Infections of the heart and circulatory system Flashcards

1
Q

Bacteraemia

A

Bacteria in blood

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

Septicaemia

A

Bacteria in blood causing clinical symptoms

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

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

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

How is plague transmitted

A

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

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

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

Immunosupression

A

Immunosuppression = predisposing factor for development of septicaemia

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

Infections of heart+Circ system: opportunistic pathogens

A
  • Pseudomonas aeruginosa
  • Stenotrophomonas maltophilia
  • Acinetobacter spp. (e.g. baumannii)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Newborn babies are vulnerable to serpticaemia caused by?

A
  • Listeria monocytogenes
  • Group B streptococcus (e.g. S. agalactiae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

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

What is DIC

A

Disseminated intravascular coagulation

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

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

What is toxic shock syndrome caused by (TSS)

A

Staph or Strep

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

TSS1

A

Toxin shock syndrome - toxin

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

TSLS

A

Toxic shock like syndrome

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

A

Vegetation

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
Q

Early prosthertic value endocaridits occurs how long after valve replacement

A

Before a year

26
Q

Early prosthertic value endocaridits is caused by contamination of what

27
Q

Early prosthertic value endocaridits is caused by what organisms

A

CoNS
S. aureus
Dipetheroids, e.g Corynebacterium spp.

28
Q

Late prosthertic value endocaridits occurs how long after post replacement

A

Post a year

29
Q

Late prosthertic value endocaridits is caused by

A

Viridians streptococci
Enterococci
CoNS
transient bacteriaemia from mouth

30
Q

How often is native valve endocaridits caused by S. aureus seen, common group and what valvue and why

A

Rare, IV drug users, tricupsid valve as it is for venous return

31
Q

Duke criteria is for what

A

Score likelihood of endocaridits

32
Q

Major duke criteria

A
  • 2x Blood cultures positive for organisms known to cause IE
  • Echocardiogram positive for IE  visualise any vegetations.
33
Q

Minor duke criteria

A
  • Predisposing factors (IV drug use, heart condition)
  • Fever
  • Vascular phenomena (emboli, conjunctival haemorrhage, Janeway lesions)
34
Q

Definitive diagnosis following Duke criteria of endocardiatis (number of major and minors scored)

A

2 major
1 major, 3 minor
5 minor

35
Q

Mycotic aneurysm

A

Infected aneurysm, arteritis. Inflammatory damage and weaking of arterial wall leading to buldging (aneurysm)

36
Q

Suppurative thrombophelbitis

A

Inflammation of vein wall, clot formation, microbial colonisation. common in IV catheters