Over Hydration Normally excess of water consumed are shade off

by body & no ill effect are there. In condition kidney ability to dilute
urine has been reduced the overload of water take place leading to
expansion of extracellular compartment fluid. It lead early diaurasis
followed by oliguria or anuria due to damage renal tubules
Causes Acute & chronic renal failure, Sever CHF, Addision`s
disease, cirrhosis liver & early post operative phase.
Clinical effect Disordered cerebral function
Nausea,vomiting,headach,confusion
Plasma changes are reduce serum electrolyte& osamolity
plasma protein & low PCV
Dehydration May be either pure water deficiency or water &
electrolyte combined deficiency
Pure water is relative uncommon firstly there is withdrawal of fluid
from interstial space & cellular depletion of water along with
potassium which in result in renal insufficiency leading to sod.
Retention & potassium depletion

Causes Deficient water intake due to obstruction,dysphagia

or excessive loss of water in diabetes
insipidus,hyperparathyroidism,hyperapnoea
Clinical effect intense thirst, mental
confusion,fever,oliguria,Plasma changes in PCV,plasma
protein Blood urea, Serum sodium
Combined sodium & water deficiency more common fall
in volume of intra vascular fluid in early stage sod. Level
remain normal but later fall
Causes GI disorder ,sever vomiting,dirrhea excessive
perspiration diurasis,excessive blood loss
Clinical effect sign & symptom of dehydration shrunken
eye thready pulse cold & calmly skin perspiration dry tongue
Plasma changes sodium,PCV,Blood urea, Plasma
protein

Hypernatremia High sodium contain of plasma normal

135 to 145 mEq/l
Causes Pure sodium excess ,Retention in Cushing
syndrome,hyperaldosteronism
Combined water & sod loss ,Excessive sweating
heat stroke,Polyurea
Pure water deficiency Lake of water
intake,dysphegia,obstruction
Hyponatremia Low Sod. Content
Cause Excessive use of Diuretics Addision
disease,Dirrhea,vomiting,chronic renal
failure,hypoaldosteronism

Hypokelemia low Potassium in serum Normal 3.8 to

4.5mEq/l
Cause Excessive retention Oliguria,Renal tubular
dysfunction,Adernal cortical insufficiency
Excessive intake of diuretic
Excessive mobilisation of intracellular Pot. Muscle necrosis,
Diabetic acidosis, Use of digitalis group of drugs
Hypokelamia Low Pot. In serum
Causes Excessive loss from G.I.,Kideny Insulin therapy

Metabolic Acidosis Fall in Blood pH due to low bicarbonat & highH+ inos in
blood
Causes Lactic Acidosis,in vigrous excerises,shock Diabetic
ketoacidosis,starvation
It stimlate respiratory center so deep & rapid respiration & fall in plasma
bicarbonate
Metabolic alkalosis cause due to loss of H+ ions & in bicarbonate
Causes sever & prolonged vomiting,Adminstration of strong alkaline salt
like sod.bicarbonate,Hypokalaemia
Cinically characterised by respiration Renal function with Uremia blood
bicarbonate level
Respiratory Acidosis Fall of Blood pH due to Pco2 leading
underventilation
cause co2 retention & acidosis
Causes Airway obstruction in Asthma,Chronic Bronchitis
Restractive respiratory movement Pleural effusion,Ascitis,Pregnancy
Impaired Neromuscular function Poilomylitis,Polyneuritis
Clinically peripharal vasodilation& Intracrainal pressure Due to Co2
retention Pt. Develop confusion,drowsiness & coma

Respiratory Acidosis Fall of Blood pH due to Pco2 leading

underventilation
cause co2 retention & acidosis
Causes Airway obstruction in Asthma,Chronic Bronchitis
Restractive respiratory movement Pleural
effusion,Ascitis,Pregnancy
Impaired Neromuscular function
Poilomylitis,Polyneuritis
Clinically peripharal vasodilation& Intracrainal pressure Due
to Co2 retention Pt. Develop confusion,drowsiness & coma
Respiratory Alkalosis blood pH due to lower Pco2 due to
hyperventilation of lung
Causes Hysterical overbreathing,Working at high
temparature,At high altitude,Meningitis,encaphalitis
Clinically there is peripharal vasoconstraction headach,teneny

Type
Acidosis
Metabolic
Plasma Bicarbonate Diabetic
Bicarbonate, sever

Coma,Starvation,Prolonged
blood

excerise,Asthama,Uremia ,Shock

Alkalosis

Respiratory Co2 clerance,pco2, Blood pH

loss,pco2,Blood pH
COPD,Emphysma,Asthama
hypoxia ,high
Pulmonary oedema,
alltitude,convelsion,high fever
Unconsciousness
Combined
pco2 with Lactic acidosis
bicarbonate
circulatory failure cardiac
for acidosis
arrest, respiratory distress

Plasma
dehydration, massive
transfusion,
co2
Hyperventilation in

septicaemia
pco2 with loss of
excessive treatment

HYPEREMIA ( ACTIVE )
CONGESTION ( PASSIVE )
Acute
Or
Chronic

Increased volume of blood in dilated blood vessels of

organ or tissue
Increase volume of blood in arteries or arterioles is
active hyperemia
Impaired drainage of blood from venous drainage called
venous congestion
ACTIVE HYPERMIA
Inflammation any where cause hyperemia in local part
Blushing response of emotions
Menopausal flush
Muscular exercise
High grade fever

Dilation of veins & capillaries due to impaired

venous return is passive hyperemia or venous
congestion
It may be local in any part of body due to obstruction
or in case of portal hypertension or due to pressure
on vessels in tight bandage plasters tumors
pregnancy hernia etc.
Systemic venous congestion
Due to heart failure Right side failure all systemic
organ except lung
Left sided failure cause
congestion lung

CHRONIC VENOUS CONGESTION ( C.V.C )

LUNG

CHRONIC VENOUS CONGESTION ( C.V.C )

LIVER

CHRONIC VENOUS CONGESTION ( C.V.C )

SPLEEN
12

Occur in left sided failure due to rheumatic mitral stenosis ,sever M.I.
Mechanism CHFreduce blood flow to lungChronic passive pulmonary
congestionIncrease pressure in alveolar capillaries & filles with blood
Consequences
Micro haemorrhage minute haemorrhage in alveolar capillaries Relase
of RBC Hb breakdown liberation of haemosidrin engulf by alveolar
macrophages.
Pulmonaery odema
Fibrosis
Pulmonary hypertension
Gross Lung is heavy firm on cut section surface dark brown congested
called brown induration of lung
Microscopically Alveolar septa widened due to edema & dilated
congested blood vessels. Capillary slightly thickened. Rupture of capillaries
cause intra alveolar hemorrhage. Breakdown of RBC released hemosiderin
pigment which are taken up by macrophages giving brown discoloration
called heart failure cells

C.V.C. LUNG

14

C.V.C LIVER
Occur in right sided failure rarely in constractive
pericarditis & obstruction of inferior venacava
Mechanism Dilatation of central veinTransmission of
pressure to sinusoiddilartion of sinusoidischemic
necrosis of centrilobular region
Grossly liver enlarge tender tense capsule cut surface
show nutmeg appearance red & yellow mottled
appearance
Microscopically centrilobular congestion lead to
hypoxia at periphary causes fatty changes .
Centrilobular hepatocyte undergo hemorrhagic
necrosis healed by fibrosis & causes distortion of
lobular structure leading to cardiac cirrhosis

Due to right-sided cardiac DE

compensation :
Enlarged , tense , cyanotic liver with
rounded edges
Congestion of centrilobular sinusoids
Atrophic centrilobular hepatocytes
Markedly attenuated liver cell cords

Left-sided cardiac failure or

shock :
17

Leads to hepatic hypo perfusion and

Combination of hypo perfusion

and congestion
Leads to centrilobular hemorrhagic
necrosis
Variegated mottled appearance
Sharp demarcation of viable perioral
&
necrotic centrilobular
hepatocytes
Red-brown depressed areas
( centrilobular )
Tan coloured surrounded areas
( periportal )
18

21

C.V.C.LIVER

23

Occur in right sided failure

Grossly In early stage spleen is moderately enlarge
up to 250 gm in comparison normal 150 gm. In
progressively failure it may weigh 500 to 1000gm.
Deeply congested capsule tense cyanotic cut surface
grey tan color
Microscopically Red pulp shows congestion &
marked sinusoidal dilation with area of recent & old
hemorrhage. Hemorrhage gate organize & formed
Gamma Gandy bodies ( Siderofibrotic nodule) which
have deposit of hemosiderin pigment calcium
deposit & fibrosis. Reticulin net work& fibrous
network thickened

C.V.C. SPLEEN

26

Escape of blood from vessel either out side or in internal

organ is hemorrhage
Extravasation of blood into skin called Hematoma
Purpara are small areas of hemorrhage less than 1cm. In
size
Petechiae are minute pinheaded hemorrhage
Causes of Hemorrhage
Trauma of vessels or penetrating wound Road side
accident
Spontaneous hemorrhage rupture aneurysm, Bleeding
diathesis,vericose veins Peptic ulcer
Neoplastic invasion
Vascular disease
Elevated pressure in Blood vessels

Effect depend on 3 main factors

The amount of blood loss
The speed of blood loss
The site of hemorrhage
Loss of 20% suddenly or slowly up to 50 % have little
clinical effect
A sudden loss of 33% may cause death while loss up
to 50% slowly in 24 hours is not fatal