Veterinary Physiology Phase 3

What is the normal pH of the body?

Between 7.35-7.45 (venous and arterial blood).

pH below 7 = acidic.

pH above 7 = alkaline.

Movement out of this range will affect metabolism.

An abnormal pH of the body will cause proteins to become denatured with enzymes losing their ability to function.

What affects pH in the body?

Changes on acids and bases in the body affect pH.

Increase in acid and decrease in base lowers blood pH - acidaemia.

Increase in base and decrease in acid elevates blood pH - alkalaemia.

Hydrochloric acid is an example of an acid.

Bicarbonate is an example of a base.

What does the alteration of pH affect?

Osmolarity.

Body fluid enzymes.

Enzyme activities.

Transportation.

Membrane potentials.

Nerve and muscle function.

How do hydrogen ions link to pH?

The function of all body systems are affected by abnormal H+ concentrations.

pH is another way of writing H+ concentrations.

H+ concentrations must be regulated and maintained within narrow limits.

Its regulation is termed acid-base balance.

Hydrogen is inversely related to pH.

A high pH = alkalotic = decreased H+ ions.

A low pH = acidic = increased H+ ions.

Where do hydrogen ions come from?

Carbon dioxide: large amount of carbon dioxide (CO2) is formed by cellular metabolism within the body.

Inorganic acids: hydrogen produced by normal metabolism of protein.

What is acidosis?

H+ is increased.

pH of blood is

What is alkalosis?

H+ is reduced.

pH of blood is >7.45.

Excitability of CNS, convulsion/tetany, death if respiratory muscle affected.

What is pH like in dogs and cats?

Cats are slight more on the acidic side in comparison to dogs.

How does the body regulate acid base?

Three systems in place:

* 1st line of defence - the body’s buffer systems (buffers including bicarbonate) - act within seconds to resist changes in pH.
* 2nd line of defence - lungs - work to resist changes in hydrogen ion concentration.
* 3rd line of defence - kidneys - play a large role in regulating acid-base balance.

How do the buffer systems help regulate acid-base balance?

Resist changes in H+ concentration in the body.

Bicarbonate (HCO3-), phosphate and proteins act as buffers.

React very quickly.

Act to keep pH as near to normal as possible.

Prevent dramatic fall in pH when H+ ions are added to the body or if large amount of hydrogen ions are being produced by metabolism.

How do the lungs help regulate acid-base balance?

Second line of defence against changes in pH of the body.

An increase in H+ ions causes a fall in pH of the blood - termed acidosis.

Drop in blood pH → stimulates breathing → increased pulmonary removal of CO2.

This respiratory compensation is rapid.

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pH is detected by specialised receptors called chemoreceptors, these are situated in the brain. These chemoreceptors are stimulate by a lowering of pH (due to an increase in the levels of dissolved CO2), An increase in the level of dissolved CO2, will cause a lowering of pH of the CSF (cerebrospinal fluid) that will stimulate these chemoreceptors. This causes an increase in the rate and depth of breathing to try and eliminate any excess CO2.

CO2 is a source of hydrogen ions which lower the pH of the body, therefore when the pH is low, the lungs start blowing out more CO2 trying to reduce the hydrogen ions and return the pH to normal.

When more CO2 is being blown out, it stimulates more hydrogen ions to react with HCO3 which forms carbon dioxide in the tissue fluid.

How do the kidneys help to regulate acid-base balance?

Respond differently depending whether the animal is suffering from acidosis or alkalosis.

During alkalosis they excrete HCO3- in urine.

During acidosis they excrete H+ and produce HCO3- in an attempt to decrease the acidity of the body fluid.

What is primary acid-base disorder?

An animal may be suffering from:

* Respiratory acidosis or alkalosis.
* Metabolic acidosis or alkalosis.

What is respiratory acid-base disturbances?

Respiratory acidosis.

Respiratory alkalosis.

Limited to amount of CO2 dissolved in the blood.

What is the clinical context of respiratory acidosis?

Lungs fail to eliminate carbon dioxide as fast as it it being produced in the body.

The concentration of CO2 rises in the body → fall in blood pH (acidosis).

Impaired respiration can quickly lead to life-threatening acidosis.

What are the potential causes of respiratory acidosis?

Lung disease - (e.g. pulmonary oedema or pnuemonia) which means the lings are not working at their optimum level.

Reduced activity in the respiratory centre (e.g. periods of apnoea during GA due to certain drugs).

Any obstructions in the airways.

What is the pathophysiology of respiratory acidosis?

Increased carbon dioxide dissolves in water to produce carbonic acid which lowers pH (acidosis).

So decreased ventilation:

* Increased carbon dioxide levels (as CO2 is not being blown off as it should).
* Decreased pH.
* Termed respiratory acidosis.

Is compensated by the kidneys by them producing HCO3- to normalise pH (this happens slowly).

Because the production of CO2 in the body is extensive, if this is not being excreted by normal breathing then life threatening acidosis can develop within a matter of minutes. If respiration is severely impaired.

What is respiratory alkalosis?

Less common.

The concentration of CO2 falls in the body → rise in blood pH (alkalosis).

Caused by hyperventilation.

Tends to be self-correcting as reduced CO2 is detected by the brain so hyperventilation rarely continues for long enough to become critical.

Pain, stress, respiratory disease, hyperthermia etc - they are blowing off large amounts of CO2 therefore the pH of the body increases - alkalossi and because this is caused by the respiratory alkalosis.

Why may a dog be hyperventilating?

Can occur for a number of reasons:

* Pain.
* Stress.

Things to look out for when nursing patient.

It can be caused by abnormal stimulation of the respiratory centre (ammonia toxicity, fever) or indirectly through hypoxia.

What is hypoxia?

A state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis.

What is the metabolic acid-base disturbances?

Acid-base disturbances not caused by abnormal removal of CO2 by the respiratory system.

* Metabolic acidosis.
* Metabolic alakalosis.

What is metabolic acidosis?

Occurs commonly.

Can occur for a variety of reasons:

* Increased lactic acid production (heavy exercise).
* Reduced renal excretion of H+ with kidney disease.
* Severe diarrhoea (loss of HCO3- in faeces).

What is metabolic alkalosis?

Can be caused by persistent vomiting.

Gastric vomiting causes a loss of gastric acid.

This causes a loss of hydrogen and chloride as hydrochloric acid.

This is often a result of pyloric or proximal small intestine obstruction, such as a foreign body - this the most common cause

What is extracellular fluid?

Fluid outside of the cells.

What is intracellular fluid?

Fluid in the cytoplasm and skeletal muscle.

What is the interstitial fluid?

Fluid cells are bathed in.

What is plasma water fluid?

Fluid proportion of the blood which the cells are suspended in.

What is transcellular fluid?

Specialised fluid produced by active secretory mechanisms.

E.g. CSF and GI secretions.

What are the normal ways fluid goes into an animals body?

Drinking.

Eating.

What are the normal ways fluid goes out of the body?

Urine.

Faeces.

Skin - sweat.

Respiratory tract.

What are the abnormal ways fluid exits the body?

Polyuria - urinating more frequently.

Diarrhoea.

Vomiting.

Blood loss.

Evaporation (during surgery - opening of the abdominal cavity).

What is the daily maintenance of fluid balance?

Every losses need to be replaced to maintain fluid balance.

* Faeces = 10mls/kg/day.
* Urine = 20mls/kg/day.
* Skin & respiration = 20mls/kg/day.

Total maintenance = 50mls/kg/day.

What are the components of the kidney?

Cortical blood vessels.

Interlobar blood vessels.

Renal hilum.

* Renal vein.
* Renal nerve.
* Renal artery.

Medulla.

Ureter.

Capsule.

Arcuate blood vessels.

Minor calyx.

Major calyx.

Renal pelvis.

Pyramid.

Papilla.

Renal column.

Cortex.

What is the renal pelvis?

The central area located in the indentation (or hilus) of the kidney. It is where blood enters via the renal artery from the aorta, and exits via the renal vein into the caudal vena cava. Following production in the nephrons, urine exits at the pelvis via the ureter. It is made of fibrous connective tissue hence it is off-white in colour.

What is the cortex?

The outer area that encaspulates the entire kidney. It is dark red in colour because of the number of glomeruli (and therefore blood supply) is more concentrated here.

What is the medulla?

The middle area located between the cortex and the pelvis. It is slightly paler in colour to the cortex. The triangular renal pyramids are located here which contain the collecting ducts and the tissue between the pyramids contain the loops of henle.

What is a nephron?

Functional unit of the kidney.

Responsible for the filtration of blood and production of urine.

Consists of:

* Renal corpuscle.
* Bowman’s capsule (cortex).
* Glomerulus (cortex).
* Proximal convoluted tubule (cortex).
* Loop of henle (medulla).
* Distal convoluted tube (cortex).
* Collecting duct (medulla).

How does fluid pass through the Bowman’s capsule, glomerulus and renal corpuscle?

Blood enters the kidney via the renal artery and is carried to the dense ball of capillaries known as the glomeruli.

Blood pressure is high in the glomeruli as the blood supply has arrived to the kidney via the renal artery which stems directly from the aorta. The efferent arteriole also has a much smaller diameter than the afferent arteriole therefore building the blood pressure within.

As the blood pressure is extremely high within the glomeruli, fluid and small molecules are forced out of the blood stream and into the pores located on the Bowman’s capsule surface. Larger molecules such as RBCs remain within the arterioles. This is known as ultrafiltration. The solution produced from this ultrafiltration is often known as ‘glomerular fluid’.

How does fluid pass through the proximal convoluted tubule?

The glomerular filtrate passes into the PCT which is where approximately 65% of all resorption back into the arterioles occurs.

80% of all the Sodium (Na) and chloride ions (Cl) found within the glomerular filtrate are actively reabsorbed, and in response to this water moves back into the blood supply via osmosis. Removal of water concentrates the levels of urea in the PCT. In a healthy animal all glucose within the glomerular filtrate will be reabsorbed into the blood supply at this stage.

Certain drugs within the blood supply are actively secreted into the filtrate at the PCT. Most notably drugs of the penicillin family transfer and are carried in the urine at this early stage - hence why it is useful for infections of the urinary tract.

How does fluid pass through the loop of henle?

Descending limb: the filtrate is then carried along the loop of Henle where the filtrate concentration and volume is regulated. The descending limb tubule is permeable to water. The fluid surrounding the loop of Henle, known as peritubular fluid of the vasa recta, is highly concentrated in Na ions therefore water is drawn out of the tubule via osmosis. As a result of this, the filtrate becomes more concentrated the further down the loop it goes, reaching maximum concentration at the loop turn.

Ascending limb: is impermeable to water but it actively reabsorbs Na ions back into the peritubular fluid and blood supply. This active transport of Na out of the tubules maintains the process of osmosis from the descending limb described earlier. At this stage the filtrate becomes less concentrated as it ascends the tubule because of the Na removal. The end result of the process is that the filtrate actually remains the same concentration when it entered the loop of Henle when it finally exits, however the removal of water has reduced the total volume.

How does fluid pass through the distal convoluted tubule?

The filtrate then moves into the DCT where the final adjustments are made. What happens here is dependent on the health of the animal and the status of the extra-cellular fluid. Further reabsorption of Na occurs here but in smaller quantities then previously in the PCT. Potassium is excreted into the filtrate at this stage also. Certain drugs are also secreted into the filtrate at this stage.

The pH of the blood is controlled at the DCT. Normal blood pH is 7.4. If pH is low (acidic blood) the kidney excretes hydrogen (H+) ions into the urine via the DCT to return pH to normal. If the pH is high (alkaline blood), the kidney stops excreting H+ ions and retains them in the blood to ensure the pH falls to a normal level.

How does fluid pass through the collecting duct?

The filtrate now follows the tubules into the collecting ducts - the final stage in urine production. The hormone antidiuretic hormone (ADH) can change the permeability of the collecting duct walls to water. Dependent on the hydration status of the animal, water may be drawn out of the ducts via osmosis due to the presence of high Na concentrations in the tissue surrounding the collecting ducts.

The collecting ducts carry the filtrate, which can now be referred to as urine, to the renal pelvis and out of the kidney via the ureter which connects to the bladder for urine storage.

What is the order of the nephron filtration?

Bownan’s capsule, glomerulus and renal corpsucle.

Proximal convoluted tubule.

Loop of henle.

* Descending limb.
* Ascending limb.

Distal convoluted tubule.

Collecting ducts.

What is the function of the kidney?

Osmoregulation.

Acid-base balance.

Excretion.

Hormone secretion.

* Eryhtropoietin - formation and maturation of erythrocytes.

Enzyme secretion.

* Renin.

What is osmoregulation?

To regulate the chemical composition and volume of bodily fluids.

Ensures homeostasis of blood contents is maintained.

Control of water loss and salt loss (NaCl).

Prevent dehydration.

Dehydration will lead to decreased blood pressure (baroreceptors) and increased osmotic pressure (osmoreceptors).

What control factors regulate fluid balance?

Renin.

Angiotensinogen.

Anfiotensin II.

Aldosterone.

Antidiuretic hormone (ADH)/ Vasopressin.

Baroreceptors.

Osmoreceptors.

How does renin regulate fluid balance?

Produced by juxtaglomerular cells in the glomeruli in response to low arterial pressure. Splits angiotensinogen into angiotensin II.

How does Angiotenisinogen regulate fluid balance?

Converted to angiotensin I by renin. Angiotensin I is converted into angiotensin II by angiotensin converting enzyme (ACE) - enzyme produced in the lungs.

How does angiotensin II regulate fluid balance?

Causes vasoconstriction of afferent and efferent arterioles.

Stimulates release of Aldosterone from adrenal glands. Increases Na+ reabsorption.

How does aldosterone regulate fluid balance?

Secreted by adrenal cortex, acts on distal convoluted tubule and collecting tubules (less effect) to increase Na+ reabsorption.

How does Antidiuretic hormone (ADH)/Vasopressin regulate fluid balance?

Secreted by the posterior pituitary gland, acts on collecting ducts to increase permeability to water.

How do baroreceptors regulate fluid balance?

Found in the walls of blood vessels, monitor arterial blood pressure.

How do osmoreceptors regulate fluid balance?

Found in the hypothalamus; monitor the osmotic pressure of the plasma, affect the thirst centre of the brain and influence secretion of ADH.

What is the effect of the antidiuretic hormone (ADH)?

Low blood pressue/increased osmotic pressure.

Increased ADH secretion by the posterior pituitary gland.

Permeability of collecting ducts increased.

Increased reabsorption of water from the ducts into the medulla and associated blood vessels.

Volume of ECF including blood plasma increases.

Rise in blood pressure.

What are the different types of excretion?

Water and ions (osmoregulation).

Nitrogenous waste (urea).

Products of detoxification (often deactivated by the liver and excreted by the kidneys).

* Hormones.
* Drugs.
* Poisons.

What are the different types of renal disease?

Acute kidney injury (acute renal failure).

Chornic renal disease/failure.

What are the symptoms of renal disease?

Hallmark features:

* Azotaemia.
* Elevated BUN.
* Elevated serum creatinine.

Uraemia.

* Nausea, vomiting, diarrhoea.
* GI haemorrhage.
* Stomach ulcers.
* PUPD.
* Anaemia.
* Hypertension.
* Isosthenuria.

What is the BUN test?

Measures the amount of nitrogen in the patient’s blood that comes from the waste product urea. Urea is made in the liver, passes through the kidneys and is excreted in the urine. When kidneys start to fail, they are unable to remove the urea normally, thus causing an elevation in BUN.

What is uraemia?

A term used to describe most of the clinical sings and biochemical findings that occur with renal failure. The most common uraemic complications are the appearance of gastrointestinal symptoms, such as nausea, vomiting and diarrhoea. Gastrointestinal signs can escalate to include haemorrhage of the gastrointestinal tract and ulcers in the stomach caused by an increase in gastric acid (40% if gastrin is metabolised within the kidneys); additionally, ulcers in the mouth may occur, and patients may be termed as having ‘uraemic breath’. Other signs of uraemia inlcude polyuria, polydipsia (caused by an impaired ability to concentrate urine), hypertension and anaemia. The pet may also experience isosthenuria, where urine is excreted that has not been concentrated by the kidneys and has the same osmolality as that of plasma.

What is acute kidney injury?

Dramatic drop in glomerular filtration rate due to pre-renal, intrinsic renal or post-renal causes.

Reversible if diagnosed and treated early.

What is the cause of pre-renal acute kidney injury?

Inadequate blood supply to the kidneys.

What is the cause of intrinsic renal acute kidney injury?

Damage to kidney parenchyma caused by toxins, ischaemia, infectious agents.

What is ischaemia?

Blood flow and oxygen is reduced to a part of the body.

What is the cause of post-renal acute kidney injury?

Urinary tract obstruction (uroliths, mucous plugs, masses, blood clots).

What are the systemic disease of acute kidney injury?

Pancreatitis.

Heat stroke.

Pyelonephritis - occurs secondary to a lower urinary tract infection.

Lymphosacroma.

What are the clinical signs of acute kidney injury?

Sudden onset.

Anorexia.

Depression.

Dehydration.

Oral ulceration.

Vomiting.

Diarrhoea.

Oliguria, anuria or polyuria.

Hyperkalaemia - may result in bradycardia and ECG abnormalities.

May cats with AKI are anuric or oliguric.

Cats presenting with AKI may be in good body condition previously healthy and now seriously unwell, often with only moderate levels of azotaemia.

What is the diagnosis of acute kidney injury?

History - toxin exposure.

Physical exam - kidney enlarged and painful.

* Non-specific = dehydration, hypothermia, depression and ulcers.
* Normal or enlarged kidneys.
* Monitor urine output for anuria, oliguria or polyuria.

Blood sample.

* Elevated BUN, creatinine, phosphorous.
* Hyperkalaemia
* Metabolic acidosis.

Lab.

* Reduced GFR (glomerular filtration rate) therefore increased parameters. If ethylene glycol poisoning then may also see hypocalcemia.
* Hypercalcaemia tends to be associated with CRF (complete renal failure).

Urine analysis.

* SG: 1.007-1.017.
* Proteinuria.

What is hyperkalaemia?

High potassium levels in the blood.

What is the treatment and nursing care for acute kidney injury?

Treat cause.

* Induce emesis - as long as the patient is alert enough to protect its airway.
* Activate charcoal - absorbent for may toxins, aiding patient decontamination.
* Stop nephrotoxic drugs.

Fluid therapy.

* Often hypovolaemic and dehydrated.
* IV bolus 0.9% NaCl over 20 minutes, reassess and repeat as necessary.

Monitor urine output.

* Indwelling urinary catheter.
* Maintain >0.5ml/kg/hr urine production.
* Hyperkalaemia often resolves once urine output restored.

Prompt treatment is essential.

What does hypovolaemic mean?

A condition that occurs when the body losses fluid like blood or water.

What is the prognosis of acute kidney injury?

Depends on cause and length of time until treated.

Poor prognosis:

* Ethylene glycol toxicity.
* Failure to improve azotaemia with 3 days of treatment.

Recovery possible with early aggressive treatment.

What is chronic renal disease?

Commonly affects older dogs and cats.

Progressive irreversible damage affects kidney function.

* Weeks-years.

Damage nephrons = decreased GFR and accumulation of waste products.

Azotaemia occurs when >60% nephrons lost.

Uraemia occurs when >70% nephrons lost.

What are the possible causes of chronic renal disease?

Idiopathic - cause unknown.

Polycystic kidney disease - inherited disease seen mainly in Persian and related cats where normal kidney tissue if gradually replaced by multiple fluid filled cysts.

Neoplasia - lymphoma.

Infectious agent.

* Pyelonephritis - infection of the kidney.
* Feline infectious enteritis.

Toxins.

Drugs - NSAIDs.

Golmerulonephritis - inflammation of the glomeruli (individual units in the kidneys that filter the blood) - they may become inflammed for various reasons and if prolonged this can lead to CKD.

Hyperthyroidism.

What are the clinical signs of chronic renal disease?

PUPD.

Weight loss.

Vomiting.

Reduced appetite.

Lethargy/weakness.

Blindness - due to hypertension.

CNS depression, convulsions, coma, death.

Sudden onset deterioration and collapse = acute on chronic disease.

What can be observed in a clinical examination to help diagnose chronic renal disease?

Dull unkempt hair coat.

Halitosis - bad smelling breath.

Mouth and GIT ulceration.

Anaemia (non-regenerative).

Hypertension.

Small kidneys.

Hypertensive retinopathy.

Hypoproteinaemia.

What is chronic renal disease diagnosed?

History.

Phyiscal examination.

Blood sample:

* Elevated BUN and creatinine.
* Elevated phosphorus (hyperphosphataemia).
* Hypokalameia.
* Hypercalcaemia (elevated total calcium but low/normal ionised calcium).
* Non-regenerative anaemia.
* Metabolic acidosis.

Urinalysis.

* SG 1.008-1.012 (isothenuria).

Radiography - small irregular kidneys.

Hypertension.

What is the pathophysiology of polyuria and polydispia (PUPD) with chronic renal disease?

Decreased functional nephrons causes increased filtration in healthy nephrons.

Rapid fluid flow through DCT and collecting ducts.

Water reabsorbed less efficiently = less concentrated urine.

Severe CRF:

* Large volumes of dilute urine produced.
* Drink excessive quantities of water to maintain water balance.

What is the pathophysiology of vomiting and GIT ulceration with chronic renal disease?

Decrease GFR leads to decreased excretion of waste products creatinine and urea.

Creatinine and urea build up in the blood stream (azotaemia).

Cells damaged by accumulation of toxic products - especially GIT cells.

What is the pathophysiology of non-regenerative anaemia in chronic renal disease?

Erythropoietin (produced by kidneys) is needed for the formation and maturation of erythrocytes.

Kidney damage means decreased production of erythropoietin.

Therefore reduced formation of erythrocytes.

What are erythrocytes?

A red blood cell.

What is the pathophysiology of weakness in chronic renal disease?

Acid-base imbalance leads to acidosis = weakness.

Large quantities of dilute urine leads to dehydration = weakness.

What is the pathophysiology of hypertensive retinopathy in chronic renal disease?

60% dogs and 20% cats are hypertensive.

High blood pressure → retinal detachment or retinal haemorrhage.

Sudden onset blindness most commonly seen in elderly cats.

Why is renal disease staged?

Important, as it allows monitoring of disease progression and formation of treatment protocols according to stage; it also provides prognostic evaluation.

What is the initial evaluation for renal disease stages?

Serum or plasma creatinine.

The initial stage is determined by serum creatinine levels.

Creatinine should be measured once the patient has been rehydrated (where necessary), to reduce any pre-renal component that could influence the allocated stage. Ideally, serial creatinine measurements are taken, as staging should be performed on patients with stable CKD (ideally indicated by obtaining two similar readings).

Why do we substage renal disease?

Once a stage has been allocated based on serum creatinine, measurement of urine protein and systolic blood pressure allows allocation of substages. Substaging of CKD is important for monitoring of disease and identification of treatment targets. Proteinuria has also been shown to influence prognosis for survival in CKD.

What is urine protein and what is its importance?

Proteinuria is a negative prognostic indicator in CKD and should be targeted during treatment. Measurement of urine protein and determination of the urine protein:creatinine ratio it therefore recommended. Pre-renal proteinuria and post-renal proteinuria should be excluded. Initially a dipstick examination can be performed and a UPC requested is protein is evident. A negative dipstick results allows classification as non-proteinuric (NP).

Why is blood pressure important in chronic renal disease?

Cats with CKD may be hypertensice, resulting in progression of CKD and other clinical signs associated with the hypertension. Blood pressure should therefore be measured in all cats with CKD and a blood pressure substage allocated. Assessment for end-organ damage (also called target-organ damage) should be performed.

What is the management of chronic renal disease?

Discontinue any potentially nephrotoxic drugs.

Fluid therapy - correct dehydration and/or electrolyte abnormalities.

Manage systemic complications.

Manage any concurrent illnesses.

Most cases of CKD occur in older cats and therefore comobrid disease is common (cardiac disease, OA/DJD, hyperthyroidism, diabetes mellitus, dental disease, neoplasia). Failure to manage these conditions can reduce the effectiveness of strategies to manage CKD; for example dental disease may reduce intake of food, including renal prescriptive diets.

Why is nutrition important in cases of chronic renal disease?

Renal friendly diet results in longer survival times.

Features of most renal diets include:

* Reduced phosphate sodium and protein (but of high nutritional quality).
* Increased potassium, calorific density (fat) and B vitamins.
* Non-acidifying.
* Antioxidants.
* Polyunsaturated fatty acids.

Dietary intervention is appropriate for IRIS stage II and upwards. It is best introduced when the cat has a reasonable appetite rather than during a period of nausea/anorexia. A renal prescription diet is beneficial, but reduced calorie intake or starvation if the prescription diet is refused is more detrimental than eating the old familiar diet. A cat with CKD will benefit even if the renal diet only makes up a proportion of the diet as a whole.

What are the tips for giving a renal diet?

Do not offer the new diet during hosptialisation or the initial stabilisation period, as the presence of nausea or pain could result in food aversion and a negative association with the new diet.

Manage nausea or pain as appropriate.

Try more than one brand in initial brand is refused; and try wet and dry formulations as tastes and textures vary.

Some older cats will change their food preference every few days or weeks, so owners can stock a variety of flavours/brands of renal diets and rotate them.

Although a slow transition via mixing a component of the old diet with the new diet is often recommended, some cats dislike a mixture of flavours. It is often better to offer the new diet and the old diet separately at the same time, slowly reducing the volume of the old diet and increasing the volume of the new diet.

Warm the new diet to increase odour.

Ensure that older cats in particular have an accessible quiet area in which they can eat.

Appetite stimulants may be used when initially changing diet.

What are the less common forms of management for chronic renal disease?

Drugs.

* Anti-hypertensive agents.
* Anti-emetics.
* Appetite stimulants.
* Antibiotics.
* Phosphate binder.

Nasogastric feeding tube.

Subcutaneous fluid therapy and increase oral water intake.

What is the prognosis of chronic renal disease?

Poor prognosis - impossible to regenerate damaged nephrons.

Treatment aimed at slowing disease.

Good management can increase lifespan and quality of life.

What is endocrinology?

The study of the endocrine system.

What is the structure and function of the endocrine system?

It is one of the major control systems of the body working to maintain a more or less constant level of environment.

The endocrine system is comprised of glands that release hormones (chemical messengers) directly into the circulation.

These hormones then a physiological effect on the target organ.

When the hormone reaches the target cell it will bind to a reception on/in the cell and elicit its action on that cell.

What are hormones?

Chemical messengers.

Carry information from endocrine cells to target cells which are hormone sensitive.

Produced in endocrine glands and also in individual cells.

What are the 3 types of hormones?

Classical hormones - cell signalling molecules synthesised by the endocrine cells.

Neurohormones - chemicals released from the nervous system.

Local hormones - act on the cells around them.

What are the important endocrine glands?

Hypothalamus.

Pituitary gland.

Parathyroid glands.

Thyroid gland.

Pancreas.

Adrenal glands.

Ovaries.

Testes.

What is the hypothalamus?

Region within the brain that is the regulatory centre for the endocrine system.

Many important functions of the endocrine system are regulated by the hypothalamus.

Controls most of the endocrine glands in the body, mainly via stimulation of the pituitary gland - just below the hypothalamus.

Hypothalamic hormones control the secretion of anterior pituitary hormones.

What is the pituitary gland?

Situated at the back of the skull.

Consists of 3 parts:

* The posterior pituitary.
* The anterior pituitary.
* The intermediate lobe.

The controller of many of the endocrine glands in teh body.

The master gland.

What are the hormones secreted by the posterior pituitary gland?

The 2 hormones secreted are:

* Antidiuretic hormone (ADH).
* Causes water reabsorption in the kidneys (collecting ducts).
* Oxytocin.
* Elicit milk let down.
* Increase uterine contractions.