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HISTOPATH > Lecture | Part 2 Hemodynamic disorder > Flashcards

Lecture | Part 2 Hemodynamic disorder Flashcards

1
Q
  1. EXTRAVASATION beyond vessel
  2. “HEMORRHAGIC DIATHESIS”
  3. HEMATOMA (implies MASS effect)
  4. “DISSECTION”
  5. PETECHIAE (1-2mm) (PLATELETS)
  6. PURPURA <1cm
  7. ECCHYMOSES >1cm (BRUISE)
  8. HEMO-: -thorax, -pericardium, -peritoneum, HEMARTHROSIS
  9. ACUTE, CHRONIC
A

hemorrhage

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2
Q

manifestations on hemorrhage:

very small 1 to 2 mm millimeters

A

petechiae

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3
Q

manifestations on hemorrhage:

little larger than petechiae

A

purpura

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4
Q

manifestations on hemorrhage:

large areas with hemorrhage more than 1 centimeters

A

ecchymoses or bruise

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5
Q

blood in the thorax

A

hemothorax.

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6
Q

blood in the pericardial space

A

hemopericardium

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7
Q

blood in the peritoneal space

A

hemoperitoneum

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8
Q

blood in the joint spaces

A

hemarthrosis

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9
Q

from acute to chronic so blood may be manifest as color

A

BROWN or red brown

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10
Q

from hemoglobin it will be transformed into bilirubin and eventually become

A

hemosiderin.

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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

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12
Q

hemorrhage in the head

A

epidural hematoma or subdural

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13
Q

one of the layers of your meaninges– covering of your brain

A

dura

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14
Q

means above the dura

A

epi

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15
Q

means down or under so under the dura

A

subdural

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16
Q

follows skull fracture

A

epidural

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17
Q

follows close head trauma

A

subdural hematoma

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18
Q

have texture and usually ADHERE to a vessel wall.

A

Pre-mortem clots

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19
Q

have a jelly or chicken fat consistency.

A

Post-mortem clots

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20
Q

opposite of thrombosis

A

hemostasis

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21
Q
  1. PRESERVE LIQUIDITY OF BLOOD
  2. “PLUG” sites of vascular injury
A

hemostasis

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22
Q

3 components of hemostasis

A
  1. VASCULAR WALL
  2. PLATELETS
  3. COAGULATION CASCADE
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23
Q

One important or fundamental aspect on blood

A

it should be in a liquid state

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24
Q

thrombus formation is usually needed ?

A
  1. when there are vascular injury
  2. thrombus is used to plug the blood vessel injury
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25
Q

to achieve this hemostasis there are three important factors or participants

A
  1. vascular wall
  2. platelets
  3. coagulation cascade
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26
Q
  1. Reflex Neurogenic
  2. Endothelin, from endothelial cells
A

ARTERIOLAR VASOCONSTRICTION

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27
Q
  1. Adhere and activate platelets
  2. Platelet aggregation
A

THROMBOGENIC ECM at injury site
 Adhere and activate platelets

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28
Q

TISSUE FACTOR released by endothelium activates coagulation cascade to form

A

thrombin

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29
Q

first reaction in vascular injury

A

arteriolar vasoconstriction

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30
Q

exposure of the sub
endothelial matrix is called

A

thrombogenic

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31
Q

cause platelets to activate and adhere to each other called platelet aggregation

A

thrombogenic

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32
Q

1° hemostasis

A

platelet aggregation

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33
Q

a plug that is considered a soft blood because it is composed mainly of platelets

A

primary hemostasis

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34
Q

tissue factor activates the

A

coagulation cascade

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35
Q

tissue factor activates the coagulation cascade resulting to

A

thrombin formation

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36
Q

the purpose of thrombin in tissue factor is to form

A

fibrin

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37
Q

1° Hemostasis

A

fibrin

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38
Q

polymerizes the platelet plug–makes it
more durable and makes it quite hard

A

fibrin

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39
Q

plug that is acted upon by fibrin make it stronger

A

secondary plug

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40
Q

when the blood vessel wall is already repaired, the fibrin plug or what you call secondary plug will be

A

lyse

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41
Q

players that participate in thrombus formation

A
  1. Endothelium
  2. Platelets
  3. Coagulation “Cascade”
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42
Q

–?– formation is not in response to the blood vessel injury but to abnormalities and pathogenic

A

thrombus

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43
Q

normal endothelial properties

A
  1. Antiplatelet properties
  2. Anticoagulant properties
  3. Fibrinolytic properties
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44
Q

in injury of endothelium secretes

A

Pro-coagulant properties

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45
Q

in injury the endothelium will secrete pro-coagulant properties and trigger

A

coagulation cascade

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46
Q
  1. Protection from the subendothelial ECM
  2. Degrades ADP (inhibit aggregation)
A

ANTI-Platelet PROPERTIES

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47
Q
  1. Membrane HEPARIN-like molecules
  2. Makes thrombomodulin which is used for synthesis of
    protein c
  3. tisse factor pathway inhibitor
A

ANTI-Coagulant PROPERTIES

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48
Q

protein c has what type of property

A

anti-thrombin

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49
Q

makes vWF, TISSUE FACTOR, & Plasminogen inhibitors

A

PROTHROMBOTIC PROPERTIES

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50
Q

binds Platelets→Collagen

A

vWF

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51
Q

in injury, endothelium will be prothrombotic and enhanced formation of thrombus due to

A

Von Willibrand factor

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52
Q

factor that binds platelets to the sub endothelial matrix

A

Von Willibrand factor

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53
Q

PROTHROMBOTIC PROPERTIES of endothelium is activated by

A

Infectious agents, Hemodynamics, & Plasma

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54
Q

Alpha granules

A
  1. Fibrinogen
  2. Fibronectin
  3. Factor-V, Factor-VIII
  4. Platelet factor 4, TGF-beta
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55
Q

Delta granules (dense bodies)

A

ADP/ATP, Ca+, Histamine, Serotonin, Epinephrine

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56
Q

platelet phases

A
  1. Adhesion
  2. Secretion (I.e., “release” or “activation” or “degranulation”)
  3. Aggregation
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57
Q

platelet adhesion is regulated by

A

Von Willebrand factors

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58
Q

during platelet adhesion, this bridges the receptors in the platelet surface through the extracellular matrix collagen

A

Von Willebrand factors

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59
Q

in the subendothelial layer, this will be exposed upon injury

A

in the sub endothelial layer this will be exposed upon injury

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60
Q

Primarily to the subendothelial ECM

A

platelet adhesion

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61
Q

the release of the substances found in the alpha and delta granules of the platelets

A

platelet secretion

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62
Q

Binding of agonists to platelet surface receptors and intracellular protein PHOSPHORYLATION

A

platelet secretion

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63
Q

substances that will enhance platelet aggregation

A

ADP and thromboxane a2

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64
Q

platelet events

A
  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
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65
Q

formation of thrombus which is emphasized will now be abnormal in a

A

disease condition; pathologic condition because there is blood clot formation

66
Q

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

A

coagulation cascade

67
Q

Vit-K dep. factors:

A

II, VII, IX, X, Prot. S, C, Z

68
Q

triggered when there is release of your tissue factor

A

coagulation cascade

69
Q

enhances the cascade

A

coagulant properties

70
Q

coagulation cascade inhibitors in the presence of

A

1.protein c
2. protein s
3. anti-thrombin
4. plasminogen inhibitors

71
Q

checks for your intrinsic pathway

A

activated protrumbin time

72
Q

will look at your extrinsic pathway

A

protrumbin time

73
Q

check the number of platelets

A

Bleeding time

74
Q

Platelet-count

A

150,000-400,000/mm3

75
Q

Bleeding time checks the number of platelets for how many mins

A

2-9min

76
Q
  1. Pathogenesis
  2. Endothelial Injury
  3. Alterations in Flow
  4. Hypercoagulability
  5. Morphology
  6. Fate
  7. Clinical Correlations
  8. Venous
  9. Arterial (Mural)
A

thrombosis

77
Q

person is prone to thrombus formation because of this abnormalities contributed by these three factors

A
  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
Q

Thrombosis will occur due to Virchow’s triangle which are the

A
  1. endothelial injury
  2. abnormal (non-laminar) flow
  3. hyper-coagulation
79
Q

any perturbation in the dynamic balance of the pro- and antithrombotic effects of endothelium, not only physical “damage”

A

ENDOTHELIAL “INJURY”

80
Q

disruption on the laminar flow of blood will bring the platelets

A

platelets into contact with the endothelium and or the extracellular matrix

81
Q

two forms of hypercoagulability

A

inherited & acquired

82
Q

most common inherited hypercoagulability

A

Factor V and Prothrombin defects

83
Q

common inherited hypercoagulability are mutation in

A

prothrombin gene & methyltetrahydrofolate gene

84
Q

rare inherited hypercoagulability

A
  1. Antithrombin III deficiency
  2. Protein C deficiency
  3. Protein S deficiency
85
Q

Very rare inherited hypercoagulability

A

Fibrinolysis defects

86
Q
  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)
A

acquired hypercoagulability

87
Q

Risk for thrombosis:

A
  1. Cardiomyopathy
  2. Nephrotic syndrome
  3. Pregnancy
  4. Oral contraceptive use
  5. Sickle cell anemia
  6. Smoking, Obesity
88
Q

thrombosis morphology adherence to vessel wall, such as

A
  1. HEART (MURAL)
  2. ARTERY (OCCLUSIVE/INFARCT)
  3. VEIN
89
Q

most important thing to remember that has clinical outcome of a thrombus formation

A

OBSTRUCTIVE vs. NON-OBSTRUCTIVE

90
Q

thrombosis color

A

RED, YELLOW, GREY/WHITE

91
Q

mural thrombus in the heart can be found in

A

chambers or valves of the heart

92
Q

an example of an obstructive form of thrombus

A

mural thrombus

93
Q

fate of thrombi

A
  1. PROPAGATION (Downstream) 
  2. EMBOLIZATION
  3. DISSOLUTION
  4. ORGANIZATION
  5. RECANALIZATION
94
Q

add up more cluttered blood along its
way

A

Propagation

95
Q

formation of small lumen within the thrombus that can make the blood pass through

A

recanalization

96
Q

the thrombus dissolved and almost get there’s no remnantsthat can be seen

A

resolution

97
Q

thrombus become part of the wall; it’s incorporated into the blood vessel wall

A

organize

98
Q

thrombus that occurs in the arteries, there is a complete seal off on the blood vessel so blood cannot pass through anymore

A

occlusive arterial thrombus

99
Q

DVT

A

deep vein thrombosis

100
Q

CHF is a huge factor and fairly common occurrence and it is due to inactivity

A

deep vein thrombosis

101
Q

dvt is usually trauma, surgery, burns, injury to vessels, and there is prolonged immobilization to the

A

lower leg (calf, thigh, pelvic)

102
Q

Procoagulant substances from tissues and Reduced t-PA activity

A

deep vein thrombosis

103
Q

old atherosclerosis + fresh thrombosis

A

ACUTE MYOCARDIAL INFARCTION

104
Q

ARTERIAL THROMBI also may send fragments in what direction

A

DOWNSTREAM

105
Q

ARTERIAL THROMBI also may send fragments that may contain

A

flecks of PLAQUE

106
Q

PROPORTIONAL to the % of cardiac output the organ receives,

A

LODGING

107
Q

not a primary disease and considered as complications to obstretic complications, difficult child birth, in advanced malignancies, and shock.

A

Disseminated intravascular coagulation

108
Q

Disseminated intravascular coagulation is a serious condition due to

A

consumptive coagulopathy

109
Q

prone to bleeding. An example are reduced platelets, fibrinogen, F-VIII and other consumable clotting factors, brain, heart, lungs, kidneys, MICROSCOPIC ONLY

A

consumptive coagulopathy

110
Q

other materials that can act as an embolus

A

fat globules, bubbles of air, amniotic fluid, and tumor cells

111
Q

type of embolus it is usually fatal

A

saddle type

112
Q

consistency of cluttered blood when the patient is still alive

A

pre-mortem blood clot : Friable, adherent, lines of ZAHN

113
Q

consistency of cluttered blood when the patient is dead

A

post mortem blood clot : Current jelly or chicken fat, not adherent

114
Q

most common source of pulmonary embolism

A

thrombus from the deep veins of the legs

115
Q

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

A

pulmonary embolism

116
Q
  1. “PARADOXICAL” EMBOLI
  2. 80% cardiac; 20% aortic
A

SYSTEMIC EMBOLI

117
Q

Embolization lodging site is proportional to the degree of flow (cardiac output) that area or organ gets, i.e., brain, kidneys, legs

A

SYSTEMIC EMBOLI

118
Q

based on the proportional degree of the flow of the cardiac output.

A

SYSTEMIC EMBOLI

119
Q

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

A

amniotic fluid

120
Q

deep sea divers are
not advised to arise to the surface of the ocean rapidly due to this emboli

A

bubbles of air

121
Q

fat along this may act as an embolus

A

long bone fractures

122
Q

Defined as an area of necrosis secondary to decreased blood flow

A

infarction

123
Q

INFARCTION FACTORS

A
  1. NATURE of VASCULAR SUPPLY
  2. RATE of DEVELOPMENT
    - SLOW (BETTER)
    - FAST (WORSE)
  3. VULNERABILITY to HYPOXIA
    - MYOCYTE vs. FIBROBLAST
  4. CHFvs.NOCHF
124
Q

3 cells that are vulnerable to hypoxia

A
  1. cardiac cells
  2. renal tubular cells
  3. neurons (brain cells)
125
Q

death of tissues due to loss of blood supply

A

infarction

126
Q
  1. Pathogenesis
    - Cardiac
    - Septic
    - Hypovolemic
  2. Morphology
  3. Clinical Course
A

shock

127
Q

manifested as loss of tissue perfusion

A

Shock

128
Q

collapse in the circulatory system such that there is a lack of blood flow to important organs

A

Shock

129
Q

defines as cardiovascular collapse

A

shock

130
Q

common pathophysiologic features of shock

A
  1. INADEQUATE CARDIAC OUTPUT
  2. INADEQUATE BLOOD VOLUME
131
Q

general results of shock

A
  1. INADEQUATE TISSUE PERFUSION 2. CELLULAR HYPOXIA
  2. UN-corrected, a FATAL outcome
132
Q

type of shock : Acute, Chronic Heart Failure

A

CARDIOGENIC

133
Q

type of shock : Hemorrhage or Leakage

A

HYPOVOLEMIC

134
Q

type of shock : “ENDOTOXIC” shock, #1 killer in ICU

A

SEPTIC

135
Q

type of shock : loss of vascular tone

A

NEUROGENIC

136
Q

type of shock : IgE mediated systemic vasodilation and increased vascular permeability

A

ANAPHYLACTIC

137
Q

cardiogenic shock equates to

A

failure of the heart to pump adequate blood

138
Q

equates to inadequate blood volume

A

hypovolemic shock

139
Q

due to massive infection and activation of the inflammatory mediators resulting to low blood pressure

A

Septic shock

140
Q

IgE

A

allergy-hypersensitivity reactions

141
Q

cause systemic visodilatation; slowing down the flow of blood and there is increased vascular permeability.

A

anaphylactic shock

142
Q

causes cardiogenic shock

A
  1. MYOCARDIAL INFARCTION
  2. VENTRICULAR RUPTURE
  3. ARRHYTHMIA
  4. CARDIAC TAMPONADE
  5. PULMONARY EMBOLISM (acute RIGHT heart failure or “corpulmonale”)
143
Q

causes cardiogenic shock when there is an external force that constrict the pumping action of the heart oroutside force that impinged on the heart

A

Cardiac tamponade

144
Q

causes cardiogenic shock when contraction of the heart is irregular

A

Arrhythmia

145
Q

one of the most common causes of cardiogenic shock

A

myocardial infarction

146
Q

caused by overwhelming infection and when gram-negative bacteria enter the blood that results to low blood pressure

A

Septic shock

147
Q

polyclonal T-lymphocyte activators that induce systemic inflammatory cytokine cascades similar to those occurring downstream in septic shock

A

SUPERANTIGENS

148
Q
  1. OVERWHELMING INFECTION
  2. “ENDOTOXINS”
  3. FUNGAL
  4. “SUPERANTIGENS
A

Septic shock

149
Q

prime example of “toxic shock” antigens

A

Staphyloccoccus aureus

150
Q

TOTAL BODY inflammatory response

A

Septic shock

151
Q

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

A

ENDOTOXINS

152
Q

clinical stages of shock

A
  1. NON-PROGRESSIVE
  2. PROGRESSIVE
  3. IRREVERSIBLE
153
Q

clinical stage of shock known as compensatory mechanisms, action is done by catecholamine, and vital organ perfused

A

NON-PROGRESSIVE

154
Q

clinical stage of shock known as acidosis, early organ failure, hypoperfusion, and oliguria

A

PROGRESSIVE

155
Q

HEMODYNAMIC CORRECTIONS of no use

A

IRREVERSIBLE

156
Q

cause acidosis and this is manifested in a low ph.

A

Lactic acid

157
Q

Death of the cardiac cells because again lack of oxygen

A

myocardial necrosis

158
Q

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

A

acute tubular necrosis

159
Q

simultaneous bleeding and thrombose formation

A

DIC

160
Q

clinical progression of symptoms of shock

A
  1. Hypotension
  2. Tachycardia Tachypnea
  3. Warm skin →→ Cyanosis
  4. Renal insufficiency
  5. Obtundance
  6. Death
161
Q

increase heart rate increase breathing

A

tachycardia

HISTOPATH (4 decks)

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