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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.

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2
Q

Hyperemia

It is of two types:
________ and _______

A

physiological and pathological.

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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.

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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

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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.

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6
Q

Morphology of congestion

Cut surfaces are ________ and ______

A

hemorrhagic and wet

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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

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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.

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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

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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.

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11
Q

Liver micro architecture

Divided into 1-2mm-diameter _______ shaped lobules oriented around the __________ or ________

A

hexagonal

Terminal Hepatic Venules or central veins

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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

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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

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14
Q

Hemorrhage

Means extravasations of blood due to _________

A

vessel rupture.

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15
Q

Haematoma: ______________________

A

accumulation of blood within tissue

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16
Q

Petechiae: hemorrhages of __-___ mm into the _______,______, or ______

A

1 to 2

skin, mucous membranes or serosal surfaces

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17
Q

Petechiae

most commonly associated with locally increased _________, ____ platelet counts (thrombocytopenia), or ______ platelet function

A

intravascular pressure

low

defective

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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

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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

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20
Q

Hemostasis can be defined simply as the process by which ______ form at sites of vascular injury.

A

blood clots

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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

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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

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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.

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24
Q

Sequence of events in hemostasis

Arteriolar vasoconstriction
◦ Injury→ Arteriolar vaso________ (mediated by _______ mechanism and ______).

This is _________

A

constriction; reflex neurogenic

endothelin

transient

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25
Q

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)

A

von Willebrand Factor[Vwf] & collagen

adherence & activation

aggegration

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26
Q

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

A

tissue factor

factor VII

fibrin+platelets

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27
Q

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.

A

fibrin and platelet

contraction

tissue plasminogen activator,

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28
Q

The endothelium

After injury it exerts procoagulant functions

T/F

A

T

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29
Q

The endothelium possesses antithrombotic properties

T/F

A

T

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30
Q

The endothelium has Platelet inhibitory effects

T/F

A
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31
Q

The endothelium doesn’t posses fibrinolytic properties.

T/F

A

F

It does

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32
Q

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

A

subendothelial vWF & collagen.

dilators; aggregation

endothelium

Adenosine diphosphatase

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33
Q

Thrombin is one of the most potent activators of platelets.

T/F

A

T

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34
Q

Endothelial cells bind and alter the activity of thrombin

T/F

A

T

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35
Q

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

A

thrombomodulin

endothelial protein C

heparin

tissue factor pathway

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36
Q

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 ________________

A

cofactors; antithrombin III

Thrombomodulin and endothelial protein C receptor

factors Va and VIIIa.

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37
Q

The endothelium

Fibrinolytic properties
______________ promotes fibrinolytic activity which cleaves plasminogen to form plasmin

A

Tissue type plasminogen activator (t-PA)

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38
Q

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.

A

bacterial endotoxins

TNF, IL-1; tissue factor

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39
Q

Prothrombic properties of injured endothelium

Antifibrinolytic Effects: activated endothelium secretes _____________ which limit fibrinolysis favouring _________

A

Plasminogen activator inhibitors (PAIs)

thrombosis

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40
Q

Intact endothelium is ___coagulant while injured endothelium is ___coagulant.

A

anti

pro

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41
Q

Platelets

They are ____ shaped __nucleate cell fragments shed into the blood by _____________.

A

disc
A

marrow megakaryocytes

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42
Q

Platelets

Their function depends on several ___________, a contractile ______, and two types of ___________

A

glycoprotein receptors

cytoskeleton

cytoplasmic granules

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43
Q

Platelets

cytoplasmic granules :

alpha-granules contain ______,_______,______,____,______.

Dense granules contain ______,_____,______,______,______

A

P-selectin, fibrinogen, factors V & VIII, PDGF, TGF-beta

ATP, ADP, calcium ion, histamine , serotonin

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44
Q

Platelets

After injury on contact with subendothelial connective tissue [Vwf, collagen] platelets undergo three major reactions:

_____________,
____________________
_________

A

Adhesion and shape change

Secretion [release rxn] of granule contents

Aggregation

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45
Q

Platelet Adhesion is mediated via interactions with _____ which acts as a bridge between _______ and _____

A

vWF

platelet and exposed collagen.

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46
Q

Genetic deficiencies of vWF( _____________ ) or it’s receptor[GpIb] ( ___________ )result in bleeding disorders

A

von Wilebrand disease

Bernard-Soulier syndrome

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47
Q

Platelets

Shape change- Platelets rapidly change shape following ____, being converted from __________ to ________ with greatly _____eased surface area.

A

adhesion

smooth discs to spiky “sea urchins”

Incr

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48
Q

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.

A

platelet activation

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49
Q

Activated platelets also secrete thromboxane A2 (TxA2)

T/F

A

T

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50
Q

Platelet aggregation follows _____,______, and ________ and leads to formation of ___________

A

adhesion, shape change and granule release[activation]

primary hemostatic plug.

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51
Q

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 __________

A

IIb/IIIa

fibrinogen

Glanzmann thrombasthenia

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52
Q

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.

A

thrombin

cytoskeleton

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53
Q

Definitive hemostatic plug

Thrombin converts _____ into ________, cementing the platelets in place and creating the definitive secondary hemostatic plug

A

fibrinogen

insoluble fibrin

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54
Q

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____.

A

endothelial ; inhibits; dilator

platelet; activates; constrictor

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55
Q

Aspirin an (reversible or irreversible?) ______ inhibitor is given to persons at risk of coronary _______ to (temporarily or permanently?) block platelet TxA2 synthesis.

A

irreversible

cycloxygenase

thrombosis

permanently

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56
Q

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.

A

antithrombin III ; thrombin; Xa

Va and VIIIa.

fibrin

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57
Q

fibrin spilt products which is depressed in DIC

T/F

A

F

Elevated

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58
Q

The two known plasminogen activators are _____ -like PA and ________ PA (t-PA)

A

urokinase

tissue type

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59
Q

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

A

von Willebrand factor and uremia

hemophilias

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60
Q

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 _______

A

solid or semi-solid

Thrombus

platelets and the coagulation system.

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61
Q

Thrombosis

Three major factors ( _____) that predispose to thrombosis

Endothelial injury or altered endothelial function
Alteration in the normal blood flow
________

A

Virchow’s triad

hypercoagulability

62
Q

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.

A
63
Q

_______ is the most important factor in thrombus formation .

A

Endothelial injury

64
Q

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.

A

arterial and cardiac

venous

65
Q

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.

A

Turbulence and stasis

laminar

66
Q

Hypercoagulability leading to thrombosis

Secondary/ _______

Trauma, prolonged _______ or ______, _________ infarction, atrial _____, cancer, DIC, Heparin induced ______, and late _____

A

Acquired

bed rest or immobilisation

myocardial; fibrillation

thrombocytopaenia; pregnancy

67
Q

Primary/ genetic

Inherited causes e.g. ____ mutation, involves factor ___ mutation that makes it __________

Inherited deficiency or lack of anticoagulants e.g. _____,______,_____

A

leiden

V

resistant to inactivation by activated Protein C.

antithrombin III, Protein C or Protein S

68
Q

Morphology of Thrombi

Thrombi may be

_____
______
_____

A

White; arterial

Red; venous

Mixed

69
Q

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.

A

Zhan; pale layers of platelets

fibrin and darker

red cells.

thrombus

70
Q

Thrombus can be formed in the heart chambers, arteries, veins or capillaries.

T/F

A

T

71
Q

Heart or aorta : Thrombi occurring in heart chambers or in the aortic lumen are designated ______

A

mural thrombi.

72
Q

Mural thrombi

Causes: Heart- arrhythmias, dilated cardiomyopathy, or myocardial infarction or endomyocardial injury while _________ and __________ are the precursors

A

ulcerated atherosclerotic plaque and aneurysmal dilation

73
Q

Arterial thrombi: the common sites are _____,______,______ and ________

They are composed of ____,_____,______ and degenerating ______.

A

descending aorta, coronary artery, cerebral and femoral arteries.

platelets, fibrin, rbc

leucocytes

74
Q

Arterial thrombi

The thrombi are usually adherent to the _____ and they are ______

A

arterial wall

gray white

75
Q

Arterial thrombi tend to grow ______, while venous thrombi extend in the direction of ______; thus both propagate toward the ______

A

retrograde

blood flow

heart

76
Q

Venous thrombosis( _____________ )

A

phlebothrombosis

77
Q

Venous thrombosis:

The thrombi are known as _____ and _____ thrombi because they contain _____ and ________

A

red or stasis

more rbc and relatively few platelets.

78
Q

Veins easily thrombose because _________.

A

Blood flow is slow

79
Q

90% of phlebothrombosis occur in the veins[superficial or deep] of _________

A

lower extremities.

80
Q

Venous thrombi are (weak or firm?) , are focally attached to the vessel wall

A

Firm

81
Q

Venous thrombi do not contain lines of Zahn.

T/F

A

F

They do

82
Q

What distinguishes venous thrombi from postmortem clots?

A

Venous thrombi are firm, are focally attached to the vessel wall, and contain lines of Zahn.

83
Q

Post mortem clots are ______ with a _____ dependent portion where rbc have settled by gravity(_______) and the overlying _____ clot which represents _______ without ______ called _______________

A

gelatinous

dark red

currant jelly; supernatant

coagulated plasma without red blood cells

yellow chicken fat supernatant.

84
Q

Post Morten clots are attached to the vessel wall

T/F

A

F

They are not

85
Q

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.

A

vessel obstruction

dislodge

fibrinolysis by fibrinolytic

Extensive fibrin deposition and cross linking

86
Q

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.

A

ingrowth of connective tissue elements

firm and greyish white.

new lumina ; endothelial cells

organised

87
Q

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.

A

embolize to the lungs.

occlusion of a critical vessel

88
Q

Embolism

Is the process of ______ and transference of intravascular _______ mass to a site distant from it’s point of origin.

The mass is an ________.

A

detachment

solid, liquid or gaseous

embolus

89
Q

The commonest (99%) embolus is a _______

A

fragment of thrombus.

90
Q

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.

A

deep leg veins

Right

pulmonary trunk

91
Q

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 _______________

A

saddle

multiple emboli

go unnoticed.

92
Q

Systemic emboli

Most systemic emboli (80%) arise from __________ thrombi

_________ wall infarcts
left atrial _______ and ______

A

intracardiac mural

left ventricular

dilation and fibrillation

93
Q

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 ___________

A

fractures of long bones

soft tissue trauma and burns.

94
Q

Most patients of fat embolism are assymptomatic

T/F

A

T

95
Q

In fat and marrow embolism

______________ is the term applied to the (minority or majority?) of patients who become symptomatic.

A

Fat embolism syndrome

Minority

96
Q

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.

A

frothy masses

distal ischemic

97
Q

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.

A

100 cc

98
Q

Decompression sickness

Occurs when individuals experience ______________ eg either from high pressure to normal pressure.

A

sudden decrease in atmospheric pressure

99
Q

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 _______.

A

Incr

nitrogen

come out of solution as minute bubbles

fatty tissue; nitrogen

100
Q

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 _______.

A

bends

101
Q

Decompression sickness

In the lungs gas bubbles within the vasculature cause ______,_______,______, or _______ causing respiratory distress called _______ .

A

edema, haemorrhage, focal atelectasis or emphysema

chokes

102
Q

Acute decompression sickness is treated by placing the patient in _____________ followed by ___________

A

high pressure chamber

slow decompression

103
Q

In _____ disease which is a chronic form of decompression sickness , multiple form of _______ may occur affecting ______

A

Caissons

ischaemic necrosis

femoral heads.

104
Q

Amniotic fluid embolism

Amniotic fluid embolism (AFE) is a ______ complication that causes _______ life-threatening conditions. Mortality rate is up to ____%.

A

pregnancy

Maternal

80

105
Q

Amniotic fluid embolism

It happens when _____________________ cells, hair, or other debris make their way into the _________ via ___________ or rupture of ________.

A

amniotic fluid or fetal (squamous)

maternal blood

tear in placental membranes

uterine veins

106
Q

AFE is common

T/F

A

F

Rare

107
Q

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

A

dyspnea

cyanosis and shock

108
Q

An infarct is usually due to occlusion of arteries by _______ or _____
Other uncommon causes include ______________ to ovaries, testes or loop of bowel.

A

thrombosis or embolism.

twisting of vessels

109
Q

Infarcts caused by venous thrombosis are likely in organs with ____ venous outflow e.g. ______ and _____.

A

single

testes and ovary

110
Q

Types of infarcts

Can be divided on the basis of colour or infection
_______ or ________
_______ or ______

A

White or haemorhagic (red).

Septic or aseptic

111
Q

Types of infarcts

White infarcts occur in _____ occlusion and in solid organs with ______ circulation e.g. heart, kidneys, spleen.

A

arterial

end-arterial

112
Q

Spleen

Red or white Infarct

A

White

113
Q

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 _____

A

venous; lungs

infarcted

double

lung and small intestine.

114
Q

Septic infarcts are caused by ____ emboli.

The _____ in the emboli invade the dead tissue and cause ______ leading to _____ formation.

A

septic

bacteria

suppuration

abscess

115
Q

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.

A

poorly

better

Narrow; hyperemia

inflammatory response

116
Q

Arterial occlusions in organs without dual blood supply become progressively ______ and more sharply defined with time.

A

paler

117
Q

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

A

macrophages

haeme iron into haemosiderin

haemosiderin

brownish

118
Q

Demonstration of frank necrosis in tissue is seen ___-____ hours

A

4 to 12

119
Q

An inflammatory response begins to develop along the margins of infarct within ______ and becomes well developed within ___-___

A

few hours

1 to 2 days

120
Q

Congestion is (active or passive?) process resulting from reduced _________ of blood from a tissue/organ.

A

Passive

venous outflow

121
Q

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.

A

congestive heart failure

liver, spleen, and kidneys.

leg; deep venous thrombosis ; lower extremity.

Bandage; tumors, pregnancy, hernia,

122
Q

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 _________
A

shock

right-sided heart

venous outflow is reduced.

123
Q

Chronic venous congestion of lungs

Causes
•_________
•_______ heart failure

A

Mitral stenosis

Left-sided

124
Q

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.

A

flow of blood out of the lungs

Passive ; congestion

pressure in the alveolar capillaries

125
Q

Gross morphology of Chronic venous congestion of lungs

Lung is ____ in weight

Lung is _____ color due to _____

Lung is (loose or firm?) due to _____

A

Heavy
Rusty brown; Hemosiderin

Firm; fibrosis

126
Q

Microscopical morphology of Chronic venous congestion of lungs

____ and ——— of _____ in the alveolar septa

_______ alveolar septa

_______ cells are seen in the lungs

A

Distension and congestion of capillaries

Thickened

Heart failure cells

127
Q

CHRONIC PASSIVE CONGESTION OF LIVER

Causes
– ______-sided heart failure is the most common cause.
– Rare: Constrictive pericarditis, _____ stenosis and obstruction of _______ and _______ .

A

Right-

tricuspid

inferior vena cava and hepatic vein

128
Q

CHRONIC PASSIVE CONGESTION OF LIVER

Mechanism:
Dilatation of central veins → transmission of increased venous pressure to ________ →_______ of ——— → ———- of hepatocytes in the ______ region.

A

the sinusoids

dilatation of sinusoids

ischemic necrosis

centrilobular

129
Q

Gross morphology of CHRONIC PASSIVE CONGESTION OF LIVER

Liver increases in _____ and ____
Cut section shows alternate ——- and —— areas and resembles cross section of a _______

A

Size and weight

Light and dark

Nutmeg

130
Q

Central vein

Aka

_______

A

Terminal hepatic venule

131
Q

Nutmeg liver

-centrilobular area appears _____ due to _____
-periportal area appears ——— due to _____

A

Dark red brown; necrosis

Yellow and pale; fatty change and better oxygenation

132
Q

Microscopical morphology of CHRONIC PASSIVE CONGESTION OF LIVER

———- and ______ in the central veins

_____ of central veins

Periportal ______

A

Congestion and hemorrhage

Thickening

Fatty change

133
Q

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 _____

A

susceptibility to bleeding or bruising.

clotting process

134
Q

Which is associated with inflammation, hyperemia or congestion

A

Hyperemia

135
Q

Edema that is dependent on gravity is termed _______

A

Dependent edema

136
Q

Edema in the eyelids is called _____ and is characteristic of a severe ______ disease

A

Periorbital edema

Renal

137
Q

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

A

Anti
Anti
Pro
Anti
Anti
Anti
Anti
Pro
Pro
Anti
Anti
Anti
Pro

138
Q

Adenosine diphosphatase

Antithrombic or prothrombin

A

Anti

139
Q

Three primary abnormalities can lead to formation of a thrombus and
constitute __________. These include:
1.____________
2.—————
3. __________

A

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
Q

Normal blood flow is _____, in which platelets (and other blood cellular elements) flow ______, separated from endothelium by ________

A

laminar

centrally

a slower moving layer of plasma.

141
Q

Turbulence (disturbed movement of blood): It can produce thrombus in the _____ and _____

Stasis: It is a major cause for _____ thrombosis

A

arteries and heart.

venous

142
Q

Hypercoagulability state (also known as ________)

A

thrombophilia

143
Q

MTHFR Gene

Pro or antithrombic

A

Anti

144
Q

Homocystonuria

Pro or antithrombic

A

Pro

145
Q

Increased hepatic synthesis of coagulation factors and decreased anticoagulant synthesis can be seen in _________ and _______

A

Usage of oral contraceptive pill

Hyperestrogenic state as seen in pregnancy and post partum

146
Q

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

A

Injury to endothelium; stasis

Rapid; slow

Mural; occlusive

Arteries; veins

Gray white; red blue

More prominent; less prominent

Retrograde; anterograde

147
Q

POSTMORTEM CLOTS VS ANTEMORTEM CLOTS

Attachment of vessel wall
Shape
Appearance
Lines of zahn
Mechanism
Consistency

A

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
Q

Fate of thrombi

A

PEDOR:
P: Propagation E: Embolism
D: Dissolution
O: Organisation R: Recanalisation

149
Q

Mural thrombus: It is attached to the wall and ___________, without _________. It occurs in heart chambers or in the aortic lumen.

A

projects into the lumen

complete occlusion of the lumen

150
Q

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.

A

occludes

veins

151
Q

Vegetation: It is a thrombus on ______ and appears as _____ projecting into the lumen (e.g. ___________ ).

A

heart valve

polypoid mass

infective endocarditis

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