Hyperemia, Congestion, Thrombosis, Emobolis Flashcards
1
Q
Hyperemia
it refers to an increased ______ in a ______.
It is a/an (active or passive?) process resulting from __________
A
blood volume
tissue
Active
arteriolar dilatation.
2
Q
Hyperemia
It is of two types:
________ and _______
A
physiological and pathological.
3
Q
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 ____________
A
muscle; meals
inflammation; redder; oxygenated blood.
4
Q
Congestion :
It is a/an (active or passive?) process due to __________________
The affected tissue is _______ in color .
A
Passive; impaired venous drainage.
bluish red
5
Q
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 ________
A
venous compression
Congestive cardiac
chronic hypoxia, cell degeneration and or death.
6
Q
Morphology of congestion
Cut surfaces are ________ and ______
A
hemorrhagic and wet
7
Q
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.
A
alveolar capillary ; septal; capillaries with haemorrhages.
thickened and fibrotic
haemosiderin
8
Q
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 _______
A
Dark
Red
central vein and sinusoids; central hepatocyte
periportal; fatty change.
9
Q
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.
A
reddish brown
depressed; loss of cells
nutmeg liver
10
Q
Liver microscopy:
◦_________ necrosis, hemorrhage, ____________ macrophages
In prolonged severe congestion (CCF) there may be _______ commonly called ________
A
Centrilobular; haemosiderin laden
hepatic fibrosis
cardiac cirrhosis.
11
Q
Liver micro architecture
Divided into 1-2mm-diameter _______ shaped lobules oriented around the __________ or ________
A
hexagonal
Terminal Hepatic Venules or central veins
12
Q
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.
A
triangular
hepatic artery and portal vein
13
Q
Liver micro architecture
Acinus is divided into three zones 1,2,3 (_______,________,_______ zones, respectively).
Zone ___ is closest to the blood
A
periportal, mid zone, perivenular
1
14
Q
Hemorrhage
Means extravasations of blood due to _________
A
vessel rupture.
15
Q
Haematoma: ______________________
A
accumulation of blood within tissue
16
Q
Petechiae: hemorrhages of __-___ mm into the _______,______, or ______
A
1 to 2
skin, mucous membranes or serosal surfaces
17
Q
Petechiae
most commonly associated with locally increased _________, ____ platelet counts (thrombocytopenia), or ______ platelet function
A
intravascular pressure
low
defective
18
Q
Purpura:___ mm or more associated with many of the disorders that cause ____ or can be secondary to _____, vascular ______(——), or increased vascular _____ (e.g., in ______)
A
3
petechiae; trauma
inflammation (vasculitis)
fragility; amyloidosis
19
Q
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
A
1 to 2cm
red-blue
biliverdin; bilirubin
blue-green; yellow
hemosiderin; gold-brown
20
Q
Hemostasis can be defined simply as the process by which ______ form at sites of vascular injury.
A
blood clots
21
Q
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.
A
bleeding; insufficient
blood clots
intact blood vessels
chambers
22
Q
DIC [_______________] is a disease condition where ________________________________ obtain
Generalized _______________ paradoxically producing _______ due to the ________________
A
disseminated intravascular coagulation
both hemorrhagic and thrombotic disorders
activation of clotting factors ; bleeding
consumption of coagulation factors
23
Q
Sequence of events in hemostasis at the site of vascular injury
Arteriolar _________
________ hemostasis: the formation of the _________
———— hemostasis: deposition of ________. Clot _________ and ________
A
vasoconstriction
Primary; platelet plug.
Secondary; fibrin
stabilization and resorption.
24
Q
Sequence of events in hemostasis
Arteriolar vasoconstriction
◦ Injury→ Arteriolar vaso________ (mediated by _______ mechanism and ______).
This is _________
A
constriction; reflex neurogenic
endothelin
transient
25
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
26
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](secondary Hemostasis) →permanent plug
tissue factor
factor VII
fibrin+platelets
27
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,
28
The endothelium
After injury it exerts procoagulant functions
T/F
T
29
The endothelium possesses antithrombotic properties
T/F
T
30
The endothelium has Platelet inhibitory effects
T/F
31
The endothelium doesn’t posses fibrinolytic properties.
T/F
F
It does
32
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
33
Thrombin is one of the most potent activators of platelets.
T/F
T
34
Endothelial cells bind and alter the activity of thrombin
T/F
T
35
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
36
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.
37
The endothelium
Fibrinolytic properties
______________ promotes fibrinolytic activity which cleaves plasminogen to form plasmin
Tissue type plasminogen activator (t-PA)
38
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
39
Prothrombic properties of injured endothelium
Antifibrinolytic Effects: activated endothelium secretes _____________ which limit fibrinolysis favouring _________
Plasminogen activator inhibitors (PAIs)
thrombosis
40
Intact endothelium is ___coagulant while injured endothelium is ___coagulant.
anti
pro
41
Platelets
They are ____ shaped __nucleate cell fragments shed into the blood by _____________.
disc
A
marrow megakaryocytes
42
Platelets
Their function depends on several ___________, a contractile ______, and two types of ___________
glycoprotein receptors
cytoskeleton
cytoplasmic granules
43
Platelets
cytoplasmic granules :
alpha-granules contain ______,_______,______,____,______.
Dense granules contain ______,_____,______,______,______
P-selectin, fibrinogen, factors V & VIII, PDGF, TGF-beta
ATP, ADP, calcium ion, histamine , serotonin
44
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
45
Platelet Adhesion is mediated via interactions with _____ which acts as a bridge between _______ and _____
vWF
platelet and exposed collagen.
46
Genetic deficiencies of vWF( _____________ ) or it’s receptor[GpIb] ( ___________ )result in bleeding disorders
von Wilebrand disease
Bernard-Soulier syndrome
47
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
48
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
49
Activated platelets also secrete thromboxane A2 (TxA2)
T/F
T
50
Platelet aggregation follows _____,______, and ________ and leads to formation of ___________
adhesion, shape change and granule release[activation]
primary hemostatic plug.
51
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
52
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
53
Definitive hemostatic plug
Thrombin converts _____ into ________, cementing the platelets in place and creating the definitive secondary hemostatic plug
fibrinogen
insoluble fibrin
54
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
55
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
56
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
57
fibrin spilt products which is depressed in DIC
T/F
F
Elevated
58
The two known plasminogen activators are _____ -like PA and ________ PA (t-PA)
urokinase
tissue type
59
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
60
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.
61
Thrombosis
Three major factors ( _____) that predispose to thrombosis
Endothelial injury or altered endothelial function
Alteration in the normal blood flow
________
Virchow’s triad
hypercoagulability
62
Endothelial injury in thrombus formation
Causes of endothelial injury include
endocardial injury in myocardial infarction, ulceration of atherosclerotic plaques, hemodynamic stress in hypertension, bacterial endotoxins, radiation injury, cigarette smoke, immunologic injury etc.
Endothelial injury exposes the subendothelial collagen, vWF, activation of platelets, exposure of tissue factor then coagulation.
63
_______ is the most important factor in thrombus formation .
Endothelial injury
64
Turbulence is important in _________ and ______ thrombosis e.g. in atherosclerotic plaques.
Stasis is a major factor in ______ thrombosis. Arterial aneurysms, myocardial infarction, arrhythmias, mitral valve stenosis lead to stasis.
arterial and cardiac
venous
65
Alteration in normal blood flow leading to thrombosis
______ and _____ are the two e.g.. The two result in loss of _____ flow and allow platelets to come in contact with and adhere to the endothelium. They can also cause endothelial cell injury and activation.
Turbulence and stasis
laminar
66
Hypercoagulability leading to thrombosis
Secondary/ _______
Trauma, prolonged _______ or ______, _________ infarction, atrial _____, cancer, DIC, Heparin induced ______, and late _____
Acquired
bed rest or immobilisation
myocardial; fibrillation
thrombocytopaenia; pregnancy
67
Primary/ genetic
Inherited causes e.g. ____ mutation, involves factor ___ mutation that makes it __________
Inherited deficiency or lack of anticoagulants e.g. _____,______,_____
leiden
V
resistant to inactivation by activated Protein C.
antithrombin III, Protein C or Protein S
68
Morphology of Thrombi
Thrombi may be
_____
______
_____
White; arterial
Red; venous
Mixed
69
Morphology of the thrombus
Thrombi may have grossly or microscopically lines of _____ which show alternating _____ of _____ mixed with _____ and ____ layers containing more ____
Such laminations signify that a ______ has formed in flowing blood.
Zhan; pale layers of platelets
fibrin and darker
red cells.
thrombus
70
Thrombus can be formed in the heart chambers, arteries, veins or capillaries.
T/F
T
71
Heart or aorta : Thrombi occurring in heart chambers or in the aortic lumen are designated ______
mural thrombi.
72
Mural thrombi
Causes: Heart- arrhythmias, dilated cardiomyopathy, or myocardial infarction or endomyocardial injury while _________ and __________ are the precursors
ulcerated atherosclerotic plaque and aneurysmal dilation
73
Arterial thrombi: the common sites are _____,______,______ and ________
They are composed of ____,_____,______ and degenerating ______.
descending aorta, coronary artery, cerebral and femoral arteries.
platelets, fibrin, rbc
leucocytes
74
Arterial thrombi
The thrombi are usually adherent to the _____ and they are ______
arterial wall
gray white
75
Arterial thrombi tend to grow ______, while venous thrombi extend in the direction of ______; thus both propagate toward the ______
retrograde
blood flow
heart
76
Venous thrombosis( _____________ )
phlebothrombosis
77
Venous thrombosis:
The thrombi are known as _____ and _____ thrombi because they contain _____ and ________
red or stasis
more rbc and relatively few platelets.
78
Veins easily thrombose because _________.
Blood flow is slow
79
90% of phlebothrombosis occur in the veins[superficial or deep] of _________
lower extremities.
80
Venous thrombi are (weak or firm?) , are focally attached to the vessel wall
Firm
81
Venous thrombi do not contain lines of Zahn.
T/F
F
They do
82
What distinguishes venous thrombi from postmortem clots?
Venous thrombi are firm, are focally attached to the vessel wall, and contain lines of Zahn.
83
Post mortem clots are ______ with a _____ dependent portion where rbc have settled by gravity(_______) and the overlying _____ clot which represents _______ without ______ called _______________
gelatinous
dark red
currant jelly; supernatant
coagulated plasma without red blood cells
yellow chicken fat supernatant.
84
Post Morten clots are attached to the vessel wall
T/F
F
They are not
85
The fate of thrombi
Propagation. Thrombi accumulate additional platelets and fibrin which may lead to __________
Embolisation: thrombi may _______ and travel to other sites within the vasculature.
Dissolution: This is as a result of _______ by _____ agents in a recent thrombus. In older thrombi ________ renders them more resistant to lysing.
vessel obstruction
dislodge
fibrinolysis by fibrinolytic
Extensive fibrin deposition and cross linking
86
The fate of thrombi
Organisation: older thrombi may have ___________________ which causes the thrombus to become ______ and _____
Recanalisation is a process by which ________ lined by _______ form in ________ thrombus.
ingrowth of connective tissue elements
firm and greyish white.
new lumina ; endothelial cells
organised
87
Clinical features of thrombi
Venous thrombi can cause painful congestion and edema distal to an obstruction, but of great concern to the clinician is their tendency to ______
Although arterial thrombi can also embolize and cause downstream infarctions, the chief clinical problem is more often related to _____ (e.g., a coronary or cerebral artery), which can have serious or fatal consequences.
embolize to the lungs.
occlusion of a critical vessel
88
Embolism
Is the process of ______ and transference of intravascular _______ mass to a site distant from it’s point of origin.
The mass is an ________.
detachment
solid, liquid or gaseous
embolus
89
The commonest (99%) embolus is a _______
fragment of thrombus.
90
Pulmonary embolism
The thrombi usually originate from the ________ pass through the (left or right?) side of the heart into the pulmonary vasculature.
Massive ones may block the ________ or both of it’s branches causing sudden death.
deep leg veins
Right
pulmonary trunk
91
Pulmonary embolism
The _____ embolism impacts across the bifurcation of the artery.
Shower embolism is when there are _______. Less massive ones may cause acute right ventricular failure.
The very small ones may _______________
saddle
multiple emboli
go unnoticed.
92
Systemic emboli
Most systemic emboli (80%) arise from __________ thrombi
_________ wall infarcts
left atrial _______ and ______
intracardiac mural
left ventricular
dilation and fibrillation
93
Fat and marrow embolism
Microscopic fat globules, sometimes with associated hematopoietic bone marrow can be found in the pulmonary vasculature after _______ or, rarely, in the setting of ___________
fractures of long bones
soft tissue trauma and burns.
94
Most patients of fat embolism are assymptomatic
T/F
T
95
In fat and marrow embolism
______________ is the term applied to the (minority or majority?) of patients who become symptomatic.
Fat embolism syndrome
Minority
96
Air embolism
Gas bubbles within the circulation can coalesce to form ______ that obstruct vascular flow (and cause _______ injury). eg a very small volume of air trapped in a coronary artery during bypass surgery or introduced into cerebral circulation, can occlude flow with dire consequences.
frothy masses
distal ischemic
97
Generally, more than ____ of air are required to have a clinical effect in the pulmonary circulation.
This volume of air can be inadvertently introduced during obstetric operations, chest wall injuries, intravenous infusion of blood and fluid, angiography etc.
100 cc
98
Decompression sickness
Occurs when individuals experience ______________ eg either from high pressure to normal pressure.
sudden decrease in atmospheric pressure
99
In deep sea divers, under water construction workers who descend to high atmospheric pressure, ____eased amount of atmospheric gases (particularly ______) are dissolved in blood and tissue fluid.
When such an individual ascends rapidly the gases __________ as _______, particularly in _______ which has high affinity for _______.
Incr
nitrogen
come out of solution as minute bubbles
fatty tissue; nitrogen
100
In decompression sickness
The bubbles may coalesce to form large air emboli in muscles and supporting tissues around the joints which is responsible for a painful condition called the _______.
bends
101
Decompression sickness
In the lungs gas bubbles within the vasculature cause ______,_______,______, or _______ causing respiratory distress called _______ .
edema, haemorrhage, focal atelectasis or emphysema
chokes
102
Acute decompression sickness is treated by placing the patient in _____________ followed by ___________
high pressure chamber
slow decompression
103
In _____ disease which is a chronic form of decompression sickness , multiple form of _______ may occur affecting ______
Caissons
ischaemic necrosis
femoral heads.
104
Amniotic fluid embolism
Amniotic fluid embolism (AFE) is a ______ complication that causes _______ life-threatening conditions. Mortality rate is up to ____%.
pregnancy
Maternal
80
105
Amniotic fluid embolism
It happens when _____________________ cells, hair, or other debris make their way into the _________ via ___________ or rupture of ________.
amniotic fluid or fetal (squamous)
maternal blood
tear in placental membranes
uterine veins
106
AFE is common
T/F
F
Rare
107
AFE can cause death during labor or shortly after birth.
The onset is characterised by sudden severe _____, ________ and ______ followed by neurologic manifestations such as headache, seizures and coma
dyspnea
cyanosis and shock
108
An infarct is usually due to occlusion of arteries by _______ or _____
Other uncommon causes include ______________ to ovaries, testes or loop of bowel.
thrombosis or embolism.
twisting of vessels
109
Infarcts caused by venous thrombosis are likely in organs with ____ venous outflow e.g. ______ and _____.
single
testes and ovary
110
Types of infarcts
Can be divided on the basis of colour or infection
_______ or ________
_______ or ______
White or haemorhagic (red).
Septic or aseptic
111
Types of infarcts
White infarcts occur in _____ occlusion and in solid organs with ______ circulation e.g. heart, kidneys, spleen.
arterial
end-arterial
112
Spleen
Red or white Infarct
White
113
Red or haemorhagic infarcts occur with ______ occlusion (ovarian or testicular torsion), in loose tissues eg ______ where blood can collect in _____ zones and in tissues with _______ circulation eg____ and _____
venous; lungs
infarcted
double
lung and small intestine.
114
Septic infarcts are caused by ____ emboli.
The _____ in the emboli invade the dead tissue and cause ______ leading to _____ formation.
septic
bacteria
suppuration
abscess
115
Few hours after infarct the margins are ______ defined. Several days after, the margins become _____ defined by a (wide or narrow?) rim of _______ due to _____ caused by diffusion of dead cells.
poorly
better
Narrow; hyperemia
inflammatory response
116
Arterial occlusions in organs without dual blood supply become progressively ______ and more sharply defined with time.
paler
117
In haemorrhagic infarcts eg in the lungs extravasated red cells are phagocytosed by _________ which convert ______ into ______ .
In massive haemorrhage the _______ deposit is substantial enough to leave a firm _______ residuum
macrophages
haeme iron into haemosiderin
haemosiderin
brownish
118
Demonstration of frank necrosis in tissue is seen ___-____ hours
4 to 12
119
An inflammatory response begins to develop along the margins of infarct within ______ and becomes well developed within ___-___
few hours
1 to 2 days
120
Congestion is (active or passive?) process resulting from reduced _________ of blood from a tissue/organ.
Passive
venous outflow
121
Types & Causes of congestion
Systemic: e.g._________, congestion involves _____,_____,_______
Local: examples
• Congestion of ___ veins due to _____→ edema of the ______
• Local congestion at various sites due to compression of veins: e.g. tight ______, plasters, ____,_______,________ etc.
congestive heart failure
liver, spleen, and kidneys.
leg; deep venous thrombosis ; lower extremity.
Bandage; tumors, pregnancy, hernia,
122
Onset
1. Acute congestion: It develops during ____, or sudden ______ failure. It may occur in lung and liver.
2. Chronic passive congestion: It usually produces edema in the organ/tissue in which the _________
shock
right-sided heart
venous outflow is reduced.
123
Chronic venous congestion of lungs
Causes
•_________
•_______ heart failure
Mitral stenosis
Left-sided
124
Chronic venous congestion of lungs
Mechanism
• Chronic left ventricle failure → reduces the ________ → leads to chronic (active or passive?) pulmonary ______ → increases _____________ and they become excessively filled with blood.
flow of blood out of the lungs
Passive ; congestion
pressure in the alveolar capillaries
125
Gross morphology of Chronic venous congestion of lungs
Lung is ____ in weight
Lung is _____ color due to _____
Lung is (loose or firm?) due to _____
Heavy
Rusty brown; Hemosiderin
Firm; fibrosis
126
Microscopical morphology of Chronic venous congestion of lungs
____ and ——— of _____ in the alveolar septa
_______ alveolar septa
_______ cells are seen in the lungs
Distension and congestion of capillaries
Thickened
Heart failure cells
127
CHRONIC PASSIVE CONGESTION OF LIVER
Causes
– ______-sided heart failure is the most common cause.
– Rare: Constrictive pericarditis, _____ stenosis and obstruction of _______ and _______ .
Right-
tricuspid
inferior vena cava and hepatic vein
128
CHRONIC PASSIVE CONGESTION OF LIVER
Mechanism:
Dilatation of central veins → transmission of increased venous pressure to ________ →_______ of ——— → ———- of hepatocytes in the ______ region.
the sinusoids
dilatation of sinusoids
ischemic necrosis
centrilobular
129
Gross morphology of CHRONIC PASSIVE CONGESTION OF LIVER
Liver increases in _____ and ____
Cut section shows alternate ——- and —— areas and resembles cross section of a _______
Size and weight
Light and dark
Nutmeg
130
Central vein
Aka
_______
Terminal hepatic venule
131
Nutmeg liver
-centrilobular area appears _____ due to _____
-periportal area appears ——— due to _____
Dark red brown; necrosis
Yellow and pale; fatty change and better oxygenation
132
Microscopical morphology of CHRONIC PASSIVE CONGESTION OF LIVER
———- and ______ in the central veins
_____ of central veins
Periportal ______
Congestion and hemorrhage
Thickening
Fatty change
133
Bleeding diathesis refers to an increased ______________ or ________
It can occur as a result of a wide variety of underlying disorders, most of which typically affect the _____
susceptibility to bleeding or bruising.
clotting process
134
Which is associated with inflammation, hyperemia or congestion
Hyperemia
135
Edema that is dependent on gravity is termed _______
Dependent edema
136
Edema in the eyelids is called _____ and is characteristic of a severe ______ disease
Periorbital edema
Renal
137
Answer with pro or anti coagulant
CD39
Heparan sulfate
VWF
tPA/uPA
Thrombomodulin
Proteins S
Prostacyclin
Thromboxane
Tissue factor
NO
Tissue factor pathway inhibitor
protein C
PAI-1
Anti
Anti
Pro
Anti
Anti
Anti
Anti
Pro
Pro
Anti
Anti
Anti
Pro
138
Adenosine diphosphatase
Antithrombic or prothrombin
Anti
139
Three primary abnormalities can lead to formation of a thrombus and
constitute __________. These include:
1.____________
2.—————
3. __________
VIRCHOW’S TRIAD
Injury to endothelium (changes in the vessel wall)
Stasis or turbulent blood flow (changes in the blood flow)
Hypercoagulability of the blood (changes in the blood itself)
140
Normal blood flow is _____, in which platelets (and other blood cellular elements) flow ______, separated from endothelium by ________
laminar
centrally
a slower moving layer of plasma.
141
Turbulence (disturbed movement of blood): It can produce thrombus in the _____ and _____
Stasis: It is a major cause for _____ thrombosis
arteries and heart.
venous
142
Hypercoagulability state (also known as ________)
thrombophilia
143
MTHFR Gene
Pro or antithrombic
Anti
144
Homocystonuria
Pro or antithrombic
Pro
145
Increased hepatic synthesis of coagulation factors and decreased anticoagulant synthesis can be seen in _________ and _______
Usage of oral contraceptive pill
Hyperestrogenic state as seen in pregnancy and post partum
146
Differentiate between arterial and venous thrombus under the following
Main cause
Rate of blood flow
Usual type of thrombus
Common sites
Color
Lines of zahn
Propagation
Injury to endothelium; stasis
Rapid; slow
Mural; occlusive
Arteries; veins
Gray white; red blue
More prominent; less prominent
Retrograde; anterograde
147
POSTMORTEM CLOTS VS ANTEMORTEM CLOTS
Attachment of vessel wall
Shape
Appearance
Lines of zahn
Mechanism
Consistency
Not attached; attached
Takes shape of the vessel; may or may not
Currant jelly or chicken fat; alternate light and dark areas
Absent; present
Gravity fractionated stagnant blood; Virchow’s triad
Gelatinous, soft, rubbery; dry, granular , firm, friable
148
Fate of thrombi
PEDOR:
P: Propagation E: Embolism
D: Dissolution
O: Organisation R: Recanalisation
149
Mural thrombus: It is attached to the wall and ___________, without _________. It occurs in heart chambers or in the aortic lumen.
projects into the lumen
complete occlusion of the lumen
150
Occlusive thrombus: It ______ the lumen of the blood vessel and prevents the flow of blood. It usually occurs in ____ or smaller or medium sized arteries.
occludes
veins
151
Vegetation: It is a thrombus on ______ and appears as _____ projecting into the lumen (e.g. ___________ ).
heart valve
polypoid mass
infective endocarditis
