Hyperemia, Congestion, Thrombosis, Emobolis Flashcards
Hyperemia
it refers to an increased ______ in a ______.
It is a/an (active or passive?) process resulting from __________
blood volume
tissue
Active
arteriolar dilatation.
Hyperemia
It is of two types:
________ and _______
physiological and pathological.
Hyperemia
Physiological : increased flow to the _____ during exercise and increased flow to the gut after _____.
Patholog: hyperemia in ________.
The affected tissue is ______ than normal because of ____________
muscle; meals
inflammation; redder; oxygenated blood.
Congestion :
It is a/an (active or passive?) process due to __________________
The affected tissue is _______ in color .
Passive; impaired venous drainage.
bluish red
Congestion
It may occur locally as a result of __________ e.g. by a tumour.
_________ failure causes systemic congestion.
In chronic passive congestion, stasis of poorly oxygenated blood causes _________,_________, and or ________
venous compression
Congestive cardiac
chronic hypoxia, cell degeneration and or death.
Morphology of congestion
Cut surfaces are ________ and ______
hemorrhagic and wet
Morphology of congestion
Lungs
In acute congestion: ________ congestion, alveolar ________ oedema, ruptured _______ with _______
Chronic congestion: ___________ and ______ alveolar septa, _______ laden macrophages (heart failure cells) within the alveolar spaces.
alveolar capillary ; septal; capillaries with haemorrhages.
thickened and fibrotic
haemosiderin
Liver
Acute congestion- the cut surface is (dark or light ?) , _____ color , tense and oozes out blood.
The _______ and ______ are distended with blood and there may be _______ degeneration.
The _____ hepatocytes that are better oxygenated may develop _______
Dark
Red
central vein and sinusoids; central hepatocyte
periportal; fatty change.
Liver
Chronic passive congestion; grossly the central regions of the hepatic lobules are _______ and slightly _______ due to ______.
The surrounding zones are congested and tan giving rise to the so called ________ appearance.
reddish brown
depressed; loss of cells
nutmeg liver
Liver microscopy:
◦_________ necrosis, hemorrhage, ____________ macrophages
In prolonged severe congestion (CCF) there may be _______ commonly called ________
Centrilobular; haemosiderin laden
hepatic fibrosis
cardiac cirrhosis.
Liver micro architecture
Divided into 1-2mm-diameter _______ shaped lobules oriented around the __________ or ________
hexagonal
Terminal Hepatic Venules or central veins
Liver micro architecture
Acini- roughly _______ shape with the terminal twigs of ______ and _____ extending out from the portal tracts at their bases and the THV at their apices.
triangular
hepatic artery and portal vein
Liver micro architecture
Acinus is divided into three zones 1,2,3 (_______,________,_______ zones, respectively).
Zone ___ is closest to the blood
periportal, mid zone, perivenular
1
Hemorrhage
Means extravasations of blood due to _________
vessel rupture.
Haematoma: ______________________
accumulation of blood within tissue
Petechiae: hemorrhages of __-___ mm into the _______,______, or ______
1 to 2
skin, mucous membranes or serosal surfaces
Petechiae
most commonly associated with locally increased _________, ____ platelet counts (thrombocytopenia), or ______ platelet function
intravascular pressure
low
defective
Purpura:___ mm or more associated with many of the disorders that cause ____ or can be secondary to _____, vascular ______(——), or increased vascular _____ (e.g., in ______)
3
petechiae; trauma
inflammation (vasculitis)
fragility; amyloidosis
Ecchymoses: __-___ or more (bruises)
RBCs are phagocytosed and degraded by macrophages; the hemoglobin (_____ color) is then enzymatically converted into ______ then _____ ( _____ color, _____) and eventually into ______ (______ color), accounting for the characteristic color changes in a bruise
1 to 2cm
red-blue
biliverdin; bilirubin
blue-green; yellow
hemosiderin; gold-brown
Hemostasis can be defined simply as the process by which ______ form at sites of vascular injury.
blood clots
Hemostasis
Issues is divided into two groups.
A) In hemorrhagic disorders, characterized by excessive ______, hemostatic mechanisms are ______ to prevent abnormal blood loss.
B)in thrombotic disorders, ______ form within _______ or within the _______ of the heart.
bleeding; insufficient
blood clots
intact blood vessels
chambers
DIC [_______________] is a disease condition where ________________________________ obtain
Generalized _______________ paradoxically producing _______ due to the ________________
disseminated intravascular coagulation
both hemorrhagic and thrombotic disorders
activation of clotting factors ; bleeding
consumption of coagulation factors
Sequence of events in hemostasis at the site of vascular injury
Arteriolar _________
________ hemostasis: the formation of the _________
———— hemostasis: deposition of ________. Clot _________ and ________
vasoconstriction
Primary; platelet plug.
Secondary; fibrin
stabilization and resorption.
Sequence of events in hemostasis
Arteriolar vasoconstriction
◦ Injury→ Arteriolar vaso________ (mediated by _______ mechanism and ______).
This is _________
constriction; reflex neurogenic
endothelin
transient
Sequence of events in hemostasis
Primary hemostasis: the formation of platelet plug.
Distruption of endothelium - exposure of subendothelial ________ and ______ →platelet _______ and _____ → recruitment of additional platelets which undergo ________ →hemostatic plug (primary. Hem)
von Willebrand Factor[Vwf] & collagen
adherence & activation
aggegration
Sequence of events in hemostasis
Secondary hemostasis[deposition of fibrin]
◦
Release of _______ from the subendothelial cells of vessel wall →activation of ______ - the coagulation cascade- thrombin →formation of ________fibrin meshwork →permanent plug
tissue factor
factor VII
fibrin+platelets
Clot stabilization and resorption.
Polymerized ______ and _____ aggregates undergo ______ to form a solid, permanent plug that prevents further hemorrhage.
Counterregulatory mechanisms (e.g.,__________ t-PA) are set into motion that limit clotting to the site of injury and eventually lead to clot resorption and tissue repair.
fibrin and platelet
contraction
tissue plasminogen activator,
The endothelium
After injury it exerts procoagulant functions
T/F
T
The endothelium possesses antithrombotic properties
T/F
T
The endothelium has Platelet inhibitory effects
T/F
The endothelium doesn’t posses fibrinolytic properties.
T/F
F
It does
The endothelium
Antithrombotic properties
Platelet inhibitory effects:
endothelium prevents platelets from coming in contact with _______ and ______
Prostacycline and nitric oxide (vaso______, inhibitors of platelet ______) synthesised by the _______ prevent platelet activation and impede adhesion to the endothelium.
_____________ degrades ADP and inhibits platelet aggregation
subendothelial vWF & collagen.
dilators; aggregation
endothelium
Adenosine diphosphatase
Thrombin is one of the most potent activators of platelets.
T/F
T
Endothelial cells bind and alter the activity of thrombin
T/F
T
Endothelium
Anticoagulant effects
Normal endothelium shields coagulation factors from tissue factor in vessel walls.
Expresses multiple factors that actively oppose coagulation such as:
__________, ________ receptor, _____-like molecules, and _______________________ inhibitor
thrombomodulin
endothelial protein C
heparin
tissue factor pathway
The endothelium
Anticoagulants
Membrane associated heparin-like molecules act as _____ with _______ to inactivate thrombin
__________ and ________ bind thrombin and protein C.
The complex formed activates protein C/ protein S. Activated protein C is a potent inhibitor of ________________
cofactors; antithrombin III
Thrombomodulin and endothelial protein C receptor
factors Va and VIIIa.
The endothelium
Fibrinolytic properties
______________ promotes fibrinolytic activity which cleaves plasminogen to form plasmin
Tissue type plasminogen activator (t-PA)
Prothrombic properties of injured endothelium
Von Willebrands Factor (vWF) is a cofactor for platelet binding to collagen of subendothelial extracellular matrix.
Activation of clotting factors: endothelial cells are induced by ________ or cytokines(_______ ) to synthesise ________ which activates extrinsic clotting pathway.
bacterial endotoxins
TNF, IL-1; tissue factor
Prothrombic properties of injured endothelium
Antifibrinolytic Effects: activated endothelium secretes _____________ which limit fibrinolysis favouring _________
Plasminogen activator inhibitors (PAIs)
thrombosis
Intact endothelium is ___coagulant while injured endothelium is ___coagulant.
anti
pro
Platelets
They are ____ shaped __nucleate cell fragments shed into the blood by _____________.
disc
A
marrow megakaryocytes
Platelets
Their function depends on several ___________, a contractile ______, and two types of ___________
glycoprotein receptors
cytoskeleton
cytoplasmic granules
Platelets
cytoplasmic granules :
alpha-granules contain ______,_______,______,____,______.
Dense granules contain ______,_____,______,______,______
P-selectin, fibrinogen, factors V & VIII, PDGF, TGF-beta
ATP, ADP, calcium ion, histamine , serotonin
Platelets
After injury on contact with subendothelial connective tissue [Vwf, collagen] platelets undergo three major reactions:
_____________,
____________________
_________
Adhesion and shape change
Secretion [release rxn] of granule contents
Aggregation
Platelet Adhesion is mediated via interactions with _____ which acts as a bridge between _______ and _____
vWF
platelet and exposed collagen.
Genetic deficiencies of vWF( _____________ ) or it’s receptor[GpIb] ( ___________ )result in bleeding disorders
von Wilebrand disease
Bernard-Soulier syndrome
Platelets
Shape change- Platelets rapidly change shape following ____, being converted from __________ to ________ with greatly _____eased surface area.
adhesion
smooth discs to spiky “sea urchins”
Incr
Platelets
Secretion: release reaction of granule content occurs with change in shape [referred to as _________].. This happens soon after adhesion. Platelet activation is triggered by thrombin, ADP etc.
platelet activation
Activated platelets also secrete thromboxane A2 (TxA2)
T/F
T
Platelet aggregation follows _____,______, and ________ and leads to formation of ___________
adhesion, shape change and granule release[activation]
primary hemostatic plug.
The conformational change in glycoprotein ___/___ that occurs with platelet activation allows binding of ______ between adjacent platelets, leading to their aggregation.
Inherited deficiency of GpIIb-IIIa results in a bleeding disorder called __________
IIb/IIIa
fibrinogen
Glanzmann thrombasthenia
Platelet contraction
activation of ______ stabilizes the platelet plug by causing further platelet activation and aggregation, and by promoting irreversible platelet contraction. Platelet contraction is dependent on the _______ and consolidates the aggregated platelets.
thrombin
cytoskeleton
Definitive hemostatic plug
Thrombin converts _____ into ________, cementing the platelets in place and creating the definitive secondary hemostatic plug
fibrinogen
insoluble fibrin
Platelet -endothelial cell interactions
The ______ cell derived prostaglandins, PGI2 (prostacycline) (activates or inhibits?) platelet aggregation and is a vaso_____ conversely the ——— derived prostaglandins Thromboxane A2 (activates or inhibits?) platelet aggregation and is a vaso____.
endothelial ; inhibits; dilator
platelet; activates; constrictor
Aspirin an (reversible or irreversible?) ______ inhibitor is given to persons at risk of coronary _______ to (temporarily or permanently?) block platelet TxA2 synthesis.
irreversible
cycloxygenase
thrombosis
permanently
Natural Anticoagulants
Antithrombins e.g. ______ which inhibits the activity of ______ and coagulation factor _____
Proteins C and S inactivate factors ____ and ______
Plasmin derived from circulating plasminogen breaks down ______ and interferes with its polymerisation.
antithrombin III ; thrombin; Xa
Va and VIIIa.
fibrin
fibrin spilt products which is depressed in DIC
T/F
F
Elevated
The two known plasminogen activators are _____ -like PA and ________ PA (t-PA)
urokinase
tissue type
Hemorrhagic disorders
Among the most common causes of mild bleeding tendencies are inherited defects in _________ and ______ (renal failure). The latter alters platelet function through uncertain mechanisms.
Between these extremes lie deficiencies of coagulation factors (the _________ ), which are usually inherited and lead to severe bleeding disorders if untreated
von Willebrand factor and uremia
hemophilias
Thrombosis
Is defined as the formation of _____ or ______ mass from the constituents of the blood within the heart or the vascular system during life.
The solid mass formed is referred to as a ________
It is characterized by events which involve both the _________ and _______
solid or semi-solid
Thrombus
platelets and the coagulation system.