Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical Studies 1 > 4.1 Cardiac Electrophysiology and Arrhythmias > Flashcards

4.1 Cardiac Electrophysiology and Arrhythmias Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Other than the endocardium, what other structures can be involved in endocarditis?

A
  • Chordae tendinae
  • Cardiac devices
  • Interventricular septum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the names of lesions that characterise endocarditis? What do they contain?

A
  • Vegetations
  • Mass of platelets, fibrin, and inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common/less common causes of myocarditis

A
  • Most common: viral
  • Others: other infections, toxins, vaccines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Effect of myocarditis on cardiac enzymes and inflammatory markers

A
  • Raised cardiac enzymes
  • inflammatory markers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Most common cause of pericarditis (hint: it’s the same as that of myocarditis)

A

Viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List some less common causes of perdicarditis (i.e. other than viral)

A
  • Bacterial
  • Uraemic
  • Ischaemic
  • Malignancy
  • Radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pericarditis ECG changes

A

ST elevation (this is why we need to be careful when diagnosing STEMI)

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

Which three types of fluid can cause pericardial distension?

A
  • Serous
  • Blood
  • Pus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute vs chronic pericardial distension

A
  • Acute: Can be very bad; compressing blood vessels and even ventricles, resulting in cardiac tamponade
  • Chronic: pericardial space dilates, allowing slow accumulation of fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which tissues are inflamed during serositis?

A

Serous tissues, pleura, pericardium, peritoneum

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

Common treatment of pericarditis

A
  • NSAIDs (e.g. aspirin, ibuprofen)
  • Corticosteroids
  • Immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an immune complex?

A

The molecule formed by the binding of a SOLUBLE antigen to an antibody (i.e. the antigen is not connected to another cell)

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

List some common clinical signs of infective endocarditis

A
  • Osler’s Nodes
  • Janeway lesions
  • Splinter hemorrhages
  • Roth spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the pathophysiology of infective endocarditis.

A
  • Endothelial damage occurs to endocardium (e.g. due to turbulent blood flow)
  • Platelets and fibrin adhere to damaged surface
  • If bacteremia is occuring, then some bacteria may bind to these platelet-fibrin complexes, forming vegetations
  • Vegetations can produce septic emboli, which travel throughout the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is type 3 hypersensitivity also known as?

A

Immune Complex Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an Arthus reaction?

A

Localised immune complex mediated hypersensitivity reaction of dermal blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why don’t immune complexes cause type 3 hypersensitivity reactions when antibodies are present in roughly equal proportion to antigens? What is this called?

A

Because the immune complexes form a lattice, and can be removed by mononuclear phagocytes.

This is known as “equivalence”

18
Q

Describe the four common steps of the inflammatory response

A
  1. Cell surface pattern receptors recognize detrimental stimuli
  2. Inflammatory pathways are activated
  3. Inflammatory markers are released
  4. Inflammatory cells are recruited
19
Q

Describe how surface receptors lead to activation of inflammatory pathways and release of cytokines

A
  1. Ligand binds to receptor
  2. Leads to increase transcription and translation of inflammatory cytokines
  3. Cytokines either recruit other inflammatory cells, or have a direct effect
20
Q

What are the four main receptor pathways by which the inflammatory response can be triggered?

A
  • Pattern recognition receptors
  • NF-kB pathway
  • MAPK pathway
  • JAK-STAT pathway
21
Q

What does it mean that cytokines are pleiotropic?

A

They can exert multiple different types of cell responses, often on different cell types

22
Q

What does it mean that cytokines are redundant?

A

If one cytokine is inactivated, others can step in an do its job (much the same as coronary autoregulation)

23
Q

How can cytokine redundancy reduce treatment effectiveness?

A

If a medication inactivates a single cytokine, then - over time - others may take its place, and so the underlying pathology will remain.

24
Q

Are all cytokines elevated in all diseases at the same time?

A

No.
They are all elevated in all diseases at different times!

25
Q

Why is it important to understand that cytokines can be clustered into groups?

A

Because, depending on the specific inflammatory pathway, T helper cells will release different cytokines, helping you to localise the source of inflammation.

26
Q

Why is it clinically important that different cytokines are released at different stages of “a” disease?

A

Because one drug may not work for every patient, and it will not work for the entire duration of a disease.

27
Q

How does strep A most commonly manifest in terms of disease presentation?

A
  • Pharyngitis
  • Tonsillopharyngitis
28
Q

List some major clinical features of Acute Rheumatic Fever

A
  • Carditis & valvulitis
  • Arthritis
  • Erythema marginatum
29
Q

How do M proteins on streptococci cause autoimmune complications?

A
  • M protein is similar to proteins in glomeruli, valvular tissue etc.
  • Therefore, the body may mistakenly misdirect the immune response towards itself
30
Q

Effect of M protein on complement system and phagocytosis

A

Decrease/inhibit

31
Q

Describe the diagnosis of streptococcal infection

A
  • The bacteria may be cultured using a throat swab or blood samples
  • Alternatively, specific antibodies may be measured using enzyme-linked immunosorbent assay (ELISA)
32
Q

Describe how molecular mimicry may enable pathogens to cause autoimmune issues

A
  • Antigen presenting cells (e.g. dendritic cells) present foreign peptide (which “mimics: endogenous proteins) to T cells
  • Leads to B cell activation, producing antibodies that may mistakenly bind to endogenous proteins, thus causing an autoimmune response
33
Q

Describe how bystander activation may enable pathogens to cause autoimmune issues

A
  • Inflammatory response is mounted to correct antigen as usual
  • Leads to activation of immature dendritic cells that present self-peptide
  • Leads to autoimmune response
34
Q

What percentage range of strep A patients developed ARF?

A

0.05-0.1%

35
Q

What is the main class of factor that influences an individuals risk of developing ARF after Strep A?

A
  • Genetic differences
  • (there are others)
36
Q

Describe an alternative pathogenesis for rheumatic fever involving the basement membrane.

A
  • Strep A bacteria use their M proteins to bind to collagen in the basement membrane
  • Creates an immunogenic neoepitope
  • Leads to autoimmune response against collagen, thus influencing factors throughout the body (including heart muscles)
37
Q

Provide a super basic pathogenesis of acute rheumatic fever

A
  • Strep A infection
  • Invades epithelium (most commonly upper resp)
  • Foreign Strep A antigens are detected, and the body mounts an immune response
  • Antibodies bear structural similarity to autonantibodies that could bind to certain self tissues
  • This can lead to damage of skin, brain, joints, and heart
38
Q

Describe the pathogenesis of inflammatory heart disease in ARF

A
  • GAS antibodies bind to endothelial surface
  • Leads to activation of VCAM1, leading to adherence of T cells
  • Subsequent inflammatory response leads to endothelial damage and valve remodelling
39
Q

What is chorea?

A

Chorea is a movement disorder that causes involuntary, irregular, unpredictable muscle movements.

40
Q

Pathogenesis of chorea

A
  • Basal ganglia neurons targeted by cross reactive GAS antibodies
  • Alters intrracellular signalling pathways, leading to increased activity of tyrosine kinase
  • Leads to increased dopamine production and secretion, causing abnormal movements or behaviours
41
Q

Pathogenesis of arthritis in rheumatic fever

A

Cross-reactive antibodies bind to synovium, causing localised inflammation and pain.

42
Q

Pathogenesis of erythema marginatum/subcutaneous nodules (they are different)?

A

Erythema marginatum: cross-reactive GAS antibodies bind with keratin
Subcutaneous nodules: granulomatous lesion (accumulation of white blood cells)

Medical Studies 1 (90 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions