Endema and Gout — Sodium — Potassium — Magnesium — Videos

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Legs Up the Wall (Viparita Karani)

Edema: Part 1

Edema: Part 2

Capillaries | Biology | Anatomy

Explaining Puffy Outer Ankles

What is the Best Way to Diagnose Gout in the Foot?

How To Reduce Uric Acid Levels

Gout Diet Dos & Don’ts

Nutrition : How to Reduce Uric Acid in Your Diet

How to Treat Gout Naturally

Help Prevent Inflammation

Uric Acid Foods


What is Gout?

Vascular Physiology (Capillary: part 1/6)

Vascular Physiology (Capillary: part 2/6)

Vascular Physiology (Flow rate and Flow velocity: part 3/6)

Vascular Physiology (Total cross-sectional area: part 4/6)

Vascular Physiology (Metabolic hyperaemia: part 5/6)

Vascular Physiology (Organ blood supply: part 6/6)

Cell Transport Physiology (part 1/5)

Cell Transport Physiology (part 2/5)

Cell Transport Physiology (part 3/5)

Cell Transport Physiology (part 4/5)

Cell Transport Physiology (part 5/5)

Capillary Exchange Lecture

Principle of Bulk Flow and Transcapillary Exchange

Sodium Homeostasis: Part 1

Sodium Homeostasis: Part 2

Potassium Homeostasis: Part 1

Potassium Homeostasis: Part 2

Dr Donsbach Manila 1-7 Nutrient Deficiencies

Dr Donsbach Manila 1-8 Edema and Potassium

Dr Donsbach Manila 1-9 Dificiency Diseases

Background Articles and Videos


“…Edema (American English) or oedema (British English; both words from the Greek οἴδημα), formerly known as dropsy or hydropsy, is an abnormal accumulation of fluid beneath the skin or in one or more cavities of the body. Generally, the amount of interstitial fluid is determined by the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or impaired removal of this fluid may cause edema.


Five factors can contribute to the formation of edema:

  1. It may be facilitated by increased hydrostatic pressure or,
  2. reduced oncotic pressure within blood vessels;
  3. by increased blood vessel wall permeability as in inflammation;
  4. by obstruction of fluid clearance via the lymphatic; or,
  5. by changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.[1]


Generation of interstitial fluid is regulated by the forces of the Starling equation.[2] Hydrostatic pressure within blood vessels tends to cause 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 of the higher level of protein in the plasma tends to suck water back into the blood vessels from the tissue. Starling’s equation states that the rate of leakage of fluid is determined by the difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with a fall in reflection coefficient.

Changes in the variables in Starling’s equation can contribute to the formation of edema either by an increase in hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in vessel wall permeability. The latter has two effects. It allows water to flow more freely and it reduces the oncotic pressure difference by allowing protein to leave the vessel more easily.

 Generalized edema

A rise in hydrostatic pressure occurs in cardiac failure. A fall in oncotic pressure occurs in nephrotic syndrome and liver failure. It is commonly thought that these facts explain the occurrence of edema in these conditions. However, it has been known since the 1950s that the situation is more complex and it is still far from completely understood.[3]

Causes of edema which are generalized to the whole body can cause edema in multiple organs and peripherally. For example, severe heart failure can cause pulmonary edema, pleural effusions, ascites and peripheral edema, the last of which effects can also derive from less serious causes.[4]

Although a low plasma oncotic pressure is widely cited for the edema of nephrotic syndrome, most physicians note that the edema may occur before there is any significant loss of protein in the urine or fall in plasma protein level. Fortunately there is another explanation available. Most forms of nephrotic syndrome are due to biochemical and structural changes in the basement membrane of capillaries in the kidney glomerulae, and these changes occur, if to a lesser degree, in the vessels of most other tissues of the body. Thus the resulting increase in permeability that leads to protein in the urine can explain the edema if all other vessels are more permeable as well.

Organ-specific edema

Left and right ring fingers of the same individual. The distal phalanx of the finger on the right exhibits edema due to acute paronychia.

Edema will occur in specific organs as part of inflammation, as in pharyngitis, tendonitis or pancreatitis, for instance. Certain organs develop edema through tissue specific mechanisms.

Examples of edema in specific organs:

  • Cerebral edema is extracellular fluid accumulation in the brain. It can occur in toxic or abnormal metabolic states and conditions such as systemic lupus. It causes drowsiness or loss of consciousness.
  • Pulmonary edema occurs when the pressure in blood vessels in the lung is raised because of obstruction to removal of blood via the pulmonary veins. This is usually due to failure of the left ventricle of the heart. It can also occur in altitude sickness or on inhalation of toxic chemicals. Pulmonary edema produces shortness of breath. Pleural effusions may occur when fluid also accumulates in the pleural cavity.
  • Edema may also be found in the cornea of the eye with glaucoma, severe conjunctivitis or keratitis or after surgery. It may produce coloured haloes around bright lights.
  • Edema surrounding the eyes is called periorbital edema or eye puffiness. The periorbital tissues are most noticeably swollen immediately after waking, perhaps due to the gravitational redistribution of fluid in the horizontal position.
  • Common appearances of cutaneous edema are observed with mosquito bites, spider bites, bee stings (wheal and flare), and skin contact with certain plants such as Poison Ivy or Western Poison Oak,[5] the latter of which are termed contact dermatitis.
  • Another cutaneous form of edema is myxedema, which is caused by increased deposition of connective tissue. In myxedema (and a variety of other rarer conditions) edema is due to an increased tendency of the tissue to hold water within its extracellular space. In myxedema this is because of an increase in hydrophilic carbohydrate-rich molecules (perhaps mostly hyaluronan) deposited in the tissue matrix. Edema forms more easily in dependent areas in the elderly (sitting in chairs at home or on aeroplanes) and this is not well understood. Estrogens alter body weight in part through changes in tissue water content. There may be a variety of poorly understood situations in which transfer of water from tissue matrix to lymphatics is impaired because of changes in the hydrophilicity of the tissue or failure of the ‘wicking’ function of terminal lymphatic capillaries.
  • In the case of human feet, the Starling forces are always a long way out of balance, because the variation in hydrostatic pressure in the vessels in the feet as compared to the face is about a metre of water. In severe heart failure the change in central venous pressure is tiny in comparison and cannot explain why edema of the feet develops simply through an effect on capillary leakage. Three other factors may be involved. If the central venous pressure rises to equal that of the thoracic lymph duct then clearance of fluid from the tissue will be impeded (see below). That is to say the edema may actually be caused by a change in output of fluid from the tissue, as much as input to the tissue. Secondly, severe heart failure is one of the most exhausting conditions there is. The sufferers tend to spend what little effort they can make trying to breathe with edematous lungs. They tend to sit up to make breathing easier and their feet hang immobile on the floor. Immobility is perhaps the commonest of all causes of edema, because clearance of fluid via the lymphatics needs muscle action. Thirdly, in severe heart failure endocrine and neural changes alter the way tissues are perfused in ways that are not fully understood.
  • In lymphedema abnormal removal of interstitial fluid is caused by failure of the lymphatic system. This may be due to obstruction from, for example, pressure from a cancer or enlarged lymph nodes, destruction of lymph vessels by radiotherapy, or infiltration of the lymphatics by infection (such as elephantiasis). It is most commonly due to a failure of the pumping action of muscles due to immobility, most strikingly in conditions such as multiple sclerosis, or paraplegia. Lymphatic return of fluid is also dependent on a pumping action of structures known as lymph hearts. It has been suggested that the edema that occurs in some people following use of aspirin-like cyclo-oxygenase inhibitors such as ibuprofen or indomethacin may be due to inhibition of lymph heart action.  …”



Capillaries (pronounced /ˈkæpəˌlɛri/) are the smallest of a body’s blood vessels and are part of the microcirculation. They are only 1 cell thick. These microvessels, measuring 5-10 μm in diameter, connect arterioles and venules, and enable the exchange of water, oxygen, carbon dioxide, and many other nutrient and waste chemical substances between blood and surrounding tissues.[1]



Blood flows from the heart to the arteries, which branch and narrow into the arterioles, and then branch further still into the capillaries. After the tissue has been perfused, capillaries join and widen to become venules and then widen more to become veins, which return blood to the heart.

The “capillary bed” is the network of capillaries supplying an organ. The more metabolically active the cells, the more capillaries they will require to supply nutrients and carry away waste products.

Metarterioles provide direct communication between arterioles and venules and are important in bypassing the bloodflow through the capillaries. True capillaries branch mainly from metarterioles and provide exchange between cells and the circulation. The internal diameter of 8 μm forces the red blood cells to partially fold into bullet-like shapes and to go into single file in order for them to pass through.

Precapillary sphincters are rings of smooth muscles at the origin of true capillaries that regulate blood flow into true capillaries and thus control blood flow through a tissue.


There are three types of Capillaries:

  • Continuous – Continuous capillaries have a sealed endothelium and only allow small molecules, like water and ions to diffuse. Continuous capillaries have tight junctions and can be further divided into two subtypes:
  1. Those with numerous transport vesicles that are primarily found in skeletal muscles, lungs, gonads, and skin.
  2. Those with few vesicles that are primarily found in the central nervous system. These capillaries are a constituent of the blood-brain-barrier.
  • Fenestrated – Fenestrated capillaries (derived from “fenestra,” the Latin word for “window”) have pores in the endothelial cells (60-80 nm in diameter) that are spanned by a diaphragm of radially oriented fibrils and allow small molecules [2][3] and limited amounts of protein to diffuse. In the renal glomerulus there are larger fenestrae which have no diaphragms (although there are pedicels (podocyte foot processes) that have slit pores with an analogous function to the diaphragm of the capillaries). Both types of fenestrated blood vessels have continuous basal lamina and are primarily located in the endocrine glands, intestines, pancreas, and glomeruli of kidney.
  • Sinusoidal – Sinusoidal or discontinuous capillaries are special fenestrated capillaries that have larger openings (30-40 μm in diameter) in the endothelium to allow red and white blood cells (7.5μm – 25μm diameter) and various serum proteins to pass, a process that is aided by a discontinuous basal lamina. These capillaries lack pinocytotic vesicles and gaps may be present in cell junctions permitting leakage between endothelial cells. Sinusoid blood vessels are primarily located in the liver, spleen, bone marrow, lymph nodes, and adrenal gland.

The membrane in the capillary is only 1 cell thick and is squamous epithelium.


The capillary wall is a one-layer endothelium that allows gas and lipophilic molecules to pass through without the need for special transport mechanisms. This transport mechanism allows bidirectional diffusion depending on osmotic gradients and is further explained by the Starling equation.

Capillary beds may control their blood flow via autoregulation. This allows an organ to maintain constant flow despite a change in central blood pressure. This is achieved by myogenic response and in the kidney by tubuloglomerular feedback. When blood pressure increases the arterioles that lead to the capillaries bed are stretched and subsequently constrict to counteract the increased tendency for high pressure to increase blood flow. In the lungs special mechanisms have been adapted to meet the needs of increased necessity of blood flow during exercise. When the heart rate increases and more blood must flow through the lungs capillaries are recruited and are also distended to make room for increased blood flow. This allows blood flow to increase while resistance decreases.

Capillary permeability can be increased by the release of certain cytokines, anaphylatoxins, or other mediators (such as leukotrienes, prostaglandins, histamine, bradykinin, etc.) highly influenced by the immune system.

The Starling equation defines the forces across a semipermeable membrane and allows calculation of the net flux:

\ J_v = K_f ( [P_c - P_i] - \sigma[\pi_c - \pi_i] )


  • ([PcPi] − σ[πc − πi]) is the net driving force,
  • Kf is the proportionality constant, and
  • Jv is the net fluid movement between compartments.

By convention, outward force is defined as positive, and inward force is defined as negative. The solution to the equation is known as the net filtration or net fluid movement (Jv). If positive, fluid will tend to leave the capillary (filtration). If negative, fluid will tend to enter the capillary (absorption). This equation has a number of important physiologic implications, especially when pathologic processes grossly alter one or more of the variables.

 The variables

According to Starling’s equation, the movement of fluid depends on six variables:

  1. Capillary hydrostatic pressure ( Pc )
  2. Interstitial hydrostatic pressure ( Pi )
  3. Capillary oncotic pressure ( πz )
  4. Interstitial oncotic pressure ( πi )
  5. Filtration coefficient ( Kf )
  6. Reflection coefficient ( σ )
Illu capillary microcirculation.jpg
  • Note that oncotic pressure is not illustrated in the image.

Dr Donsbach Manila 1-1 PCAM Opening Ceremonies

Dr Donsbach Manila 1-2 Taking Charge

Dr Donsbach Manila 1-5 Allopathic Medicine

Dr Donsbach Manila 1-6 Wholistic Medicine

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