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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

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2
Q

disease that is caused by deficiency in Gp1b

A

bernard-soulier syndrome

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3
Q

disease that is caused by deficiency in GpIIb-IIIa

A

glanzmann thrombasthenia

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4
Q

secondary hemostasis tests

A

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

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5
Q

PTT evaluates

A

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

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6
Q

PT evaluates

A

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

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7
Q

primary hemostasis test

A
  1. platelet count
  2. bleeding time
  3. von Willebrand factor
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8
Q

Check for fibrin formation and fibrinolysis

A

D dimer test: specific fibrin degredation product

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9
Q

petechiae

A

spots of blood on skin

-caused from primary hemostasis disorder

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10
Q

purpura

A

large bruising

-primary hemorrhagia

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11
Q

thrombocytopenia

A

decreased number of platelets

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12
Q

epitaxis

A

nose bleeds

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13
Q

hemophilia A

A

deficient in CF 8

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14
Q

hemophilia B

A

deficient in CF 9

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15
Q

inherited hypercoagulation

A
  1. factor 5 Leiden
  2. prothrombin mutation
  3. deficiency in protein C/protien S (antithrombin)
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16
Q

acquired hypercoagulation

A
  1. immobilization
  2. MI
  3. atrial fibrillation
  4. tissue injury
  5. cancer
  6. abnormal platelet activation
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17
Q

protective antioxidants

A
  1. superoxide dismutase
  2. catalase
  3. glutathione peroxidase
  4. ceruloplasmin, transferrin
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18
Q

protective antiproteases

A
  1. alpha-1-antitrypsin

2. alpha-2-macroglobulin

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19
Q

C5a and C3a cause

A

inflammation

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20
Q

C3b causes

A

phagocytosis

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21
Q

C5b+C6-9 causes

A

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

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22
Q

vasodilators

A
  1. histamine

2. prostaglandings

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23
Q

increases vascular permability

A
  1. TNF, IL-1
  2. histamine and serotonin
  3. C3a+ C5a
  4. leukotriene C4, D4, E4
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24
Q

chemotaxis, leukocyte recruitment and activation

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

MCM: Cardio (4 decks)

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