Brainscape's Knowledge GenomeTM

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


See full index

MCM: Cardio > Week 1 Cardiac > Flashcards

Week 1 Cardiac Flashcards

1
Q

disease that is caused by deficiency in von Willebrand factor

A

von willebrand disease

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

disease that is caused by deficiency in Gp1b

A

bernard-soulier syndrome

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

disease that is caused by deficiency in GpIIb-IIIa

A

glanzmann thrombasthenia

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

secondary hemostasis tests

A

partial thromboplastin time (PTT) and prothrombin time (PT)

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

PTT evaluates

A

12, 11, 9, 8, and 10, 5, 2 (prothrombin), and 1 (fibrinogen) (instrinsic factors)

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

PT evaluates

A

7 and tissue factor, and 10, 5, 2, and 1 (extrinsic pathway)

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

primary hemostasis test

A
  1. platelet count
  2. bleeding time
  3. von Willebrand factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Check for fibrin formation and fibrinolysis

A

D dimer test: specific fibrin degredation product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

petechiae

A

spots of blood on skin

-caused from primary hemostasis disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

purpura

A

large bruising

-primary hemorrhagia

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

thrombocytopenia

A

decreased number of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

epitaxis

A

nose bleeds

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

hemophilia A

A

deficient in CF 8

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

hemophilia B

A

deficient in CF 9

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

inherited hypercoagulation

A
  1. factor 5 Leiden
  2. prothrombin mutation
  3. deficiency in protein C/protien S (antithrombin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

acquired hypercoagulation

A
  1. immobilization
  2. MI
  3. atrial fibrillation
  4. tissue injury
  5. cancer
  6. abnormal platelet activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

protective antioxidants

A
  1. superoxide dismutase
  2. catalase
  3. glutathione peroxidase
  4. ceruloplasmin, transferrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

protective antiproteases

A
  1. alpha-1-antitrypsin

2. alpha-2-macroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

C5a and C3a cause

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

C3b causes

A

phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

C5b+C6-9 causes

A

formation of membrane attack complex (MAC) channel formation in microbe and lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

vasodilators

A
  1. histamine

2. prostaglandings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

increases vascular permability

A
  1. TNF, IL-1
  2. histamine and serotonin
  3. C3a+ C5a
  4. leukotriene C4, D4, E4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

chemotaxis, leukocyte recruitment and activation

A
  1. TNF, IL-1
  2. chemokines
  3. C3a+C5a
  4. leukotriene B4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

fever

A
  1. prostaglandin

2. TNF, IL-1

26
Q

pain

A
  1. prostaglandin

2. bradykinin

27
Q

tissue damage

A
  1. lysosomal enzymes

2. reactive oxygen species

28
Q

cytokines for acute inflammation

A
  1. TNF
  2. IL-1
  3. Il-6
  4. chemokines
  5. IL-17
29
Q

cytokines for chronic inflammation

A
  1. IL-12
  2. IFN-gamma
  3. IL-17`
30
Q

mediators of acute inflammation

A
  1. vascoactive amines
  2. arachidonic acid metabolites
  3. cytokines and chemotaxis
  4. complement system
  5. other
31
Q

acute respiratory distress syndrome cells and molecules involved in injury

A

neutrophils

32
Q

asthma (acute) cell and molecules involved in injury

A
  1. eosinophils

2. IgE antibodies

33
Q

glomerulonephritis (acute) cells and molecules involved in injury

A
  1. antibodies and complement
  2. neutrophils
  3. monocytes
34
Q

`septic shock (acute) cells and molecules involved in injury

A

cytokines

35
Q

arthritis (chronic) cells and molecules involved in injury

A
  1. lymphocytes
  2. macrophages
  3. antibodies?
36
Q

asthma (chronic) cells and molecules involved in injury

A
  1. eosinophils

2. IgE antibodies

37
Q

atherosclerosis (chronic) cells and molecules involved in injury

A
  1. macrophages

2. lymphocytes

38
Q

pulmonary fibrosis (chronic) cell and moleculesinvolved in injury

A
  1. macrophages

2. fibroblasts

39
Q

most common cause of atherosclerosis

A
  • high LDL levels in the blood
  • lower HDL and higher risk factors (modifiable and non-modifiable)
  • modifiable risks explain over 90% of occurances
40
Q

where does atherosclerosis tend to occur

A

branch points and along inner curvatures

41
Q

what is the first step of altherosclerosis

A

adaptive intimal thickening is spontaneous and may provide soil for initial lesion development
-once this happens lesion may spread to adjacent media

42
Q

How to LDLs cause atherosclerosis

A
  • LDL can accumulate in the intima where they are oxidized and aggregate
  • can then stimulate the innate and adaptive immune response
43
Q

how does the immune system respond to the LDL presence

A

-stimulates endothelial cells and smooth muscle cells to express adhesion molecules, chemoattractants, and growth factors

44
Q

macrophages come into play

A

macrophages are recruited and try to consume the LDL and become ladened with fat=foam cells`

45
Q

xanthoma

A

the fatty streaks that occur from foam cells (key characteristic of lipoprotein -driven inflammation) but are reversible and present in fetal aortas

46
Q

pathological intimal thickening

A

a lipid pool slowly starts to form below the foam cells

47
Q

how does the necrotic core grow

A

invasion of the lipid pool by macrophages causes the necrotic core to grow

48
Q

fibroatheroma

A

when a necrotic core is present the lesion is a fibroatheroma

49
Q

contents of necrotic core include

A
  1. foam cells

2. smooth muscle cells

50
Q

neovascularization of the plaque

A
  1. vessels grow into plaque from vasa vasorum and provide a new means for monocyte entry
51
Q

characteristics of these neovessels

A
  1. lack support and are weak
  2. cause leakages into plaque
  3. can expand the fibrous core
52
Q

arterial remodelin

A

during atherogenesis the vessel is remodeled in a way that the lumen is not compromised until the plaque is very large
-therefore angiography is not very helpful at determining how much plaque someone has

53
Q

vulnerable to rupture characteristics

A
  1. thin fibrous cap
  2. low levels of SMC
  3. large amounts of foam cells
    - secrete proteolytic enzymes that can degrade the fibrous cap
54
Q

lateral ECG leads

A

I, aVL, V5, V6

55
Q

what lateral ECG shows

A

circumflex artery

56
Q

Inferior ECG leads

A

II, III, AVF

57
Q

what inferior ECG leads show

A

right coronary artery

58
Q

septal ECG leads

A

V1, V2,

59
Q

what septal ECG shows

A

left anterior descending artery

60
Q

anterior ECG leads

A

V3, V4,

61
Q

what anterior ECG shows

A

right coronary artery

MCM: Cardio (4 decks)

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