Infections of the heart and circulatory system Flashcards

(36 cards)

1
Q

Bacteraemia

A

Bacteria in blood

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2
Q

Septicaemia

A

Bacteria in blood causing clinical symptoms

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3
Q

Causative agents of septicaemia, preWW2, after antibiotics, and today

A

Before WW2: Pyogenic cocci
After antibiotics: Gram-ve rods
Today: Gram+ve and Gram-ve bacteria and C. albicans

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4
Q

Gram stain and shape of Y. pestis and also the family is belongs to

A

Caused by Y. pestis. Pleomorphic and G-ve bacillus. Member of Enterobacteriaceae.

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5
Q

How is plague transmitted

A

Can be transmitted by droplets, contact, faecal-oral and vector

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6
Q

In plague how does septicaemia spread

A

Septicaemia migrates to lymph node  inflammation  necrosis (bubonic). Can go to the lungs and getting inflammation.

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7
Q

Immunosupression

A

Immunosuppression = predisposing factor for development of septicaemia

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8
Q

Infections of heart+Circ system: opportunistic pathogens

A
  • Pseudomonas aeruginosa
  • Stenotrophomonas maltophilia
  • Acinetobacter spp. (e.g. baumannii)
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9
Q

Newborn babies are vulnerable to serpticaemia caused by?

A
  • Listeria monocytogenes
  • Group B streptococcus (e.g. S. agalactiae)
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10
Q

What causes endotoxic shock. Warm shock and cold shock

A

Typical cause of symptoms found in G-ve septicaemia. Lipid A causes vasodilation and hypotension –> warm shock. Early stages, blood pressure plummets.
Peripheral blood vessels constrict to counteract –> cold shock.

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11
Q

What is DIC

A

Disseminated intravascular coagulation

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12
Q

What does DIC cause

A

coagulopathy, profuse bleeding from orifices, endotoxin induced coagulation, clotting in blood but not on any surface, all coagulation factors are used up, -> bleeding -> multisystem organ failure.

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13
Q

What is toxic shock syndrome caused by (TSS)

A

Staph or Strep

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14
Q

TSS1

A

Toxin shock syndrome - toxin

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15
Q

TSLS

A

Toxic shock like syndrome

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16
Q

N. meningitis mode of infection

A

endotoxin mediated increase in vascular permeability causes loss of protein, fluid and plasma into the tissue with pathological compensatory vasoconstriction.

17
Q

What is TSS caused by

A

TSST-1 toxin of S.aureus

18
Q

TSST-1 toxin mode of action

A
  • Nonspecific binding of MHC II with T-cell receptors by TSST-1, it is a superantigen.
  • There is polyclonal activation leading to a cytokine storm, uncontrolled inflammation.
19
Q

How many draws are taken for lab diagnosis of septicaemia

20
Q

Antimicobial treamtnet of septicaemia

A

Emperical therapy: Aminoglycoside, b-lactam, metronidazole (AnO2 effective)
Therapy modified post susceptibility testing

21
Q

Endocarditis definition

A

Infection of the lining of the heart, not the muscle, usually refering to endocardial surface (valves)

22
Q

Frequency of endocarditis based on values (list) and reason

A

Frequency: Mitral, aortic, tricuspid and pulmonic (based on SA).

23
Q

What is endocarditis typified by

24
Q

Native heart endocarditis steps (5)

A
  1. Damaged valves/prosthetic valves  disturbances in blood flow
  2. Development of microcolonies and so fibrin is deposited in an immune response which in a hypocritical way it shields the microcolonies
  3. Growing vegetations are friable (fragile so bits break off)  septic emboli.  blockage if a large part breaks off and contains pathogens, which then can grow.
  4. Vegetation is a biofilm- cidal antibiotics are required.
  5. Can remove valve via surgery
25
Early prosthertic value endocaridits occurs how long after valve replacement
Before a year
26
Early prosthertic value endocaridits is caused by contamination of what
Valve
27
Early prosthertic value endocaridits is caused by what organisms
CoNS S. aureus Dipetheroids, e.g Corynebacterium spp.
28
Late prosthertic value endocaridits occurs how long after post replacement
Post a year
29
Late prosthertic value endocaridits is caused by
Viridians streptococci Enterococci CoNS transient bacteriaemia from mouth
30
How often is native valve endocaridits caused by S. aureus seen, common group and what valvue and why
Rare, IV drug users, tricupsid valve as it is for venous return
31
Duke criteria is for what
Score likelihood of endocaridits
32
Major duke criteria
* 2x Blood cultures positive for organisms known to cause IE * Echocardiogram positive for IE  visualise any vegetations.
33
Minor duke criteria
* Predisposing factors (IV drug use, heart condition) * Fever * Vascular phenomena (emboli, conjunctival haemorrhage, Janeway lesions)
34
Definitive diagnosis following Duke criteria of endocardiatis (number of major and minors scored)
2 major 1 major, 3 minor 5 minor
35
Mycotic aneurysm
Infected aneurysm, arteritis. Inflammatory damage and weaking of arterial wall leading to buldging (aneurysm)
36
Suppurative thrombophelbitis
Inflammation of vein wall, clot formation, microbial colonisation. common in IV catheters