Download MBBS 2nd Year Extrinsic Hemolytic Anemia Notes

83-88 Extrinsic Hemolytic Anemia 83

Non 9. Mediated

Mechanical Cause

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Macroangiopathie H.A

Micro H.A

Maero Angiopathies H.A 19

Mech Cardiac valve.

tex is prosthetic aortic valve.

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- Itere is a leak at its side

while RBC passes through this leak it is destroyed)

Calcific Aortic Stenosis

March hemoglobinuria

Bongo Drummer

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Micro Angiopattries H.A.

DIC fibrin platelate T.T. PC Thrombotic

Thrombi Thrombi HUS

In Such Cases RBC are Segmented known as

Schistocyte, Triangular cells

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Helmet cells

It is an example of Intravascular hemolysis

Examples

DIC

TTP

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HUS

84

DIC:

Fibrin Intra vascular

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Hemolysis

(when RBC passes

throug fibrin strands)

Primary Problem is Widespread activation

of Coagulation system.

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Coagulation :-

Soluble fibrinogen Insoluble fibrin

Contact

XII; XIla

Intrinsic pallu

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XI xla

1x 1x2

X xa

Extrinsicpati

VI

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PIT Thrombin

Soluble

fibrinogen

Insoluble

Hion of Coagulation system fibrin

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• AML
• Septecemia (Endotoxin)
• Obstetric Complications (Amniotic fluid)
• Cancer
• Massive tissue damage...

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Not Only Anemia Occurs but later on platelate

also used Platelate No

85

As in this process Clofting facters

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cons ome d platedate anc

It is known as

Consumption Coagulopathy.

pt Start bleeding

eg PPHC Post partum Heamorrhage)

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Steps

1. wide spread Endo damage
2. actruation of Coagulation factor
3. Lot of fibrin Strands
4. A of Ruation for gmentiationic System

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5. Bleeding tendencies

Platelate Thrombi

T.T.P HUS

Platelate plug

Fibrin Around

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thiem

Primary Problem is wide spread

Platelate activammy aggregation.

86

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T.T.P:

Some many platelate thrombi are formed

that many many platelate are

used leads to small

Hearmorbo-ge ie purpura

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Cause This Pr

ADAMTS13 Normily cuts

VWF vwf &

Prevent

Extra accombe

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Any defect in this pr

leads to T.T.P.

1. In berite d defect
2. Acquired defect (auto antibodia)

This is one of Metaloproteinase Enzyme

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then level of VWF Des

they help the plate late to Stick

to each other & to Endothelium

So all platelate Consumed leads to

Thrombotic thromocytopenic purpure

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Clinically:

• Fever
• Microangio pathic H.A
• Ischemia Renal sys due to blockage
• damage ?CNS of Micro circulation

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87

• Transief Neorological deficit
• Renal failure (Nephropathy)
• Jedplatedate

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HUS:

they have eaten Undercooked food

with special type of Ecoli

0157 Mz

pt in Childhood developed Ecoli

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induced Sastroenteritis

Shiga toxin is also produced by

Ecali

It damges Endo platelate stick

Endothelium & Platelate frogmot

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Intravascular Hemolysis.

In this case Renal damage is more

than those in T.T.P such Sevhe

damage to glomeruli leads to

Uremia

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CNS does not Suffer

TIT.P HUS

1. Micro angiopathic HA Mico angropattettem
2. Plate la te def platelate def
3. CNS Involumant No CNS Involvenet

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4. ces Renal damage More Renal damage
5. Normal, P.T & PTTT PTCT Normal
6. dense platelate age dense Platelate oss

88

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DIC

(prothrombin time) P.T ?

(partial Thromboplastin P.T.T ?

time)

d dimer (aclivaled fibrin)

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Immue Medecked

9so Ab Auto Ab

Warm Cold Cold

ABO RH agglutinn Hemolysis

Incompatibility

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