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Summary Understanding Pathophysiology, ISBN: 9781771721172 Pathophysiology (NURS1164)

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Pathophysiology (NURS1164)

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Vancouver Community College (VCC )

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Understanding Pathophysiology

This document describes the understanding pathophysiology textbook so students can ace their final exams.

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CLASS 1 • Virulence – the capacity of a pathogen to cause
severe disease (measles has low virulence, ebola
Mechanisms of infectious diseases: are highly virulent)
• Nosocomial infections • Pathogenicity – the ability of an agent to produce
disease – success depends on communicability,
infectivity, extent of tissue damage, and virulence
• Portal of entry – the route by which a pathogenic
microorganism infects the host
• Toxigenicity – the ability to produce soluble toxins
or endotoxins, factors that greatly influence the
pathogens degree of virulence.

• Factors that influence the capacity of pathogens 3 Types of Host Microorganism interaction
to cause disease - 577 • Commensalism: Where the pathogen benefits while
• Viral Vaccines – p601? ACTIVE the host gains nothing
IMMUNIZATION • Mutualism: Occurs when both the pathogen and
• Bacterial Vaccines p601? ACTIVE the host benefit
IMMUNIZATION • Parasitism: Occurs when the pathogen benefits but
the host is harmed
Terminology
• Epidemiology: study of factors, events, and
Agents of Infectious Disease
circumstances that influence transmission of
a. Prion
infectious disease among humans
• Prion diseases are rare, fatal, degenerative
• Incidence: number of new cases of infectious
brain disorders that occur worldwide
disease within a defined population
• Misfolded amino acid chains that can
• Prevalence: number of active cases of infectious
transmit their misfolded shape onto health
disease at any given time
amino acid chains of the same type
• Host - any organism capable of supporting
b. Virus
nutritional and physical growth requirements for
another organism • Second smallest pathogen: no organized
• Colonization – presence of living organisms on or cellular structures
within a host • Consist of only a protein coat that
• Microflora - bacteria inhabiting exposed surfaces of surrounds a strand of nucleic acid DNA or
the body RNA
• Virulence - disease-inducing potential • Incapable of replication outside host, or
• Infectious disease: WHO defines as disorders living cell
caused by pathogenic microorganisms that can be c. Bacteria
passed from person to person or organism to • Prokaryote: Nucleus not separated or
organism enveloped by membrane
• Pathogen: A pathogen is a microorganism (virus, • Asexual reproduction by cellular division
bacteria, fungi , parasites etc…) that causes illness • Contain RNA and DNA
in the host organism. • Classified by Microscopic appearance
• Saprophyte: Plant, fungus or microorganism that (cocci, etc.)
lives on dead or decaying organic matter. • Classified by Staining of cell (Purple or Red)
• Eukaryote: membrane bound intracellular • Gram-positive organisms: stained purple
compartments called organelles that includes a by primary basic dye (usually crystal violet)
well-defined nucleus. • Gram-negative organisms: not stained by
• Prokaryotes contain no organelles and lack a crystal violet but counterstained red by
distinct nucleus. second dye (safranin)
• Communicability - the ability to spread from one d. Parasites
individual to others • Establish a relationship which the parasite
• Infectivity - the ability of the pathogen to invade benefits at the expense of other species.
and multiply in the host. E.g. HSV can survive for Parasites range from unicellular protozoa to
long periods in latent stage large worms.
• Protozoa
• Helminths and arthropods

, e. Rickettsiaceae, Anaplasmataceae, Coxiella Portals of Entry
• Organisms with combined characteristics of • Penetration (open skin)
virus and bacteria, & produce disease in • Direct contact (mucous membranes)
humans • Ingestion (GI absorption)
• Obligate intracellular pathogens like virus • Inhalation (Respiratory tract)
• Rigid peptidoglycan cell wall
• Reproduce asexually by cellular division Symptoms
• Contain RNA and DNA similar to bacteria • Specific by organism: reflect site of infection
i. Rickettsiaceae- Rocky mountain • diarrhea, rash, convulsions, hemorrhage
spotted fever • Nonspecific: shared by number of diverse
https://www.sciencedirect.com/to infectious diseases
pics/medicine-and- • symptoms such as fever, myalgia, headache
dentistry/spotted-fever • Obvious: predictable patterns
ii. Anaplasmataceae- Tick/fish/animal • chickenpox and measles
vector diseases such as sennetsu • Covert: may require laboratory testing to detect
fever https://rarediseases.org/rare- • hepatitis or increased white blood cell count
diseases/sennetsu-fever/
iii. Coxiella: ca be used as Stages of Infectious Disease
biologicalwarfare Infection in • Incubation period: the period of time between
humans is often asymptomatic, but exposure to an infectious agent and the
it can manifest as an acute disease appearance of the first symptoms, microbes have
(usually a self-limited flu-like been introduced and are starting to multiply
illness, pneumonia, or hepatitis) or • Prodromal period: microbes continue to multiply,
as a chronic form (mainly onset of symptoms usually vague symptoms such as
endocarditis, but also hepatitis and fever, malaise, headache…
chronic fatigue syndrome). C. • Acute stage: signs and symptoms are most obvious
burnetii infection in pregnant and severe
women may result in abortions, • Convalescence: pathogen numbers tend to
premature deliveries, and decrease as immune system mounts a response,
stillbirths. Infection in nature is host may become susceptible to developing
maintained and transmitted by secondary infections
ticks as the principal vector and • Resolution stage: Host generally returns to normal
reservoir. Cattle, sheep, and goats functioning, immune system removes pathogen
are the most important source of and traces of pathogen, however there may be
human infections residual damage that cannot be repaired

Incidence of Disease Tuberculosis
• Endemic: incidence and prevalence of infectious • Tuberculosis is airborne and is spread by infected
disease is expected and relatively stable, in a person coughing
particular geographic region • Incubation period: 2-12 weeks
• Epidemic: Incidence of infectious disease increases • Prodromal phase: 2- 4 days with nonspecific
abruptly and unexpectedly symptoms such as fever and malaise
• Pandemic: incidence of infectious disease moves • Acute phase: Up to 3 years, symptoms include
beyond continental boundaries coughing, hemoptysis, weight loss
• Recovery phase: Unless treated patient will not go
Sources of Infectious Disease into recovery phase treatment can take 6-9 months
• External Locations before cure is possible
• Nosocomial: acquired in hospitalized • Chronic phase: disease is not removed from body
environment and host continues to have TB but now known as
• Community acquired: acquired outside of latent TB
health care facilities
• Host/Vector
• Object or substance from which infectious
agent was acquired
• Can be endogenous or exogenous

, Laboratory Diagnosis of Infectious Agent
Factors Influencing Virulence of • Culture (blood or bodily fluids)
• Serology or detection of characteristic antigens
Infectious Disease • Genomic sequences or metabolites produced by
• Type of pathogen pathogen
• Portal of entry
• Competence of the host immunologic defense Tuberculosis
system • Toxins: Tuberculosis necrotizing factor
Note: • Adhesion factors: Multiple adhesion factors known
- Biofilms still working to determine additional adhesion
- Antitoxins factors
- Exotoxins • Evasive factors: Infect macrophages and trigger
- Enzymes to counteract immunity macrophage apoptosis
- Antibiotic resistance • Invasive factors: Waxy outer coating of the bacteria
- Endotoxins protects it from Abx treatment
For viruses: • Diagnostic procedures:
- Antigenic variation • Interferon Gamma Release Assay or IGRA
- Antigenic drift (BW)
• Chest X-ray or CT Scan
Categories of Virulence Factors • Sputum test for Mycobacterium (C+S)
• Toxins - Compound excreted by the bacteria
Some bacterial toxins, such as Botulinum Nonpharmacological Intervention
neurotoxins, are the most potent • Surgical intervention
natural toxins known. • Providing access to infected site by antimicrobial
• Adhesion factors - how well do the microbes stick agents (drainage of an abscess)
to the host cells • Cleaning of site (debridement)
https://link.springer.com/chapter/10.1007/978-1- • Removing infected organs or tissue (e.g.,
59259-224-1_4 appendectomy).
• Evasive factors - how well the microbes can hide
from the immune system Types of Antimicrobial Agents
https://www.ncbi.nlm.nih.gov/books/NBK8526/ • Antibacterial
• Invasive factors • Antiviral
• Antifungal
Diagnosis of Infectious Disease • Antiparasitic
• Recovery of probable (or suspected) pathogen, or
evidence of its presence from infected site(s) of Antibiotic Mechanisms
diseased host • Interfere
• Accurate documentation of clinical signs and • Interfere with specific step in bacterial cell wall
symptoms (symptomatology) compatible with a synthesis
known infectious process • Inhibit
• C+S (swabs, blood, sputum etc) • Inhibit bacterial protein synthesis
• Antibody testing • Interrupt
• Interrupt bacterial nucleic acid synthesis
Diagnostics • Interfere
• Culture: For a culture, a sample of body fluid or • Interfere with normal bacterial metabolism
tissue is added to a substance that promotes the
growth of microbes Classification of Antibiotic Action
• Serology: Looking at the blood serum to identify • Bactericidal—causes irreversible and lethal damage
antibodies to bacterial pathogen
• Antigen: Looking at the blood or bodily fluids to find • Bacteriostatic—inhibitory effect on bacterial
foreign toxins or substances growth
• Metabolite: Looking at the blood or bodily fluids to
find any by-products of bacterial metabolism
(nitrates/nitrites)
• Molecular detection: Looking at blood and bodily
fluids for genetic markers of infectious agents

, Classification & Target Site of Antibacterial Agents • AKA: Methicillin-resistant Staphylococcus aureus
• Penicillins: cell wall (MRSA)
• Cephalosporins: cell wall • Caused by misuse, overuse and underuse of
• Monobactams: cell wall antibiotic medications such as penicillin, oxacillin,
• Aminoglycosides: ribosomes and cloxacillin
• Tetracyclines: ribosomes • Hospital - associated MRSA strains are mostly
• Macrolides: ribosomes resistant to macrolides, clindamycin, gentamicin
• Sulfonamides: folic acid synthesis and quinolones and may be resistant to tetracycline
• Glycopeptides: ribosomes and timethoprim-sulfamethoxazole. May be
• Quinolones: DNA synthesis sensitive to vancomycin and linezolid
• In other words, use of antibiotics caused S. aureus
Intravenous Immunoglobulin and Cytokine Therapy mutation
• Supplementing or stimulating a host’s immune
response so the spread of a pathogen is limited or MRSA Risk factors:
reversed • increased age
• Pathogen-specific antibodies given to patient as an • Admissions to hospital, extended stay in acute care
infusion to facilitate neutralization, phagocytosis, or intensive care units
and clearance of infectious agents above and • debilitated and /or bed bound requiring extensive
beyond capabilities of the diseased host hands on care
• invasive procedures
Tuberculosis drugs: • the presences of invasive indwelling devices
• Isoniazid: inhibits cell wall synthesis • recurrent antibiotic use
• Rifampin: inhibits DNA-dependent RNA polymerase • presence of surgical wounds, decubitus ulcer, or
activity in susceptible Mycobacterium tuberculosis other chronic wounds
organisms. • contact with/proximity to patient colonized or
• Ethambutol: Bacteriostatic in action, although the infected with MRSA with draining skin lesion or
exact mechanism of action has not been fully wounds not covered by dressings, or copious
elucidated, the drug appears to inhibit the synthesis uncontrolled respiratory secretion
of one or more metabolites. • malnutrition
• Pyrazinamide: acts to acidify the interior of M. • Immunosuppressed
tuberculosis and may disrupt the function of fatty
acid synthase According to BCCDC:
• 20-30% of healthy people are colonized with S.
Drug Resistance and Super Bugs aureus bacteria in nasal passages
• Bacterial resistance mechanisms • 30-60% of hospitalized patients that are colonized
• Inactivate antibiotics with MRSA develop MRSA infections
• Genetically altered antibiotic binding sites • 5-15% of residents in LTC facilities are likely to
• Bypass antibiotic activity develop MRSA infections
• Changes in bacterial cell wall • According to PHAC, between 1995 and 2003, MRSA
• Antiviral resistance mechanisms rates in Canadian hospitals (participating in a study)
• Nucleoside analogs increased from 0.46 cases per 1,000 admissions, to
• Protease inhibitors 5.10 per 1,000 admissions
• Need for combination or alternating therapy with
multiple antiretroviral agents PATHOGENESIS of MRSA
• Usually result of genetic mutations that can be • Colonization involves host contact with S. aureus;
transmitted directly to neighboring microorganisms • Adheres to host tissues and prosthetics
by plasmid exchange or incorporation of free DNA. • S. aureus evades hosts immune response by
Some microorganisms can inactivate antibiotics forming biofilm on surfaces
(understanding patho book, p. 189) • Biofilm also protects S. aureus from antimicrobials
• S. aureus can invade and survive inside epithelial
MRSA cells and endothelial cells, which may allow it to
• Mutation of Staphylococcus aureus (Staph) bacteria escape host immune defenses
commonly found on skin and nares of healthy • S. aureus is able to form small colony variants (SCV)
people (normal flora) which may contribute to persistent and recurrent
• Strain of staph bacteria that developed resistance infections
to methicillin antibiotics

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