Hypersensitivity, virus Flashcards

1
Q

Hypersensitivity Reactions

A
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2
Q

Penicillin Allergy

A
  • Most commonly reported medication allergy. However, more than 90% of patients who report the allergy are found to not be allergic
  • Important to dustinguish between immediate and delayed reactions (because IgE mediated reactions can lead to anaphylaxis and death)
    • Immediate - begin within one hour of last administered dose (need initial sensitization before patient develops symptoms). IgE mediated
    • Delayed - appear after multiple doses, typically days or weeks after administration.
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3
Q

Clinical Presentation allergic reaction

A
  • Pruritis
  • Flushing
  • Urticaria (hives)
  • Angioedema
  • Bronchospasm (wheezing, chest tightness, difficulty breathing, repetitive dry cough)
  • Laryngeal edema (throat tightness or change in voice quatity)
  • Abdominal distress (cramping, nausea, vomiting, or diarrhea)
  • Hypotension
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4
Q

Viruses

A
  • Basic life form made up of a protain coast (capsid) that surrounds genetic material
  • Do not have organelles or ribosomes
  • Genetic material is either DNA or RNA
    • Genetic material is replicated when virus takes over host cell’s synthetic macinery (viruses contact the genetic material but not the enzymes needed to replicate it).
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5
Q

Virus - Nucleic Acid

A
  • RNA virus
    • Positive stranded - acts like mRNA and can be immediately translated by host’s ribosomes into protein
    • Negative stranded - not able to be translated immediately. First, must be transcribed into positive stranded RNA. This is done via RNA dependent RNA polymerase (enzyme held in RNA capsid).
  • DNA virus
    • Must first be transcribed into mRNA and then translated into proteins
    • Have both a negative strand and a postive strand (negative strand is read)
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6
Q

Retroviruses

A
  • Viruses with the ability to incorporate their RNA into host genome. The RNA is transcribed in reverse fashion. Requries enzyme reverse transcriptase.
  • Ex. HIV
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7
Q

Capsides

A
  • Protein shell of the virus
  • Two types
    • Icosahedral - polypeptide chains organized into globular protein subunits and then arranged into a equilateral triangle. 20 of these triangles are put together to form the icosahedral.
    • Helical - protein bound to RNA is coiled into a helical nucleoprotein capsid
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8
Q

Viral Envelope

A
  • Viruses may or may not have a lipid bilayer membrane coat
  • Viruses acquire this by budding through host cell nuclear cytoplasmic membrane
  • Those without the membrane are called naked or nonenveloped. Those with it are called enveloped.
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9
Q

Viral Replication

A
  • Viruses can’t reproduce on their own - must invade cell and take over machinery to build enzymes and new viral proteins. Next, viral genetic material is place is newly made virus and they exit the host cell.
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10
Q

Steps of viral replication

A
  • Adsorption and penetration - viral particle binds to host cell membrane and is internalized via endocyotisis or fusion of virio envelop with host cell membrane
  • Uncoating the virus - nucleic acid (DNA or RNA) is released from capside into nucleus or cytoplasm
  • Synthesis and assembly of viral products (as well as inhibition of host cells own DNA, RNA, and protein synthesis).
  • Release of virions (signal virus particle) from host cell (either by lysis or budding)
    • Naked virions - cells may lyse and release virions, or virions may be released via exocytosis
    • Enveloped virions - naked virions gains envelop by budding through lipid bilayer
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11
Q

Host cell outcome from viral infection

A
  1. Death
  2. Transformation - infection can activate or introduce oncogenese - causes uncontrolled and uninhibite growth.
  3. Latent infection - virus survives in sleeping state. Certain factors can cause reactivation.
  4. Chronic slow infection - some viruses cause disease only after many year of indolent infection.
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12
Q

Immune response to virus

A
  1. Barriers - passage across the mucosa of respiratory, genitourinary, or GI tract accounts for most instnaces of viral transmission. Virus may also enter through broken skin.
  2. Innate immune system - innate immune system responds to viral infectio via PRR recognition of PAMP - initiates activation of NK cell that induce lytic acticity and destroy virally infected cells
  3. Virus invade the cells of the host to survive and replicare. Once inside the cell, the cell uses MHC I to display pieces of protein from inside the cell - since the cell is infected it shows fragements of proteins made by the virus. This cell is than presented to CD8+ cells in the lymph, where it is activated and undergoes clonal selection. Killer T cells (CD8+) and they travel through the tissue and kill infected cells.
  4. Interferones - virally infected cells produce and release interferones. Interferons prevent viral replication by interfering with viruses ability to replicated within the cell. Interferones act as signalling molecules to warn nearby cells of the viral presence - induces neraby cells to increase MCH I molecules on cell surface so that killer T cells can identify and eliminate them faster.
  5. Antibodies - APC may endocytose peices of viruse (ex. capsule, fragments) and present this on MCH II. APCs then go to the lymph nodes and present the molecule to helper T cells (CD4+), which will activate the proliferation of B cells into plasma cells (antibodies) and memory cells (for future infection).
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13
Q

Viral Spread in animals

A
  1. Local spead - infection is mainly confined to mucosal surface or organ
  2. Primary hematogenous spread - virus is introduced directly into blood stream (ex. insect transmitted) and then disseminates to target organs
  3. Secondart hemotogenous spread - initial virus infection and replication occur on mucosal surface with subsequant issemination to target organ via blood stream
  4. Nervous system spread - viruses disseminate via nervous system
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14
Q

Viral Transmission

A
  • For infection to spread there must be 3 components. If any component is mission the potential for infection is eliminated:
    1. A susceptible host
    2. A biological agent sufficent to cause diseas
    3. A mode of transmission
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15
Q

Mode of viral transmission

A
  1. Contract spread - susceptible person has contact with infected source or reservoice and contact is either direct or indirect by drople
    • Direct patient contact - physical contract between source and susceptobe person results in expsoure to skin and body secretion
    • Indirect patient contact - infect host or other reservoice are transmitted to susceptible host via inanimate body
    • Droplet transmission - transmission of infectiour agents in droplets expelled from respiratory secretions by coughing, sneezing, or talking (cannot be transmitted beyond a radius of several feet from source).
  2. Airborne spread - organisms that have a true airborne phase in route of dissemination (i.e., distance more than several feet (ex. varicella and TB).
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16
Q

Pharyngitis

A
  • Direct inflammation of the pharyngeal tissue usually casing sore throat
  • Majority of cases are viral (50-80%) with 15-30% in children and 10% in adults due to GAS
17
Q

Differential Diagnosis Pharyngitis

A
  1. Distinguish between non-infectious and infectious causes
    • Non-infectious causes are ruled out via history and physical
      • Non-infectious - allergy, irritant exposure, GERD. More likely with a positive irritant/allergen exposure history, symptoms of allergic rhinitis, and no history or recent onset of illness.
      • GERD - history of sore throat accompanied by dypepsia and waterbrash. Symptoms usually occur following meals, at night, and early in the morning. Sore throat is relieved after several days of antacid use and H2 blockers/PPIs
  2. Once non-infectious is ruled out, differentiate between GEBHS, infectious mononucleosis, and viral pharyngitis
18
Q

Viral pharygitis

A
  • Most likely diagnosis for sore throat
  • Presenting symptoms - typical upper respiratory tract infection symptoms - nasal congestion, rhinorrhea, sneezing, and sore throat. Patient may also present with cough, fever, and palpable posterior cervical lymph nodes.
  • Usual culprits - common cold viruses (rhinovirus, coronavirus, respiratory syncytial virus, parainfluenze virus), adenovirus, herpes virus, and coxsackie virus.
  • Treatment - antiboitics are NOT indicated. Can use NSAIDS, aspirin, and acetaminophen for symptom relief. Can also use topical therapies to the throat.
19
Q

Group A B-hemolytic Streptococcal infection

A
  • Suspect GABHS with
    • Patient <15
    • Presence of tonsillar swelling and exudate
    • Tender anterior cervical lymph nodes
    • Absence of cough
    • Fever > 38C
    • Sore scratchy throat accompanied with dysphagia
  • Patients may also complain of myalgia, chills, and headaches
  • Treatment: Antiobiotics have been the traditional treatment to speed recovery. However, symptomatic improvemnt is only slightly better with antibiotics tha without (24-48hrs faster)
    • Adult first line: Penicillin
    • Children first line: Penicillin or amoxicillin
20
Q

Infectious Mononcleosis (IM)

A
  • Presents similar toGABS, but IM usually presents with history of significant fatigue
  • Typically occurs in children and teens and follows a 3-5 day period of malaise, fever, myalgia, and headache
  • Also characterized by fever, posterior cervical lymphadenopathy, palatal petechia, jaundice, rash, and absence of cough. Splenomgealy is present in 50% of patients.
  • Causes by Epstein - Barr virus
  • Treatment: Supportive. 95% of cases resolve in 2-3 weels with rest and analgesics
21
Q

Complications of IM and GABHS

A
  • Life threatening situations associated with IM and/or GABHS include peritonsillar abscess, splenic rupture, and upper airway obstruction
  • Peritonsillar abcess - patients have toxic appearance (fever and chills), altered mental status, and hoarse/muffled voice. Tonsil on affect side is pushed toward midline, giving it asymmetric appearance.
22
Q

Life threatening conditions appearing with sore throat

A
  • Epiglottitis
  • Retripharyngeal abscess
  • Lateral Pharyngeal abscess
  • Peritonsillar abscess
  • Tonsillar hypertrophy secondary to Epstein Barr virus
  • Diphtheria
  • Lemierre’s syndrome
  • Suspect a more serious cause with inability to move neck, toxic appeatance, respiratory distress or difficulty swallowing