Thursday, 28 February 2013

Abnormalities of Haemostasis

Hi, in this post we'll take a look at what happens when the haemostatic mechanism doesn't work properly. We'll take a look at haemorrhage, thrombosis, and emboli.


Haemorrhage is the loss of blood from a damaged blood vessel. It can occur externally, into a body cavity or into tissue spaces. Haemorrhage can be caused by several factors including:
  • Mechanical trauma: eg a bruise (which is also known as a contusion)
  • Congenital or acquired vessel wall weakness: eg arteriosclerosis
  • Toxic damage to the endothelium: eg arsenic poisoning
  • Disorders of the clotting mechanism: this can be seen in hemophilia. 
Small, pinpoint haemorrhages in mucous membranes and the skin are called petechiae. Grossly, these look like little red dots on the skin or mucous membrane. Larger haemorrhages that cause lesions similar to petechia are ecchymoses. Petechiae are less than a centermeter in diameter while ecchymoses are 2-3cm in diameter.


Diapedesis refers to the microscopic leakage of a small amount of blood cells through intact vessels into the surrounding extravascular tissue. It is not true haemorrhage.   


Haemorrhage may occur in several parts of the body and the nomenclature reflects this. For example: a haemorrhage in the thorax is known as haemothorax and a haemorrhage in the pericardium is referred to as haemopericardium. Similarly, haematemesis refers to the vomiting of blood and haematuria is blood in the urine.   

The Resolution of a Significant but Non-Fatal Haemorrhage

Once a significant but non-fatal haemorrhage has occurred the body employs several mechanisms to increase the blood volume and to return blood pressure to its normal level. This occurs in three phases:

Phase 1
In this phase the body tries to maintain blood flow to the vital organs.
  1.  The blood remaining in the body is redistributed.
  2. This lowers the venous return.
  3. This results in a decrease in cardiac output
  4. Arterial blood pressure falls 
  5. The carotid and aortic bodies detect this and stimulate the vasomotor centres which send out a strong sympathetic signal.
  6. The superficial blood vessels as well as those leading to and from the spleen (splenic vessels) narrow. This causes blood to be directed towards the vital organs (the brain and respiratory muscles). 
  7. Tachycardia occurs.
  8. Adrenalin and Noradrenalin are released
  9. Noradrenalin is a general vasoconstrictor but causes coronary arteries to dilate.
  10. The fall in blood pressure also causes the kidneys to release renin which cause the production of angiotensin which is a strong peripheral vasocontrictor. Aldosterone is also released, this causes more sodium to be reabsorbed at the kidneys which means that more water is retained in the blood.
Phase 2
In this phase the body tries to restore the blood volume.
  1. Despite the mechanisms utilised by the body in phase 1, the blood volume is bound to fall. 
  2. Due to the loss of blood, some plasma proteins have been lost. However, most plasma proteins remain in the blood vessels. This creates an osmotic force which pulls the fluid from the extravascular spaces into the circulation.  
Phase 3
  1. Erythropoiesis occurs and the red blood cell and haemoglobin content of the blood is restored to normal. The liver also increases its production of plasma proteins. 
  2. Reticulocytes and metarubricytes (immature red blood cells) circulate the blood after about 4 days.  

 The Resolution of Haemorrhage at Tissue Level
  1. Haemorrhage releases many red blood cells (RBCs) into the area as well as plasma and some other cell types. 
  2. RBCs breakdown, releasing haemoglobin. Most RBCs stay at the site of the haemorrhage but some will enter the circulation. 
  3. In the tissues, macrophages are attracted to the site of the haemorrhage where they phagocytose RBCs through erythrophagocytosis.
  4. The haemoglobin that is within RBCs phagocytosed by the macrophages is broken down to iron and bilivedin (which makes the green colour of a bruise). Biliverdin is then metabolised to bilirubin (orange-brown) and then released into the circulation to be transported to the liver by albumin where it is excreted in bile. 
  5. Haemoglobin is also released into the circulation and is transported to the liver bound to plasma proteins and recycled into bilirubin and then excreted in bile.
  6.  Macrophages store iron from the RBCs in haemosiderin molecules. Iron is slowly recycled from these molecules. 
  7. Globin is broken down within the macrophages into amino acids which are recycled.
  8. Haemorrhage release plasma proteins, including fibrinogen into the tissues. When fibrinogen leaves the vascular system it is converted to fibrin which encourages fibroblasts to enter and produce fibrous connective tissue (fibrosis).
As mentioned in the previous post, thrombosis occurs when the haemostasis mechanism isn't activated properly or there is "too much" haemostasis. Sluggish blood flow, irregularities in the vascular wall, and hypercoagulability of the blood predispose a region to thrombosis.

The Consequences of Thrombosis

Once a thrombus has been formed there are three potential four potential outcomes which may occur:
  1. Cause immediate death: particularly if the vessel supplies a critical organ (eg. brain, heart).
  2. Be lysed by the fibrinolytic system: plasmin causes fibrin to break down.
  3. Undergo Organisation: If the thrombus does not completely block the lumen of the vessel, endothelium may migrate over the thrombus to restore vascular integrity. Fibrocytes then cause collagen to be produced over the fibrin, causing it to contract and the size of the thrombus decreases. If the thrombus does occlude the vessel, cells may migrate through the thrombus to create small vascular channels for blood to flow through.
  4. Produce emboli.
An emboli is a plug of some material that travels throughout the circulation system. When the embolus reaches a part of the system where it is too narrow for it to pass through, it causes a blockage called an embolism. Often the embolus comes from a thrombus but it may arise from air, fat, parasites, bone marrow etc.

How much damage a thrombus or embolus causes depends on the vascular anatomy of the area which it blocks. If the tissue has an end arterial blood supply, infarction (death) of the tissue will occur. This can occur in the brain, heart, spleen, kidney and intestine. If the contents of the embolus have a high tendency to cause the formation of more thrombi, disseminated intravascular coagulation may occur. If a collateral circulation of the region affected by the embolus is present, it is likely that there will be no effect.

Thrombus vs Post-Mortem Clot

Once an animal dies, its blood is likely to form clots and it is important to be able to distinguish between post mortem clots and thrombi.

Clots tend to be moist, granular and rough while thrombi are dry, smooth and shiny. Thrombi are white or buff in colour while clots are red or yellow. In addition thrombi form attached to the vascular wall and are stratified as layers of fused platelets are added to the damaged endothelium during blood flow in a living animal. Clots are not attached to the vessel walls and are uniform in consistency as they develop from fibrin in a stagnant column of blood in the dead or dying and contain all blood elements trapped in the fibrin. The vascular endothelium remains intact.  Finally, thrombi may be partially organised and vary in shape while clots are never organised and mould the blood vessels like jelly. 

That's it for this post, see you next time :)



Hello, in this post we'll be taking a look at how the body prevents blood from escaping its vessels - a process called haemostasis. We'll take a look at how haemostasis works and how it is regulated which will include an explanation of the coagulation cascade. 


Haemostasis is the arrest of the escape of blood from a blood vessel. This is achieved through the formation of a thrombus: a compact mass of aggregated platelets and fibrin that build up in a blood vessel of an animal. It is formed by the interaction between platelets, blood vessel walls and clotting factors and is the end-product of coagulation. After a vessel ruptures, the thrombus slows down the blood flow which initiates healing.

When the coagulation system is functioning properly this is referred to as haemostasis. When there is "too much" haemostasis or the mechanism isn't activated properly, it is referred to as thrombosis. "Too little" haemostasis leads to haemorrhage.

How does Haemostasis Work? 

Haemostasis occurs as a result of interactions between blood vessel walls, platelets and soluble clotting factors.

Blood Vessel Walls

Blood vessels leading to and from capillary beds contain a layer of smooth muscle in their walls. This smooth muscle promotes laminar flow. If there are irregularities on the lining of the vessel, turbulent flow occurs and this may lead to blood clotting and the formation of thrombi. Endothelial cells release a variety of substances which have opposing effects to try and counterbalance haemorrhage and thrombosis.

The mechanisms used by the endothelial cells to prevent clotting include antiplatelet factors, anticoagulant factors, and fibrinolytic factors. Antiplatelet factors include:
  • A physical barrier: the endothelial cells separate the platelets and subendothelial collagen.
  • Vasodilators: these include prostacyclin and nitric oxide
  • Adenosine diphosphatase: this degrades ADP and inhibits platelet aggregation.
The endothelial cells also secrete substances that prevent coagulation from occurring. These include:
  • Heparin-like molecules: these bind to AT-III (Antithrombin 3) and increases its ability to inactivate thrombin.
  • Thrombomodulin: this binds to thrombin and converts it to an anticoagulant which activates Protein C. Protein C inhibits coagulation.
Fibrinolytic factors, such as t-PA, are also secreted. t-PA promotes fibrinolytic activity to clear fibrin deposits from endothelial cells.

Endothelial cells have products with prothrombotic properties. These are:
  • Von Willebrand Factor: this is a cofactor of Factor VIII and helps platelets stick to collagen
  • Tissue Factor: this is also known as Factor III and activates the extrinsic clotting cascade. 
  • Inhibitors of plasminogen activators: these prevent plasminogen from being converted to plasmin and so fibrin remains intact. 
  • Endothelins: these are potent vasoconstrictors.   

Platelets and Soluble Clotting Factors

The following diagram provides an overview of haemostasis and shows how the platelets and soluble clotting factors (which make up the coagulation cascade) work together. 

Overview of Haemostasis

The job of the platelets in haemostasis is to form the primary haemostatic plug which works to prevent blood from escaping the vessel. This plug works well in the short term but it isn't quite stable as the process is reversible. The formation of the primary haemostatic plug occurs in three stages: platelet adhesion, platelet secretion and platelet aggregation.

  • Platelet Adhesion: when the wall of the blood vessel is damaged, the platelets become exposed to the subendothelial collagen. Prostacyclin (a substance that prevents platelet activation and causes vasodilation) production decreases and this encourages platelets to adhere to the irregularity in the vessel wall. 
  • Platelet Secretion: platelet adhesion cause the synthesis and secretion of substances that will augment platelet adhesion and encourage platelet aggregation. These include:
    • ADP which attracts more platelets to the area which results in more ADP release and a positive feedback loop.
    • Thromboxane A2 which causes vasoconstriction and platelet aggregation. 
    • Serotonin, this also causes vasoconstriction
    • Von Willebrand Factor, this helps the platelets stick to the collagen. 
    • Platelet factor 3 which participates in the formation of thrombin and factor VIII
    • Platelet factor 4. This inhibits the action of heparin (heparin prevents clotting) and Fibrin Degradation Products (FDPs)
    • Fibrinogen. This is used in the formation of the secondary haemostatic plug
    • Tissue Factor: this triggers the coagulation cascade.
  • Platelet Aggregation: when the platelets have stuck to the exposed collagen and have secreted their prothrombotic substances they also change shape which encourages more aggregation. This causes the primary haemostatic plug to form. 
The tissue damage also directly activates coagulation and causes the vascular endothelium to become prothrombotic. Since the coagulation cascade was triggered by the release of Tissue Factor by the platelets, thrombin is formed and this promotes further platelet aggregation. Thrombin also causes the conversion of fibrinogen to fibrin and this firmly "glues" the primary haemostatic plug in place, forming the secondary haemostatic plug which is irreversible. 

The diagram above also explains how the process is regulated (the red, purple and navy writing). We'll explore that part when we take a closer look at the coagulation cascade and how it is regulated and that should help you to make sense of that part of the diagram.

The Coagulation Cascade

Okay, so here's where it gets a bit complicated. I've drawn a diagram (below) to try and simplify the process. I would definitely sit down and take some time to try and fully understand the process :) I'll be referring to this diagram during my explanation.

The coagulation cascade can be broken down into three pathways: the intrinsic, extrinsic and common pathways.

The Extrinsic Pathway

This is the simplest of the three. Tissue damage causes the release of Tissue Factor (TF - also known as Factor III). Tissue factor causes factor VII to be activated (VIIa). Factor VII and Ca ions work together to activate factor X and initiate the common pathway. 

 The Intrinsic Pathway
Tissue damage triggers the intrinsic pathway by causing the activation of Factor XII which in turn activates Factor XI (XIa). Factor XIa then forms a complex with Factor VIIIa and Ca ions which goes on to activate Factor X (triggering the common pathway).

The Common Pathway

Activated Factor X along with activated factor V and Calcium ions cause the conversion of Factor II to Factor IIa (Thrombin). Thrombin causes the conversion of fibrinogen to fibrin and Factor XIIIa catalyses the formation of covalent bonds which cross link adjacent fibrin molecules, making them insoluble.This fixes the thrombus in place.

Regulation of the Coagulation Cascade

There are three main groups of substances which are used to regulate the coagulation cascade:
  • Fibrinolytic agents: they promote the breakdown of fibrin and try to reduce the size of the thrombus and prevent additional fibrin from forming. This group includes:
    • Plasmin which causes fibrinolysis. Plasmin is converted from plasminogen when tissue damage occurs
    • Protein C: this inhibits alpha 2 - antiplasmin (which antagonises plasmin), thus promoting fibrinolysis. 
  • Coagulation Inhibitors: These work to prevent coagulation from occurring. They include:
    • Atithrombin III (AT-III): which inhibits thrombin and IXa and Xa. The inhibition of thrombin causes factors V, VIII, XI and XIII to be deactivated.
    • Protein S: this degrades factors V, VIIIa and Xa.
    • Fibrin Degradation Products (FDPs): which inhibit thrombin. 
  • Fibrinolytic Inhibitors: these try to prevent the fibrinolytic agents from working so that the thrombus can dissolve at a slow and appropriate rate. They include alpha 2-antiplasmin and PAI (Plasmin Activator Inhibitor). 

That's all for now, in the next post we'll take a look at what happens when haemostasis doesn't work properly. I hope this post will help you understand the process, if you have any questions please feel free to ask in the comments section below :)   

Friday, 22 February 2013


Hello, in this post we're going to be discussing the energy that is contained in food and how the body utilises this energy. We'll take a look at what energy actually is, how we measure it, how the body uses the energy contained in food, and finally Atwater factors and what they are used for. Enjoy!

What is Energy?

Energy is not strictly a nutrient but it is a major component of food. It is "the ability to do work" and allows reproduction, growth, lactation and the maintenance of life processes to occur in the body. Both nutrients and energy are required in feed.

Energy is an important aspect of the feed requirements of animals. If an animal's diet is energy deficient problems may arise. This includes poor growth and production, weight loss, decreased efficiency of nutrient utilisation, impaired reproductive efficiency and even a reduced ability to exercise. If an animal receives too much energy in it's diet similar problems may occur.

Units of Energy

Two units of energy are commonly used: the joule and the calorie. A calorie is the amount of heat energy required to raise the temperature of 1 gram of water from 14.5° C to 15.5° C. 1 calorie equals 4.184 joules and 1 joule = 0.239 calories.  

Partitioning of Energy 

The partition of energy is a system that determines the amount of energy available to the animal after digestion, metabolism, maintenance of homeostasis, and production requirements have occurred. This website has a good flow diagram which illustrates this process. (Figure 2.5, its about 1/2 down the page.)  

In Australia we use Digestible Energy (DE), Metabolisable Energy (ME), and Net Energy (NE) to describe energy in feed. DE is used in diets for horses, poultry and pigs. ME is used for ruminants, dogs, cats and humans. NE can also be used for cattle and pigs. 

Gross Energy

 Gross energy (GE) is the total energy content of a feed. It is measured by complete combustion of the sample in a bomb calorimeter. GE doesn't have a biological value because the utilisation of energy in an animal is never 100% efficient.

Digestible Energy

This is the amount of energy that is absorbed by the gastrointestinal tract. It gives us an idea of the amount of energy the animal has available to use. However, it only partially accounts for the energy lost during the utilisation of the nutrients. DE is the difference between the gross energy and the faecal energy (the energy that isn't digested or absorbed and is lost in faeces.) Ie:
DE = GE - faecal energy
 Faecal energy includes undigested feed, enteric microbes and their products, excretions into the GIT and cellular debris from the GIT. Now, when it comes to faecal energy (FE), you can get either true FE or apparent FE. Apparent FE doesn't take into consideration the endogenous contributions to faecal energy. True FE does take into consideration the metabolic contributions from the gastrointestinal tract, bacteria and protozoa. 

Metabolisable Energy

Metabolisable Energy (ME) is the amount of chemical energy that is available for use by the cells. It is the difference between the energy available for absorption by the GIT (DE) and the energy lost in urine (UE) and the gaseous products of digestion (GDP). Ie:
ME = DE - (UE + GDP) 

It can be quite difficult to measure how much energy is lost in urine and the gaseous products of digestion and so conversion formulae are often used. For example, in ruminants, ME = 0.81 x DE. In pigs ME = 0.96 x DE.

Net Energy

Net energy (NE) represents the true amount of energy available for maintenance, work and production. "It's what's left over at the end". It is calculated using the formula:
NE = ME - heat increment
The heat increment is the heat produced from digestion and absorption and comes mainly from the viscera. There are four sources of heat increment:
  1. Heat of digestion: the heat given off by the chemical reactions in the digestive tract
  2. Heat of fermentation: this is given off by chemical reactions in the bacteria of the digestive tract
  3. Heat of waste product formation: this is given off in the making of waste products, especially urea and uric acid.
  4. Heat of nutrient metabolism: this is the total heal from all other sources. 
Net Energy can be divided into the energy required for maintenance and the energy required for production. 


Maintenance energy is the amount of energy required by the animal for the continuation of simple life without change in body composition or weight. There are three components to maintenance energy: Basal Metabolic Rate (BMR), muscular work, and thermoregulation.  

BMR is the energy used to keep cells alive and to maintain organ function. In order to measure BMR, the animal must be awake and at rest, it must be in a thermoneutral environment, and no nutrients must be absorbed during measurement. BMR is affected by several factors including:
  • Body Size: larger animals require a higher energy input for maintenance but smaller animals use more energy per kilogram of body weight. This is due to an increased surface area to volume ratio which makes thermoregulation more expensive in terms of energy requirements. 
  • Sex: males tend to have higher BMRs than females. 
  • Age: younger animals have higher BMRs than older ones.
  • Previous level of nutrition: animals that have been fasted will have a lower BMR as their bodies' have adapted to a lower energy intake.
  • Species: BMRs differ between species.
  • Climate: if the climate does not match the animals thermoneutral zone, the animal needs to use more energy to increase or decrease its body temperature affecting BMR.
 Some of the maintenance energy is used for muscular work. This includes normal activity levels for an animal that leads a simple life (ie. not a racehorse or working dog). The intensity and duration of work will affect the amount of energy required. 

The regulation of temperature also requires energy which falls under the maintenance category. If an animal is too hot or too cold it will spend energy trying to heat or cool itself. 


If the energy in an animal's food exceeds the maintenance requirement, the left-over energy is known as retained energy. This energy is used by the body to produce milk, muscle, to support pregnancy, wool etc. However, the retained energy is never the same as the true amount of energy in excess after the maintenance energy has been supplied. This is because some energy is used up in the process of producing the meat, wool, milk etc. 

Atwater Factors

Atwater factors are used to predict the energy content of foods from the proximate analysis. Atwater factors work well for highly digestible foods (such as sugars and starches) but they may not be applicable for diets high in fibre. Modified Atwater factors are used for dogs and cats and take in to consideration the digestibility of the carbohydrates, fats and protein in pet food.

That's all for this topic, if you have any questions please feel free to ask :)

Abnormalities of Blood Flow

Hello :) The next few Pathology posts will discuss the effects of vascular disturbances in the body. This post will address abnormalities in blood flow which may occur, particularly hyperaemia, blood volume expansion and ischemia. 


Simple put, hyperaemia occurs when there is too much blood in a part of the vascular system. Hyperaemia can be active of passive and both types can be acute (rapidly developing) or chronic (slowly developing). 

Active Hyperaemia

Active Hyperaemia occurs when the blood vessels leading to an area of the body actively dilate and cause an increased flow of blood to that area. Active hyperaemia appears as a red/pink region on the surface of an organ (this is due to the increased supply of oxygenated blood). It may be pathological (occurs as a part of disease) or physiological (occurs normally). Active hyperaemia is pathological when it occurs as part of inflammation. If the active hyperaemia is pathological, inflammatory cells and engorged blood vessels will be seen histologically. Examples of when physiological hyperaemia may occur include:
  • Blushing
  • During Digestion
  • Muscles during exercise
 Passive Hyperaemia

Passive hyperaemia is always pathological and is also known as congestion. It occurs because the venous drainage leading from a part of the body is reduced. Passive hyperaemia is usually quite a problem because the affected area does not receive a good oxygen supply. In addition, because poor drainage is present metabolic wastes build up and add further insult to injury. Passive hyperaemia appears as a dull red colour on the surface of an organ. An example of passive hyperaemia is when a tourniquet has been applied to a limb and the outflow of blood is obstructed.

Blood Volume Expansion

When there is too much blood flowing in the circulatory system (this may be due to polydipsia, high salt intake or done intentionally [eg. blood doping]) the body uses mechanisms to try and reduce the amount of blood in the system. The increase in blood volume causes an increase in atrial stretch and pressure. This stimulus triggers the cardiomyocytes to release ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide) which causes a reduction in the extracellular fluid volume and blood pressure by causing:
  • Vasodilation: this causes more blood to enter tissues and so less is able to return back to the heart, reducing atrial stretch and pressure. 
  • Increased glomerular filtration rate: this increases the amount of blood that is filtered by the kidneys and also allows more Na to be excreted in the urine (increasing urine production). 
  • Increased sodium excretion: Since water tends to follow sodium in the body, this reduces the amount of water drawn into the blood by Na.
  • Inhibition of the Renin-Angiotensin-Aldosterone System (RAAS): this prevents the hypertension that is caused by the RAAS (see this post).
  • Increased vascular permeability: this increases the amount of blood that enters the tissues. 
  • Inhibited endothelin release (endothelins normally constrict blood vessels and increase blood pressure)
  • Inhibited vascular smooth muscle, endothelial cell and cardiac myocyte proliferation: this prevents the blood vessels from narrowing.


Ischemia occurs when there is not enough blood in a region of the circulatory system. It may be caused by anaemia (generalised ischemia), an intramluminal blockage of the vessel (eg a blood clot) or an extraluminal blockage of the vessel (eg by a tumor) - the latter two would be considered localised ischemia. Ischemic regions of an organ appear pale and will feel cool in a live animal. If the ischemia occurs rapidly, the cells in the affected area are likely to die to due a poor oxygen supply. However, if ischemia progresses slowly, tissues may be able to adapt.  

That's all for now, see you next time :)

Processes in Animal Disease

Hi :) Another unit I'll be taking this semester is called Processes in Animal Disease, which is basically General Pathology. Pathology is the study of structural and functional abnormalities (disease) in cells, tissues, organs and body systems. There are nine basic pathological processes:
  1. Circulatory Disturbances
  2. Acute Inflammation
  3. Healing and Repair
  4. Chronic Inflammation
  5. Necrosis and Calcification
  6. Adaptive Tissue Responses
  7. Storage diseases, Pigments and Infiltrates
  8. Neoplasia
  9. Teratology
 We'll be learning about these throughout the semester and I'll be publishing posts which explain these processes as I learn them myself. 

I hope you enjoy these series of posts - it seems like it's going to be a very interesting unit. If you have any questions, comments, or ideas about how I can improve my posts please let me know in the comments at the end of each post :)

Wednesday, 20 February 2013

Feed Analysis

Hello :) As explained in the previous post, the composition of feed can be variable. Because of this, it is important to measure the nutritive values of a feed. How can we do this? This post will address this question by introducing you to the major chemical analyses of feeds used in animal nutrition. We'll take a look at proximate analysis and how it can be used to figure out Dry Matter, Crude Protein, Crude Fat, Crude Fibre, Ash and Nitrogen Free Extract that is in the food we give to animals.

Proximate Analysis 

This method of analysis separates the components of food into broad chemical groupings. The proximate analysis can be conducted using wet chemistry or NIR. 

Wet chemistry is more traditional and accurate, but can be time consuming and expensive. NIR is a faster and cheaper alternative but its accuracy relies on the technique and calibration used.

Proximate analysis separates feed contents into six groups: Moisture, Crude Protein (CP), Crude Fat, Crude Fibre, Ash, and Nitrogen Free Extract. 

This website has an excellent flow diagram that summarises the process that I will explain below. I recommend following this diagram as we go through the process in detail. 


The original sample of food is either freeze dried or oven dried and the remainder of the sample is termed the moisture-free sample. This represents the amount of dry matter in the food. Thus the amount that evaporated represents the amount of moisture in the food. 

The formula to calculate dry matter (expressed as a percentage) is:
 DM = weight after drying / weight before drying X 100 
This information is used to express the content of the other nutrients on a "dry matter basis" (without moisture) or "as fed" (with moisture).

 Crude Protein

The nitrogen content of food is used to estimate the amount of protein present. There are two methods to measure nitrogen content: LECO and Kjeldahl. The LECO method is the most widely used method today. Crude protein relies on the fact that an average protein has approximately 16% nitrogen. Thus Crude Protein may underestimate or overestimate the true amount of protein present. It is also a poor indicator of protein quality. 

Crude protein is calculated as follows:
Crude Protein = N concentration X 6.25

 Crude Fat

Crude Fat (aka Ether Extract) represents the proportion of food that is soluble in a solvent. Thus in order the calculate this value, the sample is now placed in a solvent. The amount remaining after this step is used to calculate Crude Fat as shown below:
Crude Fat = Sample of food - fat free residue
 This amount is then divided by the amount of dry matter and the answer multiplied by 100 to calculate Crude Fat on a DM basis.


The sample is now boiled in acid and then boiled in alkali and then burnt in a furnace. The residue remaining after this is the Ash content of the food. It represents the inorganic component of the food, particularly minerals and may give an indication of diet quality. Diets high in ash are typically of lower quality or may be contaminated with other substances. This can be calculated on a dry matter basis as follows:
Ash (%) = Ash (in grams) / DM (g) X 100
Crude Fibre

This is the substance that remains after the sample is boiled in acid and alkali and burnt. 
Crude Fibre = % fat free residue - % ash 
 Crude fibre is the least accurately determined component as miscalculations earlier on in the process may be compounded during this step. The availability of this fibre for energy is also dependent on the type of fibre present and the ability of different species to digest fibre. 

Nitrogen Free Extract
Nitrogen free extract (NFE) is calculated by subtracting all the other components of the feed from the original sample of food. Ie:
NFE = 100% - (%Crude Protein + %Crude Fat + %Crude Fibre + %Ash + %Moisture) 
 NFE provides a reasonable indicator of the quantities of readily available carbohydrates, such as sugar and starch, in the food. It represents everything that we haven't yet measured in the proximate analysis.

That's it for now, if you have any questions please feel free to ask in the comments section below :)


Hello, this post will start off the first module of our Veterinary Nutrition and Animal Toxicology unit. We'll take a look what a nutrient is, some important definitions, the 8 categories of feedstuffs as well as the variation in the proportions of nutrients in different feedstuffs.

What is a Nutrient?

A nutrient is defined as any chemical compound that is required for normal reproduction, growth, lactation, or maintenance of life processes. Sometimes we can get compounds that are not required by the body but are still useful to it. This includes things such as starch and fibre which aren't absolutely essential but are still helpful to the body. The major nutrients that can be found in food include proteins, fats, carbohydrates, minerals, vitamins and water. 


An animal's diet needs to supply it with both nutrients and energy. Energy is stored in the chemical bonds that are present in food and this energy is released after digestion, absorption and intermediary metabolism (see the Biochemistry posts for more info on these processes). Energy isn't strictly considered a nutrient but it is a main component in food. It is the "ability to do work" and allows normal reproduction, growth, lactation and the maintenance of life processes to occur.

Important Definitions

Before we continue on with the rest of this nutrition unit, it is helpful to understand the meaning of a few terms:
  • Food: is an edible material that provides nutrients to the animal
  • Feed: is used to describe animal food
  • Feedstuff: this is any material that is made into or used as feed.  There are 8 categories:
    1. Dry forage ( hay and pasture)
    2. Pasture, range plants, feeds that are cut and fed green.
    3. Silages
    4. Energy concentrates (cereal grains, fats, and oils)
    5. Protein supplements
    6. Minerals
    7. Vitamins
    8. Additives
  • Diet: this is a mixture of feedstuffs which supply nutrients to the animal.
  • Ration: a daily allocation of food. 


The amount of a certain nutrient that is contained in a feedstuff is variable between ingredients as well as within ingredients. For example young grass can be composed of 5% protein but soybean meal can contain 46.7% protein. In addition, the protein content of oaten hay can range from 4 - 12.5%.

Rations need to take into consideration this variation to ensure that the animal receives the required amount of nutrients and energy.

Feedstuffs that originate from plants generally contain a higher amount of carbohydrates than animal-based foods. However, the composition of plants is more variable than between animal species.

The proportions of nutrients will change in an animal with age. As the animal gets bigger, fat content increases and water content decreases. 

That's it for this post, see you next time :)

Tuesday, 19 February 2013

Veterinary Nutrition and Animal Toxicology

Hi, I hope you all had a good Christmas and New Year :) I'm back from our summer holidays here in Australia and I'm ready to get back into the swing of things at uni!

One of our units this semester is called Veterinary Nutrition and Animal Toxicology. There are seven components of the unit: nutrients, feed analysis and feed stuffs; vitamins and minerals; equine nutrition; ruminant and camelid nutrition; pigs and poultry; companion animals; and finally toxicology.

I'll publish new posts which will cover each aspect of these modules as I learn them myself. It seems like it will be an interesting and unit to study. I'm sure the things we'll learn will be very useful for us to know in the future. 

As always, if you have any questions or comments about anything I mention in the posts please feel free to let me know in the comments section at the end of each post. Your questions and feedback are very welcome :)