXA2 gets released from platelets
o Stage 2  Formation of Platelet Plug:
 vWF gets released from the endothelium to
bind to platelet receptors

26
  Causes adhesion of the platelets to the
exposed collagen fibers
 As the platelets adhere to the collagen fibers
on the damaged vessel wall, they become
activated & release ADP & TXA2
Step 2
 Attracts additional platelets for
platelet aggregation
o Stage 3  Blood Coagulation:
 Formation of the insoluble fibrin clot
 Activation of the intrinsic or extrinsic
coagulation pathway
o Stage 4  Clot Retraction:
 Within a few minutes of a clot forming
 Actin & myosin in the platelets that are Step 3
trapped in the clot begin contracting like
muscles
 Fibrin strands of the clot get pulled
towards the platelets
 Any serum (plasma without fibrinogen)
gets squeezed out from the clot to allow
it to shrink
o Stage 5  Clot Dissolution or Lysis:
 Begins shortly after the clot is formed
 Begins with activation of plasminogen plasmin Step 4
 Plasminogen plasmin:
o An inactive precursor of the
proteolytic enzyme
 t-PA (powerful activator) gets slowly released
from injured tissues
 Vascular endothelium converts plasminogen to
plasmin
 Plasmin then digests any leftover fibrin strands
to dissolve the clot
 Disseminated Intravascular Coagulation:
o Individuals have widespread
clotting & bleeding in the
vascular compartment
o Causes small blood clots to
form in vessels & cutting off
the supply of oxygen to distal
tissues
o Unregulated thrombin
explosion:
 Subsequent to too much
tissue factor
 Leads to microvascular thrombosis & target organ damage (TOD)

27
 o Increased plasmin generated:
 Subsequent to thrombin explosion
 Results in fibrinogenolysis & fibrinolysis
 Leads to increased coagulation times & hemorrhage

Leukocytic & Lymphoid Disorders

 White blood cells (WBCs) originate in the bone marrow
 Granulocytes:
o Neutrophils:
 60% of all WBCs
 Primary pathogen-fighting cells
 Maintain nonspecific, normal host defense
 Mobile:
 During inflammation process, they will migrate to infected site
o Eosinophils:
 Less than 5% of total cells
 Contains granules that are stained
 Helps control allergic responses by eosin
 Fights parasites
 Releases toxins towards offending agents
o Basophils:
 Less than 1% of total cells
 Circulates through blood
 Releases heparin, histamine, & other inflammatory mediators
o Mast cells:
 Promotes inflammation
 Tissue cells of the CT of dermis
 Releases heparin, histamine, & other inflammatory mediators
 Involved in allergic reactions
 Agranulocytes:
o Lymphocytes:
 Makes up 30% of total cell count
 Responsible for immune response & recognizing antigens
 B cells:
 Formed in bone marrow
 Produces y-shaped antibodies
o Marks the cells for destruction for other cells
 Fights bacteria & viruses
 T cells:
 Formed in thymus & other lymphatic tissues
 Activates immune response
 T-helper cells (CD4+):
o Activates immune response by secreting cytokines
 Cytokines:

28
  Chemical signals that bind to * activate
other immune system cells
 Cytotoxic T cells (CD8+):
o Cell-mediated immunity
o Kills infected body cells & cancer cells
o Natural Killer Cells:
 Kills antigenic cell, tumor, & virus-infected with the help of B cells
 Important in innate immunity
o Monocytes  Macrophages:
 Makes up 5% of total cell count
 Largest WBC that the body has
 Performs phagocytosis
 Phagocytosis:
o Ingestion & elimination of pathogens
 Antigen-presenting cells
 Produces inflammatory mediators
 Leukocyte Development:

 WBC Deficiencies:
o Normal WBC count  4,500-10,000
o Leukopenia:

29
  A decrease in total number of WBCs in the blood
 Can affect all WBCs, but mostly neutrophils
 Can be at risk for infection
 Low count  Immunocompromised
 High count  Fighting off infection
o Neutropenia:
 A low neutrophil count of less than 1,500
 Normal range would be between 1,500-8,000
 Can be at increased risk for bacterial infections
o HIV:
 Immunodeficiency disorder
 Defects with cellular immunity & controlling proliferative cells
 Attacks healthy WBCs
 Impaired T-cell immunity
 Can be passed via sex, transfusions, sharing needles, or during birth
o Aplastic anemia:
 A low RBC, neutrophil, & platelet count of less than 1,000
 Mutation of myeloid stem cell line
 Can be at higher risk for hypoxia, bleeding, & bacterial infection
o Anemia:
 Low RBC, hematocrit, & hemoglobin count
 Low total volume of blood
 RBCs could be a different shape
o Infectious mononucleosis:
 A lymphoproliferative disorder caused by Epstein-Bar virus
 Aka “mono”
 Proliferation of bone marrow cells that give rise to lymphoid cells &
reticuloendothelial cells (macrophages)
 How does it spread?
 Saliva
 Bodily functions
 Large incubation period
 Won’t know of symptoms until too late
 Clinical Manifestations:
 Swollen lymph nodes
 Sore throat
 Fatigue
 Fever
 Myeloid Neoplasms:
o Consists of mainly granulocytes, RBCs, & platelets
o Mutation of the myeloid cell line
o New abnormal growth of tissue/blood cells that arise from bone marrow stem
cells
o Overproduction of abnormal monocytes or granulocytes
o Replaces normal bone marrow cells
 What complications can occur from this?

30
  Impacts formation & structure of bone marrow cells
o Due to T lymphocytes originating in bone marrow
 Can also impact immunity
o Acute & chronic myelocytic leukemia
 Lymphoid Neoplasms:
o Mutation of the lymphoid cell line
o Results from B & T lymphocyte precursor cells or their descendent cell types
o Overproduction of abnormal immune cells
o Results in:
 Overproduction of B & T cells
 Lymphocytic (B-cell & T-cell) leukemia
 Hodgkin & non-Hodgkin lymphomas
 Leukemias:
o Means “white blood” due to the ratio between WBCs & RBCs being off
o Malignant neoplasms of hematopoietic stem cells
o Originate from myeloid or lymphoid tissue cells
o Classified by where the mutation occurs in the cell lineage
 Lymphocytic:
 ALL  Acute lymphocytic leukemia
o Rapid onset
o More common in kids
o Overproduction of lymphocytes
o Clinical Manifestations:
 Fatigue
 Bone pain
 Anemia
 Inflammation of spleen & liver due to enlarged cells
o Treatment:
 Blood transfusion
 Chemotherapy:
 1st line of treatment
 Since this disease circulates through the
blood, this treatment can be used to stop
replication
 Bone marrow treatment (stem cell replacement):
 A procedure that infuses healthy blood-
forming stem cells
into the body to
replace bone
marrow that’s not
producing enough
healthy blood cells
 Very high risk due
to infection
 CLL  Chronic lymphocytic leukemia

31
 o Abnormal numbers of relatively mature lymphocytes
predominate in the marrow, lymph nodes, & spleen
o More common in adults over the age of 40 or more
o Has more differentiation in their cells
o Contains more mature cells proliferating
o Slower onset of disease process
o Clinical manifestations &
treatment are similar to ALL
 Myelocytic:
 ALL  Acute myelocytic leukemia
 CLL  Chronic myelocytic leukemia
 Biphenotypic acute leukemia (BAL):
 A mixture of both types of AML &
ALL
o Creates abnormal WBCs
o Characteristics:
 WBCs proliferate rapidly
 They aren’t supposed to
 Live longer than normal
 PCD isn’t happening
 Will “crowd-out” healthy cells in the marrow
 No room for new cells
 Will infiltrate widely
 Most often seen in children
o What makes something acute vs. chronic?
 Acute:
 Can get rid of it
 Can be controlled or managed
 Has the potential to become chronic
 Chronic:
 Can’t get rid of it
 Needs to be managed continuously
 Has the potential to become acute in certain situations
 Lymphomas:
o Non-Hodgkin’s Lymphomas (NHL):
 Any neoplasm that originated in lymph nodes
 Absent Reed-Sternberg cells
 Solid tumors (not blood based)
 Composed of neoplastic lymphoid cells
 Varying characteristics
 Spreads early & rapidly to other lymphoid tissues in the body
 Types:
 B cell  Most common
 T cell
 Clinical Manifestations:

32
  Uncontrollable lymph node growth
 Bone marrow involvement & swelling
 Fever
 Fatigue
 Weight loss
 Nausea
 Vomiting
 Diagnosis:
 Bone biopsy
 Blood biopsy
 What can these diagnoses do?
o Can give an understanding to what type of lymphoma it is
& its behavior to normal cells
 Grading (how it looks:
 Low-grade
 Intermediate
 High-grade
 Treatments:
 Varies for each type
 Radiation
 Chemotherapy
 Surgery
o Hodgkin’s Lymphomas (HL):
 Occurs in lymph nodes of the neck & chest
 Can create a solid tumor mass in lymph nodes
 Malignant B cells invade lymphoid organs
 Has Reed-Sternberg cells
 Has 6 variations
 Starts in a single lymph node
 Can spread to other lymph nodes, spleen, & sometimes bone
marrow
 In order to spread, it has to be connected to the original lymph
node
 Clinical Manifestations:
 Uncontrollable lymph node growth
 Bone marrow involvement & swelling
 Fever
 Fatigue
 Anorexia
 Weight loss
 Nausea
 Vomiting
 Diagnosis:
 Blood biopsy
 Lymph node biopsy

33
  Can tag lymph nodes with radioactive dye to se where the infected
areas are
 Treatments: Reed-Sternberg Cells
 Can depend on degree & location
 Radiation
 Chemotherapy
 Reed-Sternberg Cells:
o Specific to lymphoma
o Originating component of development & spread of
cancer
o Germinal cells
 Myeloma:
o Occurs in blood-making cells found in the red bone marrow
o Abnormal cell production of plasma cells
 Can caus an increase in serum levels of abnormal antibodies of a single
plasma cell
o Main site  Bone marrow/bone
o Clinical Manifestations:
o Can result in kidney failure or heart fialure
 Clinical manifestations of kidney failure:
 No urination
o Urine & sodium stay in the body for longer
 Both get retained by body & blood
o Can cause a high BP
o Hard for other organs to work
o Heart has to work even harder, which can tcause low BP
o Treatment:
 Chemotherapy:
 1st line of therapy
 Anything that can help suppress pain
 Steriods to decrease inflammation
 Stem cell therapy/transplant
 Last line of defense
 Can cause infection

Infection & Infectious Diseases

 Terminology:
o Host:
 The environment where the bacteria wants to live in
 Provides life-sustaining properties to the consumer
o Infection/Colonization:
 Could result in infectious disease
 The multiplication of the affect agent in target cells
o Microflora:
 Good inhabited bacteria within a host
 Is having a presence of this an infection?

34
  Only if it becomes opportunistic
 Ex  GI bacteria
o Commensalism:
 When the host doesn’t benefit or get harmed, but the organism gets a
benefit out of the relationship
 Ex  GI bacteria
 Needs nutritional support from the body, but doesn’t do any harm
o Mutualism:
 When the host & organism gets a benefit out of the relationship
o Parasitic:
 Organism feeds off of host, but host doesn’t benefit from the relationship
 Results in an infectious disease
o Infectious Disease:
 Caused by a pathogen
 Can be spread
 Result from a parasitic relationship
 Where the organism in the relationship gets an injury
 Ex  Malabsorption & inflammation
o Virulence:
 The disease-causing potential of an organism
 What can impact an organism’s virulence?
 Antibodies increase it
 Immunocompromised individuals decrease it
o Pathogens:
 Disease-carrying agents
 Microorganisms that are so virulence that are rarely found in the absent of
disease
 Ex  COVID-19
o Saprophytes:
 Lives on dead or decaying organic matter
 Majority of all microorganisms
 Any organism that obtains nutrients from decayed or dead organisms
 Can cause infections, but many to humans
 Ex  Mushrooms, mold, fungus
o Opportunistic Pathogens:
 Able to cause disease
 Takes the opportunity to infect/thrive when a body defense is reduced or
compromised
 Grows in parts of the body that isn’t natural to them
Prions

35
  Ex  Staph infection enters the skin through
a cut
 Agents of Infectious Disease:
o Prions:
 Unique with no individualized genome
 Small, modified, infectious proteins
 Abnormally shaped versions of their own
proteins
 Can bind together & damage other cells
 Most damage causes degenerative
diseases in CNS (neurological)
 Why don’t we hear a lot about prions?
 Mostly thrive in non-human animals
 Very few can go into humans
o Very gradual change in neurological abilities
 Examples:
 Creutzfeldt-Jakob Disease:
o Can be transmitted into humans
o Presents as rapidly progressive dementia with ataxia &
startle myoclonus
 Ataxia:
 Cerebellum involved
 Startle Myoclonus:
 Involuntary contractions of muscle with
minimal stimulation
 Due to exposure to prion-infected human
tissue
o Death within 1 year
 Chronic Wasting Disease:
o Can be transmitted into humans
o Starts in deer that are decaying or are dead
 Bovine Spongiform Encephalopathy:
o Aka “mad cow disease”
o Can be transmitted into humans from cows
o Viruses:
 Smallest intracellular pathogens that humans are exposed to
Viruses

36
  Replicates within a host body
 Will then multiply by
damaging/destroying cells & releasing
new particles into surrounding area
 Protein coat surrounding unclean acid core
 Some have envelopes
 DNA/RNA
 No organized cellular structure
 Cannot reproduce without a host
 Wants to thrive
 Host cell’s normal metabolic activity makes new
viruses
 Some viruses can remain dormant for years
(Herpes & Shingles) while others can start
multiplying right away (Influenza)
 Latent  No present clinical manifestations
 Might not show symptoms right away, but they might have oncogenesis
properities
 Impacts DNA/RNA enough to cause cancer
 Ex  EBV & HIV
 How do viruses spread?
 Close contact (Food, body fluids, droplets)
 Can live on surfaces for periods of time
o Bacteria:
 Prokaryotes
 Unicellular
 No nucleus
 Can replicate on their own
 Contain RNA/DNA
 Produce Biofilms
 Outer layer that protects colonies so they can thrive & stay healthy
 A surface-coating colony of 1 or more species of prokaryotes that
engage in metabolic cooperation
 Has a cytoplasmic membrane & a cell wall
 Why is it important to understand a bacteria’s structure?
 Important to understand how one can break down bacteria
 Use hosts for food & shelter
 Live in colonies
 How can you classify & describe bacteria?
 Classified by genus & species
 Described by morphological appearance, oxygen dependence, &
staining
o Morphological (physical) Appearance:
 Spherical/“Cocci”  Shape
 Most common

37
  Rod-shaped/“Vacilli”  Shape
 Most common
 Spiral/“Spirilla”  Shape
 Most common
 Cork-screwed/“Spirochaetes”
 Comma/“Vireos”
o Oxygen dependence:
 Aerobic (oxygen dependence) or anaerobic (oxygen
independent)
o Staining/gram stains:
 What is the cell wall like?
 Looking for the characteristics of the bacteria
o Mycoplasmas:
 Smaller than bacteria (1 1/3rd of size)
 No defined cell walls
 A lot harder to kill
 Have significantly less DNA
 Can’t affect as easily (virulence)
 Naturally resistant to bacteria
 Common mycoplasma can cause walking pneumonia
o Rickettsiacaea & Chlamydiacae:
 Less common
 Have both bacterial & viral characteristics
 Viral-like:
o Obligate (binds) intracellular pathogens
 Bacterial-like:
o Contains DNA/RNA
o Have cell walls
o Fungi:
 Natural & normal
 No means of movement
 Gets food by breaking down substances in their surrounding & absorbing
the nutrients
 Has cell walls, but different from bacteria
 Most require much cooler temperature than “normal” core body
temperature
 Can be found anywhere
 Few are capable of causing disease
 Most infections are on body surfaces such as superficial skin &
nail infections
o Skin  Have a shiny & waxing appearance
o Nails  Has a cloudy & coarse appearance
 2 single-celled categories:
 Yeasts:
o Single-celled
o Lives in damp places

38
 o Reproduce by budding process
 Splices from parent cell
 Keeps reproducing
o Shiny skin appearance
o Cloudy/coarse on nails
 Mold:
o Longfuldiment structures
 Ex  Cancer
o Doesn’t affect humans
 If they affect humans, the budding filaments act like
cancer cells & grab onto the host in groups of 3
o Parasites:
 Bigger than bacteria & viruses
 Members of the animal kingdom
 Protozoa:
 Unicellular
 Complete cellular components & nucleus
 Ex  Malaria, amebic dysentery, giardiasis
 Arthropods:
 Include vectors of infectious disease (ticks, mosquitos, flies,
ectoparasites, mites, lice, fleas)
 Infects by direct contact or eggs on host
 Helminths:
 Wormlike parasites
 Lives in or another organism
 Deriving nourishment at the expense of the host, usually without
killing it
 Depend on & reproduce in host
 Drain from the host
 Most are found in the GI tract
 Clinical Manifestations:
o Malnutrition
o Bloating
o Nausea
o Diarrhea
 Ex  Roundworms & tapeworms
 Mechanisms of Transmission:
o Portal of Entry:
 How is something going to be transmitted to a new reservoir or host
 Most common ways that a disease can be transmitted:
 Penetration
 Direct Contact
 Ingestion
 Inhalation
o Virulence Factors:

39
  Has impact on ability to cause disease
 Traits used to establish themselves the host
 Determines the degree of tissue damage that has occurred
 Different factors:
 Toxins:
o Are the toxins going to break down the infection or are they
going to help them?
 Adhesion Factors:
o What helps the infection adhere to the host?
 Evasion Factors:
o How is the infection stay protected from the body
defenses?
 Invasion Factors:
o What facilitates infection &/or replication?
o How do they break down the barrier?
 Clinical Course of Infectious Diseases:
o Steps:
 Infection:
 Person is exposed to the organism
 Organism dominates host
 Starts using virulence
factors
 Incubation:
 Occurs after host is
broken down
 The period for the
organism to replicate
inside of the host
 No recognizable
symptoms
 Prodromal:
 Early clinical
manifestations start to
appear
 Acute
 When an infection stays at or above critical threshold
o Body should be able to stop disease using naturally disease
 If it stays below critical threshold, it is a subclinical disease
 Most essential step in stopping disease & identifying infection
 Convalescent/Resolution:
 Body will begin to attack
 Symptoms began to subside
 Outcome 1  Death
o Body didn’t break the infection down
o Infection takes over

40
 Outcome 2  Resolution
o Body broke down the infection
o Body goes back to normal
 Outcome 3  Chronic Disease
o Started to thrive & take over the body
o Body fought back a bit
o Infection never got below the clinical threshold
o Ex  HIV
o Primary Prevention (prophylaxis):
 Immunization
 Quarantine
 Hand hygiene
o Eradicate Pathogen:
 Eliminate before reaching host
o Pharmacology:
 Antibiotics:
 Inhibit cell wall, protein, nucleic acid synthesis
 Antivirals:
 Inhibit DNA/RNA synthesis
 Inhibit binding to cells
 Antifungals:
 Bind to form cell membrane holes
 Inhibit synthesis

 Diagnostics:
o Clinical Manifestations:
 Malnutrition
 Anorexia
 Swelling
 Nausea
 Fever
o Clinical History:
 Determines what the patient is at risk for
o Complete Blood Count (CBC):
 WBC  Under 10,000
 WBC (Diff.)
 RBC
o Bacterial Infections:
 Gram Stain  Bacterial structure
 Oxygenation
 Cell shape
 Cell walls
 Culture & Sensitivity:
 Describes what antibiotics the bacteria is resistant to
o Viral Infections:
 Antibody Titers:

41
  Measures amount of a specific type of antibody is present in
plasma
 Polymerase Chain Reaction:
 Determines how viral infection is replicated
 Produces thousands of DNA segment copies using the enzyme
DNA polymerase

Inflammation & Inflammatory Responses

 Basics of Inflammation:
o Non-specific response to tissue injury or infection
 Blood & oxygen rushes to the area
o Purpose is to minimize effects of injury/infection, remove damage tissue/injured
cells/debris, generate new tissue, and facilitate healing
o Cellular involvement with inflammation
o Acute/chronic
o Local/systemic manifestations
o Fever
 Only bad when it becomes chronic
 Cells of Inflammation:
o Endothelial cells:
 Allow for vascular & selective
permeability
 Chemical mediators that leak
out of vasculature into
surrounding areas
 Lines interior surface of walls
in blood vessels
o Platelets:
 Releases proteins that mediate
inflammatory process
o Neutrophils:
 Nonspecific
 First & fastest responders to any
sort of inflammation
 Help with destruction of any pathogens by marking them & engulfing
them
 Present with acute infections
 Highly mobile
o Eosinophils:
 Slow to respond
 Present with chronic infections
 Respond to allergic reactions
o Basophils:
 Respond to allergic reactions
o Macrophages:
 Found within lymph nodes

42
  Engulf foreign objects/cells
 Releases proteins that help with cellular regeneration & repair cell walls
that got damaged
o Lymphocytes:
 Responsible for B & T cell
 Antigen formation & response
 Acute Inflammation:
o Early/immediate reaction to local tissues
o Aimed at removing injuring agent
o Want some of this to occur
o Minimal & short-lasting injury to tissue
o Clinical Manifestations:
 4 cardinal signs of acute inflammation (Most common clinical
manifestations that out outwardly expressed):
 Rubor  Redness
 Tumor  Growth
 Calor  Warmth
 Dolor  Pain
 Other symptoms (depends on extent):
 Loss of function
 Fever
o What could cause this?
 Bug bites
 Allergic reaction to foods
 Broken bone
o Two main stages
 Vascular:
 Allows for structural changes & vascular permeability
 Increased blood flow
 Without this stage, there isn’t the cellular stage Vascular Stage
 Steps:
o Vasoconstriction until assessment
of area is done
o Vasodilation:
 Increasing blood flow to the
injured area
 Mediators include histamine
& nitric oxide
 Increased redness & warmth
result due to histamines
delivered to area
o Capillaries become more permeable
 Allows exudate to escape
into the tissues

43
  Mediators include histamine, bradykinin, &
leukotrienes
 Swelling, pain, & impaired function result from this
 Cellular:
 Occurs with vascular stage by working together
o If one doesn’t work, then they both don’t work Cellular Stage
o No blood flow = no cells can access site
 White blood cells enter
the injured tissue:
o Destroying
infective
organisms
o Removing/eating
damaged cells
o Releasing more
inflammatory
mediators to
control further
inflammation and
healing
 4 main stages:
o Margination (adhesion):
 WBC are being released into the blood stream
o Emigration:
 The traveling of WBCs to enter the site of
inflammation
o Chemotaxis:
 The chemical migration of chemical mediators
travel to the site of inflammation
 Starts to release their chemicals
 Results in inflammation
 Inflammation starts to break down infection
o Phagocytosis:
 Engulf infected pathogens wherever it might be
 Inflammatory Mediators:
o Stops & limits the damage of the infectious agent
o Plasma Derived Inflammatory Mediators:
 Synthesized in liver
 Coagulation
 Fever
 Inflammation
 Released into plasma when needed
 Types:
 Kinins
 Coagulation & fibrinolysis proteins
 Complement system

44
 o Cell Derived Inflammatory Mediators:
 Released from cells
 Present at sites always
 Types:
 Vasoactive amines  Histamine & serotonin
 Eicosanoid family  Prostaglandins & leukotrienes
 Omega-3 polyunsaturated fatty acids
 Platelet-activating factor (PAF)
 Cytokines and chemokines  TNF-a & IL-1
 Nitric oxide (NO)
 Reactive oxygen species (ROS)

 Inflammatory Exudate:
o Accumulation of fluids, cells, & cellular debris that are released in the site of
inflammation
o Could be overproduced
 Depends on what is within it
o Do we want this to occur?
 Has WBCs in it
 Cushions the spot of injury
o Types:
 Serous:
 Watery
 Clear
 Low in proteins
 Hemorrhagic:
 Bloody due to vascular or vessel damage
 Fibrinous:
 Thick & sticky

45
  Cloudier than serous
 Yellow-tannish color
 Contains a lot of fibrinogen where clotting has occurred
 Membranous (pseudomembranous):
 Develops on membranes that are moist
 Very cloudy
 Contains dead or neurotic cells
 Ex  Mucous membranes
 Purulent (suppurative):
 Discharge from infected tissues as pus
 Loaded with WBCs that are broken
 Cloudy
 Thick
 May have an odor to it
 Lots of proteins & cell debris
 Associated with some sort of infection
 Chronic Inflammation:
o Self-perpetuating & can last longer than 4 weeks, months, and/or years
o May follow acute inflammation episode (still possible)
o Insidious process  causing tissue damage
o Evidence suggests recurrent inflammation influences cancer development because
of DNA damage
o Why could this be a bad thing?
 Prolonged cellular damage can lead to DNA gets damaged & cancer
 Impact on life for individuals with chronic inflammation
 Can lead to heart disease, cancer, allergies, & muscle degeneration
o Causes:
 Foreign agents
 Virus/bacteria
 Obesity
 Localized Inflammation:
o Redness (i.e., erythema)
o Swelling (i.e., edema)
o Heat
o Tenderness
o Loss of function
 Systemic Inflammation:
o Fever
o Increased catabolism (breaking down molecules)
 Needs more energy
 This is why we get tired when we are sick)
o Negative nitrogen balance
 Makes it harder to heal
o Labs:
 Increased erythrocyte sedimentation rate (ESR)

46
  Rate at which RBCs descent in a tube over an hour
 Non-specific
 Leukocytosis
 Abnormal increase in which WBC count is higher than 10,000
 Normal range  4,500-10,000
 Understanding Fevers:
o Types:
 Intermittent:
 Sporadic spikes & falls of temperature
 Alternates between elevated & normal temperature
 Sustained:
 More common during infections
 Constantly above
100.4F with little
fluctuation
 Remittent:
 Temperature fluctuates
a lot, but doesn’t fall
past normal level
 Baseline temperature
stays slightly elevated &
spikes again
 Relapsing:
 Has fever and then it
goes away for a few days & the come back
 Short, febrile periods of a few days are interspersed with periods of
1-2 days of normal temperature
o An elevation in body temperature produced in response to pyrogens that act by
promoting the release of prostaglandin or cytokines
o Interacts with hypothalamic thermoregulation
 Body is unable to control temperature
 Steps:
 Body sense temperature change
 Body sends signals to muscles, organs, glands, & nervous system
o What is the purpose of fevers?
 Depends on the severity of involvement
 Usually a good thing
 A chemical response/warning sign to the body that something is going on
(aka an infection)
o What are the clinical manifestations of fevers?

47
  Headache
 Chills
 Warmth
 Sweating
 Pain
o How can we manage fevers?
 Given antipyretics to get rid of
fever
 Can put cool cloth to reduce
severity of heat
o 4 stages:
 Prodromal
 Initial onset of fever
 Early symptoms
 May have a headache
 Chill phase:
 Core body temperature has significant increase
 Flushing phase:
 Skin becomes warm & flushed
 Defervescence phase:
 Reduction of fever due to decreased body temperature
 Sweating
o Fevers across the lifespan
 Children:
 Higher baseline temperature
 Elderly:
 Lower baseline temperature
 Individuals have different baseline temperatures

Immune Responses & Disorders of Immunity

 Immunity:
o Immunity:
 The protection of the body from different infectious diseases
 Immune system can distinguish self & non-self-cells
 Won’t start attacking our own cells
o Immune response:
 Coordinated response of the immune system

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 Innate vs. Adaptive Immunity:
o Innate Immunity:
 Aka natural immunity
 Early & rapid
 Within minutes
 Done to prevent any deep penetration
 Always present
 Attacks non-self-microbes
 Does not distinguish between different
microbes
 Mechanisms include:
 Epithelial barriers
 Cell messenger molecules
 Physical barriers
o Skin & mucous membranes
 Phagocytic cells
 Plasma proteins
o Adaptive Immunity:
 Aka acquired immunity
 Late stages & less rapid
 Attacks specific microbes (antigens)
 Develops after exposure to specific antigen
 Responsible for creating the memory of the organism so the body can
remember how to fight off the organism if it comes into the body again
 Mechanisms include:
 Humoral immunity:
o Mediated by antibodies from B
cells that can recognize each
individual organism
o Secreted into the bloodstream
o Function  Stop
microorganisms from invading
& colonizing different body
tissues
 Cell-mediated immunity:
o T cells defend against
intercellular microbes (viruses)
o Engage with phagocytes
o Will eat or kill the host cell that
are contain the intercellular
microbes
 Immune Cell Review:
o Regulatory cells control the immune response
 T helper cells:
 Aka CD4 cells

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  Help the activities of other immune cells by releasing cell
cytokines
o Cytokines help suppress/regulate immune responses
 T suppressor cells:
 Blocks the actions of other lymphocytes to keep the immune
system from being overactive
 Use in the treatment of cancer
 Antigen-presenting cells:
 Internalized invading antigen pieces are called epitopes
 Mediate the cellular immune response by processing & presenting
antigens to certain lymphocytes such as T cells
 Classical antigen-presenting cells include macrophages, dendritic
cells, & B cells
 Epitope:
o When invading antigens are
located in specific areas
o Epitopes attached to cell
surface MHC molecule
o Signals T cells
o Effector cells then carry out the attack on antigen
 T cytotoxic (or killer T) cells:
 Part of the innate response
 First line of defense
 Can recognize tumor cells versus
body cells
 B cells:
 Produces antibodies
 Mediates humoral immunity
 Leukocytes
 Immune Proteins:
o Cytokines:
 Proteins produced by immune cells in innate & adaptive immunity
 Regulates actions of immunity
 Pleiotropic:
 Can act on many different cell types
 Redundant:
 Has the ability to produce overlapping functions & can compensate
for one another
 Interleukins/Interferons:
 Interfere with virus multiplication
 Chemokines:
 Attract WBCs to the infection
 Promote the colonization of WBCs to the area of infection
 Colony-stimulating factors:

50
  Stimulate bone marrow to produce more WBCs to divide & mature
so they can go to the area of infection
o Complement Proteins:
 Help the body locate & destroy specific antigens that are circulating the
blood in an inactive form
 Circulate in the blood in an inactive form  highly toxic proteins 
destroy antigen
 Effector for innate & humoral immunity
 Classical pathway:
o Adaptive immunity response
o Antibodies recognize a specific antigen & bind to it or
other structures
o Most common
 Lectin pathway:
o Innate immunity response
o Mannose-binding ligands (plasma protein) bind microbial
glycoproteins/glycolipids
 Alternative pathway:
o Innate immunity response
o Recognizes microbial molecules without the use of
antibodies
 Antigen Response:
o Substances that can stimulate an immune response
o Immune cells have receptors that attach to MHC proteins & recognize these
antigen
 MHC  Major Histocompatibility Complex
 A complex that is able to attach its specific molecule to a specific
antigen/protein
o Only those T cells whose antigen receptors “fit” the antigen being displayed will
respond to it
 Only membrane-bound antigens
 Can’t recognize anything else
o Foreign macromolecules:
 Proteins
 Polysaccharides
 Lipids
 Nucleic acids
o Immunologically active sites - epitopes
 Antigens Stimulate:

51
 o Antigen-presenting cells
 Macrophages:
 Will digest & engulf different
microbes
 Dendritic cells:
 Acquire specialized functions as
antigen-presenting cells depending
on location
o T cells (MHC):
 Adaptive Immunity:
 Cell-Mediated Immunity
 Helper T cells  CD4+
 Cytotoxic T cells  CD8+
o B cells:
 Adaptive Immunity:
 Humoral Immunity
 Plasma cells
 Immunoglobulins (i.e., antibodies)
 Helper T Cells (CD4+):
o Called the “master switch”
 Due to role in adaptive immunity
o Most important cells in adaptive immunity
 Required for all responses
o Secrete cytokines
 B cells
 Secretes antibodies
 Cytotoxic T cells
 Kills infected target cells
 Natural killer (NK) cells
 Cell-Mediated Immunity:
o Involves CD8+ & CD4+ cells
 Performs inside of the toxic cells
 CD8+:
 Cytotoxic T cells
 Inside of target cells
 Releases cytotoxic proteins that are
responsible for inducing apoptosis
 CD4+:
 Help the activity of other immune cells by releasing T cell
cytokines
 Regulates/suppresses immune response
o Cytotoxicity
o Delayed hypersensitivity
o Memory
o Control
 B Lymphocytes:

52
o Main function  Production of antibodies
 In order to do this, they must first become activated
 Infectious agent must enter the body
 A piece of the agent’s protein membrane must be visible on its
surface
o Gets marked for antibodies
 Antibodies are secreted from plasma cells
o Like T cells, B cells have antigen receptors.
o T helper cells signals transformation.
 Plasma cells:
 Secrete antibodies (aka immunoglobulins)
 Memory B cells:
 Remain in the body for subsequent, quicker reactions
 Will remembered past infectious agents

53
 Classes of Immunoglobulins:
o IgG:
 Most common (75%)
 Circulates in body fluids
 Binds to antigens
 Display antiviral, antitoxin, & antibacterial properties
 Only immunoglobulin that can cross the placenta
 Responsible for protection of newborns
 Mostly found in secondary immune response
o IgA:
 Found in secretions on mucous membranes
 Prevents antigens from entering the body & attaching to epithelial cells
 Make up about 15%
 Found in salvia, tears, breast milk, GI tract, etc.
o IgM:
 Circulates in body fluids
 Has 5 units to pull antigens together into clumps
 Make up 10%
 Form natural antibodies for AB blood groups
 Found in early immune responses
 Help activate compliment
o IgD:
 Found on the surface of B cells
 Acts as an antigen receptor
 Less than .02%
 Needed for maturation of B cells

54
 o IgE:
 Found on mast cells in tissues
 Once they bind with mast cells, they trigger systemic release of
histamine
 Starts inflammation
 Involved in allergy
 Less than 0.004%
 Humoral Immunity:
o Found in body fluids
o Neutralize bacterial toxins
o Opsonize bacteria
 Optimization  A immune process in where bacteria are targeted to be
destroyed by a phagocyte
o Neutralize viruses
o Facilitation of phagocytosis
o Activation of complement cascade
o 2 types:
 Primary Immune Response:
 Antigen first presented on MHC-II
o T helper cells recognize & activate
 Triggers B-cell to proliferate & differentiate
o Plasma cells produce antibodies:
 Memory B cells for secondary response
 Plasma antibody levels rise
o Can continue to raise several weeks afterwards
 This can take 1 to 3 weeks
o Levels are highest during first couple weeks, which is when
most viruses/bacteria are attacked
 Vaccination  Produces a primary immune response
 Secondary Immune Response:
 Second or subsequent exposure to antigens
 Memory B cells respond to the antigen immediately
o Antigens have already been marked/tagged in during the
primary immune response
 Plasma antibody levels rise within days instead of weeks
 Booster shots  Cause a secondary immune response
o Makes use of memory to remind Memory B cells what the
original exposure was like
o Antibody levels will be high before the disease is
encountered

55
 o Where would you expect immunizations to begin?
 1st dose  1st antigen arrow
 Not as immediate
 Can be reinfected during drop of plasma
antibody levels
 After 5 weeks, we would need another dose to stay
strong
 Booster dose  2nd antigen arrow
 More immediate
 Higher contraction of plasma antibodies
 Active vs. Passive Immunity:
o Active: Type 1 Hypersensitivity
 Require exposure to pathogen or exposure to
antigen
 Leads to production of antibodies
o Passive:
 When a person is given antibodies for a particular
disease rather than producing them themselves
 Hypersensitivity:
o Considered a disorder of the immune response where
someone who is exposed to a particular antigen exhibits a
detectable hyperreaction with that specific antigen
o Commonly classified into 4 groups:
 Type 1:
 Most common
 Excessive or inappropriate activation of the
immune response

56
  The body is damaged by the immune response, rather than by the
antigen
 Commonly called “allergic reactions”
o IgE mediated response
 Systemic or anaphylactic reactions
 Local or atopic reactions (genetic)
o Urticaria (hives)
o Rhinitis (hay fever)
o Atopic dermatitis
o Bronchial asthma
 Food allergies
o Can develop overtime or can lose it
 Type 2:
 2nd most common
 Complement- & antibody-mediated cell destruction, inflammation,
cell dysfunction
 IgG or IgM binds antigens on cell surfaces
o On red (AB or Rh) or white blood cells
 Transfusion reactions
 Where individuals are given blood that
doesn’t react well with the body
 Drug reactions
o On tissues
 Can result in changes with cell function
 Goodpasture syndrome
 Graves disease:
 A disease of hyperthyroidism
 Autoantibodies are produced & start
attacking our own cells within thyroid
tissues
 Myasthenia gravis
 Type 3:
 Not often seen
 Free-floating antigen plus antibody  circulating immune
complex
 Immune complexes deposit on walls of blood vessels & activate
complement  damaged blood vessels’ walls
 Systemic:
o Autoimmune vasculitis
o Glomerulonephritis
o Serum sickness (antibiotics, food, venom)
o Kidney failure
 Local
o Arthus reaction:
 Localized tissue necrosis

57
  Type 4:
 Not often seen
 Cell-mediated:
o Sensitized T cells attack antigen
o Direct cell-mediated cytotoxicity
 Cytotoxic T cells
 Viral reactions
 Delayed-type hypersensitivity
o Macrophages
o T helper cells
o Tuberculin test
o Allergic contact dermatitis
o Hypersensitivity pneumonitis
o Reaction to Allergen Exposure:

 Anaphylaxis:
o Systemic response to the inflammatory mediators released in type I
hypersensitivity
 Not localized
 Histamine, acetylcholine, kinins, leukotrienes, & prostaglandins all cause
vasodilation
 What will happen when arterioles vasodilate throughout the body?
o Huge drop in blood pressure  HR increases
o Not enough nutrients are given to essential organs
 Acetylcholine, kinins, leukotrienes, & prostaglandins all can cause
bronchoconstriction
 What will happen when the bronchioles constrict?
 Harder time breathing

58
  Not enough oxygen in the lungs & body
o Development:

 HIV/AIDS:
o Human retrovirus that infects CD4+ cells
o Spread through certain body fluids
o Leads to AIDS:
 CD4+ counts < 200 cells/mm3
 Opportunistic infections & malignancies appear
 T cells are no longer in the body to help fight off infections &/or
malignancies
 Dementia (ADC):
 Decline in thinking or cognition
 Function loss in memory, reasoning, cognitive motor skills,
problem-solving
 Severely inhibited
 Wasting syndrome:
 Body starts wasting away

59
o Transmission:
 Sexual  Semen, prevaginal fluids
 Most common way
 Blood borne
 Sharing needles is a common way
 Perinatal
o Life Cycle:

o Viral Load & CD4+ Count During HIV Phases:

 No direct relationship between CD4 count & viral load
 High CD4 count & low/undetectable viral load are desirable
 Higher the CD4 count, the healthier the immune system is
 The lower the viral load, the likelier the treatment is effective

60
 o Clinical Manifestations of HIV/AIDS:

Atherosclerosis & Hypertension

 Introduction:
o Hyperlipidemia:
 Build-up of cholesterol & lipids
 Can lead to hypertension
o Hypertension:
 Can lead to high BP
 Caused by:
o Diet
o Hyperthyroidism
o Stress
o Fluid retention
 Function of Circulation:
o When BP is impacted, circulation is
impacted
o Delivers oxygen & nutrients into tissues
o Carries wastes to & from areas
o Circulates electrolytes & hormones
o Maintains balance via autoregulation
 Cardiac Contraction:
o Needed to prevent clots
o SA node is the intial pacemaker

61
  Followed by AV node then Bundle
of His
o How would each of the following affect
heart contraction?
 A calcium channel blocker:
 Calcium causes the heart &
arteries to contract more
strongly
 Works by preventing
calcium from entering the
heart & arteries
 Allows vessels to relax & open
 A Na+ channel blocker:
 Reduces the velocity of action potential transmission within the
heart
 Reduces cell excitability & conduction velocity
 A drug that opened Na+ channels
 Causes rapid depolarization
 A drug that opened K+ channels
 Causes rapid polarization
 Volume & Pressure Distribution:
o Where is blood at any point in time?
 64% veins & venules
 16% arteries & arterioles
 4% in left side of heart (i.e., left atrium & left ventricle)
 4% in right side of heart (i.e., right atrium & right ventricle)
 4% capillaries
o Difference between arteries & veins:
 Arteries:
 Fast
 Moves blood away from the heart
 Tight in order to distribute blood around the body
 Veins:
 Slow
 Moves blood to the heart
 Can stretch to allow more blood
 Factors that Affect Blood Flow:
o Pressure & resistance:
 Force against arterial walls
o Velocity:
 Speed of blood flow
o Compliance:
 Ability for vessels to stretch
 Greater in thinned-walled vessels like veins
o Viscosity:
 Thickness/density of blood

62
 o Response/regulation:
 Neural mechanisms  SNS & PNS
 Humoral mechanisms:
 Releases hormones to regulate BP
 Vasodilate/vasoconstricts vessels
 Autoregulatory mechanisms
 Blood Pressure:
o Equation  BP = CO x PR
 CO  Cardiac output
 PR  Peripheral resistance
 The higher the resistance, the higher the blood pressure is
 The resistance within vessels
 LV pushes against this
 Vessel diameter:
o More constrictions = increased blood pressure = more
blockages appear
o Equation  CO = HR x SV
 HR  Heart rate
 Chronotropicity:
o Can affect HR by changing rhythm
 SV  Stroke volume
 Amount of blood released in each constriction
 Preload:
o Amount of stretch before a contraction
 Inotropicity:
o Can change speed or force of the contraction of the heart’s
vessels
o Why is blood pressure important?
 Helps us with cardiac function
 High blood pressure impacts other organs
 Artery Cross-Section:
o Tunica adventitia:
 Outer coat
 Made of collagen & elastin
fibers
 Protects against trauma/injury
o Tunica media:
 Middle coat
 Smooth muscle that regulates
diameter
 Vasoconstriction &
vasodilation
o Tunica intima:
 Inner coat
 Endothelial cells
 Smooth coating to allow blood to flow through without resistance

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 Regulation of Flow & BP:
o Short-term (immediate):
 Neural:
 Autonomic nervous system (ANS)
 Baroreceptors
 Chemoreceptors
 Humoral:
 Causes vasoconstriction/vasodilation
 Renin-Angiotensin-Aldosterone (RAA) mechanism
 Antidiuretic hormone (ADH)
 Vascular:
 Tissue:
 Low BP  Can direct blood to other places that need them
 High BP  Can take on more blood if needed
o Long-term:
 Renal-body fluid:
 Volume
 Renal output
 Sodium intake
 Kidneys are 1st organs damaged due to hypotension/hypertension
 Vascular:
 Collateral
 Mechanisms of Blood Pressure Regulation:
o How does heart rate have an impact on pressure?
 Increased HR = Decreased pressure
 Doesn’t have time to fill
 Decreased HR = Increased pressure

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  Vasodilators:
o Why is this good?
 Lower resistance to lower BP & expands lumen
 Vessel size increases
 Lumen in arteries expand
 Smooth muscle relaxes
o Types:
 Histamine
 Serotonin
 Kinins
 Prostaglandins
 Vascular Endothelium:
o Vasodilators:
 Endothelial derived relaxing/releasing factor (EDRF)
 Nitric oxide (NO)
 Released in increased pressure situations through endothelial lining
 Prostacyclin
o Vasoconstrictors:
 Good for hypertension
 Shrinks size of lumen
 Angiotensin II:
 Angiotensin I  II
 Released in decreased pressure situations through endothelial
lining
 Most potent
 Endothelin I
 Arterial Blood Pressure:

Rapid

More velocity &

pressure in walls

Slow
Pressure is higher during
contraction because of initial Less velocity & pressure in walls
contraction is occurring

Needs oxygen distributed

 Systolic Blood Pressure (SBP):

o Pressure on walls immediately after contraction

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 o Highest amount
o Will rise slowly throughout our lives
 Diastolic Blood Pressure (DBP):
o Pressure on walls as heart is relaxing & filling itself
 Hypertension (HTN):
For risk factors, try & think
o Chronically elevated blood pressure (Stage 1):
about how these things can
 >140 mm Hg SBP lead to HTN or how HTN can
 Better indicator lead to these things
 > 90 mm Hg DBP
o Most common contributor to premature death & disability
o Risk Factors:
 Dyslipidemia:
 The imbalance of lipids such as cholesterol, low-density
lipoprotein cholesterol, (LDL-C), triglycerides, & high-density
lipoprotein (HDL)
 Diabetes
 Obesity
 Metabolic syndrome:
 A cluster of conditions that occur together, increasing one’s risk of
heart disease, stroke, & type 2 diabetes
 Sedentary lifestyle
 Obstructive sleep apnea:
 Occurs when the muscles that support the soft tissues in one’s
throat, such as the tongue & soft palate, temporarily relax
 Increasing adult age
o Prevalence:
 32% of American adults & 50+ years
 Increased prevalence:
 Comorbid cardiovascular disease
 Older adults (Isolated systolic hypertension)
 Hispanic Americans
 African Americans
o Types:
 Primary/Essential:
 Can’t control
 Needs a medical intervention to control BP
 Idiopathic:
o Relating to or denoting any disease or condition which
arises spontaneously or for which the cause is unknown
o Can’t control
 Disruption in vascular tone (autoregulation &/or baroreceptors)
 Disruption in RAA system
 Secondary:
 Can change
 to some other underlying disease (e.g., kidney disease)

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  to some other underlying condition (e.g., pregnancy)
 Iatrogenic (e.g., pharmacologic):
 Relating to illness caused by medical examination or treatment
o Clinical Manifestations:
 Early:
 Headaches
 Neurological changes
 Fatigue
 Lethargy
 Confusion
 Late:
 Affects ADLs
 Target organ damage (TOD)
o Secondary to ischemia/oxygen deprivation
 Cardiac:
o Heart attacks
o Heart failure
 Central Nervous System:
o Strokes
 Vascular:
o Aneurysms
 Respiratory:
o Shortness of breath (SOB)  Pulmonary edema
 Renal:
o Kidney failure (necessitating transplant or dialysis)
o Edema can form
 Due to fluid being retained because the heart isn’t
pumping blood to kidneys
 Kidneys can’t filter because of increased sodium
o Decreased urine output
o Decreased filtration of sodium
 Eyes:
o Retinal hemorrhages
o Blindness
 Atherosclerosis:
o Depositing lipids in vessels
o Walls thicken due to a fatty material (cholesterol) or plaque
 Aka hyperlipidemia
 Plaque accumulation is normal
o Lipid deposition in arterial intima:
 Triglycerides:
 Measuring cholesterol levels
 Most common
 Comes from foods we eat & extra calories we don’t use
o Gets converted

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  Phospholipids:
 Found in cell membranes
 Maintains cellular structure
 Cholesterol:
 Makes majority of hormones
 Humans don’t need a lot in our diets
o Lipoproteins:
 Fat-carrying proteins
 Types:
 Chylomicrons:
o 80-90% of triglycerides
o Found in blood & lymph
o Transports fat to liver, intestines, & adipose tissues
 VLDL:
o BAD kind
o 55-65% triglycerides, 10% cholesterol, & 5-10% proteins
o Very low-density lipoproteins (cholesterol, triglycerides, &
proteins)
o Helps transport cholesterol
 IDL
 LDL:
o BAD kind
 Want low levels of these (<100)
o 10% triglycerides, 50% cholesterol, & 25% proteins
o Low-density lipoproteins
o More fatty components
o Transports fats to cells in the liver
o To get rid of these, one should exercise & eat a balanced
diet
 HDL:
o GOOD kind
 Want high levels of these (Greater or equal to 60)
o 5% triglycerides, 20% cholesterol, & 50% proteins
o High-density lipoproteins
o More protein & less fatty components
o Transports fats to liver to metabolize
o Can lower other cholesterol levels
 Hypercholesterolemia:
o High levels of cholesterol within the blood
o Primary:
 Familial:
 Genetic changes that can be passed on
o Secondary:
 Obesity/high caloric intake
 Diabetes

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Coronary Artery Disease & Heart Failure
 Coronary Artery Disease:
o Due to:
 Increased levels of cholesterol
 Fatty plaque build-up
 Prevents blood flow, oxygenation, & nutrients from getting to
certain areas
o Atherosclerosis blocks coronary arteries
o Ischemia:
 Tissue not getting oxygenated
 May cause:
 Angina
 Heart attack
 Cardiac arrhythmias
 Conduction deficits
 Heart failure
 Sudden death
 Acute Coronary Syndrome:
o ECG:
 P wave:
 Contraction of atria
 Q wave:
 Repolarization of atria
 Relaxation
 QRS complex:
 T wave:
 Refilling of heart
 Abnormal changes:
 1st sign of decreased oxygenation
 T-wave inversion
 ST-segment depression or elevation
 Abnormal Q wave
o Serum cardiac markers Coronary Arteries
 Indicates ischemia
 Proteins released from necrotic heart cells
when there is ischemia
 Creatine kinase (CK & CPK):
o Ischemia to muscle tissue
o Specific to skeletal muscles
 Troponin:
o Specific
o Ischemia to muscle tissue
 Coronary Arteries:
o All supply blood to the heart
 Around not within

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  Obstruction depends on location to see what damage it might cause
 Acute Myocardial Infraction:
o Heart attack
o Results from acute coronary syndrome
o Chest pain/angina
 Severe, crushing, constrictive OR like heartburn
 Not always a sign of acute coronary syndrome
o Sympathetic nervous system response
 GI distress, nausea, & vomiting
 Tachycardia & vasoconstriction
 Anxiety, restlessness, & feeling of impending doom
o Hypotension & shock
 Weakness in the arms & legs
 Decrease in blood pressure  Cardiac output decreases  Increase in HR
due to less pressure & heart has to work harder
o Complications:
 Heart failure
 Cardiogenic shock:
 Due to decrease in cardiac function
 Pericarditis:
 Inflammation of sac
 Thromboemboli:
 A clot in the heart due to lack of blood flow
 Rupture of the heart:
 Rare
 Ventricular aneurysms
 Chronic Ischemic Heart Disease:
o Caused by:
 Smoking  Atherosclerosis
 Ischemia
 Acute coronary syndrome
o A continuous imbalance in blood supply & the heart’s O2 demands
 Angina
 Decreased blood supply  Increased HR
 Atherosclerosis
 Vasospasm
 Increased oxygen demand
 Stress
 Exercise:
o Most common
 Cold
 Unstable vs. Stable Plaque:
o Unstable:
 Plaque disruption & platelet aggregation
 Causes greater obstruction
 Growing obstruction

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  Plaque & platelet build-up
 Smooth endothelial cells
become more turbulent
 Thrombus forms due to
stagnation of blood
o Stable:
 Plaque is fixed to the wall
 Less likelihood of migration or
breaking away
 Medications & lifestyle changes
can treat this
 Encapsulated
 Angina & Associated Pains:
o Sever chest pain
o Pooling of blood  Thrombus forms
 Treatment of Coronary Related Disease:
o Who is at risk?
 Obese people
 Could be genetics
 Age
 Gender
 Family &/or personal history
 Men
 Post-menopausal women
o Why is time important?
 We want to prevent ischemia from getting worse
o Primary Prevention:
 Exercise
 Can decrease it by inducing release of enzyme that transports
LDLs back to the liver
 LDLs turn into bile & get excreted
 Diet
 Limit cholesterol
 Stop smoking
 Education
 Yearly check-ups
o Secondary Prevention:
 Monitoring levels at check-ups
 Medications:
 Anticoagulants:
o Makes blood less thick
 Antiplatelets:
o Makes platelets less sticky to walls
o Tertiary Prevention:
 Surgeries:
 Coronary Artery Bypass Grafting (CABG):

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 o Diverts blood around narrowed or clogged parts of the
major arteries to improve blood flow & oxygen supply to
the heart
 Percutaneous Coronary Intervention (PCI):
o A non-surgical procedure used to treat the blockages in a
coronary artery
o Opens up narrowed or blocked sections of the artery, which
restores blood flow to the heart
 What is there is a clot?
 Thrombolytic medication can help break down the clot
 MONA:
o Need to do everything
o Morphine:
 Treatment of pain due to stress or higher HR
 Causes dilation of veins, which causes a decrease in heart workload
o Oxygen:
 Need to hyper oxygenate in patient’s body
 Always step 1
o Nitroglycerin:
 Causes vasodilation & increased blood flow to myocardial & to the heart
o Aspirin:
 Makes sure the blood won’t clot as much & won’t stick
 Heart Failure:
o Part of the heart isn’t working as well anymore
 Decreased cardiac output
o MIs can cause this because of decreased cardiac output & inefficiency to pump
o Regulation of cardiac performance
 Preload
 Afterload
 Contractility – Inotropy
 Heart Rate – Chronotropy
o Types:
 Left-Sided:
 Common because it works harder
 Decrease in gas exchange
 Diastolic  LV does not accept enough blood from lungs
o Filling issue
 Systolic LV does not pump enough blood to body
o Muscle weakness
 Blood backs up:
o Left heart  lungs  right heart  body
o Body lacks blood
o The lungs fill with blood
 Symptoms:
o Dyspnea on exertion (DOE)
o Orthopnea

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 o Paroxysmal nocturnal dyspnea (PND):
 A sensation of shortness of breath that awakens the
patient, often after 1 or 2 hours of sleep
 Usually relieved in the upright position
o Cough
o Hemoptysis:
 Coughing up blood from lungs
o Bibasilar crackles
o S3
 Right Sided:
 Oxygenation issues
 Diastolic  RV does not
accept enough blood from
body
 Systolic  RV does not
pump enough blood to lungs
 Blood backs up:
o Right heart  body
 left heart  lungs
o Body fills with blood
o The lungs do not oxygenate enough blood
 Symptoms:
o Abdominal pain
o Anorexia
o Nausea
o Bloating
o Constipation
o Jugular venous distention (JVD)
o Hepatomegaly:
 Enlarged liver
o Hepatojugular reflux:
 A distention of the neck veins when pressure is
applied over the liver
o Splenomegaly:
 Enlarged spleen
 Systolic:
 Can’t pump enough out
 “Ejection” failure
 Clinical Manifestations:
o LV failure signs & symptoms
o RV failure signs & symptoms
o Maybe both
 Causes include:
o Coronary artery disease (CAD)
o Hypertension (HTN):

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  Increased workload & afterload  Decreased
function
o Dilated cardiomyopathy
Diastolic:
 Can’t fill heart as much
 Not getting oxygen to & through the heart
o Leads to more pulmonary diseases
 Hypertension in pulmonary arteries
 “Filling” failure
 Clinical Manifestations:
o Intermittent dyspnea
o Normal ejection fraction (EF) & left ventricular (LV) size
o Pulmonary congestion
o Pulmonary hypertension (HTN)
 Causes include:
o Pericardial disease
o Hypertrophic cardiomyopathy:
 Increased size of heart
o Restrictive cardiomyopathy:
 Restriction of blood flow
o Diagnostics:
 Based upon symptoms
 New York Heart Association Classification (I-IV):
o Class I:
 Early onset
 Symptoms someone is having based on a situation
o Class IV:
 Limits quality of life due to fatigue
 Echocardiogram:
 Looking at structures, flow, & ejection fraction
o Ejection fraction:
 Should be 55-65%
 Amount of blood pumped out of LV
 Brain natriuretic peptide:
 Indicates the severity of the heart failure
 Released from cardiac cells when cardiac tissue stretches
o Heart is overworking  Can’t ejected very good
 Should be below 100, but can be above 1,000 depending on
severity
o Treatment:
 Primary prevention!
 Preserve length and quality of life
 Pharmacologic agents:
 Reduce preload due to a filling issue
 Reduce afterload due to an ejection issue
 Increase inotropic properties of heart

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 o Increase squeezing of the heart
 Diminish chronotropic properties of heart
o Decrease HR
 Pulmonary Congestion & Edema:
o Capillary fluid moves into alveoli
 The lung becomes stiffer
 Harder to inhale
 Less gas exchange in alveoli
 Crackles
 Frothy pink sputum
o Hemoglobin not completely oxygenated

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