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Basic pathology

Dr. Mishaal
HAEMODYNAMIC
DISORDERS
LEARNING OBJECTIVES
The students should understand:
• 1. Edema. Etiopathogenetic Mechanism .Types and
Morphology of Edema. Subcutaneous Edema. Pulmonary
Edema. Edema of the Brain. Fluid Accumulation in Body
Cavities. Clinical Correlation.
• 2. Hyperemia. Active Hyperemia. Passive Hyperemia
(Congestion). Morphology. Acute and Chronic types.
Pathologic Changes in Lungs, Liver, Spleen and Brain.
• 3. Hemorrhage. Causes. Mechanisms. Types. Hematoma,
Petechia, Purpura. Ecchymoses. Large Accumulation of
blood in the body cavities.
LEARNING OBJECTIVES
• 4. Thrombosis. Pathogenesis (Virchov’s triad).
Morphology of Thrombi. Arterial system Thrombi.
Thrombosis in the Heart. Venous Thrombosis.
Phlebothrombosis. Migratory Thrombosis. (Trousseau’s
Syndrome). Fate of Thrombosis. Clinical Features.
Disseminated Intravascular Coagulation (DIC).
• 5. Embolism. Thromboembolism. Pulmonary Embolism.
Fate of Pulmonary Thromboemboli. Paradoxal Embolism.
Systemic Embolism. Arterial Emboli.Air Embolism.
Decompression Sickness. Amniotic Fluid Embolism. Fat
Embolism. Miscellaneous Emboli.
• 6. infarction : Pathogenesis. Types. Pathologic Changes in
Organs ( Heart, Kidney, Lung, Liver, Brain).
• 7. Shock: Pathogenesis.Types and Stages of Shock.
Pathologic Changes in Organs ( Heart, Kidney, Lung,
Liver, Brain).
NORMAL FLUID BALANCE
• Balance is achieved through physiologic
mechanisms that :
- Maintain vessel wall integrity, intravascular
pressure & osmolarity to keep values within
physiologic ranges
- Control coagulation process
• Imbalance can be :
- Primary: e.g. trauma, hypercoagulability disorders,
- Secondary: e.g. heart failure, sepsis,
HAEMODYNAMIC
DISORDERS:

• OEDEMA / EDEMA
• HYPEREMIA AND CONGESTION
• HAEMORRHAGE
• THROMBOSIS
• EMBOLISM
• INFARCTION
• SHOCK
Overview
• Edema (increased fluid in the ECF)
• Hyperemia (INCREASED flow)
• Congestion (INCREASED backup)
• Hemorrhage (extravasation)
• Hemostasis (keeping blood as a fluid)
• Thrombosis (clotting of blood)
• Embolism (downstream travel of a clot)
• Infarction (death of tissues /no enough blood)
• Shock (circulatory failure with collapse)
OEDEMA/
EDEMA
Normal body composition
• Water composes about 60% of total body
mass in men, 55% in women.
• 3 body compartments containing H2O:
• Intracellular fluid = 67%

• Interstitial fluid = 25%

• Plasma = 8%
Water distribution
• 60% body weight in men, 55% in women
• a man of average weight (70 kg), body water content is about
42 liters.
• 2 thirds of body water is intracellular, and 1 third is
extracellular. Interstitial
(25%)
Extracellular
(33%)
Vascular
Body water (8%)

Intracellular
(67%)
60%OF BODY WEIGHT IS WATER

blood
 plasma
8%

Intra-  
cellular Interstitial
(67%) fluid (25%)
Mechanisms control body fluids
• Generation of interstitial fluid is regulated by the
“Starling equation” {The rate of leakage of fluid
is determined by the difference between two
forces (hydro-static pressure and oncotic
pressure) and also by the permeability of the
vessel wall to water}.
Starling equation
• Arterial pressure, venous pressure, colloid oncotic
pressure, and competent lymphatic vessels are the main
factors of fluid filtration process and formation of edema.
• Jv = (kf[Pc − Pi] − σ[πc − πi])

• The Jv is the net fluid flux.


• The capital P refers to hydrostatic pressure, and
• The 𝝅 refers to oncotic pressures.

This is the Starling-Landis law also known as Starling


equation.
Starling equation
• The Starling equation
– Pc is the capillary hydrostatic pressure
– Pi is the interstitial hydrostatic pressure
– πc is the capillary oncotic pressure
– πi is the interstitial oncotic pressure
– Kf is the filtration coefficient – a proportionality
constant
– σ is the reflection coefficient
Starling equation
• The Starling equation in words is :
The net fluid flux = (the filtration coefficient[capillary
hydrostatic pressure − interstitial hydrostatic pressure] − the
reflection coefficient [capillary oncotic pressure − interstitial
oncotic pressure])
Mechanism
• Hydrostatic pressure within blood vessels
causes water to filter out into the tissue
• This leads to a difference in protein
concentration between blood plasma and tissue
• As a result, the oncotic pressure (plasma
osmotic pressure) of the higher level of protein
in the plasma tends to absorb water back into
the blood vessels from the tissue
Mechanism
• The hydrostatic forces are usually more and
there is always a net leakage of fluid out of
blood vessels
• Small (net leakage) leftover amount of
interstitial fluid is usually removed by the
lymphatics, and then back to blood through the
thoracic duct.
• Lymphatic vessels
are the Anatomic
structures which
drain excess
interstitial fluid
into venous blood
• Hydrostatic and
plasma oncotic
pressures are the
two opposing
major factors
governing fluid
movement between
vascular and
interstitial space
Mechanism
• Most water leakage occurs in capillaries or post-
capillary venules (semi-permeable membrane)
wall that allows water to pass more freely than
protein
• If the gaps between the cells of the vessel wall
open up then permeability to water is increased
Mechanism
• Changes in the variables in Starling's
equation can contribute to the formation
of edema either by:
↑ in hydrostatic pressure within the blood vessel
↓ in the oncotic pressure within the blood vessel
↑ in vessel wall permeability



 Leads to oedema
Normal Micro-circulation

Pressure Arterial Venous


Hydrostatic Pressure+ 36 + 21
Oncotic Pressure - 28 - 28
Net filtration Pressure + 8 mmHg - 7 mm Hg
(leak-out) (Reabsorb)

oedema occurs when :


↑ hydrostatic pressure within the blood vessel
↓ oncotic pressure within the blood vessel
Edema
• The Greek word edema means swelling
• Def : Excessive accumulation of abnormal
amounts of fluid in interstitial tissue spaces or
serous cavities.

– Anasarca: severe and generalized edema


– Hydrothorax (pleural effusion) : accumulation of
fluid in pleural cavity
– Hydropericardium: accumulation of fluid in
pericardial cavity.
– Hydroperitoneum (ascitis): accumulation of fluid in
peritoneal cavity.
Edema
• Site: affect different sites :
- Generalized: Anasarca
- Subepidermal in different parts of the skin
- In body cavities, e.g. hydrothorax(pleural
effusion), hydropericardium,
hydroperitoneum (ascites)
Edema
• 5 common pathophysiology
processes:
– Increased Blood Hydrostatic Pressure
– Reduced Blood Oncotic Pressure
– Lymphatic Obstruction
– Sodium/Water Retention
– Inflammation
Pathophysiology
1.Increased Blood Hydrostatic Pressure
• Local - Impaired venous outflow, such as in deep venous
thrombosis, venous obstruction or compression, burn,
lower extremity inactivity with prolonged dependency,
ascites, extravascular pressure (e.g., mass)
• Generalized - Congestive heart failure, affecting right
ventricular function, constrictive pericarditis, renal
disease, liver cirrhosis
Pathogenesis of Edema in heart failure
Pathophysiology
2.Reduced Blood Oncotic pressure
• Excessive loss or reduced synthesis of albumin
i. Excessive loss :
- Protein-losing nephropathy
e.g. Nephrotic syndrome (Leaky glomerular capillary
wall, albumin loss and generalized edema),
- Protein-losing gastroenteropathy

ii. Reduced synthesis: Diffuse liver pathology (e.g.


liver cirrhosis) or protein malnutrition - reduced albumin
synthesis
Pathophysiology
3.Lymphatic Obstruction - usually localized;
inflammatory or neoplastic, e.g.
• a. Filariasis – elephantiasis
• b. Carcinoma
i. Obstruction by the tumor
ii. Secondary to therapy – e.g. axillary node
dissection at time of diagnosis (as with
breast carcinoma) or post-irradiation

## NOTICE :Anything which DAMAGES a lymphatic


interferes with it’s function to drain ECF.
Pathophysiology
4.Sodium/water Retention
• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium
• Renal hypoperfusion  Increased renin-angiotensin-
aldosterone secretion

## NOTICE : One of the main principles in fluid


physiology is: Where the sodium goes, the fluid goes.
Pathophysiology
5.Inflammation
Edema in INFLAMMATION occur with :
- Acute inflammation
- Chronic inflammation
- Angiogenesis

##NOTICE : Areas of increased vascular permeability or


areas of increased blood vessels will appear “edematous”
Pathophysiology
• Edema occurring in hydrodynamic
derangements is usually a transudate:
protein-poor (protein content < 3 g/dl), specific gravity
< 1.012, usually with few cells
• Edema occurring in inflammatory conditions
is usually an exudate:
protein-rich (protein content > 3 g/dl), specific gravity
>1.020, often with inflammatory components e.g.
leucocytes, fibrin
Types of edema fluid
Transdate Exudate
Non inflammatory fluid Inflammatory fluid result
result from imbalances in from endothelial damage
normal hemodynamic increased vascular
forces permeability

Protein poor (<3 gm/dl) Protein rich (>3 gm/dl)

Specific gravity of <1.012 Specific gravity of >1.020

Congestive heart failure Inflammatory and


liver and renal disease immunologic pathology.
Morphology of edema
• Different distributions depending on
etiology
a. Diffuse distribution – e.g. renal dysfunction/nephrotic
syndrome
i. Affects all parts of body equally
ii. Initially may be more obvious in tissues with
loose connective tissue matrix such as eyelids
(periorbital edema)
b. Dependant - Prominent heart failure (particularly RHF)
Morphology of edema
Gross
Morphology of edema
• Pitting edema is a type
of edema in which the
skin surface, when
pressed by a finger,
leaves an indentation
“Pitting” Edema
Morphology of edema
Pulmonary edema
• Typical in left heart failure, but also in renal failure,
adult respiratory distress syndrome, infection
(pneumonia), hypersensitivity reactions
• Grossly, lungs are heavy with frothy, blood-tinged fluid
that is mixture of air, edema fluid and red blood cells
Morphology of edema
Morphology of edema

Pulmonary edema
Chest X-ray
Morphology of edema

Histology
Clinical manifestations of edema
Clinical Signs Most Likely Cause(s)
Unilateral edema of one arm in a Lymphatic obstruction
60-year-old female with a
mastectomy scar on that side
– swollen, erythematous breast extensive invasion and
)Peau d’ orange( obstruction of dermal
.lymphatics by tumor cells
Bilateral symmetrical edema of skin Increased hydrostatic
& subcutis of both legs below knees pressure in veins due to
in 57-year-old man whose only congestive heart failure
complaint is shortness of breath
Periorbital edema with slight edema Hypoproteinemia/
in all four extremities. Ascitis hypoalbuminemia. (kidney
and liver)
Unilateral edema of one
arm, after mastectomy
Peau d’orange
Inflammatory carcinoma with its classic peau
d’orange appearance.
Peau d’orange
Note the tiny little “pits” in the orange peel and the
skin here.
Clinical manifestations of edema
• Which 3 major vital organs their dysfuncrions are
main causes of edema?
- Heart / cardiac (congestive heart
failure / CHF)
- Liver/ hepatic
- Kidneys/ renal
CHF EDEMA
• TWO main reasons for edema due mainly to
cardiac causes:
- Increased venous hydrostatic pressure due to
heart failure
- Decreased renal perfusion due to heart failure
lead to triggering of RENIN-ANGIOTENSION-
ALDOSTERONE complex, resulting ultimately
in sodium retention followed by water retention
HEPATIC ASCITES
• TWO main reasons for edema due mainly to
hepatic causes:

- PORTAL HYPERTENSION : Portal


hypertension causes edema of organs and tissues
with portal circulation.
- HYPOALBUMINEMIA: Hypoalbuminemia
however, may cause systemic edema.
ASCITES

Hpoproteinemia and portal hypertension can cause


accumulation of fluid in abdominal cavity (ascites)
RENAL EDEMA
• TWO main reasons for edema due to relatively
“pure” renal causes:
- Sodium retention
- Protein losing glomerulopathies (nephrotic
syndrome)
EDEMA
PERIORBITAL OEDEMA (RENAL)
Clinical manifestations of edema
• Give example of an organ that has no space to
extend when it becomes edematous ?
- Brain / cerebral edema

• Give example of an organ in which fluid fills its


lumens when it becomes edematous ?
- Lung / pulmonary edema
CEREBRAL EDEMA
• CEREBRAL OEDEMA (closed cavity, no
expansion)
• HERNIATION of cerebellar tonsils
• HERNIATION of hippocampal uncus over tentorium
• HERNIATION, subfalcine
Edematous Brain
Edematous Brain
• Flattened gyri often
signify edema, this
occurs due to
compression against the
calvarium. This is an
example of an organ
which is edematous, but
does not have room to
swell freely.
Thanks

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