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1
Q

Name two infectious agents that can be the cause of an infectious polyarthritis

A

Tick-borne/rickettsial (eg borelliosis), Leishmaniasis, bacterial, mycoplasma, bacterial L-form associated arthritis, fungal, viral

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2
Q

If arthrocentesis is performed in a patient whom is suspected of having a secondary (or reactive) polyarthritis, what will culture of the synovial fluid reveal?

A

Sterile culture. Deposition of immune complexes in joint spaces leads to inflammation and pain. The offending microorganism will be at the inflammatory focus (endocarditis, discospondylitis, pyometra etc)

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3
Q

A colleague suggests a shar pei with a polyarthritis could have erosive idiopathic primary immune mediated polyarthritis. Why are they not likely to be correct?

A

Shar peis are more likely to have breed associated non-erosive primary immune mediated polyarthropathy. Greyhounds are associated with the erosive form of the disease

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4
Q

IMPA can be categorised into four sub-types. Describe these.

A

I idiopathic, II Infectious, III gastrointestinal or hepatic disease, IV neoplastic.

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5
Q

Which muscles are affected by masticatory muscle myositis?

A

Digastricus, temporalis, masseter, pterygoid

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6
Q

Why is measurement of CK included in the diagnostics for masticatory muscle myositis?

A

CK is muscle enzyme involved in energy storage, levels increase when there is increased muscle necrosis as a result of inflammation. If CK is high this is consistent with the disease (with appropriate clinical signs). If low, could be late disease process and false neg. Could then look to MRI.

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7
Q

Which drugs should be avoided in patients with myasthenia gravis ?

A

Drugs that reduce neuromuscular transmission (magnesium, phenothiazine, aminoglycosides, ampicillin and anti arrhythmic drugs)

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8
Q

Feline aortic thromboembolism is typically a complication of cardiomyopathy. Which underlying disease is typically associated with canine aortic thromboembolism?

A

Protein losing enteropathy, protein losing nephropathy, hyperadrenocorticism and peracute DIC

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9
Q

A patient managed chronically for protein losing enteropathy presents dyspnoeic with a history of exercise intolerance and coughing. What disease are you concerned about?

A

Pulmonary thromboembolism (May find secondary pulmonary hypertension)

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10
Q

Why might D-dimer evaluation be more effective at assessing for PTE than measurement of FDPs?

A

D dimer is a breakdown product of fibrin, specific to clot degradation. D dimers are only produced when fibrinolysis is activated by ongoing coagulation.

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11
Q

What is pythiosis?

A

Disease state caused by infection with the pathogen pythium insidiosum. It causes weight loss, vomiting and diarrhoea, as well as skin lesions. This pathogen is a water mould found in swampy areas, not endemic to the uk

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12
Q

What electrolyte and acid/base derangements would you expect from a patient with prolonged gastric outflow obstruction?

A

Hypokalaemia, hypochlorinaemia, hyponatraemia and a metabolic alkalosis.

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13
Q

Describe the pathophysiology behind the paradoxical aciduria phenomenon, in relation to gastric outflow obstruction

A
  1. Over time, the patient with gastric outflow obstruction and vomiting becomes increasingly dehydrated. They will have a metabolic alkalosis due to losses in chloride and decreased bicarb excretion.
  2. This leads to increased sodium reabsorption from urine filtrate, to increase blood volume.
  3. In doing so, hydrogen ions are preferentially excreted in favour of sodium reabsorption.
  4. This produces an acidic urine, despite a blood metabolic alkalosis
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14
Q

What clinical signs would you expect a patient with feline eosinophilic granuloma complex to present with? What might the owner have noticed?

A

Hypersalivation, oral lesions, specifically on the maxillary lip
Halitosis, change in eating habits (soft foods), reduction in grooming behaviours

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15
Q

Describe how an adult dog could become infected by Trichuris vulpis (whipworm)

A

Likely ingestion of contaminated materials containing ova (can survive 5years in the environment). Matures in the dog and burrows into the mucosal wall of the colon and caecum. Adult worm will shed ova into the animals faeces.

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16
Q

What clinical signs would expect from a dog infected with trichuris vulpis?

A

Large bowel diarrhoea, acute, chronic or intermittent. Can cause haematochezia and PLE.

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17
Q

What is toxacaris canis more colloquially known as?

A

Roundworm

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18
Q

Which species are responsible for a hookworm infection?

A

Ancylostoma species and uncinaria species

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19
Q

Why might clinical signs differ between dogs infected with whipworm (trichuris vulpis) and roundworm (toxocara canis)?

A

Trichuris vulpis (whipworm) infects large bowel, haematochezia more likely. Toxocara canis (roundworm) resides in the small intestine, and is more likely to induce Meleana.

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20
Q

In a patient with gastric / upper intestinal bleeding, why might they have an increase in BUN but not creatinine in biochemistry ?

A

Bun is digested and reabsorbed from the blood in the GI lumen. Creatinine is excreted and not reabsorbed.

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21
Q

Which bacterial organisms can provide a trigger for the development of chronic gastritis (lymphocytic-plasmacystic) ?

A

Helicobacter (cats) and physaloptera rara (dogs)

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22
Q

What type of gastric mass is probable when Identified on gastroscopy?

A

Adenocarcinoma (lymphoma typically more diffuse)

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23
Q

Why should patients with acute gastritis or suspicion of ulcers have excessive protein restricted?

A

Products of protein digestion increase gastric acid secretion. 30% dogs 40% cats.

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24
Q

Why might hypoallergenic foods be recommended for a patient with chronic gastritis?

A

It is thought that food antigens and immune modulation plays a role in pathophysiology of chronic gastritis.

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25
Q

Which hormone released by the duodenum plays a role in delaying gastric emptying. How can diet impact on this hormones release?

A

Cholecystokinin. It’s released in response to fat in the duodenal lumen, and stimulates bile release from the gallbladder. It delays gastric emptying. Lower fat diets will therefore facilitate faster gastric emptying.

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26
Q

Praziquantel and episprantel are effective treatments for what kind of parasite?

A

Tapeworm

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27
Q

Dipylidium caninum infect dog and cats via what route?

A

Fleas and ticks are intermediate hosts and infect dogs and cats by feeding

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28
Q

Which kind of tapeworm is a human health hazard?

A

Echinococus species

29
Q

Why is strongyloidiasis a severe human health concern, especially for the immune compromised?

A

It’s larvae are highly motile and can burrow into unbroken skin. Immunocompromised humans can suffer from large burdens if client education is poor.

30
Q

Which signalment is typical for infection with strongyloides stercoralis ?

A

Dogs, principally Puppies from over crowded living conditions

31
Q

On faecal flotation analysis, which oocytes should not be confused with giardial cysts?

A

Isospora species (subclass of coccidia) and tritrichomonas trophozoites

32
Q

Where do isospora live after infection in a host?

A

Obligate intracellular, live in villous epithelial cells.

33
Q

Faecal flotation is not the diagnostic method recommended for suspicion of cryptosporidia. Why is this ? What diagnostic methods are available instead?

A

Their oocytes are very small and need to be viewed on x 1000. Poor sensitivity. Can do ELISA testing, faecal PCR. Better sending sample to experienced lab.

34
Q

What are the treatment options for cryptosporidia infection ? (From the coccidia family)

A

No known reliable treatment. In immunocompetant humans and cattle they can remove the burden without treatment. Most patients die or are euthanised.

35
Q

How are cryptosporidia and isospora (of the coccidia family) similar as pathogens?

A

They are obligate intracellular pathogens, they reside in small intestinal epithelial cells (leading to diarrhoea in the host).

36
Q

Describe the clinical signs associated with cats infected with tritrichomoniasis (Protozoa)

A

Large bowel diarrhoea, faecal incontinance, defecation in inappropriate places, anal irritation. May self resolve (infection not cleared but controlled), and signs may reappear during times of stress.

37
Q

How does alimentary adenocarcinoma presentation differ between cats and dogs?

A

Dogs are more likely to have is in large intestine compared to small. Cats more likely to have adenocarcinoma of the small intestine.

38
Q

Describe the pathophysiology of canine parvovirus enteritis (6 marks)

A

Infection by the oral-faecal route. Clinical signs develop 5 -12 days post infection. The virus is non-enveloped and hardy in the environment. The virus invades rapidly dividing cells (bone marrow progenitor cells and intestinal crypt epithelium). Patients present with diarrhoea, lethargy, haematochezia, vomiting. Destruction of epithelial lining will predispose them to secondary infections.

39
Q

Name three bacteria that may cause diarrhoea in the dog

A

Clostridial diseases, salmonella, campylobacter

40
Q

What makes canine parvovirus infection different from canine coronaviral enteritis on blood work?

A

Parvovirus will induce a neutropenia whereas canine coronaviral enteritis does not affect bone marrow, there will be no neutropenia.

41
Q

Which infectious agent is responsible for a mycotic infection?

A

Fungus

42
Q

Which body systems can affect dogs infected by histoplasmosis ?

A

GI, respiratory, reticuloendothelial (phagocytes), bones, eyes

43
Q

Which breed is most affected by hereditary copper toxicosis ?

A

Beddlington terrier

44
Q

Describe normal copper metabolism

A

Reactive molecule as oxidative. When it is absorbed from the intestine it is bound to albumin. The liver processes cooper, it is either reused in circulation with a carrier protein bound, utilised within the hepatocyte for biochemical reactions, secreted into bile for faecal excretion or stored within hepatocytes.

45
Q

How is copper associated chronic hepatitis different from chronic hepatitis, in terms of pathophysiology

A

Copper associated chronic hepatitis begins with excessive stores of copper and secondary injury and hepatitis. In other forms of hepatitis, the injury and inflammation impacts on copper processing, and copper toxicosis is secondary.

46
Q

Feline cholangitis complex can be further classified into three groups. What are they?

A

Neutrophilic cholangitis, lymphocytic cholangitis and chronic cholangitis

47
Q

Describe the expected treatment options for patients with neutrophilic cholangitis, lymphocytic cholangitis and chronic cholangitis

A

Neutrophilic will need broad spectrum and then specific antibiotics. Destolit may help by increasing fluidity of bile. It is also immunomodulating, anti-inflammatory and antifibrotic. Anti inflammatory or immunosuppressive doses of glucocorticoids may be used for lymphocytic or unresponsive Neutrophilic. Chronic cholangitis is secondary to liver flukes, and anti parasitics will be utilised.

48
Q

Why might severe hepatitis cause hypoglycaemia ?

A

The liver performs gluconeogenesis, glyconeogenesis and glycogenolysis. If liver function is impaired, these processes may be impacted.

49
Q

What are the nutritional considerations for a patient with chronic hepatitis?

A

Limiting dietary copper. Protein restriction, but care as patient may be cachexic. Close monitoring essential.

50
Q

Which long term treatments might a patient with chronic hepatitis benefit from?

A
  1. Ursodeoxycholic acid. Hydrophilic bile acid and will reduce risk of cholestasis associated with liver dz.
  2. Drugs containing glutathione, antioxidants.
  3. Chelating agents eg penicilliamine may be useful if copper deposition is noted on histopathology
  4. Lactulose may be beneficial to keep ammonia within the gut lumen and reduce risk of hepatic encephalopathy.
  5. Colchicine is an antifibrotic. May be helpful in cases with evidence of fibrosis or cirrhosis identified on histopathology.
51
Q

Why is ALT the most sensitive liver enzyme for indicating liver injury?

A

ALT and AST are indicators of hepatocellular damage/injury. AST can be found elsewhere in the body, whereas ALT is specific to the liver. Therefore if ALT is high, this is indicative of hepatic injury.

52
Q

Why might measuring CK (creatinine kinase) activity help in the diagnostics and differentiatials for hepatic injury?

A

AST and ALT can be high due to pre-hepatic causes. AST is also found in muscle. If AST is high and CK is high, this indicates muscle injury and a pre-hepatic cause for raised ALT and AST.

53
Q

At what percentage loss of liver function would you expect to see:
a) hypoglycaemia
b) hypoalbuminaemia

A

A) 75%
B) 70%

54
Q

What are the three categories that characterise causes of hyperbilirubinaemia ?

A

Prehepatic (increased production by haemolysis)
Hepatic disease (decreased uptake and processing of bilirubin)
Posthepatic (impaired excretion of bilirubin)

55
Q

A client complains that their cat is still jaundiced at home, after being discharged recovering from a biliary obstruction and cholestasis. How long do you advise the pigmentation May last to manage their expectations? Explain your reasoning for how long it may last.

A

Conjugated bilirubin in plasma binds irreversibly and covalently to albumin and has a half life in circulation of 2 weeks. I would therefore expect the jaundice to start weaning at 2 weeks and be resolved by 6 - 8weeks max.

56
Q

What is meant by the term enterohepatic circulation?

A

It is the normal processing of bile acids. They are secreted in response to cholecystokinin into the duodenal lumen. They assist with the processing of dietary fats and protein. Bile acids are later reabsorbed in the ileum back into the blood and travel to the liver via the portal vein. Up to 95% of the bile acids are reabsorbed and reused in bile.

57
Q

Name the 6 clotting factors made by the liver that are vitamin K dependent.

A

Clotting factors II, VII, IX, X, Protein C, and protein S.

58
Q

How might surgical treatment for biliary cysts vary, between polycystic and solitary cystic forms?

A

Polycystic forms are more likely to be congenital/hereditary. Solitary cysts are usually acquired through trauma inflammation or obstruction. Solitary cysts can be drained, or surgically fenestrated/removed. Polycystic forms are often diffuse and are not amenable to surgical management. Fenestration can be used in the larger cysts to prevent obstruction or compression of portal blood flow.

59
Q

How might biliary obstruction play a role in coagulopathies? (3 marks)

A
  1. Reduced bile acid secretion into duodenal lumen reduces proper absorption of fats. This limits vitamin K absorption.
  2. There is therefor a reduction in production of Vitamin K dependent clotting factors (II, VII, XI, X, Protein C and Protein S).
  3. Impaired biliary excretion of waste (e.g. copper) leads to a build up within the liver and hepatocellular injury occurs. Liver injury will trigger inflammation and may contribute to coagulation dysfunction.
60
Q

Which disease has been linked to the development of a gall bladder mucocoele, increasing a patients risk by x29?

A

Hyperadrenocorticism

61
Q

Describe the pathophysiology that contributes to a gall bladder mucocoele forming

A
  1. Excess mucus / mucin production by gb epithelial cells. Could be due to cystic mucosal hyperplasia of gb.
  2. Prolonged periods of reduced gall bladder contraction (eg delayed gastric emptying, duodenal obstruction).
    Increased viscosity of bile in the gb will lead to impaired emptying and increase likelihood of gb mucocoele
62
Q

How does lactulose contribute to stabilisation of patients with hyperammonaemia ?

A

Lactulose reduces hyperammonaemia when administered orally or rectally. Rapid results rectally.
Lactulose is a disaccharide that is metabolised by colonic bacteria to form organic acids. It promotes acidification of colonic contents, trapping ammonia in the form of ammonium.
This ammonium is expelled in faeces with gut bacteria.
Lactulose also accelerates passage of faeces through the GI tract, limiting time for bacteria to form ammonia.

63
Q

Why is Protein C measurement used to differentiate portal vein hypoplasia (+/- portal hypertension) and Portosystemic shunts?

A

Protein C is a vitamin K dependent clotting protein. It can be used as a proxy for evaluating hepatic blood flow. In dogs with portal vein hypoplasia, protein C will be >70% whereas dogs with PSS will have low protein C

64
Q

What is the equation that is used to calculate a patients anion gap?

A

AG = [Na+ + K+] - [Cl- + HCO3-]

65
Q

Why is the anion gap useful in patients presenting with acid/base derangements ?

A

Differentiating between gain of acid or loss of bicarbonate can help to tailor treatment to the cause of the acidosis

66
Q

A patients anion gap is found to be high, what does this tell you about the cause of the metabolic acidosis?

A

There has been a gain in organic acid (eg hyperlactaemia)

67
Q

A patient has a metabolic acidosis with a normal anion gap. What does this tell you about the cause of the metabolic acidosis?

A

That it is due to a loss of bicarbonate buffers, or a failure to excrete hydrogen ions. There will be a corresponding increase in chloride to account for loss in bicarb.

68
Q

Describe the pathophysiology that’s leads to a metabolic alkalosis in relation to a gastric outflow obstruction

A
  1. Losses in stomach content (either vomiting or lack of absorption in upper GI tract) mean the blood is depleted of potassium, sodium and chloride.
  2. This can be compensated for in the kidney, until hypovolaemia induces aldosterone release.
  3. When aldosterone increases reabsorption of sodium, a lack of anions and cations as exchange molecules leads to bicarb being excreted in favour of sodium reabsorption.
  4. This leads to a metabolic alkalosis

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