HEMODYNAMIC DISORDERS, THROMBOLISM & SHOCK
THROMBO - SIS
Thrombo genesis is the process of forms of solid mass in circulating blood from the constituents of flowing blood.
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Thrombus: The solid mass formed is called thrombus. It consists of an aggregate of coagulated blood containing platelets other entrapped cellular elements of the blood.
PATHOGENESIS OF THROMBOSIS:
ETIOLOGY.
VIRCHOW'S TRIAD: Three primary abnormalities which can lead to the form of thrombus constitute Virchow's triad.
Endothelial injury (Changes in the wall of blood vessel).
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THROMBOSIS.
Changes in blood flow (Turbulence / Stasis).
Hypercoagulability of blood.
ENDOTHELIAL INJURY
Physical Endothelial injury
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Imp for the formation of thrombus in Heart
Mechanism
Physical loss of endothelium exposes thrombogenic subendothelial ECM
Platelets adhere to the site
Thrombotic tissue factor
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Local depletion of all antithrombotic factors-PHIL
CAUSE
Heart-chamber-endocardial injury due to MI
Valves-small thrombi found on valves-vegetations
VIRCHOW'S TRIAD
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Endothelial dysfunction
Abnormal blood flow
Normal blood flow-laminar
Hypercoagulability!!
THROMBOPHILIA
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DH+ Chronic disorder
Systemic disorder
Thrombosis
Associated with
Causes
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Blood cell state where induction by Stasis
Mechanism
Arterial ulcerated atherosclerotic plaque, vasculitis
Traumatic / inflammatory vascular injury
Capillaries vasculitis
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Valves inflammatory vascular endothelial ulceration
abnormally
to inflammatory cell
disturbs the tendency
moving layer of plasma
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Turbulence arterial
more turbulent effect of blood.
Thrombus form Heart
Arterial
disease major cause of
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Venous thrombosis
w/w prothrombotic activity MLA promotes endothelial
and thrombotic injury / dysfunction
tissue procoagulant activity
PAM, stimulation, Palurings platelets in contact with endo.
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Product of platelet tissue factor
TH12-1
Product of antithrombotic factor prevent washing of
Thrombomodulin, PEG22
turbulent endo.
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activated clotting factor.
prevents flowing out of
Causes
MI
deficiency of Antithromlister factors
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Protein C
Protein S
Antithrombin III
Increased Prothrombotic Factor
APC resistance
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Increased Prothrombin (II)
Factor 9,10,1,8,9,11
Non Milleteranet factor
Fibrinogen. (I)
Acquired disorder.
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Prolonged bed rest
MI / atrial fibrillation
Tissue injury Hungry
of fracture
cancer.
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TAP(hypertension), Causes
tunnel land for Heart / area firmer / arrhythmia
aquatic musk Arterial ulcerated Atherosclerotic plaque
yeim - saphenousy with vein contier,
Radiation injury.
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metabolic abnormalities
Homocystinuria
deep-y.
polycythemia vera.
hypocholesterolemia Rac acsoraus- en all
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anarmia.
Main cause.
Rate of blood flow
Usual type of thrombus
Common site-
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Color
Composition
Lines of Zahn
Propagation
Effects:
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Aspirin
ARTERIAL THROMBUS.
endothelial injury.
rapid
Mural thrombus - attached to the wall of the blood vessel.
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projects into the lumen (without complete occlusion
Heart chamber
aortic lumen.
Aorta, coronary A,
cerebral A, femoral A.
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gray-white
friable meshworks - fibrin, platelets,
RBC & degenerating WBC.
Retrograde manner from the
point of attachment of thrombus
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(i.e. towards the heart).
Ischemia (+tissue supply)
infarction of the area supported by A coronary
thrombus
VENOUS THROMBUS
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stasis
slow
Occlusive thrombus-Occludes the level of the vessel
small/met rise A.
superficial y vesicaritra &
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deep y. of leg.
blue-red.
more RBC,
relatively fewer platelets
less prominent
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Antegrade manner from the point of attachment of
thrombus towards the direction of blood flow
(i.e. towards the heart).
Thromboembolism,
edema, ulceration.
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Warfarin
Heparin
v. Thrombosis.
PALLEROTHROMBOSIS / VENOUS THROMBOSIS
Dy - Thrombosis of venous kupuprias veins of the
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deep veins of leg
Phelchothrombosis-
superficial venous Thrombus
site saphenous y
Pathogenesis
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Deep y. Thrombus (DVT)
Largely in leg / above knee
popliteal vein
femoral vein
iliac vein
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Primary platelet thrombus Damage to the endothelium
Coralline Thrombus platelet adhere to site of injury.
fibrin thrombus manager further.
accumulation of platelets
form
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fibrin & platelets with
(LINES of ZAHN)
alternate layer of the
trapped blood vessel
of thrombus
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Occluding Thrombus further growth of thrombus
occludes the lumen of vein
Consequtive Thrombus occluding thrombus stops releases
blood column beyond occluding thrombus
THROMBOPHLEBITIS
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to the endocarditis may lead to pneumonia
form
Thrombus form a freely started
mliore
Arterial / venous thrombosis may be formed
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Comment.
THROMBUS
Thrombus is the solid mass that is formed in circulation, from the constituents of the flowing blood.
always formed in vivo, within the circulatory system.
Activation of platelets is mandatory.
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we can conclude that a thrombus differs from a clot.
CLOT
clot is solid mass that is formed from the conversion of soluble fibrinogen
molecule polymerized fibrin
in e vivo, as well as in vitro in test tube
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Activation of platelets is not essential.
SHOCK
shock #BPK FCo
TYPES OF SHOCK:
CAUSES/ETIOLOGY:
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Blood loss
systemic vascular resist/
Total peripheral Resistance.
GIT bleed (peptic ulcer).
Abdominal aortic Aneurysm (AAA)
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Trauma.
post-partum hemorrhage. (PPH)
ectopic pregnancy.
Hemoptysis (Coughing es blood).
Non blood fluid loss.
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Severe plasma burn
excess vomiting.
diarrhea.
bowel destruction.
Pan Acute pancreatitis.
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pancratic protease
progressive proven
Q. How does the body compensates
medullary
centre
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sund AP from medulla
gou to
achial masth myk
within Tunica medes
of Wand vessel
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release choo
LIRI NE
cause the blood
Baroreceptors
Amuch cerated time)
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goes to the heart
try to THR
stroke vol
dependiono
Esv
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Aldosterone
TIG4 retwe
Enough blood vel
veret to commier (?a? a?s
Blood volume
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Blood volume
Low blood pressure followed by partially tang
Low blood volume
Increased systemic vascular Resistance.
Increased CBC. [ + hemorrhage
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hemorrhage
Acidosis
You Coss wrthe outp
puglycemia
loct. En watu
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athu.
watu u tour).
ruistanu
TBP
AP
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CLINICAL MANIFESTATIONS Blood vel
TH.R. (Tachycardia) non was tund Lond
The maracul - Hemowncentar
hematocril
CYANOSIS.- bluish cast on lepsi
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tongue tinguips, tou
Hypoxia ischemia necrom
rv fluid moune
multisystem organ failure
crystallards
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Normal
Ringu
Allumin, Stall
Herasraich w?
DISTRIBUTIVE SHOCK:
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Pathogenesis of circulatory shock:
Hypovolemic shock.
blood loss,
loss of plasma,
loss of fluid.)
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septic shock
(Gram tue septicemia,
Gram -ve septicemia)
cardiogenic shock
damage)
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Effective circulation
blood you chypri
venous Return to heart
C.O
Blood flow)
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02 supply (Hypots)
Anoxia.
newm
inflammatory mediato
SHOCKA Orga falle
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death.
10-0
BPICUR
blund ferme dilates
SYR
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? ?
deling
hypoxia
ischemia
PRISSUR
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ENDOTOXIC AU
Page
erstrilecctive thoik.
SEPTIC SHOCK. mapayasitec
thank
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DIC (Disseminated intravasculen
waguler)
Ischemia
Grame
Gram
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cam we list
damage here
Assues relea
chemical mediatan of
innamm
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P417
neconeg
Grame ?
Endotoxins.
TPAI-1
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microveruda
cun
Gat cra
Prateese
63
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65
27
most ter
PG
WBG.
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ROS
21
PP.
Chemotactic
Agents
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PAI
TRA
Usta
most elh.
Lelinas Hist
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Luckorima
Phi
Protease
the blood flow to fishe
9schemia
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I clat forum
Chemotactic Ageur
diate letond veci Iveredriam
make wood vesser vleeky (+plumeatsilery)
wood starts accumulating in tisme space
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BY+BP
monocyter & neurophet (WBG+
Release L
AL6
NEL
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Chemotactic Agent pull them out
Proteaser
3,5
blood you
B.P.
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neuroph
(39+159
I myocardies contrachtility
Gram-ve eace.
INF-2
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12-6
11-8
hypochasamu. PGE2 Fever.
liver Acute phase Reactiver like C-peptide
Pratim.
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Endothelial cells.
I permeaternity of endothelial cells.
401
yaradilar
go to hypothalam
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Release PH-EL
Change leody's thermo
reading
FIVO
goes to Live
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2-8
WAG
release ROS.7
12-2
TNF
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myocardial
Liver
contactilulity
class Aud
Disle
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Page
froducer Acite phase Reactive from
indi cetor that there is
lot of inflammat.
Other INBLS
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phagocytic Activity
I chemotaxis
Foru
I incidence of metro ve belt oldum
DIC
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Ischemia
1.4. annuatics-leroad specmem Alo
Crystalloids - 1x fhurd mitusion.
damage endothelial cells.
A/c - Vircho's riad.
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? Thromleont
NAW
AAL
DISEASES OF THE IMMUNE SYSTEM
Type I- HYPERSENSITIVITY.
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Hypersensitivity Reactions are Ag specific
AL
Ag
Ag exposure
(drug,
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pacien/
cood)
sensitisation of immune calle
(Primes the i'mmene system
against that Ag).
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Primed immune celk.
towards the Ag?
APPROPRIATE
MMUNE
RESPONSE.
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Type I
Type II
Type?
Type
wl mediated.
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19./ All. mediated
HYPERSENSITIVITY Ron Type-t
Immediate Reachan (Allergen ein tron)
occurs vay 108
invalues re
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recognit of ng lay porre the
?
nucleus gene
will produce (12-2)
Receptor for (12-2)
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gives signal to the cell
I uu-undergon mitose (clonal
expansion of tal)
moobropun
[12-4 ?
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binds to receptors Me
on B-cele
senutive. L
Bellen B cells starte mulhplyny
Jonal expansion of fate,
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B-cells cxpress receptas of
14-5
12-5-leinch to Receptor
all Race convert into
Plasma cells
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secrete IgE (Antipolla
(61
Ige has special recepto
on mast cell.
Agu picked
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up by
APL
B
ANTIGEN
(Allergen)
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Pollen
Food
brug
BCRYL
Bell-4-Receptor
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125-Recepte
Plein
secrète ante paller
Anilendia (IgE)
mast celn & leasophie dee IgE loaded
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mast
HLA
Preparation o? ? ? ?mwhacky
genes
12-2
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12-5
Chrowse
CD-4
Macrophage
74
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C83
nucleus
Thell
thelper-ach
Coll
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CYCRACO-A
are stimulated)
In repertory marep?
braktown pallen ng
on partially
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MHC-2017 Misceler
Lunca to pallen.
palle unor pueneu
degraded
pallen Ag will now bee
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of
exprested on the huface
APL)
macrophage along z
MHC-class molecu
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manaphage will musht
2N.
will find special type of
Tell having TERCIOUR
CA-Y
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Lind to MHL-?
Mype I-hypertensensitivity Rem
BULG
Goss linking of Igr
bby Allergen
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(za, Ga, Csa
brugs-codeine,
morphine
venome-snake bite/
Ree sting / And string
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phywlal Agure-
cold, heat,
physical Naums,
strong sunlight
plasma uel
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MOAL ULLE
Histamine
Tinglampratcases
midiaren
have
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Ron
mau cech
further stimulates
mast ulls.
CSA
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produce.
E.C.P
MEDIATOR
Gonage preformed
LATE
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granulse
MEDIA
neutrophil chemotactic facta (NCF)
cosinophilee"
Histamine
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vasodilaran
SECONDARY
MEDIATOR: try
CYTOKINES prese?
Hist R. on Lersuchral bussta w/
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I permeaterlity
Spasmogenic
Igrandalar ciner
pithelial cells.
Eotaxin
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bronchocomwhich
TNE
21
12-4
4-5
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12-6
GH-CSE
MIP
AA
yuw
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?-?
pathway
LT-R
Sathway
PG &
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LT-04
PGPH PG
22 F2
LT-E4
I glandulr
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spashiogene
lecer
Agent knowh
12-37J-help-2.
12-5 & mast alh LT-Cy
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? ? ?
-wnshichon var ogumie
damage
epit
sithelias
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cells
Eosinophile.
Groncho
(Major leaseipr
syspnew
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M-B-P
Type - Hypersensitivity Reaction
Immune mediated tissue damage.
Immune complex Inflamm"
Free. Ag. Exogenous.
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Endogenom
BOCHU
Fungal
Viral!
-
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SLE.
Ale
IgG
IgM
Ag the complement Achram & through
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i matiune comples
wif Lahmn alory
all (?)
INFLAMMATORY RXM.
Hype III H.R.
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yeneralised Ren.
(Serum sickness like Ron)
These days, it u
Localised exn.
(Arthur RXN
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due to duge.
IMMUNE COMPLEX MEDIATED IT-ITI HYPERSENSITIVITY RIN
infleted.
AT GEAR LULE Immune
globulini)
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Bone ma
sympand
Syster
Auto Reactive
Julh
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Myeloid
irculatory wintroduced.
Unage
Aplast
autore achive JULG.
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destrays.
no af/Raut, waatlemes than tympasyon) prarecer!!
Anemia Leukopenia
Thrombocytopme
RBU Platelet WB
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?
ymphay APLASTIC
PANCYTOPENIA
? ?
PANCYTOPENIA
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hone marrow cells destisyed Hypocellular/hypoplas
leone marrow
AMYLOIDOSIS
Amyloid depour
Amyloiasis i a disorals deve to alinormal ca
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of "pretum
on Amyloidosis
for these of connal mech.
PATHOGEN
sauce of misisided for yougraden Producion of abnormal
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tha
accumulate outside
the wlw.
nerable I self associated.
deposited as
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filerils in extracellula
spor
PATHOLOGICAL EFFECTS
of normal protein
Unknown (? Carcinogen
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monoclonal praciociation
ef Blympiseyter
plasma cells.
A Light chains of 19
Pressure on adjacew normal celu
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Atrophy of alle
imomplete
lbreak down
aut
seposition in wall of Wood Amyloid light (AL)
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