Pathophysiology Colloquium 2
Rachel Presser - Summary
1. General Etiology
Etiology is the causes for a disease.
These can be external/environmental e.g.:
Stress
Nutrition
Bacteria
Heat
Or they can be internal for example:
Genes
Aging
Environmental agents can be:
Physical
Chemical
Nutritional
Infections
Immunological
Psychological
Genetic Factors include:
Age
Genes
Etiology states that diseases are caused due to internal or external factors, they are multifactorial meaning that there is more than
one factor involved in initiating the pathological process.
Genetic factors affect acquired diseases and environment has a profound effect on some genetic diseases, for example, many people
can be predisposed to a specific illness but only half of them will develop the illness due to the environmental factors that triggered
their disease.
Risk factors – also known as predisposing factors, increase the probability of the disease occurring but these factors are not the cause
of the disease.
Precipitating Factor – asthma is precipitated by an exposure to an allergen, the allergen is not the cause of the asthma attack, yet it
lead to an asthma attack in response.
Ischemia, hypoxia and hypoglycemia no atp inhibition of Na/K pump intracellular K decreases, extracellular K increases,
cell membrane depolarizes and Cl goes into the cell cellular swelling
Glutamate increases instream of Na+ over activation of ion channels.
Increased Ca+ concentration in cytosol inhibition of mitochondrial respiratory chain ATP shortage
Oxygen shortage anaerobic glycolysis cytosolic acidosis inhibits glycolysis no ATP less ATP means that cell undergoes
oxidative damage but O2 radicals (mechanism against oxidants) are ATP dependent cell membrane is destroyed intracellular
molecules leak to extracellular space no immune tolerance activation of immune response and inflammation which damages
the cell further. This eventually leads to necrotic death.
2. General Pathogenesis
This word is derived from the greek pathos (disease) and genesis (creation) the term pathogenesis means step by step development
of a disease.
Pathogenesis is the chain of events leading to that disease due to a series of changes in the structure and/or function of a
cell/tissue/organ or physical agent.
It is the sequence of cellular and tissue events that take place from the time of initial contact with the etiologic agent until
the ultimate expression of diseases.
It also means: cause-consequence chain.
The pathogenesis of the disease is the mechanism by which a disease is caused
This term can also be used to describe the development of the disease such as acute, chronic, and reccurent.
Pathogenesis – the sequence of cellular and tissue events that take place from the time of initial contact with the etiologic agent until
the ultimate expression of diseases.
,Sanogenesis – means recovery, it involves unique processes for eliminating various types of pathology. Sanogenesis occurs at all
levels of a complex organism, from molecular and cell processes to higher systemic and intersystemic interrelations.
Pathological systems and sanogenetic anti-systems are related structurally and functionally.
Sanogenetic anti-systems are activated or induced by pathological systems.
These systems have different biological significance and represent biological antagonists.
The pathological process transforms into disease only when mechanisms of sanogenesis become irreplaceably disturbed,
and the organism fails to function to a necessary and optimum degree.
Disease periods
Latent period – incubation period of an infection or the early phase of a tumor.. it is the time between infection and the
appearance of symptoms, there are no symptoms present at this point.
Prodromal period – time that the patients have vague symptoms such as fatigue and loss of apetite.
Clinical period – manifestation of specific symptoms of the disease.
Types of diseases
Localized disease – one that affects only one part of the body, such as an eye infection
Disseminated disease – has spread to other parts, with cancer this is known as metastasis
Systemic disease – disease that affects the entire body, such as influenza or high blood pressure
3. Pathophysiology of peripheral circulation.
Hyperemia and Congestion
Both can be defined as an increase in blood volume in a particular tissue
Hyperaemia is an increase in blood flow in an organ or tissue due to dilation of arteries or arterioles i.e. active hyperaemia
While congestion is passive hyperaemia due to engorgement of veins and venules by blood.
Active hyperemia occurs as a result of an active process such as vasodilation.
o For example during exercise (physiological)
o In a splanchnic area after eating (physiological)
o In acute inflammation (pathological)
Active hyperemia is an engorgement of the vascular bed caused by increased arteriolar bood flow in the area. Hyperemia is therefore
the result of vasodilation.
Active hyperemia is a result of:
Arteriolar distension by several causes
Skeletal muscle activity
Inflammation
Reactive Hyperemia is due to an increase of blood flow after its temporary interruption
The affected tissue is redder because of engorgement with oxygenated blood.
Important Vasodilators and Vasoconstrictors
Vasodilators Vasoconstrictors
Adenosine PGE 2a
Bradykinin Thromboxane A4
Increased H+ concentration Leukotrines B4
Decreased oxygen partial pressure Endothelin 1
Increased carbon dioxide partial pressure Angiotensin 2
Histamine Increased Ca2+ concentration and increased Na+ concentration
Increased lactate Increased GMP
Increased NO Free radicals
Increased carbon dioxide
Increased K+ or Mg2+
Decreased cAMP
Antioxidants
Active Hyperemia during inflammation
Chemically mediated response of the vasculature to inflammatory mediators such as histamine, bradykinin, prostaglandins
etc.
Increased rate of blood flow
Increased volume of blood in region
Increased blood flow open new capillary beds and increased arteriolar blood pressure in small vessels.
Passive Hyperemia
Passive congestion is an increased amount of blood in an organ or tissue resulting from venous obstruction or from cardiac
failure.
Causes of passive hyperemia also termed congestion or stasis are
, o Compression of veins
o Obstruction of veins
o Impaired venous return to the heart (heart failure)
o This is always followed by dilation of venules and capillaries.
o As a result there is decreased drainage of venous blood from the affected area.
Heart failure occurs from a number of different causes, the heart is unable to efficiently pump blood and blood accumulates in the
ventricles, and consequently in the atria. The venous return coming through the pulmonary veins and the vena cava is opposed by
great pressure in the atria. The venous pressure increases and this is venous congestion which can be pulmonary or systemic.
There are three possible causes of venous congestion
Venous pressure increased
Obstruction inside the vein
Obstruction outside the vein
Systemic venous congestion
In which blood accumulates in veins all over the body as in case of congestive heart failure or sparing the lung in case of right
side heart failure.
Pulmonary venous congestion
In which blood accumulates in pulmonary veins and capillaries in case of left side heart failure or mitral stenosis
Localized venous congestion
It is due to obstruction to blood flow in a limited area or an organ. It can be acute as in mechanical obstruction or venous
thrombosis.
It can also be chronic by pressure on a vein by a tumor or by constriction of a vein by fibrosis.
Hyperemia in the right side of the heart
In right sided heart failure, there is systemic venous congestion with sparing of the lung
In congestive heart failure (both sides) there is congestion of all organs including the lungs.
Hyperemia in the left side of the heart
In left sided heart failure, there is pulmonary venous congestion but later it may cause pulmonary hypertension leading to
right sided heart failure i.e. congestive heart failure.
Clinical Features of congestive heat failure
Cyanosis – blue discolouration of the lips and nails due to the deoxygenation of blood
Congested pulsating neck veins – due to increased venous pressure
Edema of lower limbs – due to increased venous pressure
Enlarged tender liver
There are a number of signs of chronic venous congestion:
Veins – varicosities, phlebitis, thrombosis, haemorrhage from varicose veins
Skin – stasis, dermatitis, pigment changes, edema, poor wound healing; ulceration and scarring.
Ischemia
Ischemia is insufficient blood supply or blood flow to a particular area of the body
This restriction results in a lack of proper oxygen and nutrients leading to tissue damage or destruction
Ischemia can be caused by many different reasons for example:
o Atherosclerosis – lipid laden plaques block the lumen of arteries
o Thromboembolism – blood clots
o Sickle cell disease – reduced carrying capacity of abnormally shaped red blood cells
o Embolism – foreign bodies in the circulation
o Outside compression of a vessel – e.g. by a tumor
o Angiospasm
Quite often, the restoration of blood flow following ischemia which is known as reperfusion is actually more damaging than
the ischemia and reperfusion injury occurs.
Reintroduction of oxygen causes a greater production of damaging free radicals resulting in reperfusion injury.
The extent of the ischemia depends on:
Location and degree of occlusion
Amount of tissue supplied by the vessel
Duration of the occlusion
Metabolic needs of the affected tissue
Collateral vascular supplies
Infarction
, Infarction is the process of tissue death (necrosis) caused by blockage of the tissues blood supply. Infarctions are divided into two
types according to the amount of blood present:
White infarctions (anemic infarcts)
Red infarctions (hemorrhagic infarcts)
Anemic infarction also known as white or pale infarction is caused by arterial occlusion and is usually seen in the heart,
kidney and spleen.
Red infarctions (hemorrhagic) generally affect the lungs or other loose organs such as testis, small intestine etc the
occlusion consists of more red blood cells and fibrin strands.
Extent of infarction depends on
Location and degree of occlusion
Amount of tissue supplied by the vessel
Duration of occlusion
Metabolic needs of affected area
Extent of collateral circulation.
38. Arterial Hyperemia – etiology and pathogenesis, types, importance
Hyperemia and congestion are the result of excessive blood in a part of the body, they differ from haemorrhage as in haemorrhage
the blood has escaped from the blood vessels, yet in hyperemia and congestion, the blood is still contained within the vessels.
Hypermia is an active process whereas congestion is a passive.
Hyperemia is an important concept to understand as it is one of the four cardinal signs of inflammation: rubor, tumor, calor et dolor
as well as function lasea (loss of function) the rubor or redness in inflammation is as a result of hyperemia.
Etiology
The etiology of arterial hyperemia can be both physiologic or pathological.
In physiological conditions, the hyperemia is an adaptive and effective response for example when someone is exercising their oxygen
demand is higher, therefore hyperemia occurs to provide more oxygenated blood to the muscles.
Pathological arterial hyperemia does not change the function of the organ and tissue and has a disadvantageous role that is damaging
to the body. Pathological arterial hyperemia is accompanied by impared blood supply, microhemocirculation, transcapillary
exchange and sometimes haemorrhage and bleeding.
For example pathological arterial hyperemia of the brain with hypersensitive crisis. Causes:
Mechanical (something putting pressure on the area)
Physical (temperature, pressure etc)
Chemical (alcohol, aldehydes etc)
Biological (nitric oxide, prostaglandins, ACH, adenosine – vasodilators)
Social (emotional stress/trauma)
Usually arterial hyperemia is classified as being caused by an endogenous or exogenous agent.
Types of pathological arterial hyperemia according to the mechanism development:
1. Neurotonic or reflex
2. Neuroparalytic
3. Inflammatory arterial hyperemia is due to humoral and reflex mechanisms/
4. Vakat increase blood flow to the discharged space where the air pressure is reduced/
5. Postanemic increased blood flow after ischemia/
6. Postishemic increased blood flow after anemia
7. Collateral arterial hyperemia develops in sudden decrease in blood flow through the main vessel.
Mechanisms of occurrence
The pathogenesis of all types of pathological arterial hyperemia is the same and differs only in the starting moment.
Expansion of the lumen of small arteries and arterioles is achieved due to the realization of neurogenic (neurotonic
and neuroparalytic), humoral, neurohumoral and myoparalytic mechanisms or their combination.
1. Neurogenic mechanism. Distinguish between the neurotonic and neuroparalytic varieties of the neurogenic mechanism of
arterial hyperemia development.
- Neurotonic mechanism. It is in the predominance of the effects of parasympathetic nervous influences (in comparison with
sympathetic) on the walls of arterial vessels.
- Neuroparalytic mechanism. Characterized by a decrease or absence ("paralysis") of sympathetic nerve effects on the walls of
arteries and arterioles.
1) Neuroparalytic arterial hyperemia.
Rachel Presser - Summary
1. General Etiology
Etiology is the causes for a disease.
These can be external/environmental e.g.:
Stress
Nutrition
Bacteria
Heat
Or they can be internal for example:
Genes
Aging
Environmental agents can be:
Physical
Chemical
Nutritional
Infections
Immunological
Psychological
Genetic Factors include:
Age
Genes
Etiology states that diseases are caused due to internal or external factors, they are multifactorial meaning that there is more than
one factor involved in initiating the pathological process.
Genetic factors affect acquired diseases and environment has a profound effect on some genetic diseases, for example, many people
can be predisposed to a specific illness but only half of them will develop the illness due to the environmental factors that triggered
their disease.
Risk factors – also known as predisposing factors, increase the probability of the disease occurring but these factors are not the cause
of the disease.
Precipitating Factor – asthma is precipitated by an exposure to an allergen, the allergen is not the cause of the asthma attack, yet it
lead to an asthma attack in response.
Ischemia, hypoxia and hypoglycemia no atp inhibition of Na/K pump intracellular K decreases, extracellular K increases,
cell membrane depolarizes and Cl goes into the cell cellular swelling
Glutamate increases instream of Na+ over activation of ion channels.
Increased Ca+ concentration in cytosol inhibition of mitochondrial respiratory chain ATP shortage
Oxygen shortage anaerobic glycolysis cytosolic acidosis inhibits glycolysis no ATP less ATP means that cell undergoes
oxidative damage but O2 radicals (mechanism against oxidants) are ATP dependent cell membrane is destroyed intracellular
molecules leak to extracellular space no immune tolerance activation of immune response and inflammation which damages
the cell further. This eventually leads to necrotic death.
2. General Pathogenesis
This word is derived from the greek pathos (disease) and genesis (creation) the term pathogenesis means step by step development
of a disease.
Pathogenesis is the chain of events leading to that disease due to a series of changes in the structure and/or function of a
cell/tissue/organ or physical agent.
It is the sequence of cellular and tissue events that take place from the time of initial contact with the etiologic agent until
the ultimate expression of diseases.
It also means: cause-consequence chain.
The pathogenesis of the disease is the mechanism by which a disease is caused
This term can also be used to describe the development of the disease such as acute, chronic, and reccurent.
Pathogenesis – the sequence of cellular and tissue events that take place from the time of initial contact with the etiologic agent until
the ultimate expression of diseases.
,Sanogenesis – means recovery, it involves unique processes for eliminating various types of pathology. Sanogenesis occurs at all
levels of a complex organism, from molecular and cell processes to higher systemic and intersystemic interrelations.
Pathological systems and sanogenetic anti-systems are related structurally and functionally.
Sanogenetic anti-systems are activated or induced by pathological systems.
These systems have different biological significance and represent biological antagonists.
The pathological process transforms into disease only when mechanisms of sanogenesis become irreplaceably disturbed,
and the organism fails to function to a necessary and optimum degree.
Disease periods
Latent period – incubation period of an infection or the early phase of a tumor.. it is the time between infection and the
appearance of symptoms, there are no symptoms present at this point.
Prodromal period – time that the patients have vague symptoms such as fatigue and loss of apetite.
Clinical period – manifestation of specific symptoms of the disease.
Types of diseases
Localized disease – one that affects only one part of the body, such as an eye infection
Disseminated disease – has spread to other parts, with cancer this is known as metastasis
Systemic disease – disease that affects the entire body, such as influenza or high blood pressure
3. Pathophysiology of peripheral circulation.
Hyperemia and Congestion
Both can be defined as an increase in blood volume in a particular tissue
Hyperaemia is an increase in blood flow in an organ or tissue due to dilation of arteries or arterioles i.e. active hyperaemia
While congestion is passive hyperaemia due to engorgement of veins and venules by blood.
Active hyperemia occurs as a result of an active process such as vasodilation.
o For example during exercise (physiological)
o In a splanchnic area after eating (physiological)
o In acute inflammation (pathological)
Active hyperemia is an engorgement of the vascular bed caused by increased arteriolar bood flow in the area. Hyperemia is therefore
the result of vasodilation.
Active hyperemia is a result of:
Arteriolar distension by several causes
Skeletal muscle activity
Inflammation
Reactive Hyperemia is due to an increase of blood flow after its temporary interruption
The affected tissue is redder because of engorgement with oxygenated blood.
Important Vasodilators and Vasoconstrictors
Vasodilators Vasoconstrictors
Adenosine PGE 2a
Bradykinin Thromboxane A4
Increased H+ concentration Leukotrines B4
Decreased oxygen partial pressure Endothelin 1
Increased carbon dioxide partial pressure Angiotensin 2
Histamine Increased Ca2+ concentration and increased Na+ concentration
Increased lactate Increased GMP
Increased NO Free radicals
Increased carbon dioxide
Increased K+ or Mg2+
Decreased cAMP
Antioxidants
Active Hyperemia during inflammation
Chemically mediated response of the vasculature to inflammatory mediators such as histamine, bradykinin, prostaglandins
etc.
Increased rate of blood flow
Increased volume of blood in region
Increased blood flow open new capillary beds and increased arteriolar blood pressure in small vessels.
Passive Hyperemia
Passive congestion is an increased amount of blood in an organ or tissue resulting from venous obstruction or from cardiac
failure.
Causes of passive hyperemia also termed congestion or stasis are
, o Compression of veins
o Obstruction of veins
o Impaired venous return to the heart (heart failure)
o This is always followed by dilation of venules and capillaries.
o As a result there is decreased drainage of venous blood from the affected area.
Heart failure occurs from a number of different causes, the heart is unable to efficiently pump blood and blood accumulates in the
ventricles, and consequently in the atria. The venous return coming through the pulmonary veins and the vena cava is opposed by
great pressure in the atria. The venous pressure increases and this is venous congestion which can be pulmonary or systemic.
There are three possible causes of venous congestion
Venous pressure increased
Obstruction inside the vein
Obstruction outside the vein
Systemic venous congestion
In which blood accumulates in veins all over the body as in case of congestive heart failure or sparing the lung in case of right
side heart failure.
Pulmonary venous congestion
In which blood accumulates in pulmonary veins and capillaries in case of left side heart failure or mitral stenosis
Localized venous congestion
It is due to obstruction to blood flow in a limited area or an organ. It can be acute as in mechanical obstruction or venous
thrombosis.
It can also be chronic by pressure on a vein by a tumor or by constriction of a vein by fibrosis.
Hyperemia in the right side of the heart
In right sided heart failure, there is systemic venous congestion with sparing of the lung
In congestive heart failure (both sides) there is congestion of all organs including the lungs.
Hyperemia in the left side of the heart
In left sided heart failure, there is pulmonary venous congestion but later it may cause pulmonary hypertension leading to
right sided heart failure i.e. congestive heart failure.
Clinical Features of congestive heat failure
Cyanosis – blue discolouration of the lips and nails due to the deoxygenation of blood
Congested pulsating neck veins – due to increased venous pressure
Edema of lower limbs – due to increased venous pressure
Enlarged tender liver
There are a number of signs of chronic venous congestion:
Veins – varicosities, phlebitis, thrombosis, haemorrhage from varicose veins
Skin – stasis, dermatitis, pigment changes, edema, poor wound healing; ulceration and scarring.
Ischemia
Ischemia is insufficient blood supply or blood flow to a particular area of the body
This restriction results in a lack of proper oxygen and nutrients leading to tissue damage or destruction
Ischemia can be caused by many different reasons for example:
o Atherosclerosis – lipid laden plaques block the lumen of arteries
o Thromboembolism – blood clots
o Sickle cell disease – reduced carrying capacity of abnormally shaped red blood cells
o Embolism – foreign bodies in the circulation
o Outside compression of a vessel – e.g. by a tumor
o Angiospasm
Quite often, the restoration of blood flow following ischemia which is known as reperfusion is actually more damaging than
the ischemia and reperfusion injury occurs.
Reintroduction of oxygen causes a greater production of damaging free radicals resulting in reperfusion injury.
The extent of the ischemia depends on:
Location and degree of occlusion
Amount of tissue supplied by the vessel
Duration of the occlusion
Metabolic needs of the affected tissue
Collateral vascular supplies
Infarction
, Infarction is the process of tissue death (necrosis) caused by blockage of the tissues blood supply. Infarctions are divided into two
types according to the amount of blood present:
White infarctions (anemic infarcts)
Red infarctions (hemorrhagic infarcts)
Anemic infarction also known as white or pale infarction is caused by arterial occlusion and is usually seen in the heart,
kidney and spleen.
Red infarctions (hemorrhagic) generally affect the lungs or other loose organs such as testis, small intestine etc the
occlusion consists of more red blood cells and fibrin strands.
Extent of infarction depends on
Location and degree of occlusion
Amount of tissue supplied by the vessel
Duration of occlusion
Metabolic needs of affected area
Extent of collateral circulation.
38. Arterial Hyperemia – etiology and pathogenesis, types, importance
Hyperemia and congestion are the result of excessive blood in a part of the body, they differ from haemorrhage as in haemorrhage
the blood has escaped from the blood vessels, yet in hyperemia and congestion, the blood is still contained within the vessels.
Hypermia is an active process whereas congestion is a passive.
Hyperemia is an important concept to understand as it is one of the four cardinal signs of inflammation: rubor, tumor, calor et dolor
as well as function lasea (loss of function) the rubor or redness in inflammation is as a result of hyperemia.
Etiology
The etiology of arterial hyperemia can be both physiologic or pathological.
In physiological conditions, the hyperemia is an adaptive and effective response for example when someone is exercising their oxygen
demand is higher, therefore hyperemia occurs to provide more oxygenated blood to the muscles.
Pathological arterial hyperemia does not change the function of the organ and tissue and has a disadvantageous role that is damaging
to the body. Pathological arterial hyperemia is accompanied by impared blood supply, microhemocirculation, transcapillary
exchange and sometimes haemorrhage and bleeding.
For example pathological arterial hyperemia of the brain with hypersensitive crisis. Causes:
Mechanical (something putting pressure on the area)
Physical (temperature, pressure etc)
Chemical (alcohol, aldehydes etc)
Biological (nitric oxide, prostaglandins, ACH, adenosine – vasodilators)
Social (emotional stress/trauma)
Usually arterial hyperemia is classified as being caused by an endogenous or exogenous agent.
Types of pathological arterial hyperemia according to the mechanism development:
1. Neurotonic or reflex
2. Neuroparalytic
3. Inflammatory arterial hyperemia is due to humoral and reflex mechanisms/
4. Vakat increase blood flow to the discharged space where the air pressure is reduced/
5. Postanemic increased blood flow after ischemia/
6. Postishemic increased blood flow after anemia
7. Collateral arterial hyperemia develops in sudden decrease in blood flow through the main vessel.
Mechanisms of occurrence
The pathogenesis of all types of pathological arterial hyperemia is the same and differs only in the starting moment.
Expansion of the lumen of small arteries and arterioles is achieved due to the realization of neurogenic (neurotonic
and neuroparalytic), humoral, neurohumoral and myoparalytic mechanisms or their combination.
1. Neurogenic mechanism. Distinguish between the neurotonic and neuroparalytic varieties of the neurogenic mechanism of
arterial hyperemia development.
- Neurotonic mechanism. It is in the predominance of the effects of parasympathetic nervous influences (in comparison with
sympathetic) on the walls of arterial vessels.
- Neuroparalytic mechanism. Characterized by a decrease or absence ("paralysis") of sympathetic nerve effects on the walls of
arteries and arterioles.
1) Neuroparalytic arterial hyperemia.
