hyperemia&congestion 2003
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Over Hydration Normally excess of water consumed are shade o
by body & no ill eect are there. In condition kidney ability to diluteurine has been reduced the overload of water take place leading toexpansion of extracellular compartment uid. It lead early diaurasisfollowed by oliguria or anuria due to damage renal tubules
Causes Acute & chronic renal failure !ever "#$ Addision%sdisease cirrhosis liver & early post operative phase.
Clinical efect isordered cerebral functionNauseavomitingheadachconfusion
Plasma changes are reduce serum electrolyte& 'osamolity'plasma protein & low (")
Dehydration*ay be either pure water de+ciency or water &
electrolyte combined de+ciency Pure water is relative uncommon +rstly there is withdrawal of uid
from interstial space & cellular depletion of water along withpotassium which in result in renal insu,ciency leading to sod.-etention & potassium depletion
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Causes e+cient water intake due to obstructiondysphagiaor excessive loss of water in diabetesinsipidushyperparathyroidismhyperapnoea
Clinical efect intense thirst mentalconfusionfeveroliguria(lasma changes in (")plasmaprotein /lood urea !erum sodium
Combined sodium & water deciency more common fallin volume of intra vascular uid in early stage sod. 0evelremain normal but later fall
Causes1I disorder sever vomitingdirrhea excessiveperspiration diurasisexcessive blood loss
Clinical efect sign & symptom of dehydration shrunkeneye thready pulse cold & calmly skin perspiration dry tongue
Plasma changes ' sodium(")/lood urea (lasmaprotein
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Hypernatremia#igh sodium contain of plasma normal
234 to 254 m678l Causes(ure sodium excess -etention in "ushing
syndromehyperaldosteronism
"ombined water & sod loss 6xcessive sweating
heat stroke(olyurea (ure water de+ciency 0ake of water
intakedysphegiaobstruction
Hyponatremia0ow !od. "ontent
Cause 6xcessive use of iuretics Addisiondiseaseirrheavomitingchronic renalfailurehypoaldosteronism
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Hypokelemia low Potassium in serum Normal 3.8 to4.5mEq/l
Cause Excessive retention Oliguria,Renal tubular
!s"unction,#ernal cortical insu""icienc!
Excessive inta$e o" iureticExcessive mobilisation o" intracellular Pot. %uscle necrosis,
&iabetic aciosis, 'se o" igitalis grou( o" rugs
Hypokelamia)ow Pot. *n serum
Causes Excessive loss "rom +.*.,ien! *nsulin t-era(!
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Metabolic Acidosis $all in /lood p# due to low bicarbonat & high#9 inos inblood
Causes0actic Acidosisin vigrous excerisesshock iabeticketoacidosisstarvation
It stimlate respiratory center so deep & rapid respiration & fall in plasmabicarbonate
Metabolic alalosis cause due to loss of #9 ions & in bicarbonate
Causessever & prolonged vomitingAdminstration of strong alkaline saltlike sod.bicarbonate#ypokalaemia
Cinicallycharacterised by 'respiration '-enal function with :remia bloodbicarbonate level
!espiratory Acidosis $all of /lood p# due to (co; leadingunderventilation
cause co; retention & acidosis CausesAirway obstruction in Asthma"hronic /ronchitis
-estractive respiratory movement (leural eusionAscitis(regnancy
Impaired Neromuscular function (oilomylitis(olyneuritis
Clinicallyperipharal vasodilation& Intracrainal pressure ue to "o;retention (t. evelop confusiondrowsiness & coma
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!espiratory Acidosis $all of /lood p# due to (co; leadingunderventilation
cause co; retention & acidosis CausesAirway obstruction in Asthma"hronic /ronchitis
-estractive respiratory movement (leuraleusionAscitis(regnancy
Impaired Neromuscular function
(oilomylitis(olyneuritis Clinicallyperipharal vasodilation& Intracrainal pressure ue
to "o; retention (t. evelop confusiondrowsiness & coma
!espiratory Alalosis blood p# due to lower (co; due tohyperventilation of lung
Causes #ysterical overbreathing
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"ype Acidosis Alalosis
Metabolic '(lasma /icarbonate iabetic (lasma/icarbonate sever
"oma!tarvation(rolonged dehydration massiveblood
exceriseAsthama:remia !hock transfusion
!espiratory '"o; clerancepco; ' /lood p# co;loss'pco;/lood p#
"=(6mphysmaAsthama #yperventilation inhypoxia high
(ulmonary oedema
alltitudeconvelsionhigh fever :nconsciousness septicaemia
Combined pco; with 0actic acidosis 'pco; with loss ofbicarbonate
circulatory failure cardiac excessive treatmentfor acidosis
arrest respiratory distress
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HYPEREMIA ( ACTIVE )
CONGESTION ( PASSIVE )
Acute
OrChronic
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Increased volume of blood in dilated blood vessels oforgan or tissue
Increase volume of blood in arteries or arterioles isactive hyperemia
Impaired drainage of blood from venous drainage called
venous congestionAC"#$% HP%!M#A
Inammation any where cause hyperemia in local part
/lushing response of emotions
*enopausal ush
*uscular exercise
#igh grade fever
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ilation of veins & capillaries due to impaired
venous return is passive hyperemia or venouscongestion
It may be local in any part of body due to obstructionor in case of portal hypertension or due to pressure
on vessels in tight bandage plasters tumorspregnancy hernia etc.
'ystemic venous congestion
ue to heart failure -ight side failure all systemic
organ except lung 0eft sided failure cause
congestion lung
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0
CHRONIC VENOUS CONGESTION ( C.V.C ) LUNG
CHRONIC VENOUS CONGESTION ( C.V.C ) LIVER
CHRONIC VENOUS CONGESTION ( C.V.C ) SPLEEN
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=ccur in left sided failure due to rheumatic mitral stenosis sever *.I.
Mechanism "#$>reduce blood ow to lung>"hronic passive pulmonary
congestion>Increase pressure in alveolar capillaries & +lles with bloodConse(uences
Micro haemorrhage minute haemorrhage in alveolar capillaries -elaseof -/" #b breakdown liberation of haemosidrin engulf by alveolarmacrophages.
Pulmonaery odema
)ibrosis
Pulmonary hypertension
*ross0ung is heavy +rm on cut section surface dark brown congestedcalled brown induration of lung
MicroscopicallyAlveolar septa widened due to edema & dilated
congested blood vessels. "apillary slightly thickened. -upture of capillariescause intra alveolar hemorrhage. /reakdown of -/" released hemosiderinpigment which are taken up by macrophages giving brown discolorationcalled heart failure cells
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4
C+$+C+ ,-.*
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C.V.C LIVER
Occur in rig-t sie "ailure rarel! in constractive
(ericaritis 1 obstruction o" in"erior venacava%ec-anism &ilatation o" central vein2ransmission o"
(ressure to sinusoi2ilartion o" sinusoi2isc-emic
necrosis o" centrilobular region
Grosslyliver enlarge tener tense ca(sule cut sur"ace
s-ow nutmeg a((earance re 1 !ellow mottle
a((earance
Microscopicallycentrilobular congestion lea to
-!(oxia at (eri(-ar! causes "att! c-anges .
entrilobular -e(atoc!te unergo -emorr-agicnecrosis -eale b! "ibrosis 1 causes istortion o"
lobular structure leaing to cariac cirr-osis
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ue to ri!ht"#i$e$ c%r$i%c E
co&'en#%tion En%r!e$ * ten#e * c+%notic i,er -ithroun$e$ e$!e#
Con!e#tion o centrio/u%r #inu#oi$#Atro'hic centrio/u%r he'%toc+te#
M%r0e$+ %ttenu%te$ i,er ce cor$#
Let"#i$e$ c%r$i%c %iure or#hoc0
Le%$# to he %tic h o eru#ion %n$
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Co&/in%tion o h+'o 'eru#ion
%n$ con!e#tionLe%$# to centrio/u%r he&orrh%!icnecro#i#V%rie!%te$ &otte$ %''e%r%nce
Sh%r' $e&%rc%tion o ,i%/e 'erior%2 necrotic centrio/u%rhe'%toc+te#
Re$"/ro-n $e're##e$ %re%#( centrio/u%r )T%n cooure$ #urroun$e$ %re%#( 'eri'ort% )
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0
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03
C+$+C+,#$%!
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=ccur in right sided failure
*rossly In early stage spleen is moderately enlargeup to ;4? gm in comparison normal 24? gm. Inprogressively failure it may weigh 4?? to 2???gm.eeply congested capsule tense cyanotic cut surfacegrey tan color
Microscopically -ed pulp shows congestion &marked sinusoidal dilation with area of recent & oldhemorrhage. #emorrhage gate organi@e & formed1amma 1andy bodies !idero+brotic noduleB which
have deposit of hemosiderin pigment calciumdeposit & +brosis. -eticulin net work& +brousnetwork thickened
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06
C+$+C+ 'P,%%.
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6scape of blood from vessel either out side or in internalorgan is hemorrhage
6xtravasation of blood into skin called #ematoma (urpara are small areas of hemorrhage less than 2cm. In
si@e
(etechiae are minute pinheaded hemorrhage
Causes o/ Hemorrhage Crauma of vessels or penetrating wound -oad side
accident
!pontaneous hemorrhage rupture aneurysm /leedingdiathesisvericose veins (eptic ulcer
Neoplastic invasion
)ascular disease
6levated pressure in /lood vessels
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6ect depend on 3 main factors Che amount of blood loss
Che speed of blood loss
Che site of hemorrhage
0oss of ;?D suddenly or slowly up to 4? D have littleclinical eect
A sudden loss of 33D may cause death while loss upto 4?D slowly in ;5 hours is not fatal