Week 1 Cardiac Flashcards
disease that is caused by deficiency in von Willebrand factor
von willebrand disease
disease that is caused by deficiency in Gp1b
bernard-soulier syndrome
disease that is caused by deficiency in GpIIb-IIIa
glanzmann thrombasthenia
secondary hemostasis tests
partial thromboplastin time (PTT) and prothrombin time (PT)
PTT evaluates
12, 11, 9, 8, and 10, 5, 2 (prothrombin), and 1 (fibrinogen) (instrinsic factors)
PT evaluates
7 and tissue factor, and 10, 5, 2, and 1 (extrinsic pathway)
primary hemostasis test
- platelet count
- bleeding time
- von Willebrand factor
Check for fibrin formation and fibrinolysis
D dimer test: specific fibrin degredation product
petechiae
spots of blood on skin
-caused from primary hemostasis disorder
purpura
large bruising
-primary hemorrhagia
thrombocytopenia
decreased number of platelets
epitaxis
nose bleeds
hemophilia A
deficient in CF 8
hemophilia B
deficient in CF 9
inherited hypercoagulation
- factor 5 Leiden
- prothrombin mutation
- deficiency in protein C/protien S (antithrombin)
acquired hypercoagulation
- immobilization
- MI
- atrial fibrillation
- tissue injury
- cancer
- abnormal platelet activation
protective antioxidants
- superoxide dismutase
- catalase
- glutathione peroxidase
- ceruloplasmin, transferrin
protective antiproteases
- alpha-1-antitrypsin
2. alpha-2-macroglobulin
C5a and C3a cause
inflammation
C3b causes
phagocytosis
C5b+C6-9 causes
formation of membrane attack complex (MAC) channel formation in microbe and lysis
vasodilators
- histamine
2. prostaglandings
increases vascular permability
- TNF, IL-1
- histamine and serotonin
- C3a+ C5a
- leukotriene C4, D4, E4
chemotaxis, leukocyte recruitment and activation
- TNF, IL-1
- chemokines
- C3a+C5a
- leukotriene B4
fever
- prostaglandin
2. TNF, IL-1
pain
- prostaglandin
2. bradykinin
tissue damage
- lysosomal enzymes
2. reactive oxygen species
cytokines for acute inflammation
- TNF
- IL-1
- Il-6
- chemokines
- IL-17
cytokines for chronic inflammation
- IL-12
- IFN-gamma
- IL-17`
mediators of acute inflammation
- vascoactive amines
- arachidonic acid metabolites
- cytokines and chemotaxis
- complement system
- other
acute respiratory distress syndrome cells and molecules involved in injury
neutrophils
asthma (acute) cell and molecules involved in injury
- eosinophils
2. IgE antibodies
glomerulonephritis (acute) cells and molecules involved in injury
- antibodies and complement
- neutrophils
- monocytes
`septic shock (acute) cells and molecules involved in injury
cytokines
arthritis (chronic) cells and molecules involved in injury
- lymphocytes
- macrophages
- antibodies?
asthma (chronic) cells and molecules involved in injury
- eosinophils
2. IgE antibodies
atherosclerosis (chronic) cells and molecules involved in injury
- macrophages
2. lymphocytes
pulmonary fibrosis (chronic) cell and moleculesinvolved in injury
- macrophages
2. fibroblasts
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
where does atherosclerosis tend to occur
branch points and along inner curvatures
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
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
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
macrophages come into play
macrophages are recruited and try to consume the LDL and become ladened with fat=foam cells`
xanthoma
the fatty streaks that occur from foam cells (key characteristic of lipoprotein -driven inflammation) but are reversible and present in fetal aortas
pathological intimal thickening
a lipid pool slowly starts to form below the foam cells
how does the necrotic core grow
invasion of the lipid pool by macrophages causes the necrotic core to grow
fibroatheroma
when a necrotic core is present the lesion is a fibroatheroma
contents of necrotic core include
- foam cells
2. smooth muscle cells
neovascularization of the plaque
- vessels grow into plaque from vasa vasorum and provide a new means for monocyte entry
characteristics of these neovessels
- lack support and are weak
- cause leakages into plaque
- can expand the fibrous core
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
vulnerable to rupture characteristics
- thin fibrous cap
- low levels of SMC
- large amounts of foam cells
- secrete proteolytic enzymes that can degrade the fibrous cap
lateral ECG leads
I, aVL, V5, V6
what lateral ECG shows
circumflex artery
Inferior ECG leads
II, III, AVF
what inferior ECG leads show
right coronary artery
septal ECG leads
V1, V2,
what septal ECG shows
left anterior descending artery
anterior ECG leads
V3, V4,
what anterior ECG shows
right coronary artery
