UTHSC Fall 2022 D2 Par 2 Pathology (ANswered) Graded A+
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UTHSC Fall 2022 D2 Par 2 Pathology
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UTHSC Fall 2022 D2 Par 2 Pathology
UTHSC Fall 2022 D2 Par 2 Pathology
Normally, hydrostatic and osmotic forces are
balanced
T/F, T/F Normally, a lot net movement of fluid out of vessels, all are removed by lymphatic vessels
False, normally a little movement out
True
Disruption in the balance between Hydrostatic Pressure (HP) a...
UTHSC Fall 2022 D2 Par 2 Pathology
Normally, hydrostatic and osmotic forces are
balanced
T/F, T/F Normally, a lot net movement of fluid out of vessels, all are removed by
lymphatic vessels
False, normally a little movement out
True
Disruption in the balance between Hydrostatic Pressure (HP) and colloid osmotic
Pressure(COP) causes
movement of fluid out of or into the vessel
Hydrostatic Pressure (HP)
force exerted by fluid pressing against wall, blood fluid being pushed out of the vessel
colloid osmotic Pressure(COP)
Contribution of protein to blood osmotic pressure, pulls fluid from the tissue back into
the vessel
Edema
Accumulation of fluid in tissues
Effusion
Accumulation of fluid in body cavities (serosal surface involvement)
inflammatory edema
Protein-rich exudates accumulation due to increases in vascular permeability
Non-inflammatory edema
Protein-poor transudates accumulation, common in heart failure, renal disease, and
severe nutritional disorders
Transudate
The fluid component of blood that normally passes through the endothelial cell walls.
Exudate
like transudate but includes proteins as well. Caused by drastically increased
hydrostatic pressure
what factors increase hydrostatic pressure?
venous outflow obstruction, e.g., congestive heart failure
what factors decrease colloid osmotic pressure?
decreased protein Synthesis, e.g., liver disease; increased protein loss, e.g., Kidney
disease
how does heart failure lead to edema?
- Increased capillary hydrostatic pressure
- Decreased renal blood flow --> activation of RAS --> retention of Na and water -->
increased blood volume
how does malnutrition, decreased hepatic synthesis, and nephrotic syndrome
lead to edema?
-decreased plasma albumin, decreased plasma osmotic pressure
Pathophysiologic Categories of Edema
- Increased hydrostatic pressure
- Impaired venous return
- Arteriolar dilation
- Reduced plasma osmotic pressure
,- Lymphatic obstruction
- Sodium retention
- Inflammation
what are some systemic conditions that can lead to increased hydrostatic
pressure due to impaired venous return?
congestive heart failure, constrictive pericarditis, hepatic cirrhosis
what are some Localized conditions that can lead to increased hydrostatic
pressure due to impaired venous return?
venous obstruction: deep venous thrombosis, mass, lower extremity inactivity
what can cause lymphatic obstruction?
Inflammation, neoplasia, infections, fibrosis, post-surgical, post-irradiation
what can cause Reduced plasma osmotic pressure?
• Increased albumin loss due to nephrotic syndrome or gastroenteropathy
• Decreased albumin synthesis in hepatic cirrhosis or malnutrition
what can cause Increased vascular permeability?
Endothelial injury, inflammation
what can cause Sodium and water retention?
Acute reduction of renal function
Morphology and Clinical Features of Edema
- Subcutaneous edema
- Indicating of underlying cardiac or renal disease
-able to press swollen limb and a pit remains, "pitting edema."
Cerebral Edema
- Due to increased intracranial pressure
- Gross: gyri appear swollen and flat. Sulci are narrowed
- Micro: interfibrillar fluid accumulation
Angioedema (Angioneurotic Edema)
Diffuse edematous swelling of the soft tissues, commonly caused by mast cell
degranulation (histamine release), an IgE-mediated hypersensitivity reactions
-allergic reaction
Hydrothorax
collection of fluid in the pleural cavity, pleural effusion
Hydropericardium
abnormal accumulation of fluid within the pericardial sac
-pericardial effusion
Ascites
Effusion in the Peritoneal Cavity
Kwashiorkor
Malnutrition produced by a severely inadequate amount of protein in the diet. Can lead
to Ascites
Hyperemia and Congestion both indicate
a local increase in volume of blood in a particular tissue
T/F Hyperemia and Congestion have the same underlying mechanism and
consequence
False
Hyperemia
,- An active process
- Arterial dilation → increased blood flow → erythema of affected tissue
Examples of Hyperemia
site of inflammation, skeletal muscle during exercise
Congestion
- A passive process
- Resulting from reduced outflow → edema
- Systemic (cardiac failure) or localized (venous obstruction)
Chronic Pulmonary Congestion is often caused by
congestive heart failure
what are some signs of chronic pulmonary congestion?
- Thickening of the septa
- Heart failure cells: hemosiderin-laden macrophages
Chronic Passive Hepatic Congestion
nutmeg liver
- Congestion of the hepatic and portal vessels
- Congestive hepatomegaly
Hemostasis
A process involving platelets, clotting factors, andendothelium occurs at the site of
vascular injury → bloodclot formation
Hemorrhagic Disorders
Excessive bleeding due to blunted or insufficient hemostatic mechanisms
Thrombosis
Formation of blood clots (thrombi) within intact blood vessels or within the chambers of
the heart
Hemostasis Sequence of Events
- Arteriolar vasoconstriction
- Primary hemostasis: the formation of the platelet plug
- Secondary hemostasis: deposition of fibrin
- Clot stabilization and resorption
Hemostasis Sequence of Events: 1. Arteriolar vasoconstriction
- Immediate and transient
- Mediated by reflex neurogenic mechanisms and secretion of some local factors such
as endothelin, a potent endothelium-derived vasoconstrictor
Hemostasis Sequence of Events: 2. Primary hemostasis: the formation of the
platelet plug
Exposed von Willebrand factor and collagen → platelet adherence and activation →
aggregation and formation of a plug
1. platelet adhestion
2. shape change
3. granule release
4. recruitment
5. aggregation (hemostatic plug)
Hemostasis Sequence of Events: 3. Secondary hemostasis: deposition of fibrin
Exposed tissue factor → binding and activating factor VII → thrombin formation →
cleaving fibrinogen into fibrin
, 1. Tissue Factor
2. Phospholipid complex expression
3. thrombin activation
4. fibrin polymerization
Hemostasis Sequence of Events: 4. Clot stabilization and resorption
Counterregulatory mechanisms such as tissue plasminogen activator, t-pA to limit
clotting
what are platelet's role in hemostasis?
- Formation of primary plug and sealing vascular defects
- Several glycoprotein receptors
- A contractile cytoskeleton
- Two type of cytoplasmic granules: ὰ -granules and dense granules
Platelet adhesion
Mediated by interaction with vWF expressed on endothelial cells by platelet glycoprotein
Ib (GpIb)
Platelets rapidly change shape
From smooth disk to spiky "sea urchins" to increase surface area by alterations in
GbIIb/IIIa → increased affinity for fibrinogen
Secretion
• Activation by thrombin and ADP.• Production of thromboxane A2 (TXA 2) → platelet
aggregation. Aspirin inhibits this pathway
Platelet aggregation
• Aggregation and binding to fibrinogen. Thrombin stabilizes platelet contraction.
• Conversion of fibrinogen into insoluble fibrin by thrombin
Glanzmann thrombasthenia
Deficiency of fibrinogen bridging GpIIb-IIIa receptors
Bernard-Soulier syndrome
Deficiency of GpIb receptors
Von Willebrand disease
Coagulation Cascade
A series of amplifying enzymatic reactions --> Deposition of an insoluble fibrin clot
Intrinsic pathway of coagulation
adding phospholipids , calcium, and negative charged particles to plasma
Extrinsic pathway of coagulation
adding calcium, tissue factor(TF), and phospholipids to plasma
Cascade Reactions in Coagulation Phase
-Chain Reaction of enzymes and proenzymes form three pathways
-Convert circulating fibrinogen into insoluble fibrin
Prothrombin time (PT) assay
• Assessing the function of the proteins in extrinsic pathway (VII, X, V, II, and fibrinogen)
• 10-14 seconds
Partial thromboplastin time (PTT) assay
• Assessing the function of the proteins in the intrinsic pathway (XII, XI, IX, VIII, X, V, II,
and fibrinogen)
• 27-35 seconds
what is the Role of Thrombin in Hemostasis and Cellular Activation?
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