Biochemistry Flashcards
What does PP mean?
Increased/excessive appetite
What does PU mean?
Polyuria
What does WL mean?
Weight loss
What does PD mean?
Polydipsia
What is Azotaemia?
Azotaemia is a medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient or dysfunctional filtering of blood by the kidneys. It can lead to uraemia and acute kidney injury (kidney failure) if not controlled
What is Uraemia?
Uraemia is the condition of having high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess of amino acid and protein metabolism end products, such as urea and creatinine, in the blood that would be normally excreted in the urine.
What do the kidneys do?
Regulates blood pressure, blood sugar, blood volume, water composition in the blood, and pH levels.
What is urea?
Produced from the breakdown of proteins and is normally partially excreted in the kidneys
What is creatinine?
Produced as the result of normal muscle metabolism and filtered freely through the glomerulus and is not reabsorbed in the tubules
What are the pre-renal causes of azotaemia?
Reduced blood flow to the kidneys due to dehydration, haemorrhage, heart failure, toxins, illness, medications.
Usually nothing wrong with the kidney itself.
What are the renal causes of azotaemia?
The kidneys are not working = reduction of GFR to less than or equal to 25% of normal (chronic or acute renal failure).
What are the post-renal causes of azotaemia?
After leaving the kidneys successfully urinary waste products cannot exit the body E.g. Urethral obstruction, ruptured ureter or bladder (uroabdomen).
What are the diagnostic features of pre-renal azotaemia?
Presence of azotaemia with a urine specific gravity that is greater than or equal to 1.030 in dogs or greater than or equal to 1.035 in cats.
BUN, CRE, TP, PCV, USG = ^
What are the diagnostic features of renal azotaemia?
Presence of mild to marked azotaemia with a urine specific gravity that is less than 1.030 in dogs and less than 1.035 in cats (often in the isosthenuric range: 1.007-1.015)
BUN, CRE, = ^
TP, PCV, USG = v
What are the diagnostic features of post-renal azotaemia?
Presence of a mild to marked azotaemia, a variable urine specific gravity and clinical signs of obstruction (ie. Distended, turgid urinary bladder)or urine leakage (distended, fluid-filled abdomen or lack of bladder filling)
BUN, CRE, TP = ^
PCV = Normal
USG = No sample
What is the most sensitive liver enzyme to test?
ALT, it is found in liver cells.
What is released from RBC breakdown and seen in high amounts from IMHA?
Bilirubin
What is EPO?
It is a hormone secreted by the kidneys, this hormone signals the production of red blood cells.
What is acidosis?
Blood pH is too high, acidic blood.
Normal levels of blood glucose are…
6-8, slightly higher is likely from stress.
What does ALP stand for and what is it?
Alkaline Phosphatase. It is an enzyme found in the liver, intestinal mucosa, bone, kidney, placenta, leukocytes.
What does ALT stand for and what is it?
Alanine Aminotransferase. Enzymes that detect liver injury: These enzymes are found in the liver cells and leak out with injury to hepatocytes or biliary cells.
What does increased ALP indicate?
- Increased results from increased production by cells of the bile canaliculi rather than from leakage.
- High in large, growing young dogs and dogs with osteosarcoma
- Hyperadrenocorticism can cause HUGE increases
- In cats, increases in cholestatic disease (blocked bile flow in liver) such as cholangiohepatitis (inflamed liver and bile ducts), hepatic lipidosis, lymphoma
- Can rise in biliary disease and GGT will be high as well
What does increased ALT indicate?
- leaks into circulation from damaged hepatocytes. Marked increase = severe liver insult
- Mild increase = less severe insult or chronic disease
- Also found in muscle cells but AST and CK are typically elevated to a much higher degree with muscle damage
- Haemolysis will give a falsely high reading
What is renal failure?
It’s when excretory and renal endocrine function can’t maintain homeostasis.
What is BUN?
Determines the ability of the renal filtration system to remove this waste product of protein metabolism from the blood stream. Urea, which is the principle waste product of the body’s protein metabolism, is hard to determine in the laboratory. The blood concentration of urea nitrogen is proportional to the protein content of the diet and renal excretory capacity of the animal.
What does BUN stand for?
Blood Urea Nitrogen
What are the symptoms of azotaemia?
Symptoms often occur gradually over an extended period of time:
-Vomiting and lethargy
-Diarrhoea or Constipation
-Depression and Weight loss
-Increased thirst and lack of appetite (anorexia)
-Acute blindness, seizures and comas
-Blood in the urine (haematuria)
-An increase in the frequency and amount of urination
What things increase BUN?
Increased values can be seen with dehydration, urinary obstruction, uraemia, nephritis, surgical shock and intestinal obstruction. Intestinal bleeding may also increase the BUN.
What things decrease BUN?
Acute liver failure and intestinal disease. Because this value is related to protein metabolism, it is very dynamic and can change quickly based on changes in the diet as well as the condition of the kidneys.
What are the causes of increased urea?
High-protein diet
Tissue catabolism
GI haemorrhage
Drugs (Corticosteroids)
What is a promising marker for early kidney disease?
Symmetric dimethylarginine (SDMA) is a small molecule formed by methylation of arginine, and released into blood during protein degradation. SDMA is primarily eliminated by renal excretion and is a promising endogenous marker of glomerular filtration rate (GFR)
When GFR goes down through kidney Dz the SDMA goes up followed by CRE, followed by BUN. Somewhere during this process the USG goes down
Most useful when trying to decide if kidney Dz is present in the very early stages. Often used as a tie-breaker when values contradict
“This test, especially when run spontaneously by the lab as a promotional practice, is a classic example of how inappropriate screening can lead to overdiagnosis. When the prior probability of the disease is low, then the positive predictive value of the test is low. And when there is no intervention proven to alter the long-term outcome of a positive screening test, it is considered unethical to offer the test in human medicine because all we accomplish is to create anxiety. Effective screening which actually reduces morbidity and mortality requires adequate information and planning, which rarely seem available when such tests are introduced in vet med.” anonymous but not alone
What are the functions of the liver?
- Removes potentially toxic byproducts of some medications
- Prevents shortages of nutrients by storing vitamins. minerals and sugar
- Metabolizes/breaks down nutrients from food to produce energy when needed
- Produces most proteins needed by the body
- Helps your body fight infection by removing bacteria from the blood.
- Produces most of the substances that regulate blood clotting
- Produces bile a compound needed to digest fat and to absorb vitamins A, D, E and K.
What are the clinical signs of liver disease?
- Icterus (jaundice)
- Vomiting and diarrhoea (GI irritation)
- Hypersalivation (cats)
- Ascites (free abdominal fluid)
- Haemorrhage / petechiae (lack of production of coagulation factors)
- Anorexia/weight loss
What should be known about Bilirubin?
- Derived from RBC breakdown and excreted in bile
- Serum indicator of reduced hepatic function and cholestasis = accumulates in blood during cholestasis and spills into urine = bilirubinuria
- Seen with haemolytic anaemia
- In cats, mild INCREASE may accompany anorexia or severe inflammatory disease
What should be known about Albumin?
- Produced by the liver
- low Albumin = Hypoalbuminaemia decreased synthesis, inhibition of albumin release and increased volume of distribution with ascites
- high Albumin = Hyperalbuminaemia dehydration and hyperproteinaemia in acute liver disease
What should be known about Glucose?
- Decrease occurs with severe hepatic dysfunction
- Increase is only seen in end-stage liver disease or massive necrosis and puppies with portosystemic shunt.
What should be known about AST?
- Present in hepatocytes and skeletal muscle cells
- Often elevated following muscle injury
- When ALT levels are normal in the same blood sample, this indicates RBC destruction = haemolysed blood sample
What should be known about GGT?
- Marked increase = bile flow in liver is blocked (cholestasis), bile duct obstruction, liver tumours, pancreatic inflammation in cats
- Not on Gribbles form but shows up on IDEXX (REM Liver profile)
- Very sensitive for detecting liver damage (cholestasis) in cats (except for hepatic lipidosis = not that elevated)
What should be known about Cholesterol?
- Made in the liver
- Aids intestinal digestion and fat absorption
- May DECREASE in severe liver disease or portosystemic shunt
- May INCREASES in cholestasis
- DECREASES with malabsorption and protein-losing enteropathy
- INCREASES in hypothyroidism, diabetes mellitus, hyperadrenocorticism, nephrotic syndrome, acute pancreatitis
- Most common cause of HIGH cholesterol is collecting a post-prandial blood sample
What should be known about BUN?
- Ammonia comes from protein breakdown in the gut and is taken up by liver to be converted to urea
- Ammonia INCREASES with severe liver disease and porto-systemic shunt as it’s not removed by the liver = blood urea concentration is LOW in these animals (because liver not converting Ammonia to Urea)
- Ammonia is hard to analyse = volatile
When are liver function tests indicated?
For animals with suspected hepatic disease but normal serum hepatic enzyme concentrations, animals with increased serum enzyme concentrations but no clinical signs of hepatic disease, and evaluation of disease progression or response to treatment
What is a serum bile acid concentration test?
Synthesised from cholesterol, conjugated in the liver, excreted in the bile into the intestines and then almost completely resorbed into the portal circulation.
Only tiny amount lost in the faeces
The most useful measure of liver function in dogs and cats
Reduced liver function or portosystemic shunts allow bile acids to escape into the systemic circulation = INCREASED bile acids
What is a portosystemic shunt?
Abnormal vascular connections between the portal and systemic circulation that bypass the liver (toxins not removed)
What does AST stand for?
Aspartate Aminotransferase
What does GGT stand for?
Gamma Glutamyltranspeptidase
What are the acute hepatotoxins for dogs?
- Iron
- Toxic Muchrooms
- Blue Green Algae
- Xylitol
- Alphalipoic Acid
- Cycad Palm
- Aflatoxin (compost, coil, mulch)
- Paracetamol
- Leptospirosis
- Mycotoxins (green bin mould)
- Phenols
- Cockleburr
- Yellow Phosphorous
- Isoniazid
- Castor Beans
- Thiascetarsemide
- Mebendazole
What are the two functions of the pancreas?
Endocrine: secretes hormones including insulin and glucagon, which regulate blood glucose metabolism
Exocrine: secretes enzymes, amylase and lipase, that help digest carbohydrates, fats and proteins
What are the endocrine (hormonal) functions of the pancreas?
The pancreas secretes insulin and glucagon, hormones that regulate the level of glucose in the blood and other hormones. Endocrine tissue enables this process, and is made up of islets of Langerhans, regions of the pancreas that secrete hormones into the bloodstream.
secretes hormones including insulin and glucagon, which regulate blood glucose metabolism
Insulin is needed to carry glucose into cells
↓ insulin = ↑ glucose in blood increased glucose in urine = polydipsia/polyuria
Deficiency of insulin = diabetes mellitus
What are the exocrine (digestive) functions of the pancreas?
The pancreas helps with digestion of carbohydrates, fats, proteins and acids. Exocrine tissues allows this process by delivering enzymes into a network of ducts (tube-like vessels) that are joined to the main pancreatic duct, which runs the length of the pancreas.
Secretes enzymes, amylase and lipase, that help digest carbohydrates, fats and proteins
INCREASES in amylase and lipase occur with pancreatitis
DECREASES in amylase and lipase occur with exocrine pancreatic insufficiency = fatty faeces, gradual weight loss despite good appetite; diagnosed through LOW Tripsin-Like Immunoreactivity (TLI) levels in serum
What are the main diseases associated with the Pancreas?
- Pancreatitis
- Exocrine Pancreatic Insufficiency
- Diabetes Mellitus
What should be known about Pancreatitis?
Inflammation of the pancreas
Most common in overweight, middle-aged to older dogs
More common in cats than we used to think and difficult to diagnose
What would Pancreatitis serum biochemistry show?
↑ serum amylase or lipase levels
Azotaemia
Hypo- or hyperglycaemia
Hypoalbuminaemia
Mild hypocalcaemia
Increased serum hepatic enzymes
Hyperbilirubinaemia
Increased serum TLI (Tripsin-like Immunoreactivity) concentrations
What is Trypsin-like Immunoreactivity test?
Trypsinogen is a proenzyme (a non-activated enzyme) that is secreted into the small intestine by the pancreas, along with other pancreatic digestive enzymes.
When it reaches the small intestine, trypsinogen is converted to trypsin, an enzyme that is involved in the digestion of proteins.
In healthy animals, a small amount of trypsinogen escapes from the pancreas into the blood circulation, and can be measured in a blood sample by a test called trypsin-like immunoreactivity.
What are the clinical signs in cats for Pancreatitis?
Quiet, mild fever, off food, maybe painful cranial abdomen
What are the clinical signs in dogs for Pancreatitis?
Vomiting, anorexia, depression, fever, diarrhoea
What should be known about Exocrine Pancreatic Insufficiency?
Heritable in German Shepherds
Results from pancreatic acinar cell atrophy (unknown reasons)
Results in deficiency of pancreatic enzymes (amylase and lipase) = maldigestion
Diagnosed through serum biochemistry revealing LOW TLI concentration
reduced functional pancreatic tissue = less trypsinogen produced = less trypsinogen escapes into the blood circulation = low levels of serum TLI.
What are the clinical signs of Exocrine Pancreatic Insufficiency?
Weight loss despite good or ravenous appetite, small bowel diarrhoea or soft faeces
What should be known about Diabetes Mellitus?
Diabetes mellitus is caused by a deficiency of insulin. You are probably going to have to give injections of insulin as a replacement
The starting insulin dose is going to be based on averages and will be tweaked based on trial and error, depending on both test results and control of the symptoms
In a Diabetic Animal there isn’t enough insulin In fact, there may be no insulin at all. With no insulin, glucose cannot get in. Glucose is left floating around in the bloodstream in extremely high amounts. The body’s tissues are starving and the bloodstream has plenty of glucose to feed them but without insulin, the glucose is unavailable.
A lot of money can be saved if client’s get their own glucose meter and learn to do blood sampling at home (it’s easier than you think).
Using too little insulin is a problem in the long term but too much insulin is potentially an emergency in the short term. Be sure you know how to recognise hypoglycaemia and what to do about it.
What are the clinical signs of Diabetes Mellitus?
Excessive urination, excessive thirst, excessive appetite, and weight loss. Treatment should control these symptoms. Watching for these symptoms is the best way to know how your pet is doing. PD, PU, PP, WL
What is important to remember about insulin?
Tissues cannot absorb glucose unless a hormone known as insulin is present. Insulin can be considered to be a key that unlocks the door, allowing sugar in the bloodstream to enter the body’s cells. Once inside the tissues, glucose can be burned for fuel or stored, but without insulin the sugar stays in the bloodstream and cannot be used by the body.
What can happen to dogs but not cats with Diabetes Mellitus?
A specific type of cataract rapidly develops in the eye when high amounts of glucose enter the lens. Glucose normally feeds the lens but the amounts of glucose coming into a lens in the diabetic state are much higher. Excess glucose is converted to another sugar called sorbitol, which in turn attracts water. The excess water disrupts the clarity of the lens creating a diabetic cataract, which leads to blindness in almost all diabetic dogs.
What’s the difference between dog and cat Diabetes Mellitus?
Dogs:
- Permanent
- Require Insulin injections
- Similar to Type 1 in Humans
- Best diet is high fibre BID
Cats:
- Require Insulin to start but one third go into remission if controlled
- 75% are male
- Obesity and Burmese breed
- Similar to Type 2 in Humans but not really “non-insul dependant”
- 20% have another endocrine Dz such as Cushing’s or Acromegaly
- Best diet is multiple small meals daily high Protein low Carb
What is a glucose curve?
Where BGs are monitored every 2 to 4 hours or so for 12 to 24 hours. This kind of testing tells us how long the insulin injection is lasting as well as what the lowest and highest glucose levels of the day are. Often in the beginning, it takes several dose selections and several curves before the right dose is determined.
What would Diabetes Mellitus serum biochemistry show?
Hyperglycaemia and glucosuria, Hypercholesterolaemia and hypertriglyceridaemia may also be seen
Polyuria, polydipsia, polyphagia, weight loss, sudden blindness (cataracts) in dogs,
rear limb weakness / plantigrade stance in cats
What’s the treatment for Diabetes Mellitus?
Insulin given once per day: NPH, lente or ultralente insulin (dogs = NPH or lente; cats = lente or ultralente)
Glucose measurement: a few blood glucose concentrations should be evaluated after initiating insulin therapy to ensure that the blood glucose is not dropping too low
Blood glucose curve: measurement of blood glucose every 2-3 hours for at least 10-14 hours
Ideally blood glucose concentration should be 100-300mg/dl (5.6-13mmol/L)
Diet: correct obesity and minimize fluctuations in glucose
What is diabetic ketoacidosis?
sulin deficiency
leading to ketosis (ketones = byproducts
of the body breaking down fat for energy
that occurs when carbohydrate intake is
low or when there isn’t a sufficient level of
available glucose or glucose can’t be used
- diabetes) > ketonuria > urinary loss of Na
and K
What are the clinical signs of diabetic ketoacidosis?
Acute depression, weakness, dehydration, vomiting, acetone odour to the breath
What are the diagnostic findings of diabetic ketoacidosis?
Low sodium, chloride and potassiumHyperglycaemia and glucosuria,ketonaemia and ketonuria
What happens with too much Cortisol?
Too much cortisol = Hyperadrenocorticism aka HAC aka Cushing’s Dz
Normally a low USG and a very high ALP
What happens with not enough Cortisol?
Too little cortisol = Hypoadrenocorticism aka HOC aka Addison’s Dz
Resting Cortisol >2.0 ug/dL rules out Addison’s
> 90% Addisonians have resting cortisol < 1.0 ug/dL
If resting cortisol >2.0 ug/dL then Addison’s is ruled out 99% of the time
What is the endocrine system?
The endocrine system is made up from all the glands in the body that make hormones
What are the endocrine glands in the body?
Brain: hypothalamus, pituitary gland, and
pineal gland
Neck: thyroid and parathyroid glands
Between the lungs: thymus
On top of the kidneys: the adrenals
Behind the stomach: the pancreas
Pelvic region: ovaries and testicles
What thyriod disorder do dogs usually get?
Hypothyroidism
What thyroid disorder do cats usually get?
Hyperthyroidism
What is the most common hypothyriodism cause in dogs?
Infiltration of the thyroid gland with
lymphocytes or have idiopathic follicular
atrophy, leading to thyroid dysfunction.
Impaired production and secretion of
the thyroid hormones > anterior pituitary
produces more TSH to stimulate thyroid
gland to produce more T4 (and T3).
What are the clinical signs of hypothyroidism in dogs?
Lethargy, Depression, Increased sleeping
Weakness
Weight gain (despite little or no change in appetite)
Cold intolerance
“Tragic facial expression”
Bilateral symmetrical alopecia, rat tail
Hyperpigmentation, Seborrhea, Pyoderma, Otitis
Peripheral neuropathies
Ophtho issues
What are the diagnostics for hypothyroidism in dogs?
Biochem profile: hypercholesterolaemia, elevated CK and liver enzymes (fat accumulation)
Total T4 is usually significantly below the reference interval in hypothyroid dogs (~85%). Hormone levels can fluctuate throughout the day.
Consequently the vet will consider history and clinical examination as well as blood work.
A free T4 can be assessed as it is typically low in true hypothyroidism (>90% of cases).
What are reasons other than hypothyroidism for low T4 in dogs?
However, T4 can fall for a number of reasons other than hypothyroidism including presence of inflammatory disease, hyperadrenocorticism, other significant systemic disease and with administration of various medications. It is estimated that 50-60% of normal dogs have low serum T4 at some stage during the day.
What is the treatment required for hypothyroidism in dogs?
A blood sample is taken 4 to 6 hours after administration of eltroxin with the aim of getting T4 concentration to the upper half to slightly above the reference interval.
T4 is checked about 6 weeks after starting eltroxin and after adjusting dose.
What is the most common hyperthyroidism cause in cats?
Cats: Adenomatous hyperplasia of both thyroid glands = thyroid adenoma
in ~70% of cases, both thyroid lobes are enlarged.
This results in excessive secretion of the thyroid hormones, T4 and T3, resulting in signs that reflect an increased metabolic rate.
What is the most common hyperthyroidism cause in dogs?
Thyroid carcinoma (rare in cats)
What are the clinical signs of hyperthyroidism in cats?
Increased appetite
Weight loss
Unkempt appearance
Increased heart rate / murmur
Diarrhoea, vomiting
Increased respiratory rate
Agitation, excited state, behavioural changes (aggressive etc.)
Some cats: fever, hair mats due to overgrooming, voice change, hypertension and retinal detachment
Palpable thyroid nodule (70% are bilateral)
What are the diagnostics for hyperthyroidism in cats?
Remember to remind clients to fast their pets for 12 hours before blood tests
Biochemistry profile: often increased ALT, ALP, phosphorus
Total T4 and free T4
Serum Total T4 = inexpensive, provides diagnosis
5-10% of cats have normal serum T4 values
Typically T4 increases with time, so an option is to re-test in several weeks’ time
OR..
FreeT4 can be assessed - a high free T4 concentration along with consistent history and physical examination findings is diagnostic of hyperthyroidism.
What is free T4?
This is the component of T4 hormone that is not bound to plasma proteins.
It is elevated in about 98% of hyperthyroid cats.
Vets often assess total T4 first as assessing free T4 requires a fiddly test and is expensive to run.
What is the treatment required for hyperthyroidism in cats?
Prone to kidney failure - clinics should ALWAYS monitor renal function during treatment of a hyperthyroid cat.
Elevated thyroid function maintains glomerular filtration rate and as T4 falls, so does GFR and azotaemia may then develop.
The aim of treating hyperthyroidism is to increase weight, decrease T4 and reduce their frantic activity.
Radioactive iodine therapy – radioactive iodine destroys the functioning thyroid cells without destroying non-thyroidal tissue
Surgery
Methimazole – can affect kidney function by decreasing hyperthyroidism = decrease GFR and renal blood flow
When is adrenal disease a common issue?
Adrenal cortical diseases are mainly a problem in dogs with hyper- and
hypo-adrenocorticism.
Rarely reported in cats.
What is the most common cause of Hyperadrenocorticism (Cushing’s Disease)?
Mostly caused by bilateral enlargement of the adrenal cortex as a result of a pituitary tumour which causes overproduction of ACTH.
Causes excessive production of cortisol (steroid hormones) by the adrenal cortex due to stimulation of the adrenal cortex by an adrenocorticotrophic hormone (ACTH) secreted from the pituitary gland.
Symptoms can also occur due to excessive administration of glucocorticoids that are used to suppress inflammation and itching = “Iatrogenic” cause
What are the clinical signs of Hyperadrenocorticism (Cushing’s Disease)?
Polydipsia, polyuria, polyphagia
Obesity
Pendulous abdomen (redistribution of body fat, muscle breakdown, thin skin, big liver)
Hepatomegaly
Alopecia (hair thinning and hair loss especially along the trunk)
Lethargy
Muscle weakness
Anoestrus
Nerve damage, seizures, behavioural changes (with larger tumours)
Recurrent UTIs
What are the diagnostics for Hyperadrenocorticism (Cushing’s Disease)?
Dogs with this nearly always show abnormalities in their routine blood work that are non-specific but if they are absent suggest that there may be another cause for the signs.
Biochemistry abnormalities are:
Increased ALP in most cases
a stress leukogram which are seen in about 95% of cases
Increased ALT in about 50-80% of cases
Decreased BUN in some cases
Fasting hyperglycaemia in some cases and occasionally Diabetes mellitus
USG is usually below 1.020
What are the diagnostic tests done for Hyperadrenocorticism (Cushing’s Disease)?
Three specific tests commonly used:
Low Dose Dexamethasone Suppression Test (LDDS):
- Most sensitive screening test
- Dog is tested over 8 hours in hospital and must be kept calm
- Serum samples to measure cortisol levels are obtained before and then 4 and 8 hours after low dose dexamethasone is given
- normal dog = inhibition of CRH from hypothalamus = decreased ACTH release from pituitary via negative feedback = decrease plasma cortisol levels for up to 48 hours
- affected dog = no / little inhibition of ACTH release from pituitary = lack of adequate suppression of plasma cortisol = Cushing’s
Urinary Cortisol - Creatinine Ratio:
-Measures cortisol production and excretion rate
-More cortisol produced (Cushing’s) = more excreted in urine = higher the ratio
Get a morning urine sample
-Lots of false positives but is useful for ruling out hyperadrenocorticism as false negative results are rare
ACTH Stimulation Test:
-Looking for an exaggerated cortisol response after administering synthetic ACTH
-Can get false positives
What is the most common cause of Hypoadrenocorticism (Addison’s Disease)?
A result of a deficiency in both mineralocorticoids (aldosterone) and glucocorticoids due to decreased secretion of these hormones from the adrenal glands.
What are the clinical signs of Hypoadrenocorticism (Addison’s Disease)?
Dehydration
Low blood pressure
Decreased heart rate
Anorexia
Diarrhoea, vomiting
Polyuria and polydipsia
Lethargy, weakness
Weight loss
Shock
What are the diagnostics for Hypoadrenocorticism (Addison’s Disease)?
Mild anaemia - 25% of cases
Absence of stress leukogram in an ill dog
Hyponatremia - 80% of cases
Hyperkalemia - 95% of cases
Hypochloremia - 40% of cases
Azotaemia - 90% of cases (due to dehydration)
Urine specific gravity 1.007-1.030 (95% of cases)
Hypoglycaemia - 20% of cases
Hypercalcemia - 30% of cases
What are the differences between primary and secondary Hypoadrenocorticism (Addison’s Disease)?
Primary hypoadrenocorticism:
- A result of destruction of the adrenal gland, most commonly secondary to immune mediated destruction of the adrenal cortex.
- Can also be caused by overdose of adrenolytic drugs or sometimes, metastasis of tumours to the adrenal gland or infarctions.
- All layers of the adrenal cortex are affected; glucocorticoid, mineralocorticoids, sex hormones are deficient
Secondary hypoadrenocorticism:
- Due to a pituitary problem and suppression of ACTH secretion resulting in cortisol deficiency.
- This can be caused by chronic administration of corticosteroids or less commonly by tumours of the pituitary gland or trauma.
What are the diagnostic tests done for Hypoadrenocorticism (Addison’s Disease)?
ACTH stimulation is the only way to check adrenal function in this condition.
Blood sample is obtained for cortisol measurement before and 1-2 hours after administration of ACTH.
No or little increase in blood cortisol levels with administration of ACTH = Addison’s
What is Fructosamine?
A compound that is formed when glucose combines with protein.
Provides a reflection of average blood glucose over the two to three weeks prior to testing. It can be done at any time of the day.
What is Diabetes Insipidus?
DI may be caused by inadequate production of ADH – this is called Central DI (CDI) – or by kidney resistance to the hormone – this is called Nephrogenic DI (NDI).
What is ADH?
Part of kidney function = filter the blood to maintain the balance of the body’s water (homeostasis) by excreting or reabsorbing fluid as required.
Requires an adequate level of a hormone called “antidiuretic hormone” (ADH), or vasopressin > produced by the pituitary gland at the base of the brain > acts on the kidneys.
What are the causes of Diabetes Insipidus?
DI may be caused by inadequate production of ADH – this is called Central DI (CDI) – or by kidney resistance to the hormone – this is called Nephrogenic DI (NDI).
What is the cause of Nephrogenic DI (NDI)?
Lack of kidney response to ADH (NDI) can result from a birth defect, an adverse reaction to certain medications, or secondary to certain diseases (like severe infection, metabolic disorders, or advancing kidney disease).
What is the cause of Central DI (CDI)?
Inadequate production of ADH (CDI) can be caused by a birth defect, brain trauma, a tumor in the pituitary gland, or there may be no specific cause found (idiopathic).
What are the clinical signs of Diabetes Insipidus?
Polydispia and polyuria
Usually no other clinical signs!
What are the diagnostics for Diabetes Insipidus?
Urinalysis: USG is usually less than 1.010
Water deprivation test
To see if the animal secretes and responds to ADH in order to differentiate between: central and nephrogenic DI and psychogenic polydipsia.
What are the diagnostic tests done for Diabetes Insipidus?
Water Deprivation Test
Preparation - starvation for 12 hours, water withheld for 15 hours.
Bladder emptied by catheterisation first thing in the morning.
Weight of the animal recorded.
Recatheterisation every 2-4 hours and measurement of urine SG and weight taken each time.
Water is withheld until the animal has lost 3%-5% of its body weight, the USG is >1.030-1.035 or the animal becomes azotemic.
Perform ADH response test (if still no concentration - likely nephrogenic DI as the kidney is not responding to the ADH).
Do not perform if urea is elevated in the blood biochem
Normal dog / cat = dehydrated, with USG >1.030
There is little change in specific gravity in those animals with a complete lack of ADH activity, whether due to a primary loss of ADH or to unresponsiveness of the kidneys
What are T3 and T4?
The thyroid gland utilized Iodine in food to produce thyroxine (also known as T-4 or levo-thyroxine), a hormone involved with the bodies metabolic rate. T-4 secreted by the thyroid gland gets converted to T-3 in the liver. It is now called triiodothyronine (T-3), which is the active form. When T-3 circulates through the bloodstream if affects the metabolism of every cell in the body.
What are the internal organs affected by cortisol?
Muscles
Cortisol is needed for proper muscle action, yet too much can cause the muscles to atrophy (shrink).
Bone
Bone is made up of a protein matrix and calcium, both of which are affected by cortisol.
Skin
It causes atrophy of hair follicles and sebaceous glands, which leads to alopecia (hair loss).
Vascular System
Cortisol is required for maintaining the integrity of the lining of blood vessels.
Central Nervous System (CNS)
Cortisol is necessary for the normal maintenance of brain functions.
Liver
Excess cortisol will increase the workload on the liver as it converts amino acids to glycogen.
Kidney
An increase of cortisol increases the blood flow (also called GFR-glomerular filtration rate) to the kidneys.
Immune System
It decreases the inflammatory process and helps minimize an overreaction of the immune system to foreign bodies or infections. Unfortunately, it also suppresses the immune system to the point that the body has a hard time mounting a proper response.
