disorder of blood flow

1. Disorder of blood flow
By
Shatha al sulh

2. 1-Hyperemia & Congestion
hyperemia congestion
Local increase of blood Local or general (each
acute or chronic)
Due to active VD Passive dilataion (due to
incresed blood flow or
venous outflow
obstruction)
Of arteries, arterioles &
capillaries
Of veins, venules &
capillaries
e.g: inflammation

3. Acute local venous congestion
• Aetiology: sudden occlusion of vein.
• Effect: sudden venous congestion:
– Edema.
– Hrge.
– Infarction & venous gangrene (rare).

4. Chronic local venous congestion
• Aetiology: gradual incomplete venous
occlusion as in : Pregnancy, cirrhosis or
portal fibrosis , MS, LVF.
• Pathology & effects:
– Chronic dilatation of veins, venules &
capill.:
• Edema.
• Hrge.
• Stasis thrombosis.
• Gradual opening of collaterals.
• varicosities

5. Chronic local venous congestion (cont.):
• E.g:
• CVC of lungs:
– Aetiology: MS or LVF.
– Gross:
• Early: dark red, moist, heavy.
• Later: brown induration.
– M/P:
• early: congested intra-alveolar capillaries + edema + hrge +
HF cells
• Late: hemosiderin + fibrosis.
– Clinical effects: dyspnea & hemoptysis.
• Liver cirrhosis or fibrosis :  obst. of veins
portal hypertension.

6. General venous congestion
• Due to total (Rt & Lt ) heart failure So Congestion occurs all over
the body.
• 1- Acute
– in acute H.F all organs show acute rapid generalized congestion &
generalized edema.
• 2- Chronic
– Def : gradual venous congestion affecting the whole venous system.
– Causes : both Rt. Sided & left sided H.F.
• Rt. Sided H.F.: show chronic venous congestion all over the body except
lungs.
• Left sided. H.F.: show chronic venous congestion of lungs
– Pathology of Rt. Sided H.F. :
• I-General effects
– 1- Congested neck veins
– 2- Cyanosis = purple - blue coloration of lips, bed of nails ... Etc due to ++
reduced Hb & inadequate tissue perfusion & - - oxygenation.
– 3- Cardiac edema : in dependent parts of the body =Gravitational edema
( discussed later in edema )
– 4- increase blood volume due to increased Na & H2O retention.

7. Chronic generalized venous congestion
• II: local effects : (organ lesions)
herat lung liver spleen kidney Stomach,
intestine
& viscera
Marked
dilatation
of RV &
RA.
As GVC.
When cause
of RSHF
started in
the left side
of the heart
Gross:
• early: enlarged & heavy, cut
section (nutmeg appearance).
•Later: cardiac cirrhosis
(shrunken, firm,irregular
surface +/- regeneration
nodules).
Gross:
enlarged,
dark.
Gross:
enlarged
,congested
congested
M/P:
•congestion (central v. &
sinusoids) pressure atrophy
of central hepatocytes +
steatosis at perepheral cells +
hemosiderin in kupffer cells.
•Later: fibrosis +/- regeneration
nodules.
M/P:
congested
sinusoids.
Clinically:
hematuria.

8. 2- thrombosis
• Definition:
–thrombus :
• solid compact mass.
• formed inside CVS
• during life
• from circulating blood constituents
(platelets, clotted blood [fibrine+blood
cells]).

9. Aetiology:
• Endothelial injury:
– Causes: atherosclerosis, trauma, inflamm.
– Lead to:
• exposure of subendothelial collagen to which plt. Stick firmly.
• Release thrombotic & antithrombotic factors.
• Alteraion in blood flow:
• Change in blood composition: as polycythemia, leukemia,
dehydration, increased fibrinigen, macroglobulinemia.
• Hypercoagulability of blood: alteration in clotting michanisms.
– Inherited: lack natural anticoagulants.
– Acquired:(unclear michanism)e.g: OCP, HF, surgury, burn, sever trauma.
stasis turbulance
Stasis lead to platelet deviation from axial
blood stream to contact with endoth.
Deviation & destortion of bl.stream that hits vs. & cardiac
lining= plt.deviation + endoth.damage, associated with
stasis.
Causes: HF, VV, LA stais with MS, acute inflam.,
hyperviscosity states.
e.g: aneurysms, AF, vs compression from outside as by
tumors.

10. Michanism of thrombous formation:
• Exposure of subendothelial collagen & release of
endothelial thrombotic factors.
• Adhesion of platelets to the exposed collagen by
factor III.
• Platelet release reaction: platelet derived factors
(serotonin, ADP(aggregation), TXA2(contraction))
irreversible mass of aggregated plt..
• PF3: prothrombin thrombin.
• Thrombin: fibrinogen fibrin thrombus
(platelet/fibrin plug).

11. Classification of thrombi:
• Thrombus color: pale, red, mixed (coralline,
laminated).
• Occlusive or not: non- occlusive (mural),
occlusive (most common), propagating.
• Presence or absence of bacteria: sterile, infected
(septic) as septic vegetations in ABE & septic
thrombophlebitis.
• The site: arterial, cardiac (valvular [vegetations],
atrial, ventricular), venous, capillary.

12. Venous thrombi
• common: slower v. circulation & thin wall.
• Types:
phlebothrombosis thrombophlebitis
•Definition: noninflamed vein.
•Effects: congestion & edema,
pulm. Embolism , propagating
thrombus.
•E.g: in VV, in pelvic & leg v. after
labour or surgery, calf v. in HF.
•Definition: inflamed veins.
•Types:
•Aseptic (sterile): irradiation
•Septic: pyogenic bacteria lead to
pyemia.
•E.g: pelvic veins in perpural
sepsis
appendicular v. in ASA.
in vicinity of abscess or
cellulitis

13. Fate & complications
• septic thrombi septic emboli pyemia.
• Aseptic thrombi:
– Lysis: by fibrinolysins.
– Organization (fibrosis).
– Recanalization.
– calcification (phlebolith)
– Incorporation of arterial thrombi into atheroma.
– Embolization: efficacy of collaterals (poor or
good).
– Occluding thrombi: ischemia, congestion,
propagation.