Hyper Conges/ CPVC Shock Def/Septic Shk/ Classification Hypovolemic Shk Organs changes Shock

Lung,Liver, Spleen Cause(etiology) Oedema Def/ Cardiac Oedema

SHOCK 1.Acute loss of critical portion of
Defn blood volume Organs changes in shock
Hyperemia & Congestion
It is a catastrophic event caused by Eg. Massive Haemorrhage due to Hypoxic failure of multi organ
Def:Increaced volume of blood in
wide-spread tissues hypoperfusion system
affected tissues or organ. splenic rupture haemorrhagic
due to reduction in the blood 1.Brain ( ischaemic/anoxic/ hypoxic
shk
volume or cardiac output or encephalopathy)
CPVC of Lung Severity depend on
redistribution of blood resulting in -brain is vulnerable to o2 deficit
Causes: Acute & chronic passive -rate of blood loss
an inadequate effective circulating -widespread neuronal injury
congestion of lungs & consequent -D of trauma
blood volume. -Morphological changes 12-24 hrs
pulmonary oedema occur when - Hb level of blood Gross; brain enlarged, swollen, Gyri
there is L.A pressure & pulm:
Classification - cardiopulmonary status prior to widen, sulci narrowed
venouse pressure.
1.Hypovolemic or Haemorrhagic shk Histo;
1.All forms of cardiac
shock 2. Acute reduction of plasma a.early changes (12 -24 hrs)
decompensation
P.mech; inadequate blood or plasma volume -Acute neuronal cell change (Red
2.L.V Myocardial infarct
or fluid volume Eg. Extensive burns Neurone)
3.Rheumatic mitral stenosis
C.eg = profuse haemorrhage 3. Extensive depletion of fluid & Susceptible cells neurons of
Morphology:
2.Cardiogenic Shk hippocampus, cerebellum cortex
Gross: electrolyte
P.mech; failure of myocardial pump b.Subacute Change (24- 2 wks)
Lung- size & wt Eg. Severe vomiting in
due to intrinsic myocardial damage Tissue necrosis, vascular
Dusky red cyanotic Gastroenteritis
or extrinsic compression or proliferation,
C.S-excessive bloody & wet Pathophysiology
obstruction to outflow c.Repair ( after 2 wks)
Long stading-Brown induration of Stage 1. Initial nonprogressive or
C.eg = Extensive M.I, Arrhythamias, -removal of necrotic tissues
lung Early stage
Rupture of Ht Pseudolaminar necrosis
Histology;
3.Septic Shk 1.Activation of compensatory 2.Heart
1.Alveolar capillaries are engorged
P.mech; Peripheral vasodilation, reflex mechanisms a.Subendocardial ecrosis;
with blood & become tortuous with
pooling of blood, endothelial -preservation of perfusion of vital -range from isolated fibre ischaemic
small aneurysmal
activation injury, leucocyte induced organs lesion to large areas
dilatation>>minute intraalverolar
damage,activation of cytokine Mech; cardiac output remains b.Zonol lesion
Hge & breakdown & phagocytosis
cascade unchanged / no fluid 3.Kidney
of red cell debris>>appearance of
C.eg = Overwhelming microbial A R F ischaemic acute tubular
HEMPOSIDERIN LADEN redistribution
infection, Gram negative necrosis
MACROPHAGE(HEART FAILURE Initial vaso-vagal attack due to
septicaemia Shock kidney; Hemoglobinuric
CELLS) in alveolar spaces. volume deficit syncopy
4.Neuogenic shk nephrosis
2.Severe form- alveolar widened Widespread vasodilation of
P.mech; loss of vascular tone Grossl;
by dilation of alveolar capillary & arterioles ed B.P & ed
vasodilation, peripheral pooling of Cortex enlarged, pale, widen
collection of oedema fluid in cerebral blood flow
blood Medulla deep red, congested
interestitium of alveolar septa
C.eg = Anaesthetic accidents, Spinal (transient)loss of consciousness CMJ well defined
3. In time- Oedematous septa
cord injury 2. Activation of Neurohumoral Histo;
become fibrotic & together with
5.Anaphylactic Shk mechanisms Tubule;Ischaemic acute tubular
hemosiderin pigmentation >> Brown
P.mech; systemic vasodilatation, a. stimulation of baroreceptors; necrosis (Tubulorrhexis)
induration
increase V.P vasoconstriction of arterioles in Lumen; Occlusion of tubular lumina
4.Long standing congestion-
C.eg = Generalized type I skin & skeletal muscle by haline casts
progressive thickening of walls of
hypersensitivity I/S; Intestitium oedema &
pulmonary arteries & arterioles b. release of cathecholamines
Accumulation of leucocytes
Pulm: Hyertension>> Rt Ht (generalized sympathetic
SEPTIC SHOCK Glomeruli; Most cases unaffected,
failure(Chronic Cor pulmonale) activation)
-Most common cause of death 4. Lungs
-Results from spread of microbes - selective arteriolar (shock lung, adult resp; distress $)
CPVC of Liver(Nutmeg liver) vasoconstriction of skin, skeletal
from uncontrolled initially localized Gross; Heavy, firm, red, boggy
Causes: 1. R.H.F m/s, salivary glnd, intestine, liver,
infection ,S bact- infection foci of
2.Congestive Ht failure
(eg. UTI, GI infection, abcess, spleen, kidney bronchopneumonic consolidation
3.obstruction of IVC or hepatic
peritonitis) -in the kidneys cortical Histo- Pulm; congestion & intra
veins(rarely)
A. Cause (Etiology) vasoconstriction blood is alveolar H;ge
Morphology
1.Majority 70 % cause by redistributed toward medulla 5. Adrenal Gland
Gross:
endotoxin producing gram negative -vasodilatation of cerebral & Stress response
Liver-in size & wt
bacilli coronary arteries Depletion of lipids within cortical
Dusky red cyanotic
Source of infection cells - non vacuolated compact cells
C.S excessive ooze of blood & -activation of RAA axis
-infected burns -it begins within zona reticularis &
central veins may appear prominent -release of ACTH> S/W retention
-Surgical operation spreading outward towards to
with chronic congestion central -release of AGH > renal
-complication of post abortion capsule
regions of lobule become red blue conservation of W
2.G+ cocci eg Pneumococci, Staph, 6.Intestines
surrounded by yellow brown zone of Net effects
Strept Ischaemic Enterocolitis or acute
uncongested liver substances >> -increase peripheral resistance
3.Fungi haemorrhagic enteropathy)
Nutmeg Liver
4.Super antigen -increase force of myocardial Gross; oedema & thickening of
Histology:
B. Pathophysiology contraction intestinal wall and Hgic congestion
Central vein & vascular sinusoids of
Haemodynamic & metabolic -increase blood volume & venous of superficial ulcer
centrilobular region distended
alteration of septic shock is caused return Shedding of mucosa
with blood.
by lipopolysaccharide -shunting of available blood to Histo;
Central hepatocytes atrophic S to
LPS bind to CD14 molecules on vital organ -Dilatation of mucosal capillary &
chronic hypoxia
leukocytes venules
Peripheral hepatocytes less severe Clinical Features
Depending on the dosage, LPS -submucosal oedema with Hgic
hypoxia >> develop fatty change -cold, clammy sweaty skin (Cold
binding protein complex extravasation of RBC
With severe Ht failure reduction in shk)
-can directly activate vascular wall -thrombi within the v/s
circulating blood volume & hepatic Stage II,
cells 7. Liver
blood flow >> Hypoxia >> centrall Progressive or Decompensatory
-initiate a cascade of cytokines Fatty change & central Hgic necrosis
oocytescytes become necrotic & phase
mediators -begin in center of lobule &
centrilobular zone>> haemorrhagic
1.At low doses LPS, -volume deficit still uncorrected extending through entire lobule
Central Haemorrhagic Necrosis.
LPS- activate monocytes & -persistent hypoxia Fibrin thrombi + within sinusoids
In time fibrous thickening of walls of
macrophage Resultant metabolic acidosis
central vein & extension of fibrous
-direct activation of complement lowers the pH Oedema
tissues into surrounding lobule>>
- the mononuclear phagocytes -vasodilation occur Def: Abnormal accumulation of luid
Cardiac Cirrhosis
respond to LPS by producing TNF -effective circulatory blood in the intercellular(interstitial)
which in turn induces IL-1 synthesis tissues paces or body cavities.
CPVC of Spleen volume (hypovolemia)
TNF & IL-1 on endothelial cells to Cardiac Edema
Cause;1. Portal Hypertension due to Effect
produce further cytokines (eg IL6 & Cause:1.Congestive Ht failure
cirrhosis of liver(most common) With wide spread tissues hypoxia
IL8) & induce adhesion molecules 2.Constrictive pericarditis
2.Cardiac decompensation involving deteriorate the function of
Effects Dsitribution:
Rt side of Ht. vital organ
-local acute inflammatory response 1.Dependent edema-typically
a.Tricuspid or pulmonary valvular Clinical features
-improve clearance of infection influenced by gravity.eg. legs when
disease or
2. Moderate dose LPS (moderately -mental confusion & oliguria, standing
b.Chronic corpulmonale
severe infection) Upto this stage II,patient may 2.Pittying edema
c.following Lt Ht failure
-initiation of cytokine cascade return to normal state Pathophysiology of cardiac edema
3.Obstruction of Extrahepatic Portal
-release of cytokine induce Stage III, -Generalized increases in venous
vein or Splenic Vein
secondary effectors eg. NO, PAF, Irreversible shk pressue, with resulting systemic
Morphology:
C3a, C5a, bradykinin -occurs the following severe edema, occur most commonly in
Gross:First moderate enlargement
Effects congestive Ht failure, affection R>V
of spleen rarely exceeds 500 Gm cellular & tissues hypoxic injury
Systemic effecto of TNF& IL 1 cardiac dysfunction
Long Standing marked enlargement -Death usually
-fever -Although ed Venous pressure is
& Wt 1000 Gm or > , May reach -Widespread cell injury
-increased synthesis of acute phase important, pathogenesis of cardiac
5000 Gm, firm (irreversible multiorgan failure)
reactants edema is more complex.
Capsule-thickened fibrous Effects
3.Higher Dose LPS -C.H.F is associated with ed
C.S- meaty appearance & varies -myocardial depressant factor
Syndrome of septic shock cardiac output & ed renal
from gray red to deep red depend
-results in endothelial cell injury -ischaemic intestinal mucosa perfusion
on amount of fibrosis, Malpighian
-Cytokines & secondary mediators at -complete renal shutdown due to -This process leads to
corpuscles are indistinct.
high levels result in acute tubular necrosis intravascular volume & improve
Histology:
-Systemic vasodilation -Hypoxic encephalopathy cardiac output with restoration of
Early phase pulp is suffused with
-MDF + NO Diminished -ARDS normal renal perfusion.
red cells
myocardial contractility Recovery Phase -If failing Ht cant increase cardiac
With time- ingly more fibrous &
-Widespread endothelial injury & output, extrafluid load results only
cellular 80-90% healthy young patients
activation in ed venous pressure & oedema.
portal venous pressure Timely volume replacement
(adult respiratory distress $) -Unless cardiac output is restored or
deposition of collagen in B.M of Urine formation with diuresis
-activation of coagulation system renal water retension is reduced , a
sinusoidswhich appear dilated due Clinical course
DIC cycle of renal fluid retention &
to rigidity of their walls - blood Patient presents hypotesion,
-Multi organ failure worsening edema occur.
flow from cords to ashen-gray pallor; cool & clammy
- warm shock with fluching of skin
sinusoidsprolong the exposure of
-Superantigens, bacterial proteins cyanotic skin; weak rapid thread
blood cells to cordal
cause similar shock pulse,
macrophageexcessive destruction
-they are polyclonal T-lymphocyte With uncontrolled sepsis, skin is
Foci of recent or old Hge(+)
activators warm & flushed due to peripheral
Deposition of hemosiderin in
-result in clinical manifestations vasodilatation
Histiocyte
ranging from diffuse rash to
Organization of these fociGandy
vasodilation, hypotension and
Gamna nodules Foci of fibrosis
death.
containing , Iron, Ca2+ salts
encrusted on connectiove tissue &
elastic fibres.
Renal / Morpho Oedema
Renal Oedema
Cause:1. Nephrotic $
2. Acute glomerulonephritis
3. Chronic Glomerulonephritis
4.Renal failure
Distribution:Generalize oedema-
all regions of body are qually
effected but mostly in loose C.T
matrix: facial oedema,
particularly in eyelids, but
posture modifies this distribution
& with erect position- facial
edema slowly subside &
accumulate again when pt is
confined to bed.
Mechanism
a.Nephrotic $ Characterised by 1.
Heavy proteinuria
2.Hypoproteinaemia
3.generalized oedema
4.Hypercholesterolemia
2.Acute Glomerulonephritis
Oedema is first symptom of
diseases.
Important factor is Ht failure
produced by sudden systemic
hypertension & aggrevated by
blood volume due to fluid
retention.
3. Chronic glomerulonephritis
-associated with hypertension &
oedema is due to Ht failure.
Morphology & clinical importance
of oedema
1.Subcutaneous Oedema
Manifestation of cardiac failure
particularly RVF, more prominent in
lower extremities.
Dependent Oedema- Oedema is
influenced by gravity
Pitting Oedema
Renal Oedema-(Renal dysfunction &
Nephrotic $)-generalized & more
severe than cardiac oedema,affect
all parts of body equally
Initially-loose C.T matrix such as
eyelids
Later- Generalized(anasarca)
2.Pulmonary Oedema
Cause:1.LVF 2.Renal diseases
3.Shock 4.Infection within lungs
5.Hypersensitivity states
Morphology:
Gross: Site: Most marked in lower
lobe
C.S:permits free escape of frothy
sanguineous fluid representing
mixture of air & edema fluid
Histology: 1- oedema fluid
accumulates abt septal capi:with
widening of septa
3.Cerebral Oedema
Causes: Localized cerebral oedema-
Neoplsms, abscess
Generalized cerebral oedema-
Encephalitis
Trauma- Localized or generalized
oedema depend on nature
&distribution
Morphology:
Gross: Heavier than normal
Sulci-narrowed
Swollen gyri- flattened where tey
press against skull
Ventricles-compressed
C.S soft & gelatinous white matter
Histology: Widening of interfibrillar
spaces of brain substances loose
app: of white & gray matter.
-Swelling of neuronal & glial cells
Clinical correlation:
Edema may give rise to minor
clinical problems or it may be lethal.
1.Subcutaneous tissue edema-in
cardiac of renal failure is important
primarily because it indicates
underlying diseases:but, it can
impair wound healing or clearance
or infection.
2.Pulmonary edema-can cause
death by interfering with normal
ventilator function & impede oxygen
diffusion.Edema fluid in alveolar
spaces creates a favourable
environment for bacterial infection.
-Pulmonary oedema may be lethal.
3.Brain edema-is serious & can be
rapidly fatal: if severe,brain
substance can herniate through
e.g.foramen magnum or brain stem
Forminal or Tonsillar
Herniationvascular supply can be
suppressed can injure medullary
centre &death.
ICP- Headache, projectile vomiting
& convulsive seizures.
Embo/ Amniotic/Air Embo
EMBOLISM
Defn
Occlusion of some part of the
cardiovascular system by the
impaction of an embolus
Embolus : A detached
intravascular solid, liquid or
gaseous mass that is carried by
the blood to a site distant from
its point of origin.
Types
1.pulmonary E
2.systemic E
3.air or gas E
4.fat E
5.Amniotic fluid E
6.Tumor E
Amniotic Fluid
Embolism(Infusion)
Cause: Infusion of amniotic fluid
with all or its contents into
maternal circulation following a
tear in the placental membranes
& rupture of uterine & cervical
veins.
As a consequence, epithelial
squames from fetal skin, fat from
verni caseosa, mucin from fetal
resp: or GIT & bile enter into
pulmonary microcirculation.Acute
respiratory distress is due to
thromboplastin like substance in
amniotic fluid which activate
extrinsic pathway.
MECHANISM:
1.Due to
obstruction of pulmonary
circulation by particulate material
with the amniotic
fluid.eq.squames, fat globules.
2.Some humoral factor in
amniotic fluid-
pulm:vasoconstriction & impaired
cardiac contractility respiratory:
& cardiac decompensation.
3.PGF 2 level- increased in
amniotic fluid during labor(+)
C/F;
Predisposing factor: Advanced
age for pregnancy , multiparity,
tumultuous labor occur in any
obstetric setting including
abortion &Cesarean delivery
1.Sudden profound respiratory
difficulty with deep cyanosis &
cardiovascular shock.
2.If pt survive, develop
pulm:edema,excessive bleeding
from & any injuries to birth canal
3.Nonspecific C/F:chills,
apprehension, agitation.
Diagnosis: prescence of amniotic
debris in pulmonary capillary
AIR OR GAS EMBOLISM(CAISSON
DISEASES)
Def:Tis is a condition where
bubbles of air or gas enter the
circulation, obstruct vascular flow
& damage the tissues know as
barotrauma.
CAUSES:Air or gas may gain
access into circulation.
1.during delivery or abortion
2.during performance of
pneumothorax
3.when injury to lung or chest
wall
4.during intravenous therapy.
EFFECTS: depend on
1.amount introduced
2.rate of entry
3.position of patient during &
soon after entry
4.general condition of patient
Many small bubbles may coalesce
to produce frothy, gaseous
masses, sufficiently large to
occlude a major vessels, usually
in lungs or brain
C/F; 1. Lung-acute respiratory
distress
2.Brain- sudden neurologic
disturbances such as convulsion
or coma & death
3. Sudden death occur when
aggregates of larger size may
become trapped in chambers of
Right Ht & block orifice of
pulmonary artery.
About 100 cc of air is required to
produce problems.
Pulmo / Systemic Embo
PULMONARY THROMBOEMBOLISM
(Venous)
Incidence
Most common preventable cause of
death in hospitalized patient
Defn
Embolic occlusion of the large or
small arteries of the bulm; arterial
tree.
Most common & most lethal.
Origin
1.95% -arise from thrombi within
the large deep veins of the lower
legs Popliteal, femoral, & iliac
veins
2. 5% - thrombi within superficial
veins of the legs, veins of calf
muscles
3. veins in the pelvis periprostatic,
broad ligment, periovarian & uterine
veins uncommon
Pathway
Dislodgement of such thrombi
producing an embolus which flows
with the venous drainage through
the large vessels to the Rt Ht
Unless the blood clot is very large, it
passes through the capacious
chambers & valves of the Rt Ht &
enters the pulmonary arterial
circulation
-long mass impact create a saddle
embolus
-occlude a major pulm; v/s
-pass further out , to acclude smaller
vesssels
-an embolus may pass through an
interatrial or interventricular septal
defect, when pressure in the Ht
exceeds that in the Lt Ht, to gain
accesss to the systemic circulation
(paradoxical embolism)
Clinical Significance
Depends on
-size & site of occluded A
-size & no; of emboli
- proportion of entire arterial tree
obstructed
-underlying cardiopulmonary status
of pt.
1. 60-80% clinically silent
Because they are small; promptly
removed by fibrinolylsis; collateral
bronchial circulation
2. 5% sudden death
(acute Rt Ht failure)
Occur when> 60% of total pulm;
vasculature is obstructed
3. 10-15 % embolic obstruction of
middle sized arteries (pulm; Hge)
4. 10-15% obstruction of small sized
pulm; arteries (pulm; infarction)
5. Uncommonly multiple emboli
lead to Pulm; Hypertension
SYSTEMIC EMBOLISM
(Arterial)
Defn
Emboli that travel through the
arterial circulation
Origin
80-85% arise from thrombi within
the Heart
-2/3 arise within LV secondary to
MI
-1/4 from thrombi in dilated &
fibrillating LA (S to MV disease)
cardiomyopathy
Less common causes;
1.Thrombi occur in ulcerated
atherosclerotic plaques
2.Aortic aneurysm
3.Infective endocarditis
4.Valvular or aortic prosthesis
5. Paradoxical embolism from
venous thrombi
10-15% source of embolus
unknown
Pathway
Arterial emboli follow a much
shorter & move varied pathway &
almost always cause infarction.
Sites
Lower extremities ; 70-75%
Brain; 10%
Viscera 10% mesenteric, renal &
splenic
Upperlimbs; 7-8%
Clinical Significance
Determined by
-site of lodgement
-size of embolus within systemic
vessels
1. Embolic occlusion of the
femoral artery infarction of
lower extremities
2. Infarction of brain may or may
not occur
-impaction in circle or Willis, may
be compensated by collateral
flow
3. Emboli affect the spleen &
kidney
4. Emboli from infective
endocarditis produce septic
infarcts
THROMBOGENESIS
Virchows Triad
1.Endothelial injury
2.Alterations in the blood flow
3.Alteraton in the blood
constituents (hypercagulability
state)
1. Endothelial/Endocardial Injry
-most important factor
-intact vascular
endothelium/endocardium is
thromboresistant
-injury exposes subendothelial
collagen
-especially important in thrombus
formation within heart chambers
& arterial system
Causes;
-Trauma
-Not due to trauma, causing overt
or covert changes in endothelium
Causes of Overt Damage
a.myocardial infarction; tbus
formation within LV chamber
b.rheumatic endocarditis; tbus
formation within LA chamber
c.Infective
endocarditis/Rheumatic
endocarditis
d.Atherosclerosis
Causes of Covert Damage
-Hemodynamic stress of
hypertension
-turbulence
-cigarette smoking
-radiation
-hypercholesterolemia
Mechanism (thrombogenesis)
-role of endothelium in blood clot
formation
-endothelial injury
-Platelet Adhesion, activation,
aggregation
-Exposure of ECM activation of
coagulation cascade
2. Alterations in the Blood flow
Normal blood flow is central
axial/ laminar flow
Turbulence thrombosis within
the heart & arterial system
Stasis thrombosis within the
venous system
Turbulence & Stasis cause
1.Disrupt the liminar flow & bring
platelets into contact with
endothelim
2.Prevent dilution of activated
clotting factors by fresh flowing
blood
3.Retart the inflow of inhibitors of
clotting factor
4.Promote endothelial cell
activation, predisposing to local
thrombosis and other endothelial
cell effects
Clinical Examples of turbulence
1.Ulcerated atherosclerotic
plaque with superimposed
thrombi
2.Aneurysms stasis
3. Myocardial infarction
4.Mitral Stenosis with dilated LA
in healed Rheumatic endocarditis
Clinical examples of stasis
1.Varicose veins
2.Hyperviscosity $
Turbulence
-usually combine with endothelial
injury
-produce thrombosis in the
arterial system
Stasis
-usually combine with
hypercoagulability state
-produces thrombosis in the
venous system
3.Alteration in blood
Constituents
Definition
Analtered state of circulating
blood that requires a smaller
quantity of clot promoting
substance to induce intravascular
coagulation than is required to
produce comparable thrombosis
in a normal subject.
Hypercoagulability state
-stickiness of platelets
-levels of activated pro-
coagulants
-levels of inhibitors eg. ATIII,
Fibrinolysin, Protein C,S
Usually combine with stasis
Produces formation thrombosis in
the venous system
Associated with certain clinical
setting
Morphology of Thrombus
Can occur anywhere in the
cardio-vascular system cardiac
chamber, heart valves, arteries,
veins and capillaries
Size and shape variable
Types
1.Antemortem thrombus
In heart & arterial syst
-mural thrombi
-arterial thrombi
-vegetations
In venous system
-venous thrombi
2.Post mortem thrombus
Gross
1.Mural Thrombus
-non occlusive, large friable blood
clot
-occur in cardiac chambers, aorta
and great vessels
-firmly attach to the wall
-usually appear at the site of
endothelial injury
-fragmented, easily detachable
-mural thrombi have
laminations,,,,,,,,,,,known as line
of Zahn
2.Arterial Thrombi
-firm, gray white in clor
-usually occlusive
-composed of tangled mesh of
platets, fibrin, erythrocytes
-firmly attach to vessel wall
-in small arteries- no definite
appearance of line of Zahn
-Contraction of fresh thrombi
-can propagate both ways
-most common sites in
descending order coronary,
cerebral and fenoral arteries
-seen in site of endothelial injury,
artherosclerosis and aneurysm
3.Vegetations
-occur in heart valves
1.Infective vegetations
-following damage of heart valves
due to infection with bacteria or
fungus eg. Infective endocarditis
-thrombi laden with micro-
organisms
2.Non infective/ Sterile
vegetations
-non-infective valves
-non-bacterial thrombotic
endocarditis
-Verrucous endocartditis or
Libman Sack endocarditis
-due to immune complex
-seen in SLE
4.Venous thrombi
-1. Phlebothrombosis (DVT)
almost invariably occlusive,
creats long cast of vein lumen
due to stasis, un-inflammed
vessels, can embolise
2.Thrombophlebitis- associated
with vessel wall inflammation
stasis is a major cause, always
occlusive, frequent in superficial
varicose veins & rarely embolise
Morphology; redblue, ill-defined
pale gray fibrin strands, attached
to underlying wall (stasis or red
thrombi)
5.Capillary thrombi
-usually widespread, Effects
microcirculation
-associated with DIC
Fate /Clinical Thrombus
Fate of Thrombus
1.Propagation
-the thrombus may propagate &
cause obstruction of some critical
vessels
2.Embolization
Thrombi may dislodge to distal
sites in vascular tree & from
Embolus.
-follow invasion of thrombus by
bacteria septic emboli
Arterial thrombus systemic
embolism
Venous thrombi pulmonary
embolism
3.Dissolution
Thrombi may be removed by
fibrinolytic activity.
It occurs within the first days or
two.
4.Organization & Recanalization
Thombi may induce inflammation
& fibrosis.
May become recanalized
5.Dystrophic calcification
-especially in venous thrombus
(phleboliths)
Clinical Significance
Thrombi are important for 2
reasons
1.cause obstruction of arteries &
veins
2.provide possible sources of
Emboli
Venous Thrombosis
(Phlebothrombosis)
Most venous thrombi are
occlusive & arise in superficial or
deep veins of the leg.
Superficial thrombi;
Occur in saphenous system
Rarely embolize
-Cause local congestion, swelling,
pain & tenderness along the
course of involved veins
Predispose the skin to infection
from slight trauma & develop
varicose ulcer.
Deep Thrombi
Occur in larger veins of legs
-most serious
-cause deep vein thrombosis
Oedema of foot & ankle &
produce pain & tenderness on
compression of calf muscles
About of patients-
asymptomatic & recognized only
when they have embolized.
Specific Clinical settings
-cardiac failure
-severe trauma or burns
-post operation & post partum
states
-nephrotic$
-disseminated cancer
-use of oral contraceptives
-advanced age, bed rest
Arterial Thrombosis
1.Myocardial infarction
-damage to endocardium
(advanced age, bed reset)
2.Rheumatic Heart Disease
-mitral stenosis
-cardiac arrhythmia
3.Florid Atherosclerosis
-injury to endothelium
-turbulence
4.Aneurysm
-stasis
Arterial thrombosis cause
obstruction of some critical
vessels & thrombi in cardiac
chamber & aorta Fragment
systemic embolism to brain ,
kidney, spleen, legs, other tissues
or organ. infarction
Infarct / Class / Factors
INFARCTION
Def:
Infarction: Porcess of formation of
an infarct.
Infarct:An area of ischaemic
necrosis, caused by occlusion of
arterial supply or impaired venous
drainage within an organ or tissue.
Types of Infarct
1.On the basis of their color
a.Anaemic (white)
b.Haemorrhagic (red)
2.Presence or Absence of Bacterial
contamination
a.Bland infarct
b.Septic Infarct
FACTORS INFLUENCING INFART
-Occlusion of and artery or a vein
may have little or no effect or death
of tissues & of individual.
1.The General Status Of Blood &
CVS
-Any systemic alteration such as
anaemia or hypoxaemia, that
reduces O2 carrying capacity of
blood or velocity & volume or blood
flow through tissues predispose to
infarction.
a. congestive Ht failure
b.chronic obstructive airway
diseases
c.shock
d.severer anemia
e.combination with abnormal
Hb:carboxy Hb,Sulph Hb,Met
Hb,sickle cell anemia prone to
infarcton
2.NATURE OF VASCULAR SUPPLY
A.DOUBLE BLOOD SUPPLY
Eg. Lung & liver
Lung: Bronchial & pulmonary
circulation
Liver: Portal & hepatic circulation
In individuals having normal blood &
CVS-occlusion of one system, dont
give rise to infarction.
But in the (+)ce of Ht failure, severe
anaemia or oxygenation of
blood,occlusion of one system-
precipitate infarction.
B.PARALLEL ARTERIAL SYSTEM
Eg. Fore arm & brain
Forearm:radial artery & ulnar artery
-Occlusion of one artery-dont give
rise to infarction
Brain: Circle of willis
-occlusion of one of cerebral or
cerebellar arteries-infarction of
dependent region of brain
C.SINGLE ARTERIAL SUPPLY WITH
RICH INTERARTERIAL
ANASTOMOSES
Eg.S>I, Branches or superior
mesenteric artery are
interconnected by looping arcades.
-But one of division of superior
mesenteric artery or main artery is
obstructed
-arcades cant provide
compensation casue infarction
D.SINGLE ARTERIAL SUPPLY WITH
FEW ANASTOMOSES
Eg. Kidney
-occlusion of major branches of
main renal artery cause infarction
Heart: eg. Of organ having
intermediate pattern of fairly rich
anastomosis & can compensate
narrowing or occlusion of 1 of 3
main trunks of coronary arterial
system.
3.RATE OF DEVELOPMENT OF
OCCLUSION
-Slowly developing occlusion is
better tolerated than those
occurring suddenly, since they
provide opportunity for alternative
pathways & collaterals to become
activated. Eg. Heart
4.VULNERABILITY OF TISSUE TO
HYPOXIA
-Tissues of body vary widely in their
susceptibility to hypoxia.
-Neurons of CNS- most sensitive to
hypoxia
-Glial tissues resistant to hypoxia
-Myocardial cells- sensitive(20-30
min)
Epithelial cells of PCT-sensitive (3-4
hrs)
-Mesenchymal cells of body
resistant to hypoxia.