Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Patho Test 1 > TEST 2: Infection > Flashcards

TEST 2: Infection Flashcards

1
Q

$ Communicability

A

The time during which an infectious agent may be transferred directly or indirectly
Aka “infectious period”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

$ Infectivity

A

The ability to produce or transmit infection
Aka “contagious period”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

$ Immunogenicity

A

The ability of a foreign substance (antigen) to provoke an immune response in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

$ Toxigenicity

A

The ability of a microorganism to produce a toxin that contributes to the development of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

$ Pathogenicity

A

The ability of an organism to cause disease (ie harm the host)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

$ Virulence

A

The degree of pathology caused by the organism
It is usually correlated with the ability of the pathogen to multiply within the host but may be affected by other factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

$ Portal or entry

A

The way a pathogen enters a susceptible host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

$ Endemic

A

A disease or condition regularly found among particular people or in a certain area
Example: malaria, rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

$ Epidemic

A

A disease that affects a large number of people within a community, population, or region
Example: when Covid was confined to China, opioid and obesity in the US (unique problem to the US)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

$ Pandemic

A

An epidemic that’s spread over multiple countries or continents
Example: Covid when it spread continents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

$ Stages of progression of infection

A
  1. Colonization
  2. Invasion
  3. Multiplication
  4. Spread
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Colonization

A

Involves the establishment of pathogens on a hosts surface
-Successful colonization requires adhesion of pathogen to host cells (competing with normal flora)
-Affected by the presence of specific adhesion molecules on the pathogen and complementary receptors on the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

$ Invasion

A

Pathogens penetrate host epithelial barriers to enter underlying tissues or cells (triggers inflammatory response)
-Pathogens produce enzymes to degrade cell junctions and the ECM (facilitating entry)
-Successful invasion may also include mechanisms to evade the hosts initial immune defenses (ie altering surface proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

$ Multiplication

A

Once inside the host, the pathogens begins to replicate in the tissues utilizing host resources
-Often leads to disruption of normal cellular and tissues responses (causes damage)
-The immune system responds to the the increased pathogen load by implementing things like inflammation and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

$ Why do pathogen virulence factors matter?

A

They are specialized molecules/ structures that enable a microorganism to colonize a host, evade or suppress immune responses, and cause disease
-They contribute to a pathogens ability to infect and damage the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

$ Bacterial structure

A

-unicellular prokaryotes (small)
-Rigid cell wall made of peptidoglycan
-Multiple different shapes:
1. Spherical (cocci): pairs, chains or clusters
2. Rod shaped (bacilli): chain
3. Spiral / other shaped: have no particular shape, they morph to evade detection
-Bacteria secrete enzymes that degrade host tissues (hyaluronidase, collagenase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

$ General components of bacteria

A
  1. Pili: Hairlike structures that help them attach to surfaces and other bacteria
  2. Plasmid: genetic material associated with bacteria (if bacteria is abx resistant it is encoded here)
  3. Ribosomes: structures that allow them to make proteins
  4. Cytoplasm: gel that houses ribosomes and genetic material
  5. Cytoplasmic membrane: phospholipid layer (important for abx treatment)
  6. Capsule: layer around the outside the prevents bacteria from drying out or getting engulfed
  7. Flagellum: can propel them (not all bacteria have)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Bacteria Taxonomy

A

1.Gram negative
2. Gram positive
3. Acid Fast Bacilli
4. Aerobic
5. Anaerobic
6. Facultative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

$ Gram negative bacteria
(Release ENDOTOXINS)

A

Categorized as such because they do not take up the stain under microscope
-Thin cell wall but duplicates of them which make them more resistant to being destroyed
-Release ENDOtoxins from cell wall as the cell walls lyse which causes:
Fever, hypotension, DIC, septic shock
-examples: nisseria, salmonella, shigella, Klebsiella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

$ Gram positive bacteria
(Release EXOTOXINS)

A

They hold onto the stain under the microscope (turn purple)
-Single cell wall
-Release EXOtoxin:
Type 1 exotoxin: pro inflammatory cytokines
Type 2 exotoxin: damages cell membranes
Type 3 exotoxin: enters the cell itself and causes damage to the inside of the cell
Examples: clostridium, staph, strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

$ Acid Fast Bacilli

A

Unusual and opportunistic infections
-Have a really thick cell wall
-Slow growing due to lack of nutrient penetration of the thick cell wall
-Therefore, takes a longer time for culture to result positive
-Long duration of abx therapy
-Examples: TB, mycobacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

$ Aerobic vs anaerobic bacterium

A

Once you’ve classified gram negative, positive, or acid fast, can further differentiate aerobic or anaerobic
-Aerobic: must have oxygen (ie pseudomonas: lungs, anthrax: soil)
-Anaerobic: don’t need oxygen to grow (ie bacteroides: abscess or GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

$ Facultative anaerobes

A

Can grow in either aerobic or anaerobic (but prefer aerobic)
-Examples: E. Coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

$ Staphylococcus Aureus
GRAM POSITIVE COCCI IN CLUSTERS

A

Common bacteria that lives in skin flora and nasal passages
-skin and soft tissue infections: boils, abscesses, cellulitis, food poisoning, surgical wound infections
-can also cause PNA, bacteremia, endocarditis
-adheres to surface proteins in connective tissue and endothelium
-Have protective capsule around the outside that produces proteins that keep the complement system from being activated
-Is resistant to intercellular lysing (makes it hard to kill)
-There ARE resistant forms (MRSA)
-virulence factors:
1. Protein A: interferes with immune recognition and phagocytosis
2. Exotoxins: includes enterotoxins that cause food poisoning and toxic shock syndrome toxin 1 (TSST-1)
3. Biofilm formation: concerning in chronic and device related infections as there is enhanced resistance to host defenses and abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

$ Escherichia Coli
GRAM NEGATIVE RODS

A

-In the normal flora of the GI tract
-Virulence factors:
1. Pili/ fimbriae: structures that facilitate adhesion to the urinary/ intestinal tracts
2. Shiga toxin production: disrupts protein synthesis within host cells (contributes to bloody diarrhea and severe kidney damage)
-Most common cause of UTI’s (found in biofilm on foleys)
-Can cause significant GI distress (travelers diarrhea from ETEC or bloody diarrhea from EHEC)
-Severe complication: HUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hemolytic Uremic Syndrome
(HUS)

A

-A severe complication of E. Coli (EHEC) infections, particularly serotype O157:H7
-Shiga toxin binds to receptors on endothelial cells (particularly in the kidneys) that cause cell damage and death
-manifestations:
1. Hemolytic anemia (d/t destruction of RBC’s)
2. Acute renal failure (d/t damaged renal vasculature)
3. Thrombocytopenia (d/t platelet consumption in microvascuar system)
-Mechanism of damage: toxin induced injury to cells triggers microthrombi formation in small vessels, reducing blood flow (particularly to the kidneys as they have an abundance of toxin receptors in their vasculature)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

$ Mycobacterium Tuberculosis

A

Survives and grows WITHIN macrophages and phagolysosomes
-Therefore, the things that normally fight bacteria it uses to grow and survive
-Develops a thick capsule/ membrane that prevents phagocytosis
-Induces anergy (suppressing the host
response)
-As mycobacterium involves involved in forms granulomas—> tubercle—> caseates—>collagen scar—> immune response—> dormant
-very contagious, opportunistic infections can be resistant and latent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

$ Mechanisms of antibiotic resistance

A
  1. Enzymatic degradation of abx
  2. Alteration of target sites
  3. Efflux pumps
  4. Reduced permeability
  5. Bypass pathways
  6. Genetic transfer and mutation
  7. Biofilm formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
  1. Enzymatic degradation of antibiotics
A

Beta lactamases: enzymes that hydrolysis the beta-lactam ring of abx like penicillin and cephalosporins, inactivating them
-Extended spectrum beta lactamases (ESBL’s) and carbapenamases are advanced enzymes that target a wider range of antibiotics

30
Q
  1. Alteration of target sites
A

-Modification of penicillin-binding proteins (PBP’s): Bacteria alter the structure of PBP’s, reducing the binding affinity of beta lactam antibiotics
-Ribosomal alterations: structural changes in bacterial ribosomes prevent abx like macrolides, tetracyclines, and aminoycosides from binding (thus inhibiting their action on protein synthesis)

31
Q
  1. Efflux pumps
A

Active Efflux systems: Efflux pumps in bacterial membranes expel antibiotics and other toxic substances from the cell, lowering the antibiotic concentration to sub-lethal levels.
-This mechanism is common resistance against tetracyclines, fluoroquinolones, and macrolides.

32
Q
  1. Reduced permeability
A

Changes in porin channels: in gram negative bacteria, alterations or reductions in outer membrane porin channels limit antibiotic uptake into the cell (affecting drugs that need entry to reach their target).

33
Q
  1. Generic transfer and mutation
A

-Horizontal gene transfer (HGT): bacteria acquire resistance genes from othered through transformation (direct DNA uptake), transduction (transfer via bacteriophages), or conjunction (via cell to cell contact using plasmids)
-Spontaneous mutations: random mutations in bacterial DNA can offer resistance, especially under sub-lethal antibiotic exposure, fostering the selection and spread of resistant strains

34
Q

Antibiogram

A

Is an antimicrobial susceptibility summary
-summarizes the specificity of target antibiotics to prevent over use
-Allows for choosing the most appropriate antibiotic and decreasing antibiotic resistance in the future

35
Q

$ Antibiotic stewardship

A

-Coordinated strategies used to improve the use of antibiotics, enhance patient outcomes, reduce microbial resistance, and decrease the spread of infection cause by MDRO’s.
-Always draw cultures and follow them
1. Optimize ABX usage
2. Narrowing therapy as soon as able from broad spectrum abx to targeted
3. Using evidence based guidelines and promoting rapid diagnostic testing
4. Provide ongoing education for medical professionals and the public
5. Monitoring prescription patterns and resistance trends
6. Provide feedback to prescribers
7. Good infection prevention and control (follow for C diff possibility)

36
Q

$ Community VS. hospital acquired infections

A

-Hospital acquired if: less than 14 days after discharge, more than 4 days since admission, any time in long term care setting (SNF)
-Hospital acquired tend to be more virulent than community acquired
-Common hospitla acquired: CLABSI, CAUTI, VAP, surgical site infections (SSI)-
These are not reimbursable conditions
-Different pathogens usually causative so different abx may be needed and length of treatment may differ

37
Q

$ Fungi

A

Mold and yeasts
-are eukaryotic with a nucleus and organelles; more complex than bacteria
-Cell wall is composed of chitin and glucans
-Highly opportunistic (cause disease mainly in immune compromised hosts)
-T cells super important in fighting fungi (produce cytokines to activate macrophages)
-Can produce mycotoxins that are toxic to humans if ingested
-Adapt to host environment
-Can be superficial skin infection or severe systemic
-Can evade detection by capsule formation, biofilm development, and modulation of immune detection
-Cause damage by tissue destruction:
1. Direct: enzymes (preoteases) secreted degrade host tissues and toxins secreted damage fungal structures
2. Indirect: causing inflammation

38
Q

$ Candida Albicans

A

-Normal part of microbiome: skin, GI tract, mouth, vagina
-Opportunistic, yeast- like infection that affects immunocompromised
-Are dimorphic (can switch between 2 forms) which is crucial for virulence
-Hyphal transformation which is associated with tissue invasion, boosting its ability to penetrate and cause damage
-Very resistant to anti-fungals
-can form biofilms on surfaces (foleys) which enhances its ability to adhere to surfaces and resist treatment
-pathological effects:
mucocutaneous infections (ie thrush, vaginal infections)
Systemic: bloodstream infections
-Candida Auris is a new strain that is resistant this is MDRO

39
Q

$ Viruses

A

Small pathogen consisting of nucleic acid enclosed in a protein (capsid) that protects the nucleus
-Comes in various shapes (helical, icosahedral, or complex)
-Pathogenicity:
-Obligate intracellular parasites: require host cells to replicate; they hijack host machinery to produce viral components
-High mutation rates: RNA viruses in particular have high mutation rates allowing rapid evolution and evasion of immune responses
-When they hijack a cell, it usually results in cell death
-Can evade immune responses through latency and antigenic variation
-can cause indirect damage by provoking stroke immune responses leading to to tissue damage (ie inflammation)

40
Q

$ Coronavirus

A

100’s of strains
-Transmitted via droplet
-Mild to moderate URI symptoms
-Ie SARS/ MERS

41
Q

$ Covid 19

A

-Coronavirus shift (SARS-Co-V2)
-Antigen drift vs. antigenic shift ( ex influenza a and b variation)
-spike protein allows virus to infect cell
-S/s: cough, fever, loss of taste/ smell (can lead to PNA/ARDS)
-Infectious 2-3 days before symptoms appear & up to 10 days after symptoms
-Virus enters host cells by binding to ACE enzyme receptors, virus then undergoes endocytosis or direct with the cell membrane, releasing its RNA into host cell
-Replication of the virus leads to extensive immune activation—> cytokine storm and widespread inflammation
-Associated with endothelial damage, pro-thrombotic and blood clots
-Long covid: persistent fatigue, dyspnea, brain fog, joint pain

42
Q

$ Influenza

A

-Caused by influenza viruses a and b (known for high mutation rates)
-Incubation period short, however shed the virus for a long time
-S/s: sudden onset fever, chills, muscle aches (from release of pro inflammatory cytokines and chemokines TNF & Interferon), HA, resp symptoms (cough and sore throat)
-Enter the host cell via hemagglutinin binding to sialic acid receptors (viral RNA is then released and transcribed to mRNA initiating viral replication)
-Initial damage to resp epithelium can predispose to secondary bacterial infections (PNA)
-Rare neurological complications: Reye’s syndrome and Guilin barre

43
Q

$ Herpes simplex

A

-Sheds from the point of infection
-Activated by fever, fatigue, stress
-Never get rid of it always dormant and can re-activate
-HSV 1–> oral infection via saliva contact
-Moves along axon of dorsal root ganglion
-HSV 2 —> genital infection with mucous membrane contact (unprotected sex)

44
Q

$ Herpes varicella and zoster

A

-Varicella is the initial infection you get, zoster is the reactivation of the previously acquired infection
-appears as vesicles along dermatomes
-mother can transmit to neonate (very harmful)
-Post heretic neuralgia with zoster
-vaccinations available

45
Q

$ Measles Rubeola (classic)

A

-RNA virus spreads thru upper resp tract
-spreads thru local lymphatic tissues and disseminates
-s/s: maculopapular rash (head trunk and extremities), Koplick spots, buffalo mucosa
-VERY contagious
-Incubation period 6-19 days (can be contagious four days before rash and up to 5 days after)
-spread via droplet
-more outbreaks due to lower vaccinations
-complications: PNA, diarrhea, otitis media, SSPE (fatal)

46
Q

$ Rubella (aka 3 day or German measles)

A

-RNA virus sore via upper resp tract
-Also presents with the maculopapular rash
-Most dangerous in first trimester of pregnancy—> congenital rubella
Syndrome (sensorineural deafness, retinopathy, cataracts, congenital heart disease)

47
Q

$ HIV infection

A

-Caused by two main types: HIV 1 (more common, less virulent) and 2 (less common, less virulent— west Africa)
-Acute phase presents flu like symptoms
-Transmitted via bloodborne pathogens (IV drug use, sex, mother to baby)
-Chronic is often asymptomatic unless progresses to AIDS
-Patho: HIV primarily targets CD4+ T cells via binding, allowing fusion and entry
-revers transcription converts the viral RNA into DNA (integrating to the host)
-Persistent replication leads to CD4+ T cell depletion, leading to chronic immune activation and inflammation (which results in immunocompromise)
-Unprotected replication and immune system exhaustion leads to AIDS
-ART has made this chronic not fatal but can have metabolic, cardiovascular, and neurocognitive changes
-Untreated HIV can lead to opportunitistic infections and malignancy

48
Q

$ HIV Viral structure

A

Envelope: composed of lipid bilayer (acquired from host membrane) containing viral glycoproteins gp120 and gp41 which are crucial for attachment and fusion with host cells
-Capsid: shell inside the envelope made of protein p24 that encased the viral RNA and enzymes
-Two strands of RNA genetic material
-Reverse transcriptase, integrate, and protease (essential for viral replication and integration into host genome)

49
Q

$ CD4+ Cells

A

-Are central to immune response (coordinating both adaptive and innate systems)
-When they are depleted this leads to immunodeficiency and thus a higher susceptibility to infection and cancer
-Have 3 receptors on the cell membrane which help HIV infiltrate the CD4
-Eventually has apoptosis or are killed by other T cells

50
Q

$ HIV diagnosis

A

-Serological tests that detect the p24 antigen in the blood
-ELISA (Enzyme linked immunosorbent assay): initial screen for antibodies
-West blot (immunoflourescence assay): confirmatory test for HIV proteins
-NAT (nucleic acid test): detects the presence of HIV RNA (neonates)
-Viral load testing: measures the amount of HIV RNA in the blood
-CD4+ T cell count: regular monitoring required for treatment and immunity

51
Q

$ Acute HIV Infection

A

-1-6 weeks after exposure
-very nonspecific, flu like symptoms
-usually later diagnosis because of that
-common s/s: fever, lymphadenopathy, rash, myalgias, diarrhea, n/v, hepatosplenomegaly, weight loss, thrush

52
Q

$ Gold standard HIV test

A

-A combo HIV Ab/Ag test
-Designed to detect HIV infection early and diagnose acute HIV infections

53
Q

$ Possible HIV Test results

A

-If antigen is negative: person is unlikely to have acute HIV infection and is negative
-If antigen is positive: then HIV1/ HIV 2 antibody differentiation assay should be completed
-If antigen is positive and HIV 1/HIV 2 antibody differentiation assay is negative and indeterminate: an HIV viral
Load should be performed to clarify diagnosis

54
Q

$ Acquired Immunodeficiency Syndrome
(AIDS)

A

The most advanced stage of an HIV infection, characterized by severely weakened immune system due to depletion of CD4+ T cells
-Diagnosis is made when CD4+T count is LESS THAN 200 cells/ mm3 and/ or the presence of an opportunistic infection
-manifestations: sever weight loss, persistent fevers, prolonged fatigue, opportunistic infections/ malignancies

55
Q

$ Key differences in HIV vs AIDS

A

-HIV: encompasses the spectrum from initial diagnosis to final stage of AIDS
-AIDS: specifically refers to the endpoint of untreated HIV infection where severe immunosuppresion results in opportunistic infections
-HIV diagnosis: based on the presence of the virus in the body
AIDS diagnosis: based on CD4+T cell count of LESS than 200 and opportunistic infection

56
Q

$ HIV signs of immunocompromise

A

-Thrush
-Cervical carcinoma in situ/ dysplasia
-ITP
-Herpes zoster
-Frequent vaginal yeast infection
-Kaposi Sarcoma
-Pelvic inflammatory disease
-Fever for over a month

57
Q

$ AIDS defining opportunistic infections

A

Respiratory:
-Pneumocystis jirovecii PNA (PJP)/ TB

GI:
-Cryptosporidiosis/ candidiasis

Neuro;
-Toxoplasmosis/ cryptococcal meningitis

58
Q

$ Pneumocystis Jirovecii Pneumonia
(PCP)

A

-Opportunistic infection caused by a fungus
-transmitted through inhalation of airborne cysts (humans are only known reservoir)
-s/s: gradual onset of dyspnea, non productive cough, fever
-Often present with hypoxemia and diffuse interstitial infiltrates or ground glass opacities
-Organisms cause damage to alveolar epithelium leading to impaired gas exchange
-Infected alveoli become filled with foamy exudate that reduces lung compliance and oxygenation capability

59
Q

$ Mycobacterium Avium Complex
(MAC)

A

-Opportunistic infection caused by mycobacterium
-Transmitted from environmental
Sources like soil/ water (not person to person contact)
-S/s: fever, night sweats, weight loss, abdominal pain, diarrhea, cough, enlargement of lymph nodes
-MAC organisms invade the GI tract
Or lungs first then disseminate to the rest of the body
-Induces a granulomatous inflammatory response

60
Q

Generic signs of immune decline

A
  1. Chronic fatigue
  2. Weight loss
  3. Persistent fever
  4. Night sweats
  5. Lymphadenopathy
61
Q

$ Cytomegalovirus
(CMV)

A

-Opportunistic infection cause by the cytomegalovirus
-Transmitted through direct contact with body fluids
-manifestations: retinitis, esophagitis, colitis, encephalitis
-CMV can remain latent and reactivate when immunity is compromised

62
Q

Opportunistic cancers

A

-Kaposi’s sarcoma: vascular cancer causing purple/ brown skin lesions
-Non-Hodgkin Lymphoma: can affect lymph nodes, GI tract, CNS
-Invasive cervical cancer

63
Q

Antiretroviral therapy
(ART)

A
  1. Reverse Transcriptase inhibitor (RTI): prevent the conversion of viral RNA into DNA
  2. Protease Inhibitors (PI): inhibit the HIV protease enzyme, preventing the maturation of viral particles
  3. Integrase Inhibitors: block the integration of viral DNA into host genome
  4. Entry inhibitors: prevent the virus from entering host cells
  5. Fusion inhibitors: prevent the fusion of the HIV envelope with the host cell
    Membrane
64
Q

Effects of the CCR5 Mutation

A

-A genetic mutation that results in the lack of functional CCR5 receptors on the cell surface
-People who are homozygous for this mutation are HIGHLY RESISTANT to getting the HIV infection because the virus can’t effectively enter their CD4+ cells using the CCR5 pathway
-implications: could be used to advanced research and treatment options

65
Q

$ HIV in children

A

-Neonates are infected via the placenta from their mother (very rare nowadays)
-To diagnose HIV during post natal period, use HIV viral load
-2 negative viral load tests at 2 weeks and 4 weeks is presumed uninfected
-2 negative viral load tests against 1 and 4 months is definitive uninfected
-HIV without prenatal care start showing symptoms around 6 months with opportunistic infections (life expectancy no more than 3 years if untreated- rare)

66
Q

$ Streptococcal Infections
GRAM POSITIVE COCCI IN CHAINS

A

-Most common infections: Pharyngitis
(Strep throat), skin infections (impetigo and cellulitis), PNA, otitis media
-virulence factors:
1.M Protein prevents phagocytosis
2. Streptolysins: contribute to hemolysis and tissue damage
3. Exotoxins: lead to systemic responses like scarlet fever and toxic shock syndrome
4. Hyaluronic acid capsule: mimics host tissues and cloaks bacteria from the immune system aiding in evasion
-Patho: post infectious glomerulonephritis

67
Q

$ Vancomycin-Resistant Enterococcus
(VRE)
GRAM POSITIVE COCCI

A

-Normal part of GI flora
-Resistance to Vanco primarily due to the acquisition of the vanA gene (altering cell wall precursor pathways)
-Often causes healthcare associated infections (particularly in immunocompromised)

68
Q

Pyrogen definition

A

Substances that cause fever by triggering the body’s thermoregulatory system to increase the set point of body temperature

69
Q

Exogenous Pyrogens

A

-Are external substances that enter the body from the outside environment (usually microbial sources)
-Are derived from bacteria, fungi, viruses
-Normally gram negative bacteria
-They do not directly cause fever, they stimulate the hosts macrophages to produce endogenous pyrogens

70
Q

Endogenous Pyrogens

A

-Fever inducing substances produced WITHIN the body (immune system)
-Are primarily cytokines such as interleukin 1 and 6, and tumor necrosis factor alpha (produced by immune cells in response to exogenous pyrogens or signs of inflammation)
-They act on the hypothalamus, prompting the production of prostaglandins that elevate the body’s temperature set point, causing fever

71
Q

$ Lab changes with infection

A

CBC:
-Elevated WBC (bacterial)
-Increased lymphocytes (viral)
-Increased Neutrophils (bacterial)
-Increased eosinophils (parasitic/ allergies)
-Elevated CRP and ESR (bacterial/ systemic infections)
-Elevated AST/ ALT (usually viruses)
-Elevated BUN/Creatinine (severe infections/ dehydration)
-Procal (elevated in BACTERIAL infection to distinguish from viral)
-Cultures used to identify cause

72
Q

$ Common clinical manifestations of infections

A

-General: fever, fatigue, malaise
- Respiratory: cough (wet=bacterial), SOB, sore throat (often viral)
-GI: N/V, diarrhea, abdominal pain
-Skin/ Mucosa: rash, lesions/ ulcers, redness/ swelling
-Neuro: HA, confusion/AMS, seizures
-Musculoskeletal: Maylgia (viral), joint pain or swelling
-Cardio: chest pain, palpitations
-Urinary: Dysuria, increased urgency

Advanced Patho Test 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions