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basics of diseases Flashcards

1
Q

types of upper respiratory tract infections

A

1) common cold - viral rhinitis
2) sinusitis
3) pharyngitis
4) acute laryngitis

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2
Q

URTI - common cold - viral rhinitis

A
  • affect nasal passages
  • SS: sore throat, congestion, runny nose, sneezing, cough,
  • AA: rhinovirus (most common), influenza virus, coronavirus, respiratory syncytial virus (RSV)
  • rhinovirus: host immune response not drug induced tissue damage
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3
Q

URTI - sinusitis

A
  • sinus cavities
  • symptoms: congestion, facial pain & pressure, headache, runny nose
  • AA: streptococcus pneumoniae
  • pathogenesis
    1) obstruction of sinus ostia
    2) dysfunction of muco-ciliary action (infection when cannot clear mucous properly)
    3) alteration in mucous secretion (infiltration of immune cell & protein -> increase lipophilicity -> impair ciliary function)
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4
Q

URTI - pharyngitis

A
  • affect pharynx
  • SS: sore throat, congestion, pharyngeal inflammation
  • AA: adenovirus & rhinovirus (most common), streptococcus pyogenes, Group A Streptococcus (GAP) (Associated with acute rheumatoid fever)
  • inflammatory mediators: bradykinin, prostaglandin
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5
Q

URTI - acute laryngitis

A
  • larynx
  • SS: hoarse voice with decrease phonation & voice projection
  • AA: major virus & several bacteria
  • local inflammation due to trigger -> influx of WBC to site of infection -> enhance vocal cord oedema
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6
Q

types of LRTI diseases

A

1) bronchitis
2) bronchiolitis
3) pneumonia

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7
Q

LRTI - bronchitis

A
  • bronchitis
  • SS: acute cough wo signs of pneumonia
  • AA: viral (most likely), bacteria (less likely)
  • pathogenesis: direct cytopathology + host immune response -> inflammation of large and medium sized airways
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8
Q

LRTI - bronchiolitis

A
  • bronchioles
  • SS: wheezing, tachypnoea (increased respiratory rate), nasal flaring (more common in young children & infants)
  • AA: RSV (most common)
  • inflammation of small airways: airway obstruction, air trapping, hyperinflation of lungs, atelectasis
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9
Q

LRTI - pneumonia

A
  • alveoli & alveolar sacs
  • SS: fever, cough, dyspnea, sputum production, tachypnoea, systemic when severe (chest pain, fatigue, sweats, headache, nausea, abdominal pain, diarrhea)
  • AA (community acquired pneumonia (CAP)): streptococcus pneumoniae, mycoplasma pneumonia, community respiratory virus
  • defect in host immune defense (smoke/alochol)
  • pneumonia (inflammation & infection) vs pneumonitis (infection only)
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10
Q

aetiology of rhinovirus infection - general

A

loss in tight junctions between cells -> opportunity for opportunistic infection & increase cytokine/growth factor penetration

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11
Q

aetiology of rhinovirus infection - infection process

A

1) virus bind to viral receptors on epithelial cells (ICAM1, LDL-R, CDHR-3)
2) receptor mediated endocytosis
3) uncoating & genome release -> mRNA transcription
4) transcription by RNA polymerase
- error prone -> viral mutation
5) replication
6) assembly of viral core structure
7) leave cell via lytic (cell death) or non-lyric mechanisms

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12
Q

aetiology of rhinovirus infection - response to infection

A

1) TLR3/7/8 recognise rhinovirus associated proteins
2) activate NFK beta
3) increase release of inflammatory cytokines
4) activation & recruitment of immune cells

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13
Q

aetiology of rhinovirus infection - immune response to infection

A

1) innate immunity
- recruitment of WBC (neutrophil, eosinophil)
- increase release of cytokine, chemokine, inflammatory markers
- increase viral clearance & activation of adaptive immune system (humoral, cellular)

2) humoral immunity
- activate B cells: produce serologic specific antibodies to rhinovirus antigenic type
- block ligand attachment, opsonisation of cells for presentation to phagocytic cell, initiating NK cell mediated cytotoxicity

3) cellular immunity
- activate T cells to
. CD 4+ T cells: produce IFN-gamma & facilitate humoral immunity
. CD8+ T cells: kill virus infected cells

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14
Q

influenza aetiology

A

. infiltration process
1) viral entry: receptor mediated endocytosis
2) release of viral genome
3) translation, transcription, replication
4) assembly, budding, leave host, further infection

. viral surface proteins
- neuraminidase (NA): cleave sialic acid receptor to leave host cell
- haemagglutinin (HA): viral entry

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15
Q

types of mutation in virus

A

1) antigenic shift
- drastic change after genetic reassortment
- coinfection: mixing of genetic material

2) antigenic drift
- gradual accumulation of mutations

  • why is mutations relevant?
    . antigenic shift: changes viral subtype, need to come up with seasonal vaccines
    . vaccines: life-attenuated/inactivated/RNA
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16
Q

aetiology of pneumonia

A
  • hospital vs community acquired pneumonia
  • causative agents:
    1) bacterial: streptococcus pneumoniae, staphylococcus aureus, haemophilus influenzae
    2) viral: RSV (kids), Influenza A (adults)
    3) others: mycoplasma pneumoniae
17
Q

pathophysiology of pneumonia

A

1) respiratory epithelium
- MCC
- mucin, antimicrobial
- chemotactic peptides (recruit other immune cells)
- phagocytosis
- intracellular killing

2) alveolar macrophage
- pro-inflammatory & chemotactic mediators (IL-1, TNF-alpha cause fever)
- phagocytosis
- intracellular killing
- apoptosis

3) neutrophils
- pro-inflammatory & chemotactic mediators
- phagocytosis
- intracellular killing
- neutrophil extracellular traps (NETs)
- recruit other effector cells

4) platelet
- pro-inflammatory & chemotactic mediators
- interact with leukocytes
- increase NETs

18
Q

histopathology of pneumonia

A
  • when host pulmonary defenses has defects
  • stages of pneumonia
    1) early stage: congested, leaky capillaries
  • mild intra-alveolar oedema
  • congestion in capillaries cuz recruitment of immune cells to site of infection
    2) day 3-7: red hepatisation
  • accumulation of neutrophils, RBC, fibrin in alveolar spaces
  • hepatisation: tissue harden
    3) day 4-7: grey hepatisation
  • subsequent, gradual disintegration of RBC & neutrophils
    4) resolution
  • break down & clearance of RBC, macrophages, fibroblasts
  • gradual
  • cleared in sputum produced & productive cough
19
Q

how does pneumonia affect breathing

A
  • pneumonia -> inflamed & thickened alveolar wall with mucous & inflammatory cells -> lower diffusion across barrier -> shunt perfusion (constrict capillaries, shunt blood to other capillaries) -> lower ventilation/perfusion ratio (<0.8)
  • lower ventilation + constriction = hypoxia = tachypnoea
20
Q

TB

A
  • SS: cough, fever, night sweat, weight loss
  • AA: mycobacterium tuberculosis
  • types
    1) latent: asymptomatic, non-transmissible
  • bacteria affect cell, migrate to T cell for priming but does not escape granuloma
    2) active: transmissible if re-enter respiratory tract
  • increase bacteria load until escape granuloma

2154 (8 decks)

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