[P] Week 3: HEMODYNAMIC DISORDERS, THROMBOEMBOLIC DISEASES, AND SHOCK [AI generated] Flashcards
(153 cards)
1
Q
What is hemostasis?
A
The process by which we activate the clotting mechanism that prevents excessive bleeding after blood vessel damage.
2
Q
What can inadequate hemostasis result in?
A
Hemorrhage, thrombosis, or embolism.
3
Q
What is edema?
A
The increased amount of fluid in the interstitial tissue spaces.
4
Q
What are the two main opposing forces in edema?
A
- Hydrostatic pressure
- Plasma colloid osmotic pressure (oncotic pressure of plasma protein)
5
Q
What happens under normal conditions regarding fluid movement?
A
Proteins in the plasma are retained within the vasculature, leading to little net movement of water and electrolytes into the tissues.
6
Q
What is the role of lymphatic vessels in fluid accumulation?
A
They drain a small amount of fluid to prevent accumulation in the interstitial tissue space.
7
Q
What causes fluid accumulation?
A
- Increased hydrostatic pressure
- Decreased plasma colloid osmotic pressure
- Blockade in lymphatic flow
8
Q
What is the role of RMTs when fluid is aspirated?
A
Perform assays requested by clinicians, including Chemistry Analysis, Cell Count Analysis, and Culture & Sensitivity.
9
Q
What distinguishes inflammatory-related edema from non-inflammatory-related edema?
A
Inflammatory-related edema is protein-rich, while non-inflammatory-related edema is protein-poor (transudate).
10
Q
What are common clinical correlations of edema?
A
- Deep Venous Thrombosis
- Congestive Heart Failure
- Periorbital Swelling in Nephrotic Syndrome
- Low Serum Protein
- Lymphedema
- Parasitic Filariasis (Elephantiasis)
- Pulmonary Edema
- Brain Edema
11
Q
What is Deep Venous Thrombosis (DVT)?
A
Localized increase in hydrostatic pressure due to disorders that impair venous return, typically seen in the lower extremities.
12
Q
What is Congestive Heart Failure (CHF) associated with?
A
Systemic increases in venous pressure leading to widespread edema.
13
Q
What is pitting edema?
A
A type of edema where pressing on the skin leaves a depression corresponding to the size of your thumb.
14
Q
What causes periorbital swelling in Nephrotic Syndrome?
A
Decreased oncotic pressure due to massive amounts of proteins excreted in the urine.
15
Q
What are the causes of low serum protein leading to edema?
A
- Severe liver diseases (e.g., liver cirrhosis)
- Decreased protein intake (e.g., malnutrition)
16
Q
How does sodium and water retention affect hydrostatic pressure?
A
It increases hydrostatic pressure due to intravascular fluid volume expansion and diminishes vascular colloid osmotic pressure due to dilution.
17
Q
What is lymphedema?
A
Edema associated with chronic inflammation, malignancy, physical disruption, radiation damage, and certain infections due to lymphatic obstruction.
18
Q
What is parasitic filariasis and its effect on lymphatics?
A
A condition where an organism induces obstructive fibrosis of the lymphatic channels, resulting in edema, often referred to as elephantiasis.
19
Q
What is pulmonary edema characterized by?
A
Fluid-filled lungs, with frothy fluid material exuding when cut, and alveoli filled with pinkish, eosinophilic material.
20
Q
What is brain edema and its consequences?
A
Swelling of the brain causing narrowed sulci and distended gyri, potentially leading to herniation and compression of vital centers.
21
Q
What is hyperemia?
A
An active process resulting from arteriolar dilation, usually occurring at sites of inflammation.
22
Q
What is congestion?
A
A passive process resulting from reduced outflow of blood from a tissue, leading to a blue-red or cyanotic appearance.
23
Q
What is the difference between acute and chronic pulmonary congestion?
A
Acute pulmonary congestion is marked by engorged capillaries and edema within alveoli, while chronic leads to heart failure cells (hemosiderin-laden macrophages).
24
Q
What are heart failure cells?
A
Hemosiderin-laden macrophages formed from engulfed red cells in chronic pulmonary congestion
These cells are indicative of chronic conditions such as congestive heart failure.
25
What is the difference in septa between acute and chronic pulmonary congestion?
In chronic pulmonary congestion, the septa are thicker and fibrotic
## Footnote
In acute pulmonary congestion, the septa are not as thick.
26
What happens to centrilobular hepatocytes during acute hepatic congestion?
They may undergo ischemic necrosis
## Footnote
This occurs because they are farthest from the blood supply.
27
What is 'nutmeg liver' indicative of?
Chronic passive congestion of the liver
## Footnote
It is characterized by grossly red-brown centrilobular regions undergoing necrosis.
28
What are the histomorphologic findings in chronic passive congestion of the liver?
Centrilobular necrosis, hemorrhage, and abundance of hemosiderin-laden macrophages
## Footnote
Degeneration of hepatocytes is most marked around the central vein.
29
What is hemostasis?
The process by which blood clots form at sites of vascular injury
## Footnote
It is crucial for preventing hemorrhagic disorders.
30
What types of hemorrhages can occur in tissues?
Petechiae, purpura, ecchymoses
## Footnote
Hemorrhage can vary in size from small to large.
31
What is the goal of hemostasis?
To maintain blood in a fluid, clot-free state while forming a hemostatic plug at injury sites
## Footnote
This prevents or limits bleeding.
32
What are the three major components of hemostasis?
* Vascular Wall (endothelium)
* Platelets
* Coagulation Cascade
33
What induces vasoconstriction after vascular injury?
Endothelin
## Footnote
This is a neurohumoral factor that causes blood vessels to constrict.
34
What is the endpoint of primary hemostasis?
Formation of the platelet plug
## Footnote
This occurs after platelet activation and aggregation.
35
What triggers platelet adhesion in primary hemostasis?
Exposure of subendothelial collagen and the von Willebrand factor
## Footnote
This leads to platelet activation.
36
List the five steps in primary hemostasis.
* Platelet Adhesion
* Shape Change
* Granule Release (ADP, TXA2)
* Recruitment
* Aggregation (Hemostatic Plug)
37
What is the endpoint of secondary hemostasis?
Deposition of fibrin
## Footnote
This occurs as fibrin forms a meshwork among platelets.
38
What activates tissue factor in secondary hemostasis?
Exposure at the site of vascular injury
## Footnote
Tissue factor activates Factor VII, initiating the coagulation cascade.
39
What is clot stabilization?
Contraction of fibrin and platelets forms a solid permanent plug
## Footnote
This aims to prevent further hemorrhage.
40
What are the antithrombotic properties of the endothelium?
* Anticoagulant factors
* Inhibition of platelet aggregation
* Promotion of fibrinolysis
41
What role does t-PA play in hemostasis?
t-PA cleaves plasminogen to form plasmin which degrades thrombi
## Footnote
This is part of the fibrinolytic process.
42
What is the clinical significance of von Willebrand factor?
Essential for platelet binding to collagen; absence leads to defects in primary hemostasis
## Footnote
vWF disease can cause small bleeds in skin or mucosal membranes.
43
What is the role of thrombomodulin in hemostasis?
Converts thrombin from a procoagulant to an anticoagulant
## Footnote
It activates protein C, which inhibits clotting.
44
What are the procoagulant properties of the endothelium?
* Production of vWF
* Induction by endotoxins/cytokines
* Antifibrinolytic effects
45
What is the primary cause of mucosal bleeding associated with defects in primary hemostasis?
Deficiency of von Willebrand Factor (vWF)
## Footnote
Mucosal bleeding can manifest as epistaxis, GI bleeding, or menorrhagia.
46
What is the clinical significance of tissue factor?
Tissue factor is regarded as a procoagulant essential for thrombin formation
## Footnote
Thrombin facilitates the conversion of fibrinogen to fibrin.
47
What is hemarthrosis?
Bleeding in the joints, often following minor trauma
## Footnote
This is particularly characteristic of hemophilia.
48
What are the manifestations of defects in von Willebrand Factor and tissue factor?
Petechiae, purpura, ecchymoses, hemarthrosis, hematoma
## Footnote
These are examples of bleeding manifestations.
49
What are plasminogen activator inhibitors (PAIs)?
PAIs are counter-regulatory factors that inhibit fibrinolysis
## Footnote
They act against tissue plasminogen activator (t-PA), which promotes fibrinolysis.
50
What is the role of intact endothelial cells in hemostasis?
Intact endothelial cells inhibit platelet adhesion and blood clotting
## Footnote
They prevent platelets from binding to non-injured endothelium.
51
List the components that define anticoagulants.
* Prostacyclin (PGI2)
* Nitric Oxide (NO)
* ADPase
* Heparin-Like Molecules
* Thrombomodulin
* Protein C
* Protein S
* Tissue Factor Pathway Inhibitor
* t-PA
* Plasmin
## Footnote
These substances help to regulate and prevent excessive coagulation.
52
What is the primary role of platelets in hemostasis?
Platelets form the primary hemostatic plug
## Footnote
This plug limits bleeding at the site of vascular injury.
53
What are the two types of granules found in platelets?
* Alpha granules
* Dense bodies
## Footnote
Alpha granules contain proteins for coagulation and wound healing, while dense bodies contain ADP and other substances.
54
What is the receptor involved in platelet adhesion to von Willebrand Factor?
GpIb (glycoprotein Ib)
## Footnote
GpIb binds to vWF for platelet adhesion.
55
What happens during the platelet shape change step?
Platelets undergo a conformational change, developing a spiky appearance
## Footnote
This step is crucial for increasing their surface area and promoting aggregation.
56
What triggers the release reaction in platelets?
Activation by thrombin and ADP
## Footnote
This leads to the release of granules from the platelets.
57
What is the significance of thromboxane A2 (TXA2) in platelet function?
TXA2 promotes platelet aggregation and attracts other platelets
## Footnote
It is an important factor in the recruitment of platelets.
58
What does GpIIb/IIIa receptor do during platelet aggregation?
It allows binding of fibrinogen, stabilizing the platelet plug
## Footnote
Fibrinogen is converted to fibrin, which helps to consolidate the clot.
59
What is Glanzmann Thrombastenia?
A bleeding disorder caused by inherited deficiency of GpIIb/IIIa
## Footnote
This condition affects platelet aggregation.
60
What are the two primary assays for evaluating coagulation factors?
* Prothrombin Time (PT)
* Partial Thromboplastin Time (PTT)
## Footnote
PT assesses the extrinsic pathway, while PTT assesses the intrinsic pathway.
61
What is the most important activity of thrombin?
Conversion of fibrinogen into cross-linked fibrin
## Footnote
Thrombin also activates platelets and has proinflammatory and anticoagulant effects.
62
What are natural anticoagulants?
* Antithrombin III
* Protein C & S
* Tissue Factor Pathway Inhibitor (TFPI)
## Footnote
These factors help limit coagulation and prevent excessive clotting.
63
What is fibrinolysis?
The process of breaking down fibrin to dissolve clots
## Footnote
It is primarily mediated by plasmin.
64
Which is the most important plasminogen activator?
t-PA (tissue-type plasminogen activator)
## Footnote
t-PA is synthesized by endothelial cells and is most active when bound to fibrin.
65
What is thrombosis?
Formation of a clot within a vessel
## Footnote
It is associated with endothelial injury, stasis, and hypercoagulability.
66
What are the primary abnormalities leading to thrombosis?
* Endothelial injury
* Stasis or turbulent blood flow
* Hypercoagulability of the blood
## Footnote
Each factor contributes to the likelihood of clot formation.
67
What are the three components of Virchow's triad in thrombosis?
Endothelial injury, stasis or turbulent blood flow, hypercoagulability
## Footnote
Among these, endothelial integrity is the most important factor.
68
What does stasis refer to in the context of thrombus formation?
Atrial fibrillation, immobilization, non-ambulatory state
69
What is hypercoagulability?
An abnormally high tendency of the blood to clot, often caused by alterations in coagulation factors
70
What is the significance of endothelial injury in thrombosis?
It is the single most important factor influencing thrombus formation
71
True or False: Endothelial cells must be physically disrupted to contribute to thrombosis.
False
72
What are procoagulant changes associated with activated endothelial cells?
Downregulation of thrombomodulin, protein C, and tissue factor protein inhibitor
73
What do activated endothelial cells secrete that limits fibrinolysis?
Plasminogen activator inhibitors (PAIs)
74
Fill in the blank: The normal blood flow is said to be _______ where platelets flow centrally in the vessel lumen.
laminar
75
What are the effects of turbulence and stasis on thrombus formation?
* Promote endothelial activation * Disrupt laminar flow * Prevent washout of activated clotting factors
76
What clinical conditions can altered blood flow contribute to?
* Ulcerated atherosclerotic plaques * Aortic and arterial dilations (aneurysms) * Rheumatic mitral valve stenosis
77
What mutation is most commonly associated with inherited hypercoagulability?
Factor V Leiden mutation
78
What is the inheritance pattern of Factor V Leiden?
Autosomal Dominant
79
What is the prothrombin gene mutation associated with?
Elevated prothrombin levels and increased risk of thrombosis
80
What are common acquired causes of thrombotic diathesis?
* Oral contraceptive use * Hyperestrogenic state of pregnancy * Smoking * Obesity * Disseminated cancers
81
What is Heparin-Induced Thrombocytopenia (HIT)?
A serious disorder following the administration of unfractionated heparin
82
What characterizes Antiphospholipid Antibody Syndrome (APS)?
* High titer of circulating Ab against anionic phospholipid * Venous or arterial thromboses * Pregnancy complications
83
Differentiate between primary and secondary antiphospholipid syndrome.
* Primary: Hypercoagulable state without other autoimmune disorders * Secondary: Associated with a well-defined autoimmune disease
84
Where can thrombi develop in the cardiovascular system?
Cardiac chambers, valve cusps, arteries, veins, and capillaries
85
What are lines of Zahn?
Laminations in thrombi indicating formation in flowing blood
86
What are mural thrombi?
Arterial thrombi occurring in heart chambers or aortic lumen
87
What are the most common sites for arterial thrombi?
* Coronary * Cerebral * Femoral
88
What are characteristics of venous thrombi?
* Form in sluggish venous circulation * Contain more enmeshed erythrocytes * Firm and focally attached to the wall
89
What distinguishes postmortem clots from antemortem venous thrombi?
* Gelatinous consistency * Dark-red dependent portion * Yellow 'chicken fat' upper portion
90
What is the fate of a thrombus?
* Propagation * Embolization * Dissolution * Organization & Recanalization
91
What happens during the propagation of a thrombus?
Thrombi accumulate additional platelets and fibrin
92
What occurs during the dissolution of a thrombus?
Fibrinolysis leading to rapid shrinkage and total disappearance
93
What is involved in the organization and recanalization of older thrombi?
* Ingrowth of endothelial cells, smooth muscle cells, and fibroblasts * Formation of capillary channels reestablishing original lumen continuity
94
What is dissolution in relation to thrombi?
The result of fibrinolysis, leading to rapid shrinkage and total disappearance of recent thrombi
## Footnote
Fibrinolysis is also known as resolution.
95
What occurs during the organization of thrombi?
Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts
96
What is recanalization?
The formation of capillary channels that reestablish the continuity of the original lumen, albeit to a variable degree
97
What is Virchow’s Triad?
Endothelial injury, abnormal blood flow, and hypercoagulability
98
What is disseminated intravascular coagulation (DIC)?
Widespread fibrin thrombi in the microcirculation causing circulatory insufficiency and consumption coagulopathy
## Footnote
DIC is a complication of various conditions associated with systemic activation of thrombin.
99
What is an embolus?
A detached intravascular solid, liquid, or gaseous mass carried by blood to a distant site, causing tissue dysfunction or infarction
100
What are the most common types of embolism?
Pulmonary thromboembolism and systemic thromboembolism
101
What is pulmonary thromboembolism?
Pulmonary emboli that originate from deep vein thrombosis (DVT) and are the most common form of thromboembolic disease
102
What percentage of pulmonary emboli are clinically silent?
60% to 80%
103
What are the functional consequences of pulmonary emboli?
Sudden death, acute right heart failure, pulmonary hemorrhage, and pulmonary hypertension
104
What is systemic thromboembolism?
Thrombi that originate from the heart and are thrown into systemic circulation
105
Where do most systemic emboli originate from?
Intracardiac mural thrombi (80%)
106
What is fat embolism?
Presence of microscopic fat globules in the vasculature after fractures of long bones or soft tissue trauma
107
What are the clinical symptoms of fat embolism?
Pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia
108
What is the pathogenesis of fat embolism?
Mechanical obstruction and biochemical injury caused by fat microemboli and free fatty acids
109
What is air embolism?
Gas bubbles within circulation that obstruct vascular flow and cause distal ischemic injury
110
What is decompression sickness?
A form of gas embolism occurring when individuals experience sudden decreases in atmospheric pressure
111
What are the bends?
Painful condition caused by rapid formation of gas bubbles within skeletal muscles and supporting tissues
112
What are the chokes?
Respiratory distress caused by gas bubbles in the lungs leading to edema and hemorrhage
113
What is caisson disease?
Chronic form of decompression sickness characterized by persistence of gas emboli leading to ischemic necrosis
114
What characterizes infarction?
Area of ischemic necrosis caused by occlusion of arterial supply or venous drainage
115
What are the factors influencing infarct development?
Nature of the vascular supply, rate of development, vulnerability of tissue, blood oxygen content
116
What are the two types of infarction?
Red (hemorrhagic) and white (anemic) infarcts
117
What is a hemorrhagic (red) infarction?
Occurs with venous occlusion, in loose tissue, or when flow is reestablished to a site of previous arterial occlusion
118
What is anemic infarction?
Occurs with arterial occlusions in solid organs with end-arterial circulation
119
What is the classic morphology of infarcts?
Wedge-shaped, with the occluded vessel at the apex and the periphery of the organ forming the base
120
What is coagulation necrosis?
The dominant histologic characteristic of infarction, indicating ischemic coagulative necrosis
121
What histologic changes may be absent shortly before death?
Histologic changes may be absent shortly (minutes to hours) before the death of the person.
## Footnote
It takes 4 to 12 hours for the dead tissue to show microscopic evidence of necrosis.
122
When does acute inflammation typically become well defined in infarcts?
Acute inflammation is usually well defined within 1 to 2 days.
## Footnote
Acute inflammation is present along the margins of infarcts within a few hours.
123
What does the absence of a nucleus in coagulated fiber indicate?
The absence of a nucleus indicates an area of necrosis.
124
What is the exception to the generalization regarding infarcts and tissue regeneration?
The brain is an exception, as central nervous system infarction results in liquefactive necrosis.
125
What are septic infarctions?
Septic infarctions occur when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue, converting the infarct to an abscess.
## Footnote
This leads to a greater inflammatory response.
126
What is shock in a medical context?
Shock is a state of circulatory failure that impairs tissue perfusion and leads to cellular hypoxia.
127
What are the primary categories of shock?
Categories of shock include:
* Cardiogenic Shock
* Hypovolemic Shock
* Septic Shock
## Footnote
Each category has different underlying causes.
128
What defines sepsis?
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.
129
What is septic shock?
Septic shock is a subset of sepsis characterized by profound circulatory, cellular, and metabolic abnormalities with a greater risk of mortality.
130
What is Systemic Inflammatory Response Syndrome (SIRS)?
SIRS is a sepsis-like condition associated with systemic inflammation triggered by non-microbial insults such as burns, trauma, and pancreatitis.
131
True or False: Septic shock is most frequently triggered by gram-negative bacterial infections.
False.
## Footnote
Septic shock is most frequently triggered by gram-positive bacterial infections.
132
What initiates pro-inflammatory responses in sepsis?
Pro-inflammatory responses are initiated by microbial cell wall constituents engaging receptors on cells of the innate immune system.
133
What are Pathogen-associated molecular patterns (PAMPs)?
PAMPs are substances recognized by Toll-like receptors (TLRs) that trigger inflammatory responses.
134
What role do cytokines play in sepsis?
Cytokines such as TNF, IL-1, and others are released, contributing to inflammation and endothelial activation.
135
What is the effect of inflammatory cytokines on endothelial cells?
Inflammatory cytokines loosen endothelial cell tight junctions, causing vascular leakage and tissue edema.
136
What metabolic abnormalities are observed in septic patients?
Septic patients exhibit insulin resistance and hyperglycemia.
137
What are the proposed mechanisms for immune suppression in sepsis?
Proposed mechanisms include:
* Shift from pro-inflammatory (Th1) to anti-inflammatory (Th2) cytokines
* Production of anti-inflammatory mediators
* Lymphocyte apoptosis
* Immunosuppressive effects of apoptotic cells
## Footnote
These mechanisms contribute to oscillation between hyperinflammatory and immunosuppressed states.
138
What leads to multiple organ dysfunction in shock?
Multiple organ dysfunction results from systemic hypotension, interstitial edema, and small vessel thrombosis that decrease oxygen and nutrient delivery.
139
What characterizes the initial non-progressive stage of shock?
Reflex compensatory mechanisms maintain cardiac output and blood pressure, resulting in tachycardia and peripheral vasoconstriction.
140
What occurs during the progressive stage of shock?
The progressive stage is characterized by widespread tissue hypoxia and worsening circulatory and metabolic derangement.
141
What is the irreversible stage of shock?
In the irreversible stage, cellular and tissue injury is so severe that survival is not possible, even if hemodynamic defects are corrected.
142
Fill in the blank: The pro-inflammatory state and endothelial cell activation in sepsis lead to widespread vascular _______.
leakage.
143
What is the clinical significance of Waterhouse-Friderichsen Syndrome?
It is associated with adrenal insufficiency and can occur due to disseminated intravascular coagulation (DIC).
144
What is the endpoint of shock?
Multiorgan Failure
## Footnote
Main organs involved include the heart, lungs, kidneys, and gastrointestinal tract.
145
What are the main organs involved in multiorgan failure due to shock?
* Heart
* Lungs
* Kidneys
* GIT
## Footnote
GIT stands for gastrointestinal tract.
146
What characterizes the Non-Progressive Phase of shock?
Reflex neurohumoral mechanisms to maintain cardiac output and blood pressure
## Footnote
Includes tachycardia, peripheral vasoconstriction, and renal conservation of fluid.
147
What occurs during the Progressive Stage of shock?
* Widespread tissue hypoxia
* Anaerobic glycolysis with production of lactic acid
* Arterioles dilate & blood pools in microcirculation
* Subsequent DIC
## Footnote
DIC stands for Disseminated Intravascular Coagulation.
148
What happens during the Irreversible Stage of shock?
* Lysosomal enzyme leakage
* Worsening myocardial contractile function due to nitric oxide synthesis
* Superimposed bacteremia
* Complete renal shutdown (Acute Tubular Necrosis)
## Footnote
Acute Tubular Necrosis is a condition that can lead to complete renal failure.
149
True or False: The Non-Progressive Phase of shock is characterized by widespread tissue hypoxia.
False
## Footnote
The Non-Progressive Phase is about maintaining cardiac output and blood pressure, not widespread tissue hypoxia.
150
Fill in the blank: In the Progressive Stage of shock, intracellular aerobic respiration is replaced by _______.
anaerobic glycolysis
## Footnote
This shift leads to the production of lactic acid.
151
What is a consequence of lysosomal enzyme leakage in the Irreversible Stage of shock?
Worsening myocardial contractile function
## Footnote
This is due to nitric oxide synthesis.
152
What is the role of neurohumoral mechanisms in the Non-Progressive Phase of shock?
To maintain cardiac output and blood pressure
## Footnote
This phase involves tachycardia and peripheral vasoconstriction.
153
