1. Hemodynamic Disorders
Dr. Riham Abu-Zeid
Prof. of Pathology

2. EDEMA

3. What is this ? Why is there a depressed area after pressure?
Pitting :
displacing interstitial fluid leaving finger shape depression
Edema
Pitting:displacing interstial fluid leaving finger shape depression

4. Define edema
Differentiate between different types and sites of edema
Explain causes of edema
Explain pathogenesis of edema in different diseases(heart failure,renal disease,hepatic disease)

5. Approximately 60% of lean body weight is water
only 5% of total body water is in blood plasma
remainder is in extracellular compartments, mostly as interstitial fluid
two-thirds of which is intracellular

6. Factors that govern fluid movement across compartments
The movement of fluid between vascular and interstitial spaces is controlled mainly by the opposing effects of vascular hydrostatic pressure and plasma colloid osmotic pressure. Normally, the exit of fluid into the interstitium from the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end; the lymphatics drain a small residual amount of excess interstitial fluid. Either increased capillary pressure or diminished colloid osmotic pressure can result in increased interstitial fluid As extravascular fluid accumulates in either case, the increased tissue hydrostatic and plasma osmotic pressures eventually achieve a new equilibrium, and water re-enters the venules. Excess interstitial edema fluid is removed by lymphatic drainage, ultimately returning to the bloodstream via the thoracic duct

7. Osmotic pressure better named oncotic pressure
depends on plasma proteins not on salts

8. Edema: increased fluid in the interstitial tissue or spaces.

9. Edema Edema: Increased fluid in the interstitial tissue space
+body cavities
Hydrothorax
(pleural effusion)
Hydropericardium
(pericardial effusion)
Where else can fluid accumulate ?
Hydroperitoneum
(Ascites)

10. What is Anasarca?
Severe generalized edema
in subcutaneous tissue ,
viscera and serous cavities

11. Dec. Osmotic colloidal pressure
What are the causes (mechanism) of edema?
Dec. Osmotic colloidal pressure
Inc.Hydrostatic
pressure
Lymphatic obstruction
Sodium and Water retention
Increased vascular permeability

12. 1.Inc.hydrostatic pressure 2.Reduced colloidal osmotic pressure
Causes of edema
1.Inc.hydrostatic pressure
2.Reduced colloidal osmotic pressure
Liver cirrhosis
Decreased synthesis of protein
Malnutrition
Nephrotic
Increased loss of protein
(Venous congestion)
DVT
5.Inc. permeability
3.Lymphatic obstruction??
4.Sodium & Water retention
Inflammation/allergy
DVT= deep venous thrombosis

13. Classify generalized edema according to organ involved in its pathogenesis
Cardiac
Renal
Hepatic
Nutritional

14. Pathogenesis of edema

15. 1.Increased hydrostatic pressure
Local edema congestion eg. DVT
Generalized edema
RHF
DVT

16. Salt and water retention
1-Generalized increased hydrostatic pressure
CVC
Renal blood flow
COP
Rt failure
Increased cap. hydrostatic bl. Pressure
EDEMA
Renin –angiotesin
secretion
Volume overload
Salt and water retention is common in all 4 types of edema
Salt and water retention not only fails to correct the plasma volume but exacerbates edema as primary defect is low serum prt
The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance.
Salt and water retention
Aldosterone secretion

17. Inc .Hydrostatic Pressure
1. Generalized Increased Hydrostatic Pressure
Cardiac Edema (RHF)
-Aldosterone
How does edema occur in RHF
CARDIAC EDEMA?
Inc .Hydrostatic Pressure
Salt and water retention
Inc. Capillary permeability (hypoxia)
(hypoxia )Inc. Capillary permeability
Reduced CO > congestion >oozing + renal hypoperfusion
In normal ht ….inc Cardiac output ….inc renal perfusion
In HF heart cannot increase CO in response to compensatory increase in BV >>> vicious circle further congestion + hypoperfusion of Kd
Corrected by inc CO or dec retention by dec salt intake ,diueretic aldesterone antagonist
Salt and water retention is common in all 4 types of edema
Salt and water retention not only fails to correct the plasma volume but exacerbates edema as primary defect is low serum prt
The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance.
When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the prorenin already present in the blood into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.[2] Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs. Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure.[3] Angiotensin II also stimulates the secretion of the hormone aldosterone[3] from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of extracellular fluid in the body, which also increases blood pressure

18. Decreased renal blood flow Activation of renin angiotensin system
2.Reduced Plasma osmotic pressure
-Renal edema(Nephrotic Syndrome) :Protein loss -Hepatic (cirrhosis) -nutritional edema :Dec synthesis
Low prt .
edema
Decreased renal blood flow
Activation of renin angiotensin system
Salt & Water Retention
Increase blood volume
Dec. Plasma oncotic pressure

19. 2ndry Na & H2O retention 1ry :Plasma Osmotic Pressure
What is pathogenesis of edema in Hypoprotenemia- Nephrotic Syndrome -Hepatic -Nutritional def ?
1ry :Plasma Osmotic Pressure
2ndry
Na & H2O retention
When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the prorenin already present in the blood into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.[2] Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs. Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure.[3] Angiotensin II also stimulates the secretion of the hormone aldosterone[3] from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of extracellular fluid in the body, which also increases blood pressure
Summary
dec RBF >>> activate renin in blood >> activates angiotensin (formed in liver )>VC +aldosteron(adrenal ) reabsorption of sodium and water in the tubules > inc blood vol > inc pressure
dec RBF >>> activate renin in blood secreted from JGC in afferent arterioles >> activates angiotensin (formed in liver )>VC +aldosteron(adrenal ) reabsorption of sodium and water in the tubules > inc blood vol > inc pressure
+dec osmotic pressure>>increases vasopressin (ADH) secretion from the posterior pituitary .
>>increase water reabsorption in the collecting ducts of the nephron, (increases water permeability of the kidney's collecting duct .It also increases peripheral vascular resistance, which in turn increases arterial blood pressure.

20. 3.Lymphatic obstruction =Lymphedema causes of lymphatic obstruction &
its effects??
a.infiltration of superficial lymphatics by cancer
c.Filariasis >lymphatic fibrosis
b.Lymphnode resection +/or irradiation in breast cancer
There is an
extensive venous drainage of the breast, and cancer or
other focal mass lesions are not likely to cause significant edema fluid
however, the infiltrated skin is tethered by the sweat ducts such that it cannot swell, leading to an appearance like orange skin. 
Non –pitting edema

21. 3.Lymphatic obstruction =Lymphedema causes of lymphatic obstruction &
its effects??
a.infiltration of superficial lymphatics by cancer
Peau d’orange
b.Lymphnode resection +/or irradiation in breast cancer
c.Filariasis >lymphatic fibrosis
Elephantiasis
There is an
extensive venous drainage of the breast, and cancer or
other focal mass lesions are not likely to cause significant edema fluid
however, the infiltrated skin is tethered by the sweat ducts such that it cannot swell, leading to an appearance like orange skin. 
Non –pitting edema

22. 3.Lymphatic obstruction =Lymphedema
Protein rich lymph
>overgrowth of connective tissue
Elephantiasis dt obst and fibrosis
Peau d’orange infiltration of superf lymphatics by cancer ……
Edema
Peau d’orange infiltration of superf lymphatics by cancer ……edema
In the interstitium, protein and fluid accumulation initiates a marked inflammatory reaction. Macrophage activity is increased, resulting in destruction of elastic fibers and production of fibrosclerotic tissue. Fibroblasts migrate into the interstitium and deposit collagen. The result of this inflammatory reaction is a change from the initial pitting edema to the brawny nonpitting edema characteristic of lymphedema. 
Non –pitting edema .Why ?

23. 4.Sodium and water retention
Nephritic Syndrome (1ry)
2ndry (contributory )in several forms of edema)
eg.Renal hypoperfusion (eg. heart failure)
activation of renin-angiotensin-
aldosterone system>
Salt and water retention is common in all 4 types of edema
Salt and water retention not only fails to correct the plasma volume but exacerbates edema as primary defect is low serum prt
There are osmoreceptors in the hypothalamus When the osmotic pressure of blood changes This causes an afferent neural signal to be sent to the hypothalamus, which increases or decreases vasopressin (ADH) secretion from the posterior pituitary to return blood concentration to normal.
Vasopressin regulates the body's retention of water by acting to increase water reabsorption in the collecting ducts of the nephron, (increases water permeability of the kidney's collecting duct .It also increases peripheral vascular resistance, which in turn increases arterial blood pressure.
Dec osmotic pressure> ADH reabsorption of water
exacerbates edema

24. 5. increased vascular permeability ( eg. Inflammatory Edema )
Why ?
Early Increased hydrostatic pressure due to VD>>> transudate
Mainly :
>>increased vascular permeability >passage of inflamm cells+ protein
>>Increase Interstial fluid oncotic
pressure
Exudate

25. Does increased salt and H20 retention that occurs in edema due to liver disease correct plasma volume ??Why?
No it aggrevates the condition
as the primary cause is decreased albumin
Salt and water retention cause further decrease osmotic pressure +volume overload > more edema

26. a.Lymphatic obstruction Cardiac edema
Liver cirrhosis
b.Inc.hydrostatic pressure +
Peau d’orange
c.Dec. plasma colloidal osmotic pressue

27. Types of edema fluid according to its composition
colour
Assoc.with
Protein
cells
Spc gravity
What is the difference ?

28. Types of edema fluid Transudate Exudate Turbid Hemodynamic disturbance
color
clear
Turbid
Associated. With
Hemodynamic disturbance
inflammation
Protein
<1g%
>4g%
cells
Few or no cells
Many
Specific gravity
<1012
>1020
Specific gravity is the ratio of the density of a substance to the density (mass of the same unit volume) of a reference substance
a specific gravity of 1 are neutrally buoyant in water, those with SG greater than 1 are denser than water, and so (ignoring surface tension effects) will sink in it, and those with an SG of less than 1 are less dense than water, and so will float.
Spc density in kilograms per meter cubed (kg/m3) or in grams per centimeter cubed (g/cm3). Then, divide this density by the density of pure water in the same units.

29. Subcut Pulm Brain Pathological Features : mic + sites +pitting or not
Cell swelling
Clearing and separation of the extracellular matrix elements
Subcut
Cardiac?
Nephrotic-Nephrotic?
Lymphatic ?
Pulm
Brain

30. B-Pulmonary C-Brain A-Subcutaneous
Classify Types of edema according to
distribution(sites)?
A-Subcutaneous
B-Pulmonary
C-Brain

31. A-Subcutaneous Generalized Localized ( most prominent in ) -Renal
-Cardiac(dependent)
-Renal
(early periorbital)
in Loose CT
Localized
Cardiac :>in depedant parts coz its influenced by gravity where hydrostatic pressure (depends on this factor) is highest (greatest distance from the HT) and
Legs ;standing / sacrum :sitting
Localized:inflamm-DVT_lymphatic obst
Renal : > eyelids )periorbital in loose CT depends on hypoproteinemia
BOOK
Nephrotic all over more in eyelids
Nephritic less severe EARLY eye lid
Why ??
Local inc BP >
DVT
Inflammation
Lymphatic obstruction
-Liver dis
Malnutrition
LL/scrotum:standing
sacrum :sitting

32. Renal edema
Nephrotic
Dec .albumin
More severe begins periorbital & may progress to anasarca
Nephritic
Salt & water retention
Less severe

33. B-Pulmonary Mainly Due to?? LVF Heavy ,oozes frothy blood tinged fluid
Left Ventricular failure
Congestion of alveolar capillaries +edema fluid+red cells
Dt LVFDt LVF + Renal failure –resp distress syndrome hypersensitivity-infections

34. C-Brain compressing vascular supply brain herniation Leading to
brain herniation or by compressing vascular supply of the brain stem.

35. State whether the following is pitting –non pitting
localized – generalized
A.After surgery and irradiation for breast cancer a female developed left upper limb edema
B.A patient with right sided heart failure
C.A patient with liver dysfunction
D.A patient infected with filaria after mosquito bite
E. Edema due to Deep venous Thrombosis
Localized non-pitting
Generalized pitting
Generalized pitting
Inc hydrostatic pressure-Na and water retention
if you are a doctor and u don’t knowthe cause of edema u will first ask urself is it local or general b4 trying to reach the cause
Localized non-pitting
Localized -pitting

36. Extended Modular Program
History: Patient with chronic liver disease
Specimen :Ascitic fluid
Gross:15 cc of clear pale yellow fluid
Mic: Smears examined are hypocellular showing very few lymphocytes
Is this fluid transudate or exudate ?
transudate
Extended Modular Program

37. Subcutaneous Pulmonary edema Brain edema Clinical effects of edema
Impairs clearance of infection
Impairs healing
Impair
ventilation
Environment for infection
Death dt
Herniation
Compress vasculature

38. Test yourself
Give reason why edema d.t renal disease is more prominent peri-orbital while edema d.t heart failure it is more prominent in lower limbs
Renal : > depends on hypoproteinemia edema is mainly in loose CT as eyelids (periorbital edema)
Cardiac :>depends on increased hydrostatic pressure which is highest in dependent parts due to influence of gravity
Cardiac :>in depedant parts coz its influenced by gravity where hydrostatic pressure (depends on this factor) is highest
Localized:inflamm-DVT_lymphatic obst
Renal : > eyelids )periorbital in loose CT depends on hypoproteinemia

39. According to the organ affected
Causes of edema
Cardiac
Renal
Hepatic
Nutritional
Types of edema fluid
Sites of edema
SCT
Brain
Localized
Generalized?
Pulmon.