calcium oxalate

anonymous asked:

I was reading a post recently saying that if your cat or dog drinks antifreeze than alcohol(not pure rubbing alcohol I assume) will stop the acidification of organs and save your pet. Is this true?

There is a tiny grain of truth in there, but it’s a whole lot more complicated than that.

The toxic component of antifreeze is ethylene glycol. Its metabolites have multiple toxic effects and its metabolism. Its metabolism through the liver is complicated.

All metabolites of antifreeze have toxic effects.

  • Ethylene glycol causes central nervous system depression, euphoria and increased serum osmolarity.
  • Glycoaldehyde and Glycoxylate can inhibit the Krebs cycle, that thing mitochondria do to generate cellular energy.
  • Glycolate causes renal failure and acidosis
  • Oxalate aculumation in the kidney can also cause permanent renal failure.

So with all this badness, where does ethanol (drinking alcohol) come in?

Ethanol is preferentially acted upon by alcohol dehydrogenase. This means that if you have both ethanol and ethylene glycol present, alcohol dehydrogenase will spend more time acting on the ethanol. This slows down the rate that ethylene glycol is turned into its other toxic metabolites.

Because a relatively small amount of ethylene glycol is getting metabolised at one time, the other enzymes in the chain can keep up with the pace, so the most toxic metabolites don’t accumulate in super high levels before being excreted as calcium oxalate.

However, this means two things:

  • If you give ethanol 18 hours after ingestion of antifreeze, you actually make everything worse
  • Treatment with ethanol requires you to induce alcohol poisoning for about two days.

A single shot of vodka isn’t going to cut it. We usually have these dogs on intravenous fluids to keep them hydrated whilst giving ethanol in hospital (we use vodka) because these animals are often nearly comatose.

We are inducing one type of poisoning to protect against another.

And for what I hope is obvious reasons, do not try this at home.

Common Poisonous House and Garden Plants and their Symptoms

If you have children or pets or suspect someone might have ingested or handled these plants improperly, this list is for you. Most of these plants seem entirely harmless and even more of them are used every day in gardens and as indoor decoration or in spellwork. Most all the symptoms I list are symptoms of ingestion unless otherwise noted. If something is incorrect, please feel free to message me and I will fix it shortly!

Peace Lily (Spathiphylum)

Peace lilies resemble Calla lilies and are fairly popular as gifts. They contain calcium oxalate crystals that can bring on skin irritation when handled, burning of the mouth, difficulty swallowing and nausea.

English Ivy (Hedera Helix)

The berries from English Ivy can cause gastrointestinal issues and delirium or respiratory problems. Sap from the leaves can cause skin irritation and sometimes blisters.


All parts of this plant contain calcium oxalate. Repeated contact can cause reactions similar to allergic reactions and ingestion can cause abdominal pain.

Ficus trees and Rubber Trees (Ficus Benjamina/Elastica)

Ficus trees produce a form of latex that can bring on allergic reactions in some people.

Larkspur and Delphinium (consolida ajacis)

Similar to our deadly friend Aconite (monkshood), this plant can bring about the same symptoms if ingested in a large enough quantity.

Lily of the Valley (Convalina mahalis)

Contains cardiac glycosides that can cause headache, nausea, and cardiac issues.

Bleeding Heart (Dicentra)

Contains toxic alkaloids that can cause nausea, seizures, and respiratory issues.

Sweet Pea (Lathyrus odoratus)

All parts of sweet peas are mildly poisonous. New sprouts and shoots contain the most toxins, an amino acid called lathyrogen. Can cause paralysis, weakness and tremors.


Produces a highly irritating sap. Touching the bulbs can cause a reaction as well as breathing dust from the bulbs. Ingestion can cause vomiting, breathing issues, and weakness.

Hyacinth (hyacinth orientalis)

Sap and bulbs, much like tulips, are major skin irritants.

Azaleas and Rhododendrons

A toxin called grannotoxin can be found in the leaves, flowers, nectar and pollen. Ingestion can cause heart problems, vomiting, dizziness, and extreme weakness

Black Locust (Robina Psudocacia)

All parts but the flowers are poisonous. Can cause weak pulse, upset stomach, headache, and cold extremities.


All parts are toxic. Causes burning, fever, vomiting and in extreme cases kidney failure.


All parts are poisonus. Sap is a skin irritant and bright berries are deadly. Irritation of the throat, internal bleeding, weakness, and vomiting are all symptoms.

Foxglove (digitalis)

All parts can cause severe stomach upset, skin irritation, delirium, tremors, convulsion, headaches, and heart failure.

Hellebore/Christmas Rose

All parts are poisonous, and the sap is a skin irritant. Can cause bruning, vomiting, dizziness, nervous depression, and convulsions.


Often used as a cake topper, Hydrangea actually contains levels of cyanide. Ingestion leads to vomiting, headache, and muscle weakness.


Berries contain toxins that can cause visual problems, weakness, vomiting, heart problems and even death.


Contains a toxin known as Lobelamine that can cause heart problems, vomiting, tremors and paralysis.

Yellow Jessamine (Gelsimium semperviens)

All parts are toxic. Pollen and nectar are fatal to children.

Bring me the vodka!

I’ve gained so many funny and interesting stories from my work experience but this has to be one of my favourites. Bare with me, it’s a long but fun little tale.

Ethylene glycol is the main ingredient in antifreeze. It has a sweet taste so is easily consumed by cats and dogs accidentally from car radiators or garages. Last year, the vet I volunteer at had several cases of cats from the same area suffering from symptoms of ethylene glycol poisoning.  As soon as the vet realised what the problem was I remember him taking one of the nurses to one side and asking her in hushed tones to pop down the road and buy some vodka. I was very confused and began questioning his motifs.. but luckily all became clear as the case unfolded.

Once ingested, ethylene glycol is broken down through a number of metabolic processes. The first step includes the enzyme ‘alcohol dehydrogenase’ which breaks ethylene glycol down in to glycoaldehyde. Without this step the rest of the degrading can’t happen. It is the breaking down of the chemical which causes the problems within the body, as the metabolites formed are toxic. Metabolites are the intermediates and products of the metabolic process. Glycolic acid and oxalic acid are two of these metabolites known to cause the most issues. Oxalic acid combines with the calcium in the animal’s blood to form calcium oxalate which in turn blocks and destroys the nephrons in the kidneys.

Symptoms of ethylene glycol poisoning come in 3 stages. Stage 1 if from half an hour to 12 hours after ingestion and consists of neurological and gastrointestinal symptoms. The animals are often said to be acting ‘drunk’, so showing signs of dizziness, uncoordinated movements, head shaking and confusion. There’s also irritation to the stomach as the toxins are broken down causing nausea and vomiting. 

Stage 2 is 12 to 36 hours after ingestion and is a result of accumulation of the organic metabolites formed as the chemical is broken down. Symptoms include an increased heart rate, high blood pressure and hyperventilation.  Muscle spasms can also occur. The toxins created by the metabolic process can be lethal at this point. Stage 3 occurs 24 to 72 hours after ingestion and result in kidney failure. Symptoms include red blood cells or excess protein in the urine as well as lower back pain. It’s best to treat the poisoning with an antidote as soon as possible after ingestion as the toxic metabolites can begin to cause irreversible harm to the kidneys very quickly.

 A form of diagnosis is urine examination. My particular vet looked under a microscope for the presence of calcium oxalate crystals. I’ve put a picture at the bottom of the post of these crystals from the urine of a cat with said poisoning.

In order to save the animal the aim is to prevent the formation of the toxic metabolites. Here’s where our good old friend ethanol/vodka comes in! Ethanol competes with ethylene glycol for the enzyme alcohol dehydrogenase. Ethanol has an affinity 100 times greater than ethylene glycol for alcohol dehydrogenase so successfully blocks the first step of the metabolic process. Without oxalic acid formation, the toxic bodily effects can be avoided, and the ethylene glycol is eventually excreted in the urine. During recovery the animal’s blood acidity needs to be brought back up to normal too. This is done through the administration of fluids that contain sodium bicarbonate and by checking the pet’s urine or blood pH periodically to regulate the amount given. Giving intravenous fluids usually increase urine flow – so fluid administration is important to ensure the chemical is urinated out as quickly as possible.

So the vet genuinely ‘got the cat drunk’. He administered the vodka orally using a syringe but said sub-cut fluids could be infiltrated with ethanol too. He was confused that 3 or 4 cats from the same area were all suffering from the same poisoning. It was finally discovered by the RSPCA that someone had been leaving out bowls of antifreeze as they were fed up with other people’s cats defecating in their garden! Shocking!

Common Ailments in Guinea Pigs

I attended a BSAVA Clinical Club Pub talk on guinea pigs by Jill Pearson, a veterinary surgeon with lots of exotics knowledge.

So what are the common diseases of guinea pigs?

Hypovitaminosis C (Scurvy)

  • Consequences: parasitic infestation, respiratory disease, pododermatitis, malocclusion, immunosuppression, swollen and painful joints, poor wound healing
  • Treatment: 100 mg/day vitamin C supplement
    • In young animals, musculoskeletal damage can’t be reversed – euthanasia
    • Prevention: use a guinea pig diet with 800 mg/kg vitamin C

Respiratory disease

  • Bordatella bronchiseptica
    • Clinical signs: snuffles, severe depression, respiratory disease
    • Treatment: antibiotics, fluids, nutritional support, NSAIDs
  • Streptococcal pneumonia
  • Syringe feeding
    • Prevention: use a thick mixture and don’t do if guinea pig won’t swallow
  • Cervical lymphadenitis (abscesses in lymph nodes)
    • Cause: Streptococcus zooepidemicus
    • Treatment: systemic antibiotics, possibly excision of node/lancing and drainage of abscesses

Urinary problems

  • Cystic ovaries
    • Clinical signs: bilateral flank alopecia, vulval bleeding, palpable lumps in abdomen
    • Treatment: spaying
  • Cystitis or cystic/urethral calculi
    • Usually calcium oxalate calculi
    • Clinical signs: squeaking while peeing, blood in urine, urine scald
    • Treatment: use pre-boiled water to drink, add Ribena to water to increase fluids, antibiotics, diazepam (if male)

Weight loss

  • Dental malocclusion – linked to Hypovitaminosis C
    • Treatment: dentistry, adjust diet
  • Yersinia pseudotuberculosis – rare
    • Clinical signs: weight loss, diarrhoea
    • Diagnosis: euthanasia and post-mortem
  • Coccidiosis (Eimeria caviae) – rare
    • Causes: poor husbandry and overcrowding
    • Treatment: sulphamezathine/sulphadimidine in water with Ribena (because bad-tasting)
  • Tumours (lymphomas), pododermatitis, painful temporomandibular joint


  • Trixacarus caviae – most common
    • Clinical signs: crusting, hair loss, pruritus, pain, seizures, bronchospasm
    • Treatment: topical or parenteral ivermectin, NSAIDs vs pain, diazepam vs seizures, bathing to clean skin
  • Trichophyton mentagrophytes – less common
    • Clinical signs: starts at head
    • Diagnosis: microscopic examination, culture
    • Treatment: topical enilconazole
  • Pediculosis (Gyropus ovalis, Gliricola porcelli)
    • Treatment: ivermectin 3x every 7-10 days

anonymous asked:

Ever post anything about Miniature Schnauzers? I've been having constant nightmares about mine recently. (Came for the veterinary info, stayed for the breed (mythological creatures too!) info.)

.Oh my anonymous friend, let me tell you about miniature Schnauzers. I have much to say about these little dogs.

Before I go too far, these posts are about the breed from a veterinary viewpoint as seen in clinical practice, i.e. the problems we are faced with. It’s not the be-all and end-all of the breed and is not to make a judgement about whether the breed is right for you. If you are asking for an opinion about these animals in a veterinary setting, that is what you will get. It’s not going to be all sunshine and cupcakes, and is not intended as a personal insult against your favorite breed. This is general advice for what is common, often with a scientific consensus but sometimes based on personal experiences, and is not a guarantee of what your dog is going to encounter in their life. 

Originally posted by bellarinadejour

Although having said that disclaimer, there is one condition in particular that it would not surprise me at all if every miniature schnauzer ends up having at least once in their life…

Ah, pancreatitis. Mini schnauzer with abdominal pain? Pancreatitis. Vomiting? Pancreatitis. Diarrhoea? Pancreatitis. Not wagging its tail properly? Pancreatitis. There is no other breed of dog I’ve encountered that seems to be so exquisitely sensitive to this condition.

Honestly, on one occasion I saw a mini schnauzer for an ear infection, but because I did a full clinical exam identified abdominal pain and subsequently confirmed pancreatitis on a blood test.

Pancreatitis occurs when the pancreas becomes inflamed, often leaking its own digestive enzymes into itself. Symptoms vary in severity. A very mild case may result in a dog just being off their food for a day, and the owner almost calling the vet clinic, but then not bothering when the dog eats and looks normal the next morning. Or they can be so sick they present recumbent with a massive fever, can’t keep even water down, and have so much damage to their pancreas that they become diabetic.

In my experience mini schnauzers spend a lot of the time with the mild to moderate forms of pancreatitis, maybe enough to recover with a single shot each of pain relief and anti-nausea medication, or a 3-5 day stay in hospital. However if these episodes are ignored, or if a momentary lapse allows the dog access to high fat foods, they often have severe or catastrophic pancreatitis episodes. Also, the more episodes of pancreatitis they have, the more likely they are to have another, more severe episode in the future.

I don’t know if this is what you’ve been having nightmares about. Pancreatitis is more common in older dogs, which you can’t do anything about, but it’s also often triggered by diet. Many of our mini schnauzer patients end up on low fat diets for this reason, several of them on prescription ultra-low fat diets. At least this is a factor that you can control.

Related to the strict dietary control that this breed often needs, Dental Disease can be a significant problem. Bone marrow is hugely fatty, and some of these dogs will end up hospitalized if they get to chew on a bone, or chicken neck. I cannot emphasize enough how sensitive some of these dogs are to dietary fat. Consequently many of them can’t tolerate the usual things we encourage dogs to chew for dental health, and these dogs often end up needing dental treatments and extractions. 

Also related to pancreatitis, Diabetes Mellitus is more common in this breed, but considering that it can develop secondary to pancreatitis that shouldn’t be a surprise.

The breed is reputed to be prone to a number of eye diseases, but the only one I’ve come across with relative frequency has been cataracts. These can also form secondary to diabetes. 

Another possible factor that might contribute to pancreatitis in these dogs (and the hyperlipidaemia thought to cause it) is hypothyroidism. This endocrine condition slows their metabolism and produces changes in the hair coat, but also results in higher blood cholesterol and lipid levels.

A number of these dogs have historically ended up on cortisone for Allergies or Atopy. These vary in how problematic they are for the dog, but they are certainly frustrating to treat.

Ear infections are also fairly common, and while they may be worsened with allergies or atopy, it is the densely packed fur growing from the canal that traps moisture and predisposes these dogs to problems. The hairy canals are not fixed by cropping, claiming they are is a weak excuse for an outdated and unnecessary surgical modification.

Mini Schnauzers are at increased risk for developing Calcium Oxalate bladder stones, which is not the most common stone seen in dogs so diets claiming to prevent urinary crystals or stones are not always appropriate for this breed. Some are, but it’s important to check.

And lastly I see a fair number of these dogs with Back Pain, which sometimes is associated with a bulging intervertebral disc. So quite a lot to say about the miniature schnauzer, but most of it is related to consuming fat in amounts that would be normal for other dogs.
Molecule of the Day: Oxalic acid

Oxalic acid (C2H2O4) is the simplest dicarboxylic acid, and is a commercially significant commodity chemical. It is a white powder that dissolves in water to produce a colourless, acidic solution.

Oxalic acid is naturally found in many plants, such as spinach, rhubarb, and parsley. It is produced from oxaloacetate, which is produced in the Krebs cycle, via the action of oxaloacetate acetylhydrolase, which hydrolyses oxaloacetate into oxalic acid and acetic acid.

Oxalic acid is a reducing agent, and is capable of being oxidised to carbon dioxide in the presence of strong oxidising agents, such as potassium permanganate.

It is commercially used for rust removal; since oxalic acid is acidic, and its conjugate base is a bidentate ligand, it can react with rust to form the ferrioxalate anion, which is soluble. This removes the rust, revealing the inner iron layer (see below). It is also used as a mordant (dye fixative), as well as a bleaching agent for wood.

Oxalic acid is toxic if consumed; it combines with calcium ions in the body to produce calcium oxalate, which is insoluble and accumulates in the form of kidney stones. It is also the basis for the toxicity of ethylene glycol, which is found in antifreeze, as ethylene glycol is metabolised in the body to produce oxalic acid.


Anthurium dolichostachyum is in the peace lily family Araceae. It is native to South America including Ecuador and Brazil. Like many Anthuriums, this species is an evergreen shrub or vine that grows in the jungle understory. The flowers are arranged in a spike-like inflorescence known as a spadix, and develop into bright red berries. The fruits, and other parts of this plant are toxic, due to the presence of calcium oxalate crystals in the tissues. These calcium oxalate crystals are abrasive and can damage lung tissue and organ linings if ingested.

Case Study: Distressed Chameleon Part II


1. Due to limited finances, it is only feasible to perform one diagnostic test. What do you choose? Bloodwork (which test)? Radiographs? Ultrasound?

A couple of you chose to do bloodwork, which is a very reasonable choice. Bloodwork (namely, a complete blood count and a blood chemistry) would help us assess the chameleon’s calcium and phosphorus levels, along with letting us look at a number of other values: red and white blood cells, liver values, uric acid, etc. It would help us get an overall systemic picture of how the animal is doing.

However, there is one important factor to remember: hypocalcemia (low blood calcium) is often not present until very advanced stages of metabolic bone disease. The body tries very hard to keep blood calcium levels adequate, hence the pulling of calcium from the bones and formation of such a brittle skeleton. Therefore, while bloodwork is definitely a useful tool, certain values may not be what you’d expect at first glance. Oftentimes, animals with metabolic bone disease will have fairly normal bloodwork.

cacajao​ chose radiographs, which are very often taken in cases of suspected MBD. Radiographs allow us to assess the bone density of the animal, along with checking for any fractures, pathological or otherwise. Radiographs also allow us to look for other abnormalities that can result from improper care: issues like impaction, for example, caused by an incorrect substrate.

What did I do in this case? Radiographs.

This was partially due to cost, and largely due to the fact that, as some of you noted, this animal was too small and too fragile to allow for successful collection of a large enough amount of blood.

Here is the dorsoventral view of this particular patient:

This animal has extremely poor bone density. Most of his bones aren’t visible at this point, while the ones that are are very faint and, particularly in the limbs, fractured at various points. This radiograph shows an animal with advanced metabolic bone disease.

2. What aspects of this animal’s husbandry are correct? Which are incorrect? How would you keep this particular reptile?

This animal’s husbandry was a bit of a mix of good and bad. 


  • 5.0 UVB bulb (with assurance that the patient could reach its rays)
  • Low temp in the mid-70s
  • Proper light cycle
  • Proper misting and fogger
  • Adequate humidity


  • Glass tank: Screen enclosures are widely considered to allow for better ventilation needed to keep healthy chameleons (some glass tanks allow for good ventilation, but many don’t; screen is easier)
  • High temp isn’t quite high enough (95-105*F would be more ideal)
  • Initial lack of cricket supplementation: This is a huge issue. Crickets, while a popular feeder, are widely known to have a poor calcium to phosphorus ratio (0.33:1), about three units of phosphorus for every one unit calcium. The correct ratio for most reptiles is understood to be between 1.5:1 and 2:1, the complete reverse of what the cricket ratio is. This imbalance in itself can result in metabolic bone disease.

3. What is your top differential diagnosis for this patient?

This is a classic case of metabolic bone disease (MBD). MBD is actually an umbrella term for various disorders interfering with healthy bone structure. In this animal’s case, the disease is called Nutritional Secondary Hyperparathyroidism.

What this means is that his parathyroid glands, which secrete parathyroid hormone (PTH), are working in overdrive. PTH encourages calcium absorption from the gut and from the bones to increase blood calcium.  

The reason they are doing this is likely due to the imbalance in calcium and phosphorus in the animal’s diet. The high level of phosphorus in the crickets causes a binding of calcium in the gut to form insoluble calcium phosphate, decreasing absorption of calcium itself. 

Poor calcium absorption can also be caused by low temperatures, lack of vitamin D (making proper UVB lighting very important), other calcium binders (such as oxalates) in the diet, and other maladies, such as kidney or liver disease.

In order to keep blood calcium at normal levels, the glands secrete more and more PTH, which encourages the break down of the patient’s bones to provide the calcium lacking in the diet. This, in turn, results in the soft, breakable bones we seen in animals afflicted with metabolic bone disease.

So now what?

Now that we know this chameleon’s problem, what treatments do we initiate?

The floor is open!


Jack in the Pulpit…

the roots were used for a variety of Native American medicines, including pain relief, asthma and snakebite… the corm or bulb was used as a food source, but care had to be taken to inactivate the poisonous calcium oxalate… in fact, some competing tribes would try to poison each other by lacing food with calcium oxalate taken from the corm…