Week 1 Cardiac Flashcards Preview

MCM: Cardio > Week 1 Cardiac > Flashcards

Flashcards in Week 1 Cardiac Deck (61):
1

disease that is caused by deficiency in von Willebrand factor

von willebrand disease

2

disease that is caused by deficiency in Gp1b

bernard-soulier syndrome

3

disease that is caused by deficiency in GpIIb-IIIa

glanzmann thrombasthenia

4

secondary hemostasis tests

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

5

PTT evaluates

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

6

PT evaluates

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

7

primary hemostasis test

1. platelet count
2. bleeding time
3. von Willebrand factor

8

Check for fibrin formation and fibrinolysis

D dimer test: specific fibrin degredation product

9

petechiae

spots of blood on skin
-caused from primary hemostasis disorder

10

purpura

large bruising
-primary hemorrhagia

11

thrombocytopenia

decreased number of platelets

12

epitaxis

nose bleeds

13

hemophilia A

deficient in CF 8

14

hemophilia B

deficient in CF 9

15

inherited hypercoagulation

1. factor 5 Leiden
2. prothrombin mutation
3. deficiency in protein C/protien S (antithrombin)

16

acquired hypercoagulation

1. immobilization
2. MI
3. atrial fibrillation
4. tissue injury
5. cancer
6. abnormal platelet activation

17

protective antioxidants

1. superoxide dismutase
2. catalase
3. glutathione peroxidase
4. ceruloplasmin, transferrin

18

protective antiproteases

1. alpha-1-antitrypsin
2. alpha-2-macroglobulin

19

C5a and C3a cause

inflammation

20

C3b causes

phagocytosis

21

C5b+C6-9 causes

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

22

vasodilators

1. histamine
2.prostaglandings

23

increases vascular permability

1. TNF, IL-1
2. histamine and serotonin
3. C3a+ C5a
4. leukotriene C4, D4, E4

24

chemotaxis, leukocyte recruitment and activation

1. TNF, IL-1
2. chemokines
3. C3a+C5a
4. leukotriene B4

25

fever

1. prostaglandin
2. TNF, IL-1

26

pain

1. prostaglandin
2.bradykinin

27

tissue damage

1. lysosomal enzymes
2.reactive oxygen species

28

cytokines for acute inflammation

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

29

cytokines for chronic inflammation

1. IL-12
2. IFN-gamma
3. IL-17`

30

mediators of acute inflammation

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

31

acute respiratory distress syndrome cells and molecules involved in injury

neutrophils

32

asthma (acute) cell and molecules involved in injury

1.eosinophils
2. IgE antibodies

33

glomerulonephritis (acute) cells and molecules involved in injury

1. antibodies and complement
2. neutrophils
3.monocytes

34

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

cytokines

35

arthritis (chronic) cells and molecules involved in injury

1. lymphocytes
2. macrophages
3. antibodies?

36

asthma (chronic) cells and molecules involved in injury

1. eosinophils
2. IgE antibodies

37

atherosclerosis (chronic) cells and molecules involved in injury

1. macrophages
2. lymphocytes

38

pulmonary fibrosis (chronic) cell and moleculesinvolved in injury

1. macrophages
2. fibroblasts

39

most common cause of atherosclerosis

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

40

where does atherosclerosis tend to occur

branch points and along inner curvatures

41

what is the first step of altherosclerosis

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

42

How to LDLs cause atherosclerosis

-LDL can accumulate in the intima where they are oxidized and aggregate
-can then stimulate the innate and adaptive immune response

43

how does the immune system respond to the LDL presence

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

44

macrophages come into play

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

45

xanthoma

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

46

pathological intimal thickening

a lipid pool slowly starts to form below the foam cells

47

how does the necrotic core grow

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

48

fibroatheroma

when a necrotic core is present the lesion is a fibroatheroma

49

contents of necrotic core include

1. foam cells
2. smooth muscle cells

50

neovascularization of the plaque

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

51

characteristics of these neovessels

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

52

arterial remodelin

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

vulnerable to rupture characteristics

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

lateral ECG leads

I, aVL, V5, V6

55

what lateral ECG shows

circumflex artery

56

Inferior ECG leads

II, III, AVF

57

what inferior ECG leads show

right coronary artery

58

septal ECG leads

V1, V2,

59

what septal ECG shows

left anterior descending artery

60

anterior ECG leads

V3, V4,

61

what anterior ECG shows

right coronary artery