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Pathophysiology
(Complete collection of lecture notes)

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~ Table of Contents: Lecture Notes ~
Introduction to Pathophysiology …………………………………………………… 3 - 4
Inflammation and Immune Response ………………………………………………… 4 - 6
Altered Immunity ………………………………………………………………………6 - 7
HIV and AIDS ………………………………………………………………………… 7 - 8
Genetics ……………………………………………………………………………… 8 - 10
Neoplasia and Cancer ……………………………………………………………… 11 - 12
Hemostasis Disorders ……………………………………………………………… 12 - 14
Fluid and Electrolyte Balance ………………………………………………………

14 - 16

Acid-Base Balance …………………………………………………………………… 16 - 18
Renal and Urinary Tract Disorders …………………………………………………

18 - 21

Respiratory Disorders ……………………………………………………………… 21 - 25
Circulatory Disorders ………………………………………………………………… 25 - 29
Cardiovascular Disorders …………………………………………………………… 29 - 31
Neurological Disorders ……………………………………………………………… 32 - 35
Musculoskeletal Disorders …………………………………………………………

35 - 39

Endocrine Disorders ………………………………………………………………… 39 - 42
GI Disorders ………………………………………………………………………… 42 - 44

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~ Introduction to Pathophysiology ~
Defining Terms
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Pathology: The study of disorders (patho = suffering/disease)
Physiology: The study of chemical and physical functions within a living system (physis = nature or origin)
Pathophysiology: The study of changes in normal mechanical, physical, and biochemical functions
Pathogenesis: The development of disease
Health: Wellness of mind, body, and spirit
Disease: A deviation from normal structure or function; a disruption in homeostasis
“Normal” parameters: A range within which the majority of the population falls
“Abnormal” conditions: Fall outside of “normal” parameters
Homeostasis: A dynamic, steady state of internal balance
Negative feedback loop: Opposes stimulus to correct deficits or excess
o For example: Blood pressure (BP) control, body temperature
• Positive feedback loop: Enhances stimulus
o For example: Labor contractions

Levels of Disease Prevention
• Primordial: Preventing the development of risk factors
o For example: The social determinants of health (i
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access to healthcare and transportation)
• Primary: “Protection and Prevention”; improving general well-being while protecting against specific diseases
before things go wrong
o For example: Vaccines, helmets
• Secondary: Screenings; early detection and intervention to stop disease from progressing
o For example: Pap smears, BP screens
• Tertiary: Treatment of disease; the goal is to return to a state of maximum usefulness with minimal risk of
recurrence of disease or exacerbation
o For example: Medications, physical therapy, surgery

Pathophysiology of Stress
• Stress: A physical, chemical, or emotional factor that causes bodily or mental tension and may cause or
worsen disease processes
• Allostasis: The attempt to cope with stressors and adapt to maintain homeostasis
o Allostatic overload: When the body is not able to return to homeostasis
• Alarm Stage: “Fight, Flight, or Freeze” response; the hypothalamus activates the sympathetic nervous system
(SNS) which arouses the central nervous system (CNS) and provides a temporary burst of energy
• Adaptation/Resistance Stage: Long-term, chronic stress; the body will either adapt, attempt to limit the
problem, or become desensitized, whichever is most effective and advantageous
• Exhaustion Stage: Prolonged stress overwhelms the body and systems can no longer function

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Cellular Response to Injury
• Reversible: The cell withstands assault and returns to normal; swelling occurs
• Adaptation: The cell responds to persistent injury by changing shape or function
o Atrophy: Decrease in size due to (d/t) decreased work demand
o Hypertrophy: Increase in size d/t increased work demand
o Hyperplasia: Increase in number d/t increased need for divisions
o Metaplasia: The reversible change of one cell type to another; growth is ordered and controlled
o Dysplasia (atypical hyperplasia): Abnormal changes in size, shape, or organization; not a true adaptation;
typically precancerous
• Death: The response to severe, prolonged, and irreversible injury; necrosis and inflammation
o Necrosis: Cell death d/t irreversible injury; inflammation occurs
o Apoptosis: Programmed cell death via self-destruction; no inflammation occurs

~ Inflammation and Immune Response ~
Immunity
• Innate/nonspecific immunity: A generic and immediate response, regardless of self or non-self cells; no
memory or long-lasting immunity
• Acquired/specific immunity: Highly-specific to particular pathogens, recognizing self vs
...

• 3rd line: Specific immune response involving NK cells, T-cells, etc
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AIDS
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Human immunodeficiency virus (HIV): Chronic suppression of the immune response
Acquired immune deficiency syndrome (AIDS): When HIV advances to produce a profound drop in CD4
count and decreased resistance to infection

Pathway of HIV
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Binding and fusion: HIV binds to CD4 receptor and fuses with the host cell to release RNA
Reverse transcription: HIV enzyme reverse transcriptase converts single-stranded HIV RNA to doublestranded HIV DNA
Integration: HIV DNA enters the host cell’s nucleus and is hidden within its DNA by HIV enzyme integrase
o Provirus: Integrated HIV DNA; may remain inactive for several years
Transcription: The host cell receives a signal to become active; RNA polymerase creates mRNA to make HIV
protein chains
Assembly: HIV enzyme protease cuts chains into smaller HIV proteins and a new virus particle is assembled
Budding: Newly-assembled virus pushes out from host cell, stealing part of the outer envelope and moving
on to infect other cells

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Immunopathology of HIV and AIDS
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Stage 1: Infection; virus infects T-cells and impairs function; burst of virus in blood followed by response,
recovery, and seroconversion (2 weeks to 6 months); flu-like symptoms occur
o Seroconversion: The time period in which one has enough antibodies to render a test positive
Stage 2: Latency period; viral replication in lymph nodes; asymptomatic
Stage 3: Rapid virus production; CD4 T-cell count drops to <400
Stage 4: CD4 T-cell count continues to decrease and T-cells become less functional
Stage 5: CD4 T-cell counts drop lower and more symptoms are present (viral/fungal infections of skin and
mucous membranes) and immune response is weaker
Stage 6: AIDS; CD4 count <200; opportunistic infections; rapid virus production and CD4 cell turnover

Transmission of HIV
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Fluids: Blood, semen, vaginal fluid, breastmilk
Sexual: Usually male-to-male or anally from male-to-female; other STIs increase the risk of transmission
Blood: Needle-sharing, needlesticks, blood transfusion, surgery, injury
Mom-to-baby: In utero, during delivery, breastfeeding
NOT by: HIV is NOT transmitted by respiratory/oral secretion or on surfaces

HIV Prevention
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Primordial: Sex and drug education, economics (social determinants of health)
Primary: Safe sex, pre-exposure prophylaxis (PrEP), universal precautions, needle exchange programs
Secondary: Early screening, peri-natal newborn drug therapy, post-exposure prophylaxis (PEP)
Tertiary: Treatment of HIV

~ Genetics ~
Defining Terms
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Genes: Sequences of DNA that are biologic and the basic units of inheritance
Chromosome: Genetic material in a cell’s nucleus that functions in the transmission of genetic information
o Full set: 23 chromosome pairs; 22 homologous pairs of autosomes and 1 sex-linked pair
Genotype: Genetic constitution
Phenotype: Physical trait presented by the gene
Karyotype: A diagrammatic representation of chromosomes in organized pairs in descending order of size,
based on the position of centrosomes

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Cellular Reproduction
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Mitosis: Reproduction of somatic/body cells; results in two identical diploid daughter cells containing 23
chromosome pairs; errors in mitosis affect the individual
Meiosis: Reproduction of gametes; diploid cells go through a second division, resulting in four haploid cells
with 23 single chromosomes; errors in meiosis affect the offspring

Mutations
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Mutation: Any inherited alteration of genetic material
Base pair substitution: One base pair of DNA replaces another
Frameshift mutation: Insertion or deletion of one or more base pairs of the DNA molecule

Genetic Disorders
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Mendelian disorders: Result from changes in a single gene
Multifactorial/multigenic disorders: Traits are produced by multiple genes acting together; affected by
environmental factors (i
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asthma, HTN, diabetes, schizophrenia)

Aneuploidies
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Aneuploidy: An abnormal number of chromosomes, usually d/t nondisjunction
o Nondisjunction: Failure to separate during mitosis or meiosis; higher risk with higher maternal age
o Meiosis: Genetic mutations, chromosomal alterations
o Mitosis: Genetic mutations
Trisomy 21 (Down Syndrome): Extra copy of chromosome 21; higher risk with higher maternal age
Other trisomies: Not as common and usually result in early death
Klinefelter Syndrome: 2-4 X chromosomes and 1 Y chromosome; male phenotype with feminization
occurring at puberty; sterile; treated with testosterone
Turner Syndrome (Monosomy X): One single X chromosome and no second X or Y chromosome; paternal
origin; female phenotype, short, sterile, amenorrhea, congenital heart defects

Chromosomal Abnormalities
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Deletion: Broken chromosome with loss of DNA/genetic info
o Cri Du Chat: Deletion of short-arm chromosome 5; infant cry resembles a cat; developmental delays,
heart defects
Duplication: Addition of genetic material
Translocation: Switching of genetic material between non-homologous chromosomes
Inversion: Breaks occur in a chromosome and segments are re-inserted at different ends

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Sex-Linked Disorders
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Etiology: Alteration in the X chromosome; males most commonly affected
XY: Dominantly-affected (only requires one alteration)
XX: Recessively-affected (requires two alterations)
Examples: Color-blindness, muscular dystrophy, Hemophilia A

Mendelian Genetics
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Dominant presentation: Only requires one dominant gene
o AA: Homozygous affected; may cause spontaneous abortion if too many defects occur
o Aa: Heterozygous affected
o aa: Homozygous unaffected
o Examples: Marfan syndrome, Huntington’s disease
Recessive presentation: Requires two copies of the recessive gene
o aa: Homozygous affected
o AA: Homozygous unaffected
o Aa: Heterozygous unaffected; carrier (can pass trait to offspring)
o Examples: Albinism, cystic fibrosis, sickle cell anemia

Congenital Abnormalities In Utero
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Susceptibility: Depends on the amount of exposure, fetal stage when exposed, any existing maternal
conditions, and genetic predisposition of the fetus
Risk factors: Nutritional deficiencies (folic acid), chemicals/drugs, infections, radiation
Teratogen: Any agent that can disrupt embryonic or fetal development; causes congenital malformation by
interfering with cell proliferation, differentiation, or migration
o TORCH: Toxoplasmosis, Others, Rubella, Cytomegalovirus, Herpes
▪ Others: Hepatitis B, Coxsackievirus B, mumps, poliovirus
▪ Toxoplasmosis: Ingestion of raw meat or contact with cat feces
▪ Rubella: Risk up to 20 weeks gestation
▪ TORCH syndrome: Fever, feeding difficulties, hemorrhage, hepatosplenomegaly, jaundice, hearing
impairment, eye abnormalities
Fetal alcohol syndrome (FAS): Slowed growth, neurologic disorders, head/face malformations, heart defects

Periods of Fetal Vulnerability
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< 3 weeks: All or nothing; embryo either develops normally or can’t survive teratogen damage and
spontaneously aborts
3 to 9 weeks: Embryo very vulnerable to teratogens (most susceptible at 4 to 5 weeks)
3 to 9 months: Significantly less susceptible; insult results in growth retardation or injury to organs

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~ Neoplasia and Cancer ~
Cell Growth and Differentiation
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Normal growth: highly regulated; occurs in response to irritation or inflammation
o Cytokines: regulate cell growth
o Suppressor genes: stop cell division and promote apoptosis of damaged cells
o Telomeres: limit the number of cell divisions
Neoplastic growth: excessive growth of a new cell type as a result of a genetic alteration that is not
detected or fixed (tumor)
Cell differentiation: change from one cell type to another
o More differentiated: cell is specialized with a specific function in response to specific signals
o Less differentiated: cell is able to recognize other signals and provide a generalized response; leads to
tumor growth

Genetic Mechanisms of Cancer
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Proto-oncogenes: promote normal cell growth and dictate when divisions should occur
Tumor suppressor genes (TSGs): inhibit cell growth, stop division when cells are damaged, signal apoptosis
Oncogenes: mutated proto-oncogene; multiple cell proliferation, increased risk of mutation, tumor growth
Mutated TSGs: can go undetected and multiply; may appear different after undergoing many changes
Telomeres: shorten during each cell division and eventually signal apoptosis when too short
Positive feedback: loss of growth inhibition; mutations occur during cell division; more divisions → more
mutations → TSGs become overwhelmed
Malignant neoplasm: a result of multiple mutations

Types of Tumors
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Benign tumor: does not spread/metastasize; cells are differentiated, slow-growing, and usually
encapsulated; left alone until harmful
Malignant tumor: spreads to distant sites (metastasizes); interferes with normal tissue function and
regulation; less differentiated, faster-growing, and has a necrotic center
o Necrotic center: signals angiogenesis in order to survive and keep growing

Tumor Growth
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Carcinogenesis: the formation of cancer cells
o Initiation: mutation or DNA damage occurs to permit growth
o Promotion: cell growth in response to a stimulus
o Progression: entry of cell into the positive feedback system; angiogenesis, invasion, and metastasis
Angiogenesis: new blood vessel growth; promotes metastasis
Metastasis: the spread of cancer cells to distant tissues via blood or lymph; cardinal characteristic of cancer

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Grading and Staging of Tumors
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Tumor markers: biologic markers produced by cancer cells that excrete signals of increased growth;
concerning but not defining diagnoses
Grading: histological characterization by cell differentiation
o Low grade: cell looks like neighboring cells
o High grade: cell does not look like neighboring cells
Staging: numerical estimate of prognosis
o Stage I: confined to organ of origin
o Stage II: locally invasive
o Stage III: spread to regional structures
o Stage IV: spread to distant sites

Signs and Symptoms of Cancer
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Pain: occurs in later stages d/t activation of pain and pressure receptors and tissue destruction
Fatigue: most frequently reported symptom
Cachexia: a syndrome involving loss of appetite, early satiety, weight loss, and altered metabolism
Immunosuppression: some cancer cells secrete immunosuppressants that increase the risk for infection
Bone marrow depression: results in anemia, leukopenia, thrombocytopenia

Skin Cancer
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Skin cancer: most common form of cancer; usually d/t sun exposure
Melanoma: has the highest risk of metastasis; very severe
o Superficial: flat, spreading most common
o Nodular: elevated, bleeds easily
Basal cell carcinoma: pearly pink papule with central depression that bleeds easily and rarely metastasizes
Squamous cell carcinoma: warty, crusty, tough lesions that bleed easily
Warning signs: Asymmetry, Border irregularity, Color variation, Diameter >6mm, Elevation or Evolution

~ Hemostasis Disorders ~
Defining Terms
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Hemostasis: the stop of blood flow; regulated by platelets, blood proteins, and vasculature
Coagulation: the formation of a fibrin blood clot
Platelets (thrombocytes): produced in the bone marrow and located in circulation and the spleen; in an
inactivated state until triggered by vessel damage

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Clot Formation and Dissolution
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Vasoconstriction: reduces blood flow and bleeding
Adhesion: platelets adhere weakly to the sub-endothelium and form a platelet plug
Aggregation: platelets adhere to each other and stabilize the plug
Formation: the platelet plug is formed and clotting factors activate to crosslink fibrin
Clot retraction: the soft clot contracts to form a firm clot and reinforces it
Fibrinolysis: clot breakdown (lysis); clotted blood is removed from tissues and small clots are dissolved
o Plasmin: enzyme that dissolves clots and degrades fibrin and fibrinogen
o Intrinsic pathway: occurs within the blood vasculature; involves Factor XII and urokinase
o Extrinsic pathway: occurs outside the vasculature; involves T-PA

Impaired Hemostasis
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Genetic alterations: missing or defective clotting factors, altered platelet function, or missing platelets
Hereditary: primary/congenital cause
o Hemophilia A: Factor VIII missing
o Hemophilia B: Factor IX missing
o Von Willebrand Disease: von Willebrand Factor (stabilizes Factor VII) missing
Liver disease: liver unable to generate proteins that assist with clotting
Vitamin K deficiency: decreased production of clotting factors
Anticoagulants: may cause impaired hemostasis
o Warfarin: inhibits vitamin K → decreased production of clotting factors
o Heparin: prevents clotting but can cause a hypersensitivity reaction resulting in too much bleeding
Disseminated intravascular coagulation (DIC): severe systemic deregulation in response to large-scale
damage or inflammation; massive amounts of clotting → body tries to eliminate clots → excessive bleeding

Thrombocytopenia
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Thrombocytopenia: not enough clotting; low platelet count (<100,000)
o <50,000: risk for hemorrhage with minor trauma
o 10-15,000: risk for spontaneous bleeding
Etiology: increased consumption, decreased production, decreased lifespan, trapping in spleen
Heparin-induced thrombocytopenia (HIT): hypersensitivity reaction to heparin; IgG triggers platelet
activation → clotting → decreased platelet counts
Idiopathic thrombocytopenia purpura: true cause is unknown, but there is a connection to the immune
system as low platelet levels are seen after an infection
Thrombotic thrombocytopenia purpura: microangiopathy; aggregation in microvasculature leads to
blockages and increased platelet consumption

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Thrombocythemia
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Thrombocythemia: too much clotting; high platelet count (>400,000)
o >1,000,000: person becomes symptomatic; high risk for thrombosis
Etiology: increased production, ineffective removal of thrombopoietin, more platelets in circulation
Essential thrombocythemia: increased platelet production; defective receptor can’t effectively bind and
remove thrombopoietin from the blood
Status-post splenectomy: platelets that are normally stored in the spleen are now in circulation
Reactive thrombocythemia: excessive cytokine production induces platelet production

Thromboembolic Disorders
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Hereditary/primary conditions: Factor V Leiden mutation, prothrombin mutation, MTHFR mutation, protein
deficiency, antithrombin III deficiency
Acquired/secondary condition: autoimmune antiphospholipid syndrome
Virchow’s Triad: vessel injury, altered blood flow, and hypercoagulable state
Thrombus: blood clot adhered to a vessel or tissue
Embolus: undissolved mass present in the blood or lymphatic tissue with the potential to cause occlusion
Thromboembolism: a clot that was initially adhered to the vessel wall that has become detached and is
freely circulating with the potential to cause occlusion

~ Fluid and Electrolyte Balance ~
Fluids
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Total body water (TBW): the sum of all fluids within all body compartments; 45-80% of body weight
o Intracellular fluid: 2/3 of TBW
o Extracellular fluid: 1/3 of TBW; interstitial fluid (between tissues), intravascular fluid (in vessels)
Function: homeostasis, volume balance, osmolarity balance, pH

Definitions
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Solute: “sugar and lemon juice”; the substance that’s being dissolved
Solvent: “water”; the substance that’s doing the dissolving
Solution: “lemonade”; solute + solvent
Solute concentration: the ratio of solute to solvent
o Hypertonic: “sour lemonade”; highly-concentrated (more solute than solvent)
o Hypotonic: “watered-down lemonade”; diluted; lower concentration (less solute than solvent)
o Isotonic: “perfect lemonade”; balanced; same amount of solute as solvent

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Principles of Regulation
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Blood pressure: the only thing we can change or measure
Compartments: the protein and ion composition is different but their concentration is the same
o Intracellular: high in protein, potassium, and phosphate; low in sodium
o Extracellular: high in sodium and chloride
o Interstitial: low in protein
o Intravascular: high in protein
Capillary walls: control the movement of fluid between the intravascular and interstitial space; single layer
of flat endothelial cells with fenestrations for small ions and molecules to pass through
o Permeability: permeable to O2, CO2, water, and glucose; not permeable to proteins and larger cells;
varies by location and increases with inflammation

Movement of Water
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Osmotic pressure: the principal force determining the movement of water; attractive pressure pulls water
across a membrane
Hydrostatic pressure: the pressure exerted by a fluid that pushes water across a membrane
Osmolarity: the concentration of substances in a compartment
Water: moves to the area with the highest solute concentration
Osmoreceptors: sensors located in the hypothalamus that detect changes in osmotic pressure or
concentration to regulate water balance and maintain a concentration within 2%; releases ADH
o ADH: increases permeability of renal tubular cells to water so it can be reabsorbed

Filtration and Reabsorption
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Filtration: the movement of fluid out of the capillary into → the interstitial space
Reabsorption: the movement of fluid into the capillary  from the interstitial space
Four forces: interact with each other to determine filtration and reabsorption
o Capillary hydrostatic pressure (CHP): blood pressure; pushes water out of the capillary; favors filtration
o Capillary oncotic pressure (COP): pulls water into the capillary; favors reabsorption
o Interstitial hydrostatic pressure (IHP): pushes water into the capillary; favors reabsorption
o Interstitial oncotic pressure (IOP): pushes water out of the capillary; favors filtration
Starling’s Hypothesis: fluid balance must be a balance of hydrostatic and oncotic pressures
o Net filtration = (CHP + IOP) - (COP + IHP)

Edema
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Edema: excessive accumulation of fluid in the interstitial space
Etiology: lymphatic obstruction, inflammation, increased hydrostatic pressure, and decreased osmotic
concentration
o Decreased COP: d/t decrease in proteins from starvation, liver failure, or renal failure/damage

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Increased CHP: d/t fluid overload or excessive vasoconstriction; favors filtration
Decreased COP and increased IOP: d/t inflammation → increased vascular permeability → “leakage”
into the interstitial space
Lymphatic obstruction: “clogged drain”; lymph system unable to filter fluids, so they accumulate in the
interstitial space and are not absorbed by the lymph system

~ Acid-Base Balance ~
Overview
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Hydrogen ions (H+): maintain membrane integrity and speed of metabolic enzyme reactions
pH: power of hydrogen
o Lower pH: more acidic (higher [H+])
o Higher pH: more basic (lower [H+])
[H+]: concentration of hydrogen ions
o Normal value: 0
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0)

Body Acids
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Body acids: end-products of metabolism (i
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carbs, proteins, fats)
Volatile acids: can be eliminated by the lungs as CO2 gas
o Example: carbonic acid (H2CO3) dissociates into H2O and CO2
Nonvolatile acids: can be processed and eliminated by the kidneys through the urine
o Examples: sulfuric, phosphoric, and other organic acids

Buffer Systems
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Buffers: retain or release acid based on acid-base status; prevent significant changes in pH
Carbonic acid – bicarbonate buffer: operates in the lungs and kidneys
Renal buffering: kidneys secrete H+ into the urine and reabsorb bicarb (HCO3-)
Protein buffering: intracellular buffer system

Normal ABG Values
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Arterial blood gas (ABG): used for determining acid-base status
pH: 7
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45
o Low pH: risk for cardiac arrythmias
o Death: occurs when pH is <6
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8
PaCO2: 35 – 45 mmHg
HCO3: 22 – 26 mEq/L
PaO2: 80 – 100 mmHg

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Acid-Base Imbalances
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Acidemia: too much acid; pH <7
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45
o Alkalosis: systemic decrease in [H+]
o Respiratory alkalosis: loss of CO2
o Metabolic alkalosis: excess HCO3
Mixed imbalance: problems in both respiratory and metabolic systems; both acidic or both alkalotic; there is
no way for the body to compensate so the individual gets very sick

Compensation
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Compensation: body adjusts to maintain pH but does not correct it to normal levels
Correction: when body compensates enough for pH to return to normal levels
Respiratory system: changes in ventilation to maintain normal pH
o For acidosis: increases RR to blow off CO2
o For alkalosis: decreases RR to retain CO2
Renal system: changes in urine pH
o For acidosis: urine becomes acidic; conserves HCO3 and eliminates H+
o For alkalosis: urine becomes basic; eliminates HCO3 and conserves H+

Respiratory Acidosis
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Patho: pH <7
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35 d/t problems in the metabolic system resulting in loss of base or gain of acid
Etiology: diarrhea (loss of base); diabetes, starvation, alcohol, kidney failure (gain of acid)
S/S: headache, confusion, lethargy, coma, arrythmias, abdominal pain, anorexia, nausea and vomiting (N+V)
Compensation: increased RR to blow off CO2

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Respiratory Alkalosis
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Patho: pH >7
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45 d/t loss of acid or gain of base
Etiology: vomiting, gastric suctioning (loss of acid); excessive antacid use, diuretic therapy (gain of base)
S/S: weakness, muscle cramps, hyperreflexia, confusion, convulsions, neuromuscular irritability with severe
lethargy, coma, symptoms of underlying condition
Compensation: decreased RR to conserve CO2

ABG Analysis
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Determine the disorder: determine the type of acid-base problem
a
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Respiratory or metabolic?
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Metabolic: if the direction of HCO3 matches the direction of pH
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Yes: compensated
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Partially compensated: pH is abnormal
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PaO2 analysis: considered hypoxemia if PaO2 is <80

~ Renal and Urinary Tract Disorders ~
Anatomy and Physiology
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Kidney functions: filtration, reabsorption, and activation/deactivation of hormones; regulates BP, fluid
volume, pH, vitamin D conversion, and excretion of drugs and metabolic wastes
Nephron: functional unit of the kidney; glucose reabsorption, acid-base balance, K+ balance, water balance
Glomerulus: filtration; freely permeable to water but not large plasma proteins
o Glomerular CHP: the major force moving water and solutes into the Bowman’s capsule
Juxtaglomerular apparatus: stimulates secretion of aldosterone and renin synthesis
Macula densa: monitors plasma [Na+] and alerts renin-secreting cells when it increases

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Sodium chloride (NaCl): controls glomerular filtration rate (GFR) by changing the diameter of afferent and
efferent arterioles or changing the permeability of the glomerulus
o High NaCl: afferent arteriole constriction → decreases GFR
o Low NaCl: efferent arteriole constriction → increases GFR

Renal Hormones
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Antidiuretic hormone (ADH): stimulates water retention and lower output of more concentrated urine
o When absent: there is an increased output of more dilute urine
Aldosterone: regulated by RAAS; increased water reabsorption d/t increased sodium reabsorption
Atrial natriuretic peptide (ANP): secreted by cardiocytes when right atrial BP increases; increased water loss
d/t increased filtration and urine output, countering the effects of RAAS
Urodilatin: lowers BP via urination and inhibits water reabsorption
Erythropoietin (EPO): stimulates RBC production in the bone marrow in response to hypoxia
Vitamin D: hydroxylated to active form by liver and kidneys; helps body absorb calcium and phosphate

Tests of Renal Function
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Urinalysis: analyzes urine composition
BUN/Cr ratio: analyzes GFR and renal function; a higher ratio means lower GFR and poor kidney function
o Creatinine (Cr): byproduct of muscle metabolism
o Blood urea nitrogen (BUN): the level of nitrogen in the blood in the form of urea

Polycystic Kidney Disease (PKD)
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Patho: cysts develop in the nephron and destroy healthy kidney tissue
o Cysts: large, fluid-filled sacs that compress and eventually replace healthy, functional tissue
Etiology: unknown, but there is a genetic link
S/S: HTN, flank pain, abdominal tenderness, hematuria, nocturia
Complications: UTI, pyelonephritis, glomerulonephritis, chronic renal failure

Pyelonephritis
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Patho: general infection of the renal pelvis and interstitium
Acute etiology: usually d/t poorly-treated bladder infection that travelled up the ureters
Chronic etiology: persistent and recurrent infections leading to scarring and renal failure/malfunction; PKD,
renal calculi, stricture/stenosis, hydroureter, hydronephrosis, untreated UTIs/cystitis, obstruction
S/S: vary and may have symptoms of cystitis; hematuria, WBCs in urine
o Acute: fevers, chills, flank/groin pain, CVA tenderness, dysuria
o Chronic: often minimal; HTN, frequent urination, dysuria, flank pain

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Glomerulonephritis
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Patho: inflammation of the glomeruli; type III hypersensitivity reaction
Etiology: immunologic abnormalities, ischemia, free radicals, drugs, toxins, vascular disorders, systemic
diseases, obstruction, decreased blood flow
o Acute: usually associated with strep infections
o Chronic: autoimmune; chronically increased permeability and decreased ability to filter
S/S: hematuria, proteinuria, decreased GFR, oliguria

Renal Calculi (Kidney Stones)
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Patho: crystallized material forms in renal calyces and pelvis and possibly descend through the ureters
Etiology: decreased inhibitors in urine, high concentrations of stone-forming substances
S/S: renal colic, flank/groin pain, N+V, hematuria
o Renal colic: severe flank pain when stones reach the ureter
Treatment: analgesics, lithotripsy, increased fluid intake

Obstructive Disorders
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•
•
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Ureter stricture/stenosis: pinched ureter → hydroureter → hydronephrosis → pyelonephritis →
glomerulonephritis
Urethra stricture/stenosis: pinched urethra → decreased urine flow → overflow incontinence and
increased risk for cystitis → UTI → pyelonephritis
Benign prostatic hyperplasia (BPH): enlarged prostate → decreased urine flow or hydroureter
Bladder spasms: cause urge incontinence
Weak pelvic floor: causes stress incontinence

Urinary Tract Infection (UTI)
•
•
•
•

Cystitis: inflammation of the bladder d/t infection, irritation from stones, trauma, or chemical irritants
UTI: usually a bacterial infection; E
...
5 g/day
Complications: hypoalbuminemia, hyperlipidemia (HLD), edema, altered immunity, lipids in urine

21

Acute Renal Failure (ARF)
•
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•

•

Patho: decreased renal function that is generally reversible
Glomerular injury: three different categories of causes
o Prerenal: alterations in blood flow; increased blood flow → increased pressure → vessel damage;
decreased blood flow → decreased oxygenation → vessel damage
o Intrarenal: nephron damage d/t immune complexes or nephrotoxic drugs; process injury/damage
o Postrenal: outflow/urine obstruction d/t ureter stricture, PKD, or kidney stones
Phases of ARF: occurs in three phases
o Oliguria: oliguria, high BUN/Cr, uremia, azotemia, fatigue, anorexia, N+V, pruritus, neurologic changes
o Diuretic phase: excretion of large amounts of dilute urine with low specific gravity
o Recovery: renal function is healthy enough to avoid dialysis but still insufficient
Treatment: diuretics, dopamine, natriuretic peptide, temporary dialysis

Chronic Renal Failure (CRF)
•
•
•

Patho: irreversible, progressive loss of function
Etiology: most often due to uncontrolled diabetes and chronic HTN
Stages: occurs in three stages
o Decreased renal reserve: Cr at the high end of normal, minor decrease in filtration; asymptomatic
o Renal insufficiency: 25% functionality; minor increase in Cr and BUN; polyuria, nocturia
o End stage renal disease (ESRD): 10% functionality; decreased filtration; hypervolemia, hyperkalemia,
hyperphosphatemia, metabolic acidosis, uremia, hypocalcemia, osteodystrophy/osteoporosis, anemia
▪ Prevention/management: glucose control, kidney transplant, dialysis, diet restrictions (low protein,
phosphorous, potassium and sodium), supplemental calcium and vitamin D

Dialysis
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•
•

Hemodialysis: redirects blood flow via AV shunt; blood is cleaned and pumped back in
Peritoneal dialysis: placed in abdominal cavity and drained via gravity; allows for more mobility
Complications: osteodystrophy, anemia, peripheral neuropathies, infection, anorexia, weight loss

Types of Urinary Incontinence
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Urge: involuntary void d/t bladder spasms and loss of bladder control
Stress: voiding occurs with increased abdominal pressure (i
...
laughing) and weak pelvic floor muscles
Mixed: combination of urge and stress incontinence
Overflow: unable to void completely so accumulation causes leakage; d/t partial obstruction
Functional: d/t factors unrelated to the urinary tract (such as immobility)
Reflex: purely neurological; no sensory warning or awareness of the need to void
Management: bladder training, pelvic muscle strengthening (Kegel), scheduled voiding, anticholinergics,
estrogen, urethral plugs, vaginal rings, pads, surgical repair

22

~ Respiratory Disorders ~
The Pulmonary System
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•
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Components: lungs, airways, chest wall, circulation
Function: gas exchange
Ventilation: inhalation and exhalation; the physical movement of air into and out of the lungs; a volume
o Inhalation: increases gas volume in lungs
o Exhalation: decreases gas volume in lungs
Diffusion: gas exchange between air spaces in the lungs and the bloodstream
Perfusion: movement of blood from the lungs to other tissue

Anatomy and Physiology
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•
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Lungs: series of bifurcating tubes
o Bronchiolar branches: produce mucus and move it out of the airway
Lobes: three in the right lung, two in the left lung
Alveoli: functional unit of the lung; protection, gas exchange; oxygen enters the blood and CO2 is removed
o Type I cells: promote gas exchange and provide structure
o Type II cells: secrete surfactant, which decreases surface tension and stabilizes alveoli → lung expansion
Acinus: gas exchange airway; bronchioles, alveolar ducts, and alveoli
o Pores of Kohn: physically connect the alveoli and promote collateral ventilation
Nasopharynx and oropharynx: nose and mouth; ciliated mucosa warms, humidifies, and filters inspired air
Larynx: connects the upper and lower airways
Trachea: connects the larynx and bronchi; bifurcates into left and right main stem bronchi
Bronchi: main airways that enter the lungs and ventilate both sides
o R
...
8 (Q exceeds V)
Types: lungs receive oxygen but no blood flow or lungs receive blood flow but no oxygen
Etiology: hypoxemia → vasoconstriction, high altitude, hypoventilation, pulmonary HTN
S/S: worsens symptoms of lung diseases

Pulmonary Embolus
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Patho: occlusion/blockage of pulmonary vasculature by an embolus/clot
Etiology: thromboembolism, tissue fragments, lipids, foreign body, air bubbles
S/S: pleuritic chest pain, anxiety, tachycardia, tachypnea, death
Treatment: anticoagulant therapy, removal of embolus

Pulmonary Cancer
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Patho: irritation to epithelium of the respiratory tract
Etiology: cigarette smoking
S/S: cough, chest pain, hemoptysis (usually brings the pt to the doctor), dyspnea, wheezing
Management: surgical resection/removal, chemotherapy, radiation

~ Circulatory Disorders ~
Factors Affecting Blood Flow
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Blood flow: the amount of blood moved per unit of time
Pressure: the volume of blood or of space to accommodate blood

26
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Velocity: the speed of blood movement
Turbulence: turbulent = bumpy, laminar = smooth
Compliance: the “stretch” of a vessel to accommodate blood; increased elasticity → increased compliance
→ increased blood flow
Resistance: opposition of flow; inversely related to flow (increased resistance = decreased flow)
Total Peripheral Resistance: determined by changes in arterioles
Reflex control: vasodilators act locally; vasoconstrictors are systemic
Radius of vessels: narrow = decreased output flow; wide = increased output flow
Shunting: redirection of blood flow; prioritizes body’s needs

Factors Affecting Resistance
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Diameter of vessel: increased diameter → decreased resistance → increased blood flow
Viscosity of blood: dehydrated = increased resistance; overhydrated = decreased resistance
Vessel arrangement: sequential = increased resistance; parallel = decreased resistance

Arteriosclerosis
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Arteriosclerosis: thickening and hardening of vessel wall → decreased compliance, increased pressure,
increased resistance, and turbulence
Ischemia: insufficient blood flow to tissue that may result in hypoxemia
Hypoxemia: insufficient oxygen levels that may cause cell injury or death

Atherosclerosis
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Patho: form of arteriosclerosis; soft deposits of intra-arterial fat and fibrin in vessels that harden over time
o Inflammatory response: injury to arterial wall → macrophages bind to site → release of oxygen radicals
that oxidize LDL → macrophages engulf oxidized LDL and become foam cells which penetrate intima →
lesion is created (fatty streak) → becomes fatty plaque → collagen migrates and forms fibrous plaque
S/S: d/t inadequate perfusion; varies depending on site and degree of obstruction
Partial obstruction: transient ischemic events occur during exercise or stress
Complete obstruction: d/t complicated lesion; tissue infarction
Risk factors: age, sex, family hx, diabetes, smoking, diet, stress, HTN, cholesterol, sedentary lifestyle, obesity
Complications: angina, MI, sudden cardiac death, HF, stroke, PVD

Plaques
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Stable plaque: thick fibrous cap separates core from the endothelium
Vulnerable/unstable plaque: thin cap; more likely to rupture d/t continued inflammation weakening it
o Rupture: initiates clotting cascade, causing rapid clot formation and further occlusion

27

Aneurysm
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Patho: localized outpouching/dilation of vessel wall or cardiac chamber at a weak, vulnerable area
Risk factors: atherosclerosis, HTN, collagen-vascular disorders (Marfan syndrome), infections (syphilis)
Examples: abdominal aorta, brain
Burst/rupture: causes bleeding and is when symptoms begin

Cardiac Cycle
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Heart: circulates blood via contraction and relaxation
Systole: ventricular contraction; blood is ejected into aorta or pulmonary artery
o “LUB”: S1 sound; closing of tricuspid and mitral valves, opening of semilunar valve
Diastole: ventricular relaxation; blood fills the ventricles
o “DUB”: S2 heart sound; closing of pulmonary and aortic semilunar valves; pressure in aorta > ventricles
o Early stage: ventricles fill rapidly
o Later stage: ventricles “topped off” with atrial contraction

ECG/EKG
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Depolarization: contraction
Repolarization: relaxation
P-wave: atrial depolarization
QRS complex: atrial repolarization and ventricular depolarization; “LUB”
T-wave: ventricular repolarization; “DUB”

Cardiac Performance
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Cardiac output (CO): amount of blood circulated in one minute (~ 5L); SV x HR
Stroke volume (SV): amount of blood ejected during systole
Heart rate (HR): number of beats per minute
o Tachycardia: high HR (>100bpm) leading to higher CO; d/t SNS stimulation
o Bradycardia: low HR (<60bpm) leading to lower CO; d/t PSNS stimulation

Stroke Volume
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Preload: blood volume and pressure in ventricle before systole; when ventricle is relaxed
o High preload: higher SV; increased EDV, venous return, and fluid retention
o Low preload: lower SV; dehydration, small ventricular space, decreased venous return
Afterload: blood volume and pressure in ventricle after systole; contingent on pressures that must be
exerted to eject blood; ventricle contracted; BP increases as afterload increases
o High afterload: low SV; high SVR, vasoconstriction, atherosclerosis, HTN
o Low afterload: high SV; low SVR, vasodilation, vessel compliance

28
•

Inotropy: myocardial contractility; the force of heart contraction
o Affected by: changes in stretching, alterations in SNS and PSNS activation, oxygen supply
o Stronger: high SV; SNS stimulation, increased oxygen, optimal blood volume
o Weaker: low SV; PSNS stimulation, low O2, inadequate blood volume, stretched cardiac muscles

Arterial Pressure
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Arterial pressure: constantly regulated to maintain perfusion
Mean Arterial Pressure (MAP): average pressure in the arteries throughout the cardiac cycle
o Calculation: diastolic + [(systolic – diastolic) / 3]
Systemic vascular resistance (SVR): increased by vasoconstriction and decreased by vasodilation
o Regulated by: SNS, local controls, RAAS
o Alpha adrenergic receptors: cause vasoconstriction
o Beta adrenergic receptors: cause smooth muscle relaxation

Blood Pressure (BP)
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BP: measured variable controlled by the body; adjusted by changing CO and/or SVR
Baroreceptors: sense changes in pressure and reduce BP by decreasing CO; stretch when BP is elevated
Arterial chemoreceptors: sense changes in O2, CO2, and pH and make changes as needed; adjust CO, vessel
diameter, and RR
o Increase BP when: low O2, low pH, or high CO2

Factors of Blood Volume
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Aldosterone: retains sodium and water in the kidneys
Osmoreceptors: neurons in the hypothalamus that stimulate ADH
o ADH: water retention, thirst, and vasoconstriction, increased preload
Natriuretic peptides: sodium excretion, diuresis, vasodilation, oppose RAAS, decrease preload
Filtration forces: hydrostatic and oncotic forces that regulate water movement

Hypertension (HTN)
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HTN: systolic >120 or diastolic >80; “silent killer” due to lack of symptoms
Complications: stroke, renal failure, L
...
arm; N+V, dyspnea, diaphoresis
Female symptoms: unusual fatigue, sleep disturbances, dyspnea, indigestion, anxiety
Treatment: clot busters, platelet inhibitors, angioplasty stent

Cardiomyopathy
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Patho: heart wall muscle doesn’t function well → decreased CO and SV
Primary etiology: idiopathic
Secondary etiology: HTN, ischemia, genetics, valve dysfunction, pericardial problems, inflammation
Dilated cardiomyopathy: dilation of ventricular chamber → increased preload
Hypertrophic cardiomyopathy: thickened, hyperkinetic ventricular muscle → decreased preload
Restrictive: fibrotic, rigid, non-compliant ventricle

Heart Failure (HF)
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Patho: insufficient CO to meet oxygen needs → activates RAAS and SNS to increase CO and BP
Congestive HF (CHF): HF with fluid overload
Systolic dysfunction: problem with contraction; decreased ejection fraction
Diastolic dysfunction: problem with relaxation; chamber doesn’t fill effectively; normal ejection fraction
Etiology: usually d/t CHD and HTN; may be d/t cardiomyopathy
Treatment: diuretics, ACE inhibitors, beta blockers, daily weights, low-salt diet, BP control
Forward effects: trace effects forward starting at affected ventricle; fatigue
Backward effects: traffic jam; trace effects backwards from affected ventricle; edema

31

Types of Heart Failure
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L
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ventricular infarction or HTN
o Forward effects: decreased CO to systemic circulation; inadequate oxygen supply
o Backward effects: affects lungs; pulmonary congestion → increased RV afterload → RV failure
R
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ventricular infarction or pulmonary disease
o Forward: decreased CO to pulmonary circulation → decreased CO to systemic circulation
o Backward: affects body; JVD, congestion in abdomen, bloating, anorexia, ascites
Biventricular HF: L
...
sided HF

Shock
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Patho: insufficient CO to maintain adequate BP for adequate tissue and organ function
S/S: dilated pupils, cool/clammy skin, altered mental status (AMS), anxiety/panic, HoTN, narrow pulse
pressure, tachycardia, tachypnea, uncompensated mixed acidosis with hypoxemia
Compensation: RAAS and SNS activation, attempts to maintain MAP, prioritizes BF to heart/brain
Cardiogenic shock: decreased cardiac function → decreased CO → tissue hypoxia
o Treatment: inotropic meds, oxygen, intra-aortic balloon pump
Hypovolemic shock: loss of whole blood, plasma, or fluid
o Treatment: fluid resuscitation
Anaphylactic shock: type I hypersensitivity reaction; massive vasodilation, peripheral pooling, and
hypovolemia → decreased perfusion and impaired metabolism
o Treatment: EpiPen to increase BP, vasoconstriction, increase contractility, and dilate bronchi
Neurogenic/vasogenic: widespread vasodilation d/t PSNS overstimulation or SNS understimulation
o Treatment: treat or remove underlying cause
Septic: infection → bacteremia → sepsis
o Treatment: antibacterial therapy, remove source of infection, fluid resuscitation, vasoactive meds

Complications of Shock
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Acute respiratory distress (ARDS): lung inflammation, diffuse alveolocapillary injury, pulmonary edema
Disseminated intravascular coagulation (DIC): multiple clots form → tissue damage, less clotting factors
Acute renal failure (ARF): oliguria, increased BUN/Cr
Multi-organ failure (MOSF/MODS): dysfunction or failure of multiple organs with a high mortality rate

Fibrillation
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Fibrillation: uncontrolled quivering
Ventricular fibrillation (V
...
fib): atrial quiver; missing P-wave; problematic for clotting

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~ Neurological Disorders ~
Anatomy and Physiology
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Central nervous system (CNS): brain and spinal cord; cognition, consciousness, motion, sensation
o Upper motor neurons: direct, influence, and modify reflex arcs and lower motor neurons
o Lower motor neurons: directly influence muscles
Peripheral nervous system (PNS): peripheral nerves; motion, sensation; efferent neurons
o Sensory and motor neurons: “the messengers”; afferent neurons
Dermatomes: sensory designations
Myotomes: motor/muscle designations
Frontal lobe: executive functions, thinking, planning, organizing, problem-solving, emotions, behavior
control, personality
Temporal lobe: memory, language, understanding
Occipital lobe: vision
Parietal lobe: perception, spelling, math, making sense of the world
Sensory lobe: sensation
Motor lobe: movement
Neuroplasticity: the ability of the brain to rewire itself to regain loss of function from injury or disease

Amyotrophic Lateral Sclerosis (ALS)
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ALS: Lou Gehrig’s Disease; neurologically-degenerative, rapidly progressive, and fatal; weakness and wasting
of muscles under voluntary control
Muscle atrophy: d/t motor neuron degeneration and sclerosis of the corticospinal tract in the lateral column
Initial S/S: generalized weakness in muscles that progresses to flaccid or spastic paralysis
o Complications: difficulty with swallowing, secretions, communication, respiration
Death: occurs 2-5 years after onset; usually d/t respiratory failure

Traumatic Brain Injury (TBI) Assessment
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Altered consciousness: confused, lethargic, obtunded, stupor, coma
Variant breathing pattern: d/t injury to the brainstem; may be erratic/rapid or prolonged/gasping for air
Pupil changes: altered size and reactivity
Eye reflex changes: eyes remain fixed in place during Doll’s Eye Maneuver and Caloric Reflex Test
Abnormal posturing: changes in skeletal muscle motor response
o Decorticate: hemispheric damage; arms crossed over chest (“to core”)
o Decerebrate: deeper, severe injury to the midbrain; arms at sides

33

Types of TBI
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Coup injury: initial impact/force against object
Contrecoup injury: ricochet/rebound/secondary impact with the skull
Acceleration injury: person is still and then goes into motion
Deceleration injury: person is moving and then stops
Focal: specific, grossly observable lesion
Diffuse: seen with microscope; shaking effect produces strains and distortions in the brain

Spinal Cord Injury (SCI)
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Effects: damage to vertebral column (fracture/dislocation), damage to motor neurons, herniated discs,
searing of spinal cord (never move patient without stabilizing the spine first)
Complications: loss of voluntary control, flaccid paralysis, hypotonia, muscle atrophy, hyporeflexia
Extent of transection: results of the injury
o C2: quadriplegic, vent dependent
o C4: able to move head, mouth, shoulders, and diaphragm
o C6: weak hands, able to drive with hand control
o T1: paraplegic, normal upper body

Brain Bleeds
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Etiology: injury, aneurysm, burst artery in late-stage HTN, burst arterial aneurysm
Effects: shift and distort brain, herniation, compressed blood vessels, ischemia
S+S: severe headache, altered LOC, low GCS score, compromised brain stem function
Epidural bleed: between the skull and dura; mostly arterial
Subdural bleed: between the dura and arachnoid; mostly venous
Subarachnoid/intracerebral bleed: between the pia mater and brain; venous or arterial
Hemorrhagic stroke: bleeding within the brain

Stroke/Cerebrovascular Accident (CVA)
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S+S: depend on the affected area; unilateral numbness and weakness, confusion, trouble speaking or
understanding, visual disturbances, dizziness, trouble walking, severe headache
Hemorrhagic stroke: 20% of occurrences; brain bleeds; high mortality and morbidity rate
Ischemic stroke: 80% of occurrences; usually d/t blood clots or thromboembolism
o Treatment: early is crucial (within 3 hours of onset); fibrinolytic used for re-perfusion
Risk factors: HTN, A
...
pylori, meds that inhibit prostaglandins (aspirin, NSAIDs, glucocorticoids), smoking, stress,
genetics, gastric reflux
S/S: depend on location of ulcer; some asymptomatic, some with “false symptoms” with no ulcer present
o Duodenal ulcers: chronic, intermittent epigastric pain 2-3 hours after eating; relieved by food/antacids
▪ Complications: hematemesis, melena, perforation, outlet obstruction, inflammation
o Gastric ulcers: chronic epigastric pain immediately after eating; pain relieved with antacids; anorexia,
vomiting, weight loss
Treatment: aimed at relieving the cause of hyperacidity
o Acid-lowering agents: antacids, histamine blockers, PPIs
o Antibiotics: treat H
...
B
Hepatitis E: fecal-oral spread through contaminated water; no chronic state; no treatment or vaccine

44

Liver Cirrhosis
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Patho: end-stage fibrosis (scarring) of the liver; nodules d/t degeneration and scarring, disruption of
sinusoids and bile ducts; direct/acute hepatocyte dysfunction, portal HTN d/t ischemia
S/S: jaundice, ascites, portal HTN, anorexia, third spacing, coagulopathy, palmar erythema, spider
angiomata, gynecomastia, encephalopathy, anemia
o Portal HTN: ascites, esophageal varices, GI bleeds, caput medusae, splenomegaly

Jaundice
•

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Bilirubin: produced by normal hemoglobin breakdown
o Unconjugated: increases with liver disease as the liver loses function
o Insoluble: deposits in brain, skin, and sclera, producing jaundice
▪ Kernicterus: permanent brain damage in infants
Patho: overproduction of RBCs d/t chronic destruction or under-excretion of bilirubin d/t decreased
transport into liver cells



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