Lecture | Part 2 Hemodynamic disorder Flashcards
1
Q
- EXTRAVASATION beyond vessel
- “HEMORRHAGIC DIATHESIS”
- HEMATOMA (implies MASS effect)
- “DISSECTION”
- PETECHIAE (1-2mm) (PLATELETS)
- PURPURA <1cm
- ECCHYMOSES >1cm (BRUISE)
- HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS
- ACUTE, CHRONIC
A
hemorrhage
2
Q
manifestations on hemorrhage:
very small 1 to 2 mm millimeters
A
petechiae
3
Q
manifestations on hemorrhage:
little larger than petechiae
A
purpura
4
Q
manifestations on hemorrhage:
large areas with hemorrhage more than 1 centimeters
A
ecchymoses or bruise
5
Q
blood in the thorax
A
hemothorax.
6
Q
blood in the pericardial space
A
hemopericardium
7
Q
blood in the peritoneal space
A
hemoperitoneum
8
Q
blood in the joint spaces
A
hemarthrosis
9
Q
from acute to chronic so blood may be manifest as color
A
BROWN or red brown
10
Q
from hemoglobin it will be transformed into bilirubin and eventually become
A
hemosiderin.
11
Q
timing of lesion where how many days are the lesion present. Helps in the evolution of hemorrhage through
A
change in the type of pigments through time
12
Q
hemorrhage in the head
A
epidural hematoma or subdural
13
Q
one of the layers of your meaninges– covering of your brain
A
dura
14
Q
means above the dura
A
epi
15
Q
means down or under so under the dura
A
subdural
16
Q
follows skull fracture
A
epidural
17
Q
follows close head trauma
A
subdural hematoma
18
Q
have texture and usually ADHERE to a vessel wall.
A
Pre-mortem clots
19
Q
have a jelly or chicken fat consistency.
A
Post-mortem clots
20
Q
opposite of thrombosis
A
hemostasis
21
Q
- PRESERVE LIQUIDITY OF BLOOD
- “PLUG” sites of vascular injury
A
hemostasis
22
Q
3 components of hemostasis
A
- VASCULAR WALL
- PLATELETS
- COAGULATION CASCADE
23
Q
One important or fundamental aspect on blood
A
it should be in a liquid state
24
Q
thrombus formation is usually needed ?
A
- when there are vascular injury
- thrombus is used to plug the blood vessel injury
25
to achieve this hemostasis there are three important factors or participants
1. vascular wall
2. platelets
3. coagulation cascade
26
1. Reflex Neurogenic
2. Endothelin, from endothelial cells
ARTERIOLAR VASOCONSTRICTION
27
1. Adhere and activate platelets
2. Platelet aggregation
THROMBOGENIC ECM at injury site
Adhere and activate platelets
28
TISSUE FACTOR released by endothelium activates coagulation cascade to form
thrombin
29
first reaction in vascular injury
arteriolar vasoconstriction
30
exposure of the sub
endothelial matrix is called
thrombogenic
31
cause platelets to activate and adhere to each other called platelet aggregation
thrombogenic
32
1° hemostasis
platelet aggregation
33
a plug that is considered a soft blood because it is composed mainly of platelets
primary hemostasis
34
tissue factor activates the
coagulation cascade
35
tissue factor activates the coagulation cascade resulting to
thrombin formation
36
the purpose of thrombin in tissue factor is to form
fibrin
37
1° Hemostasis
fibrin
38
polymerizes the platelet plug--makes it
more durable and makes it quite hard
fibrin
39
plug that is acted upon by fibrin make it stronger
secondary plug
40
when the blood vessel wall is already repaired, the fibrin plug or what you call secondary plug will be
lyse
41
players that participate in thrombus formation
1. Endothelium
2. Platelets
3. Coagulation “Cascade”
42
--?-- formation is not in response to the blood vessel injury but to abnormalities and pathogenic
thrombus
43
normal endothelial properties
1. Antiplatelet properties
2. Anticoagulant properties
3. Fibrinolytic properties
44
in injury of endothelium secretes
Pro-coagulant properties
45
in injury the endothelium will secrete pro-coagulant properties and trigger
coagulation cascade
46
1. Protection from the subendothelial ECM
2. Degrades ADP (inhibit aggregation)
ANTI-Platelet PROPERTIES
47
1. Membrane HEPARIN-like molecules
2. Makes thrombomodulin which is used for synthesis of
protein c
3. tisse factor pathway inhibitor
ANTI-Coagulant PROPERTIES
48
protein c has what type of property
anti-thrombin
49
makes vWF, TISSUE FACTOR, & Plasminogen inhibitors
PROTHROMBOTIC PROPERTIES
50
binds Platelets→Collagen
vWF
51
in injury, endothelium will be prothrombotic and enhanced formation of thrombus due to
Von Willibrand factor
52
factor that binds platelets to the sub endothelial matrix
Von Willibrand factor
53
PROTHROMBOTIC PROPERTIES of endothelium is activated by
Infectious agents, Hemodynamics, & Plasma
54
Alpha granules
1. Fibrinogen
2. Fibronectin
3. Factor-V, Factor-VIII
4. Platelet factor 4, TGF-beta
55
Delta granules (dense bodies)
ADP/ATP, Ca+, Histamine, Serotonin, Epinephrine
56
platelet phases
1. Adhesion
2. Secretion (I.e., “release” or “activation” or “degranulation”)
3. Aggregation
57
platelet adhesion is regulated by
Von Willebrand factors
58
during platelet adhesion, this bridges the receptors in the platelet surface through the extracellular matrix collagen
Von Willebrand factors
59
in the subendothelial layer, this will be exposed upon injury
in the sub endothelial layer this will be exposed upon injury
60
Primarily to the subendothelial ECM
platelet adhesion
61
the release of the substances found in the alpha and delta granules of the platelets
platelet secretion
62
Binding of agonists to platelet surface receptors and intracellular protein PHOSPHORYLATION
platelet secretion
63
substances that will enhance platelet aggregation
ADP and thromboxane a2
64
platelet events
1. ADHERENCE to ECM
2. SECRETION of ADP and TXA2
3. EXPOSE phospholipid complexes
4. Express TISSUE FACTOR
5. PRIMARY SECONDARY PLUG
6. STRENGTHENED by FIBRIN
65
formation of thrombus which is emphasized will now be abnormal in a
disease condition; pathologic condition because there is blood clot formation
66
1.INTRINSIC(contact)/EXTRINSIC(Tissue Factor)
2. Proenzymes→ Enzymes
3. Prothrombin(II)→Thrombin(lla)
4. Fibrinogen(1)→Fibrin(la)
5. Cofactors
- Ca++
- Phospholipid (from platelet membranes)
- Vit-K dep. factors
coagulation cascade
67
Vit-K dep. factors:
II, VII, IX, X, Prot. S, C, Z
68
triggered when there is release of your tissue factor
coagulation cascade
69
enhances the cascade
coagulant properties
70
coagulation cascade inhibitors in the presence of
1.protein c
2. protein s
3. anti-thrombin
4. plasminogen inhibitors
71
checks for your intrinsic pathway
activated protrumbin time
72
will look at your extrinsic pathway
protrumbin time
73
check the number of platelets
Bleeding time
74
Platelet-count
150,000-400,000/mm3
75
Bleeding time checks the number of platelets for how many mins
2-9min
76
1. Pathogenesis
2. Endothelial Injury
3. Alterations in Flow
4. Hypercoagulability
5. Morphology
6. Fate
7. Clinical Correlations
8. Venous
9. Arterial (Mural)
thrombosis
77
person is prone to thrombus formation because of this abnormalities contributed by these three factors
1. one is endothelial injury
2. the other one is abnormalities in the flow of blood
3. and the third one is a hypercoagulability state
78
Thrombosis will occur due to Virchow’s triangle which are the
1. endothelial injury
2. abnormal (non-laminar) flow
3. hyper-coagulation
79
any perturbation in the dynamic balance of the pro- and antithrombotic effects of endothelium, not only physical "damage"
ENDOTHELIAL "INJURY"
80
disruption on the laminar flow of blood will bring the platelets
platelets into contact with the endothelium and or the extracellular matrix
81
two forms of hypercoagulability
inherited & acquired
82
most common inherited hypercoagulability
Factor V and Prothrombin defects
83
common inherited hypercoagulability are mutation in
prothrombin gene & methyltetrahydrofolate gene
84
rare inherited hypercoagulability
1. Antithrombin III deficiency
2. Protein C deficiency
3. Protein S deficiency
85
Very rare inherited hypercoagulability
Fibrinolysis defects
86
1. Prolonged bed rest or immobilization
2. Myocardial infarction
3. Atrial fibrillation
4. Tissue damage (surgery, fracture, burns)
5. Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)
6. Prosthetic cardiac valves
7. Disseminated intravascular coagulation
8. Heparin-induced thrombocytopenia
9. Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)
acquired hypercoagulability
87
Risk for thrombosis:
1. Cardiomyopathy
2. Nephrotic syndrome
3. Pregnancy
4. Oral contraceptive use
5. Sickle cell anemia
6. Smoking, Obesity
88
thrombosis morphology adherence to vessel wall, such as
1. HEART (MURAL)
2. ARTERY (OCCLUSIVE/INFARCT)
3. VEIN
89
most important thing to remember that has clinical outcome of a thrombus formation
OBSTRUCTIVE vs. NON-OBSTRUCTIVE
90
thrombosis color
RED, YELLOW, GREY/WHITE
91
mural thrombus in the heart can be found in
chambers or valves of the heart
92
an example of an obstructive form of thrombus
mural thrombus
93
fate of thrombi
1. PROPAGATION (Downstream)
2. EMBOLIZATION
3. DISSOLUTION
4. ORGANIZATION
5. RECANALIZATION
94
add up more cluttered blood along its
way
Propagation
95
formation of small lumen within the thrombus that can make the blood pass through
recanalization
96
the thrombus dissolved and almost get there's no remnantsthat can be seen
resolution
97
thrombus become part of the wall; it's incorporated into the blood vessel wall
organize
98
thrombus that occurs in the arteries, there is a complete seal off on the blood vessel so blood cannot pass through anymore
occlusive arterial thrombus
99
DVT
deep vein thrombosis
100
CHF is a huge factor and fairly common occurrence and it is due to inactivity
deep vein thrombosis
101
dvt is usually trauma, surgery, burns, injury to vessels, and there is prolonged immobilization to the
lower leg (calf, thigh, pelvic)
102
Procoagulant substances from tissues and Reduced t-PA activity
deep vein thrombosis
103
old atherosclerosis + fresh thrombosis
ACUTE MYOCARDIAL INFARCTION
104
ARTERIAL THROMBI also may send fragments in what direction
DOWNSTREAM
105
ARTERIAL THROMBI also may send fragments that may contain
flecks of PLAQUE
106
PROPORTIONAL to the % of cardiac output the organ receives,
LODGING
107
not a primary disease and considered as complications to obstretic complications, difficult child birth, in advanced malignancies, and shock.
Disseminated intravascular coagulation
108
Disseminated intravascular coagulation is a serious condition due to
consumptive coagulopathy
109
prone to bleeding. An example are reduced platelets, fibrinogen, F-VIII and other consumable clotting factors, brain, heart, lungs, kidneys, MICROSCOPIC ONLY
consumptive coagulopathy
110
other materials that can act as an embolus
fat globules, bubbles of air, amniotic fluid, and tumor cells
111
type of embolus it is usually fatal
saddle type
112
consistency of cluttered blood when the patient is still alive
pre-mortem blood clot : Friable, adherent, lines of ZAHN
113
consistency of cluttered blood when the patient is dead
post mortem blood clot : Current jelly or chicken fat, not adherent
114
most common source of pulmonary embolism
thrombus from the deep veins of the legs
115
embolism involves the lungs, usually silent, there's no premonition and you develop chest pain and have shortness of breath that can cause sudden death
pulmonary embolism
116
1. "PARADOXICAL" EMBOLI
2. 80% cardiac; 20% aortic
SYSTEMIC EMBOLI
117
Embolization lodging site is proportional to the degree of flow (cardiac output) that area or organ gets, i.e., brain, kidneys, legs
SYSTEMIC EMBOLI
118
based on the proportional degree of the flow of the cardiac output.
SYSTEMIC EMBOLI
119
emboli that carries the squames from the baby will penetrate the uterine blood vessels and lodge into the lungs of the mother during difficult childbirth
amniotic fluid
120
deep sea divers are
not advised to arise to the surface of the ocean rapidly due to this emboli
bubbles of air
121
fat along this may act as an embolus
long bone fractures
122
Defined as an area of necrosis secondary to decreased blood flow
infarction
123
INFARCTION FACTORS
1. NATURE of VASCULAR SUPPLY
2. RATE of DEVELOPMENT
- SLOW (BETTER)
- FAST (WORSE)
3. VULNERABILITY to HYPOXIA
- MYOCYTE vs. FIBROBLAST
4. CHFvs.NOCHF
124
3 cells that are vulnerable to hypoxia
1. cardiac cells
2. renal tubular cells
3. neurons (brain cells)
125
death of tissues due to loss of blood supply
infarction
126
1. Pathogenesis
- Cardiac
- Septic
- Hypovolemic
2. Morphology
3. Clinical Course
shock
127
manifested as loss of tissue perfusion
Shock
128
collapse in the circulatory system such that there is a lack of blood flow to important organs
Shock
129
defines as cardiovascular collapse
shock
130
common pathophysiologic features of shock
1. INADEQUATE CARDIAC OUTPUT
2. INADEQUATE BLOOD VOLUME
131
general results of shock
1. INADEQUATE TISSUE PERFUSION 2. CELLULAR HYPOXIA
3. UN-corrected, a FATAL outcome
132
type of shock : Acute, Chronic Heart Failure
CARDIOGENIC
133
type of shock : Hemorrhage or Leakage
HYPOVOLEMIC
134
type of shock : "ENDOTOXIC" shock, #1 killer in ICU
SEPTIC
135
type of shock : loss of vascular tone
NEUROGENIC
136
type of shock : IgE mediated systemic vasodilation and increased vascular permeability
ANAPHYLACTIC
137
cardiogenic shock equates to
failure of the heart to pump adequate blood
138
equates to inadequate blood volume
hypovolemic shock
139
due to massive infection and activation of the inflammatory mediators resulting to low blood pressure
Septic shock
140
IgE
allergy-hypersensitivity reactions
141
cause systemic visodilatation; slowing down the flow of blood and there is increased vascular permeability.
anaphylactic shock
142
causes cardiogenic shock
1. MYOCARDIAL INFARCTION
2. VENTRICULAR RUPTURE
3. ARRHYTHMIA
4. CARDIAC TAMPONADE
5. PULMONARY EMBOLISM (acute RIGHT heart failure or "corpulmonale")
143
causes cardiogenic shock when there is an external force that constrict the pumping action of the heart oroutside force that impinged on the heart
Cardiac tamponade
144
causes cardiogenic shock when contraction of the heart is irregular
Arrhythmia
145
one of the most common causes of cardiogenic shock
myocardial infarction
146
caused by overwhelming infection and when gram-negative bacteria enter the blood that results to low blood pressure
Septic shock
147
polyclonal T-lymphocyte activators that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock
SUPERANTIGENS
148
1. OVERWHELMING INFECTION
2. "ENDOTOXINS"
3. FUNGAL
4. "SUPERANTIGENS
Septic shock
149
prime example of "toxic shock" antigens
Staphyloccoccus aureus
150
TOTAL BODY inflammatory response
Septic shock
151
Usually Gram-negative bacteria, Degraded bacterial cell wall products, Also called "LPS", because they are Lipo- Poly-Saccharides, Attach to a cell surface antigen known as CD-14
ENDOTOXINS
152
clinical stages of shock
1. NON-PROGRESSIVE
2. PROGRESSIVE
3. IRREVERSIBLE
153
clinical stage of shock known as compensatory mechanisms, action is done by catecholamine, and vital organ perfused
NON-PROGRESSIVE
154
clinical stage of shock known as acidosis, early organ failure, hypoperfusion, and oliguria
PROGRESSIVE
155
HEMODYNAMIC CORRECTIONS of no use
IRREVERSIBLE
156
cause acidosis and this is manifested in a low ph.
Lactic acid
157
Death of the cardiac cells because again lack of oxygen
myocardial necrosis
158
vulnerability of the renal tubular cells so it is manifested as oliguria; no formation of urine so it is an early or acute renal failure
acute tubular necrosis
159
simultaneous bleeding and thrombose formation
DIC
160
clinical progression of symptoms of shock
1. Hypotension
2. Tachycardia Tachypnea
3. Warm skin →→ Cyanosis
4. Renal insufficiency
5. Obtundance
6. Death
161
increase heart rate increase breathing
tachycardia
