21 Flashcards

1
Q

What gives rise to the jugular venous a, c, and v waves?

A

a wave- atrial contraction
c wave- ventricular contraction
v wave- atrial filling against tricuspid valve

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2
Q

Which heart murmur is associated with weak pulses?

A

Aortic stenosis (pulsis paris et tardis)

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3
Q

What are 4 high yield findings associated with Elhers Danlos Syndrome?

A
  • easy bleeding/ bruising
  • hypermobile joints w/ frequent dislocaiton
  • hyper mobile skin
  • aneurysms (esp berry!)
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4
Q

Describe the process mediating type I hypersensitivity.

How long does this take?

A

Free Ag x-links IgE on presensitized mast/ basophils–>
Degranulation of histamine and bradykinin–>
Vasodilation, ^ vascular permeability –>
Edema/ urticaria/ hives
Takes 15 min

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5
Q

Describe the process mediating type II hypersensitivity:

A

Abs (potentially autoAbs) + CELLULAR Ags–>

Complement/ MQ phagocytosis/NK cells destroy

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6
Q

Describe the process mediating type III hypersensitivity:

A

Abs + SOLUBLE Ags in blood–>
Ab/Ag complex deposition in tissue–>
Complement/ MQ phagocytosis/ NK cells destroy

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7
Q

Describe the process mediating type IV hypersensitivity.

How long does this take?

A

T cell + Ag–>
T cell releases IL2, IFN-g –>
Activation of MQs, tissue damage
Takes 4-12 hrs

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8
Q

Describe activation of the classical complement pathway.

What is one inhibitor of this process?

A

IgG/IgM + Ag–> C1 ACTIVATION

*Inhibited by C1 INHIBITOR/ ESTERASE INHIBITOR protein

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9
Q

Describe activation of the alternative complement pathway:

A

Does not require Abs

Can self activate/ bind microbial surface directly

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10
Q

Describe activation of the lectin pathway:

A

Mannose biniding protein–> Mannose on microbial surface

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11
Q

Common end result for all complement pathways:

A

MAC COMPLEX + CELL DISTRACTION

C5b, 5, 7, 8, 9

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12
Q

Hereditary angioedema:
What is the deficient protein/ disease presentation
What should you be wary about when prescribing drugs to these patients?

A

Deficient C1 esterase inhibitor –> ^ Bradykinin
Patients present with angioedema surprise
NEVER GIVE ACEi’s !!!

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13
Q

Deficient C3 Protein: How does this present?

A

Recurrent sinus infections/ RTIs

  • strep penumo
  • H flu
  • ^ risk of Type III hypersensitivities
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14
Q

Deficient MAC forming proteins:

How does this present?

A

Deficient C5b, 6, 7, 8, 9

- ^ risk neisseria bacteremia

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15
Q

DAF/ CD55 Deficiency:

How does this present?

A

This deficiency causes failure in protection of “self” from complement mediated destruction
- Red cell lysis/ PNH

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16
Q

Describe Paroxysmal nocturnal hemoglobinuria:

  • What are the two deficient membrane surface molecules
  • List 3 clinical features
A
  • Deficient CD55 (GPI anchor for DAF)
  • Deficient CD59 (MAC inhibitory protein)

Patients present with:

  • chronic intravascular hemolysis
  • hemosidenuria
  • thrombosis
17
Q

Describe Paroxysmal nocturnal hemoglobinuria:

  • 2 methods of dx
  • 3 methods of tx
A
  • Ham’s Test (cells will lyse in low pH)
  • Flow cytometry for CD55 and CD59

Treat with transfusion, warfarin, Eculizumab

18
Q

Two opsonins in complement pathway:

A

C3b, IgG

19
Q

Two mediators of anaphylaxis in complement away (chemokine):

A

C3a–> mast, basophil activation

C5a –> recruits neutrophils

20
Q
Asthma 
Bee sting allergy 
Eczema 
Peanut Allergy 
Seasonal allergic rhinitis are all...
A

Type I hypersensitivity

21
Q
Acute hemolytic transfusion reaction 
Acute rheumatic fever 
Graves Disease 
ITP 
Myathemia Gravis are all...
A

Type II hypersensitivity

22
Q

Arthur’s reaction
PAN
Post-strep GN
RA are all…

A

Type III hypersensitivity

23
Q

Contact Dermatitis
GVHD
MS are all…

A

Type IV hypersensitivity

24
Q

A patient who suffers from recurrent neisseria infections may have…

A

MAC formers’ deficiency (C5b, 6, 7, 8, 9)

25
Q

Which complement is responsible for neutrophil chemotaxis:

A

C5a