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Pathology Term 2 > Week 2 - HEAD & NECK > Flashcards

Week 2 - HEAD & NECK Flashcards

Pyrexia of Unknown Origin, Arboviral Fevers, Tropical Infections, Malarial Microscopy

1
Q

What is the definition of pyrexia/fever?

A
  • increase in body temp by 1-4 degrees
  • protective mechanism
  • NOT fully understood
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2
Q

What is the term for substances that produce fever and what are the 2 types?

A

Pyrogens

  1. Exogenous
    - bacterial products, LPS
  2. Endogenous
    - IL-1, IL-6, TNF-alpha
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3
Q

What is meant by a bacteria being coagulase + and give an example?

A
  • produces an enzyme causing clot formation to prevent immune system from penetrating the area of infection
  • coagulase test distinguishes between S. aureus and other types of Staph.
  • S. aureus = coagulase +
  • All other Staph. = coagulase -
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4
Q

What is meant by a bacteria being catalase + and give an example?

A
  • produces an enzyme that catalyses the conversion of H2O2 –> water
  • distinguishes between Staph and Strep
  • Staph = catalase +
  • Strep = catalase -
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5
Q

How do pyrogens produce fever?

A

Pyrogens –> increase COX –> increase synthesis of prostaglandins –> PGE2 in hypothalamus –> resets thermal clock –> FEVER

  • peripheral vasoconstriction
  • central vital organ vasodilation (increase core body temp)
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6
Q

What class of drug is commonly use to provide fever relief and how do they function?

A

NSAIDs

  • inhibit COX in hypothalamus
  • decrease PGE2
  • decrease systemic effects of pyrexia

*ALSO –> decrease local tissue injury without significantly affecting defense/immune mechanism (unline steroids)

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7
Q

What is the key difference between NSAIDs and steroids?

A

NSAIDs do NOT significantly affect immune function while steroids have immunosuppressant effects

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8
Q

Give an example of defective inflammation

A

Diabetes Mellitus

  • abnormality of BVs
  • immunosuppression results in increased infections
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9
Q

What are the systemic protective effects of inflammation?

A

Brain

  • fever via PGs in hypothalamus
  • IL-1, 6, TNF-alpha

Liver

  • increase acute phase proteins
  • IL-1, 6

Bone Marrow

  • stimulates leukocyte production
  • IL-1, 6, TNF-alpha
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10
Q

What are the systemic pathological effects of inflammation?

A

Heart

  • decrease CO; shock in case of septicemia
  • TNF-alpha

Endothelium/BVs

  • thrombosis
  • vascular damage
  • increase permeability
  • TNF-alpha

Multiple tissues

  • defective muscle metabolism due to insulin resistance
  • weakness
  • loss of weight
  • IL-1, TNF-alpha
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11
Q

What is the definition of PUO and its 4 types?

A

*Lack of Dx. of cause of fever

  1. Classic PUO - >38, >3wks
  2. Nosocomial PUO - >38.3, >1wk inpatient OR >3days intensive Ix.
  3. Neutropenic PUO - >38.3, <1x10^9 neutrophils
  4. HIV-associated PUO - >38.3, >4wks outpatient/>3days inpatient
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12
Q

What are the common causes of PUO?

A
  1. Infective
    - hidden abscess, TB, viral, parasitic
  2. Malignant
    - HL/NHL
  3. Inflammatory
    - giant cell arteritis, SLE, ARF, sarcoidosis, rheumatic
  4. Undetermined
    - MI, PE, drugs, endocrine, hepatic, CVA, allergic, etc

*UNKNOWN IN 19% cases

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13
Q

True or False?

Arboviral infections cannot spread from person to person

A

True

  • Arbo = insects
  • insects –> man
  • zoonotic (therefore infections of wild animals)
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14
Q

Why is there an increase incidence of arboviral infections nowadays?

A

Global Warming –> epidemics

-causes increased mosquito numbers = increased vectors for spread of infection

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15
Q

What arbovirus commonly causes polyarthralgia?

A

RRV

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16
Q

Which arbovirus is the commonest for fever and rash?

A

Dengue

RRV also

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17
Q

What are the common alphaviruses and flaviruses?

A

Alphavirus:

  • RRV
  • BFV
  • Chikungunya

Flavivirus:

  • Kunjin
  • Dengue
  • MVE
  • JE
  • WNE
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18
Q

Where are arboviruses more common?

A

Tropical areas

-NQ/NT/Asia Pacific

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19
Q

What is Australia’s most prevalent arbovirus and what is it also referred to as?

A

RRV

-endemic polyarthritis (as pts. have long term joint pain)

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20
Q

What type of arbovirus is RRV and what mosquito transmits it?

A

ALPHAVIRUS

-Culex/Aedes mosquito

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21
Q

What is the IP and classic presentation of RRV?

A

-IP approx. 3-11days
Symptoms:
-fever, fatigue, arthritis, rash (red, non-pruritic, maculopapular rash), headache, lymphadenopathy

*self-limited (4-7mths)

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22
Q

What is the rough IP for most arboviruses?

A

1 week

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23
Q

What is ross river disease?

A

-NO fever present

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24
Q

How is RRV diagnosed?

A

Serology:

-4-fold increase in serum IgG/IgM confirms Dx.

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25
Q

True or False?

There is a cure and effective Tx. for RRV

A

False

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26
Q

What vector is responsible for Dengue and what is interesting about it?

A

Aedes aegypti - “white band”

  • it feeds during the DAY
  • other mosquitos are night-time feeders
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27
Q

What are the symptoms of dengue and what is it also referred to as?

A

Sx.

  • fever/rash
  • myalgia/arthralgia
  • abdominal pain
  • headache
  • serositis

Marked muscle + joint pains –> AKA: breakbone fever

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28
Q

What is significant about the fever pattern in dengue?

A

Fever 5-7 days

  • biphasic
  • initially high fever, drops down, then back up again
  • SADDLEBACK FEVER CURVE
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29
Q

True or False?

Adults are affected by dengue more commonly than children

A

False

30
Q

What are the 2 clinical forms of dengue?

A
  1. Febrile form (flu-like)

2. Classic dengue fever (DF) –> muscle/joint pain

31
Q

What are the 2 immune complications of dengue fever?

A
  1. DHF
  2. DSS

*v. high mortality rate :(

32
Q

What is the pathophysiology of denge?

A
  • infection (with potential Ab-dependent enhancement)
  • inflammatory rush with cytokines/activated T cells
  • endothelial damage
  • plasma + protein leakage –> severe dehydration, shock, hypoalbuminemia –> ascites
  • platelet activation –> thrombocytopenia
  • serositis + hepatitis –> ascites from serositis
  • SHOCK –> due to severe dehydration
33
Q

Define DHF and what are the 4 grades?

A
  • fever/recurrent Hx. of fever
  • haemorrhagic manifestations
  • decreased platelet count –> endothelial damage (severe bleeding)
  • objective evidence of leaky capillaries –> increased Hct, ascites, plearual effusions, hypoalbuminemia

Grades:

  1. fever + non-specific Sx.
  2. spontaneous bleeding
  3. circulatory failure
  4. profound shock (DSS)
34
Q

What are the initial warning signs of DHF?

A
  • disappearance of fever (saddleback fever curve)
  • decreased platelets
  • increase Hct
35
Q

What are the 4 criteria for DHF?

A
  1. Fever
  2. Haemorrhagic manifestations
  3. Increased capillary permeability
  4. <100 x 10^9 platelets (thrombocytopenia)
36
Q

What are the alarming signals of DHF?

A
  • shock
  • prolonged vomiting
  • fever –> hypothermia
  • altered LOC
37
Q

What is the name of the bacteria that are being used (trialled) to kill dengue infected mosquitos?

A

Wolbachia

38
Q

What vector causes MVE?

A

Culex mosquito

39
Q

What are the Sx. of MVE and what can manifest in severe forms?

A

Sx.

  • fever
  • headache (increased ICP)
  • nausea/vomiting

Severe:

  • meningitis/encephalitis
  • drowsiness
  • confusion
  • convulsions
40
Q

How is MVE diagnosed?

A

Serology

  • 4-fold increase in serum IgG/IgM
  • viral culture of blood/CSF
41
Q

True or False?

MVE, WNV and Kunjin have cross-reacting Abs?

A

True

-positive serology could mean ANY of these 3 are the cause

42
Q

What virus does Chikungunya have cross-reacting Abs with?

A

RRV (similar Sx.)

-but chikungunya prevalent in India, Malaysia, Thailand (therefore Travel Hx. = very important)

43
Q

True or False?

BFV is the 2nd commonest arbovirus in Aus. and it is “truly aussie” - i.e. only seen in Australia

A

True + True

44
Q

What vector causes BFV and what are the Sx.?

A 
vector = Aedes mosquito
Sx. = fever, rash, headache, myalgia/arthralgia
45
Q

True or False?

NSAID use is beneficial for arboviral infections

A

False

-can cause more damage than benefits due to increased bleeding

46
Q

What is the causative organism of leptospirosis and how is it transmitted?

A

Leptospira icterohemorrhagica

  • bacterial spirochaete
  • zoonotic disease in wild animals
  • spreads to humans through contact with water, food or soil containing the URINE of infected animals –> because the bacteria resides in renal tubules
47
Q

Why is leptospirosis referred to as a biphasic illness?

A
  1. First flu phase: -fever, chills, myalgia, headaches

2. Second (Weil’s Disease): - jaundice, fever, haemorrhage (rash), renal/liver/CNS involvement

48
Q

How is leptospirosis diagnosed?

A

CULTURE

  • blood (<1wk)
  • urine (>1wk)
49
Q

What is the causative organism of melioidosis (whitmore’s disease) and how is it transmitted?

A

Burkholderia pseudomallei

  • facultative intracellular gram negative bacteria
  • saprophyte - in soil/fresh surface water in endemic regions (Northern Aus in wet season = hyperendemic)
  • spread via contact with contaminated soil/water
  • IP = 9days
50
Q

What are the Sx. of melioidosis?

A
  • pneumonia
  • multiple abscesses (splenic/liver/lung)
  • cough/pleuritis
  • bone/joint pain
  • cellulitis
  • fever, chills, rigors, cough, sputum
  • cutaneous melioidosis at site of organism entry
  • subacute/chronic presentation –> hemoptysis + night sweats (DDx. = TB)
51
Q

What is the characteristic clinical feature of melioidosis?

A

Multiple abscesses

  • splenic
  • liver
  • lung
52
Q

What is the causative organism of Q fever and how is it transmitted?

A

Coxiella burnetii

  • highly infectious (bioterrorism)
  • reservoir in cattle, sheep, goats, etc. (increased on farms) OR in contaminated dust/milk –> inhalation/ingestion

*IP = 9-40days

53
Q

What are the Sx. of Q Fever? And what is the characteristic/unique feature?

A

Sx.

  • fever
  • headache
  • fatigue
  • myalgia/arthralgia
  • most recover BUT some develop chronic fatigue, endocarditis + hepatitis

*CHARACTERISTIC FEATURE = Granulomas in Liver

54
Q

What are the 2 phases of Q Fever?

A
  1. Acute phase:
    - 7-14 days
    - flu-like Sx. + severe headache, myalgia, arthralgia, cough + pneumonia
  2. Chronic phase:
    - Q fever endocarditis –> in susceptible (IC) patients or people with previous valvular damage
55
Q

How is Q fever diagnosed?

A

Serology: - IgG/IgM

*increased IgG + IgA in Q fever endocarditis (chronic phase)

56
Q

What are prevention techniques and Tx. for Q fever?

A

Prevention:

  • vaccine
  • pasteurisation of milk
  • safe animal product handling

Tx.

  • acute: - doxycycline (3wks)
  • chronic: - doxycycline + quinolones (3yrs)
57
Q

What is an important precaution with administration of the Q fever vaccine?

A
  • pre-vaccine testing for previous exposure to Q fever is imperative
  • previous exposure to Q fever produces a severe reaction to the vaccine
  • test for previous exposure –> wait 7 days –> if negative, give vaccine. If positive, NO VACCINE
58
Q

What mosquito causes malaria and what are the 2 commonest malaria species?

A

Anopheles mosquito

  1. Plasmodium falciparum
  2. Plasmodium vivax
59
Q

Why is mild jaundice seen in malaria?

A

RBC hemolysis

60
Q

What are the clinical features of malaria?

A
  • fever
  • chills
  • rigors
  • fatigue
  • mild jaundice, splenomegaly, anemia –> chronic ?
61
Q

What is the most severe malaria species and what can it cause?

A

P. falciparum

  • acute renal failure –> malarial hemogobinuria (BLACKWATER FEVER)
  • coma
  • severe acidosis
  • extensive RBC breakdown

*due to adhesion proteins that make RBCs clog deeper veins ?

62
Q

How is cerebral malaria caused?

A
  • cerebral BVs clogged by parasites

- v. little inflammation

63
Q

Why is there a cyclical fever in malaria?

A
  • due to cyclical rupture of RBCs with subsequent release of merozoites causing fever.
  • P. falciparum = 48hrly
  • P. malariae = 72hrly
64
Q

What is the pathophysiology of malaria?

A
  • anopholes mosquito injects sporozoites into human
  • sporozoites invade hepatocytes
  • merozoites formed and released from liver
  • merozoites invade RBCs
  • merozoites –> trophozoites (ring form) in RBCs
  • trophozoites –> schizonts –> RBC rupture
  • RBC rupture releases more merozoites and produces cyclical fever
  • released merozoites invade further RBCs (blood stage)
  • some trophozoites –> gametocytes –> more mosquitos
65
Q

How is malaria diagnosed?

A

PfHRP2 Ag

  • Ab-based detection (“pan malaria”)
  • test = + even after clearing parasitemia with artemisinin Tx.
66
Q

What is the most common stage of parasite seen in peripheral blood film of a malaria patient?

A

Trophozoite (ring form)

67
Q

What is the commonest malaria species?

A

Plasmodium vivax

68
Q

What is a characteristic microscopic feature of P. falciparum?

A
  • increased parasitemia (can be >1 malaria parasite/RBC –> wheras P. vivax = 1 per RBC)
  • smaller rings (trophozoites) –> whereas P. vivax can have v. large rings
  • can also see gametocytes/schizonts
69
Q

What is a hypnozoite?

A

Malaria parasites that lie dormant in heaptocytes (hepatic dormancy) –> can lie dormant for years

*P. vivax + P. ovale

70
Q

What is the gold standard for Dx. of malaria? And what are other diagnostic tests?

A

Blood film microscopy

  • Thick film –> to determine presence of malaria
  • Thin film –> to distinguish which parasite is present

Other Dx. tests:

  • Ag detection by RDT
  • PCR molecular diagnosis
  • Serology –> ELISA

Pathology Term 2 (6 decks)

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