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VetMed Year 3 -Term 1 > e) w/c 14-Oct-13 > Flashcards

e) w/c 14-Oct-13 Flashcards

1
Q

Types of cytology

A

Fine needle aspirate, fine needle biopsy, imprints

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2
Q

Difference between FNA and FNB?

A

Fine needle aspirate requires negative pressure. Fine needle biopsy = NO NEG PRESSURE.
Only do FNA (NEG PRES) if previous method unrewarding

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3
Q

Smear preparation method

A

Remove needle from syringe, draw air into syringe, replace needle, expe aspirated fiod from needle lumen with air filled syringe. WANT THIN areas with good cell spread, minimise cell damage and minimise BLOOD content

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4
Q

What must be done before imprints are taken?

A

Use fresh cut surface, BLOT until dry before INPRINT.

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5
Q

What pot should be used for a) Clot presentation b) Bacteriology

A

a) EDTA

b) Bacto: Sterile pot

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6
Q

How to differentiate Inflammation from Neoplasm on a slide?

A

Inflammation: Sample dominated by inflamm cells (neutropgils, eosino, lymphocytes
Neoplasm: Sample dominated by tissue cells
Can have both = EXPERIENCE

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7
Q

If the slide contains a mixed population i.e. inflammatory cells and tissue cells; what are the two possibilities it could be?

A

Inflamm with secondary dysplasia
OR
Neoplasm with secondary inflammation

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8
Q

In an inflammatory sample, how can we tell if its septic?

A

Contains bacteria/ organisms.
Degenerate neutrohpils
Bacteria must be intraceullar within neutrophils to be significant. If extracellular may be contaminants.
DEGENERATIVE CHANGES IN NEUTROPHILS: NUCELAR CHANGE, SWELLS AND LOOSES LOBATION

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9
Q

The sample has increased number of macrophages. What would be the most likely cause?

A

Granulomatous inflammation (Mycobacterium sp). If Macrophages and Neutrophils = Progranulomatous inflamm - Fungal infection???

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10
Q

Is cytology or histology better for examining round cells?

A

Cytology. Can be indicitive of round cells tumour.

Lymphoma, Plasmacytoma, Histiocutoma, Mast cell tumour

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11
Q

What are the cellular and nuclear criteria of malignancy?

A

Need at least for malignancy otherwise could be dysplastic.

  • Anisoctosis
  • Macrocytosis
  • Cell crowding
  • Anisokarosis
  • Multiniucleation
  • Macrokaroysis
  • Increased mitotic figures
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12
Q

Strongest nuclear criteria of malignancy?

A

Macrokaroysis

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13
Q

How do the serological markers vary between the INNATE and ADAPTIVE immune system?

A

INNATE: Acute phase proteins e.g. serum amyloid A,
ADAPTIVE: Antibodies and Cytokines

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14
Q

When would you look for ANTIGEN rather than ANTIBODY in an ELISA

A

Indirect= looking for ANTIBODY.

You would look for antigen if recent exposure (<5days) and antibody if longer.

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15
Q

Difference between virus neutralisation test and Immunofluorescence assay?

A

IFA tells you if the antibody is present (similar to ELISA but flourence marker instead of enzyme).
VN tells you if antibody is effective (measures whether any CYTOPATHIC effects)

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16
Q

Why is a +ve culture result for E-coli from a faecal sample of affected calves be of little use?

A

Non pathogenic E-coli are very common in faeces. ONLY determining the presence of F4/F5 toxins confirm presence of ETEC

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17
Q

How does pooling samples for Johnes disease reduce cost?

A

Pool 5 faecal samples, from 5 different cows.

If the pool sample is positive test those cows individually.

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18
Q

Aetiology of PPE in pigs

A

Porcine Proliferative Enteritis is caused by Lawsonia intracellularis; an intracellular gram negative rod.
It has a non-haemorragic form and haemorragic (less common).
Present with sudden onset diarrhoea and yellow fibronecrotic casts from ilium.

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19
Q

How is bilrubin exreted?

A

Needs to become water soluble. Conjugated with Glucaronic acid in liver (RATE LIMITING STEP)
Can then be exreted in urine

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20
Q

Explain enterohepatic recycling

A

The bilrubin conj with glucaronic acid is converted by bacteria in the lower UTI to urobilinogen.

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21
Q

Excessive drooling is known as…….

A

ptyalism (TIE-A-LISM)

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22
Q

Difficulty passing urine is known as

A

Dysuria

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23
Q

How do you differentiate a) pre-hepatic and hepatic

b) hepatic- post hepatic

A

a) pre-hep and hepatic. PCV <30 = PRE

b) heptatic and post hepatic. Ultrasound and X-ray

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24
Q

Increased liver enzymes are indicative of….

A

Mostly indicitive of reversible liver DAMAGE.

Liver has huge regenerative capacity

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25
Q

What is the most specific liver enzyme?

A

ALT is most specific.

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26
Q

What iatrogenic increase in liver enzyme is only found in the dog…

A

Cortisol-induced increase in AP

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27
Q

What is liver failure?

A

When the liver’s capacity to regenerate is overwhelmed

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28
Q

What are the indications for liver failure on the chemistry profile?

A

Low albumin, low cholesterol, low glucose, low BUN (Urea). If just low ALP = only damage

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29
Q

What are the clinical signs of hepatic encephalopathy and what CAUSES these clinical signs?

A

Digestion of proteins, NH3 and AA go directly into blood without passing through liver; exposure of CNS to shunted toxins therefore neurological signs.
Head pressing, seizures, ptyalism, bizarre behaviour

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30
Q

Two diseases causing hepatic encephalopathy in CATS and DOGS

A

Cats: Acute liver failure, Hepatic Lipodosis, Neoplasm
Dogs: Portosystemic shunt, liver failure (acute), liver failure (chronic)

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31
Q

Icterus is also known as

A

Hyperbilribunaemia

32
Q

Why do you need to be careful diagnosing icterus in horses?

What is the most common cause of icterus in horses?

A

10-15% of normal horses look mildly icteric.

Anorexia is the most common cause in horses

33
Q

What is the agent that is formed by bacteria in the gut and is thought to contribute to photosensitisation?

A

Phylloerythrin. Exposure to UV light causes cell membrane damage and necrosis

34
Q

State three specific liver tests for the HORSE

A

Bile acids, succinate dehydrogenase (SDH) - raised in acute liver disease. G

GT. Increased in cholestasis

35
Q

What is the protein responsible for uptake of unconjugated bilrubin into the liver?

A

Ligandin.

Therefore anorexia/icterus could be the result of a shortage of ligandin

36
Q

What are some causes of haemolysis in horses

A

Neonatal isoerythrolysis, infections, drugs, toxins (onions), autoimmune HA.

37
Q

When might GGT increase

A

Cholestasis i.e. suggests a billary dysfunction. SDH is also liver specific but indicates hepatocellular dysfunction

38
Q

Why might mannitol be used when a horse is suffering from hepatic encephalopathy>

A

Mannitol is a HYPERtonic solution that can be used to decrease cerebral oedema

39
Q

What is the difference between anuria and dysuria

A 
Anuria = non passage of urine
Dysuria = painful urination
40
Q

Example of a Pyrrolizidine alkaloid plant. When would this cause disease

A

Ragwort is a PA containing plant.
It only causes disease after long term ingestion (4-12 weeks). It is metabolised by the liver to toxic pyroole derivatives which are antimitotic; this causes megalocyte production therefore death and fibrosis

41
Q

What would be seen on histopathology of a liver biopsy from a horse after PA toxicity?

A

Megalocyte production, subsequent fibrosis

42
Q

Difference between Theiller’s disease and Tyzzer’s disease?

A

Theiller’s: Widespread necrosis. Small liver at PM.

Tyzzer’s: Only seen in foals 7-42days. Clostridium piriformis

43
Q

Where else does the liver enzyme AST come from?

A

Muscle cells

44
Q

In which breeds is hyperlipemia common? Why does it occur?

A

Obese shetland ponies and miniature breeds. Occurs due to a negative energy balance. The negative energy balance activates a hormone sensitive lipase

45
Q

How is hyperlipemia diagnosed? When would regular testing be recommended?

A

Plasma Tg levels. Regular testing is advised in at rest horses if they are off their food (due to increase risk of NEB).
At risk horses include minature breeds and shetlands.

46
Q

Why would insulin be useful in treating hyperlipemia?

A

Insulin inhibits hormone sensitive lipase.
This will help reverse the NEB.
Could also encourage feeding/ enteral/ parenteral feeding)

47
Q

What tubes should you use for an exudate anaylysis. What will be measured?

A

EDTA to stop it clotting.

Measurements: Total nucleated cell count, cell identification, protein concentration, enzymes, urea, creatinine

48
Q

Describe a transudate + its causes

A

Transudate: Passive process (due to increased hydrostatic pressure/ decreased osmotic pressure). IS CLEAR.
Mesontheial cells/ Macrophages.
Causes: Hypoalbuminaemia

49
Q

Describe a modified transudate + its causes

A

YELLOW TO CLOUDY IN COLOUR.
Mesotheial cells, macrophages, non-degen neutrophils, small lymphocytes
Causes: Cardiac disease, lymphatic blockage

50
Q

Describe an exudate + its causes

A

TERBID RED/WHITE. High nucleated cell count.
Neutrophils (degenerate or not) and macrophages.
Can be septic or non-septic
Causes: Inflammation
Septic if intracellular

51
Q

What is it important to determine if we find haemorrage exudate? What can we use to work it out

A

Did we cause the haemorrage while sampling???!

If on-going haemorrage sidophores and haemotoidin will be present

52
Q

What diet would be recommended for a horse with suspected liver disease?

A

Low high quality protein feed,

High amounts of protein can exaggerate the CVS signs due to the ammonia breakdown products. e.g. beat pulp and corn

53
Q

What is a Chylous effusion? What happens on centrifugation

A

Oquaue, milky. Formation of ‘cream top’.

When centrifuged it does not seperate

54
Q

What are the indications for liver DAMAGE?

A

ALT (mostly commonly used for dogs/cats), AST, SDH (Sorbitol dehydrogenase), GLDH = LEAKAGE

55
Q

Why can ALT not be used in large animals?

A

Very low, so use SDH or GLDH (Glutimate dehydrogenase)

56
Q

If AST is raised what other enzyme should be checked?

A

AST is not liver specific so should check Creatine kinase (CK) which is muscle specific.
Problem is CK peaks and decreases quickly

57
Q

In choliestasis which two enzymes would be elevated? Why do we need to check the age of the animal before anaylsing results?

A

ALP (from bile duct cells), Gamma Glutimyltransferase (GGT).

ALT is always higher in growing animals. Also can be cortisol induced.

58
Q

Is bilrubinuria more significant in the cat or dog?

A

ALWAYS significant in the cat.

Low levels are normal in the dog urine

59
Q

What further specific diagnostic test can be used to reliably assess liver disease?

A

Bile acid concentration.
Measure fasted level and post prandial. Released from gall bladder after feeding, tests hepatic function.
Horses measure single sample (no gall bladder).
Can also do bile acid challenge test.

60
Q

Explain the normal occlusion

A

Maxillary insisors infront of mandibular.
Premolar zigzag pattern.
Upper PM4 should be buccal to mandibular PM1

61
Q

Why do lingually displaced canine teeth need to be removed?

A

Can lead to extensive palatal defects if left untreated.Painful impingement.

62
Q

When puppy/kitten is teething it is said to have a ____

A

Mixed dentition.

63
Q

If the permanent tooth is present at the same time as the temporary tooth it is said to have a

A

Persistant deciduous tooth which is a pathology. Can lead to malocclusion. Take radiograph to determine if any physiological reabsorbtion is present

64
Q

A missing tooth could be due to:

A

1) Hypodontia (congenital absence)
2) Impacted tooth
3) Previous extraction
4) Traumatic crown fracture, below ginigival margin
USE DENTAL RADIOGRAPHY

65
Q

What is the condition called when the enamel develops before eruption?

A

Hypoplastic enamel

66
Q

Dark brown circles on a tooth could indicate what two things

A
  • Pulp exposure (softer)
  • Secondary dentine (harder)
    USE DENTAL PROBE (sedate)- is it soft?
67
Q

If one side of of the 4th pre molar has more calculus than the other; what could this be indicitive of?

A

A upper premolar fracture.

Important to COMPARE sides and beware of calculus hiding fractures

68
Q

How would you be able to see if a fractured tooth has lead to a root abscess

A

Take radiograph assess for radiolucency.

Loss of lamina dura (white line of alveolar bone surrounding tooth roots)

69
Q

A mouth lesion is more likely to be malignant in a ____

A

CAT.

More likely to be BENIGN in a DOG

70
Q

What does the term mesial mean?

A

Towards the point of the two central incisors

71
Q

When does teeth eruption start in puppies.

When do the permanent teeth start to erupt

A

PUPPIES: 3-4 weeks. Compelte by 2-3 months.
PERMANENT: Between 3-7months of age

72
Q

Dental formula for cat

A

2(I 3/3, C1/1, PM3/2, M1/1)

have 30 teeth (c.f. dogs have 42)

73
Q

Gingival sulcus depth in dogs and cats

A

dogs 1-3mm§

cats 0.5-1mm

74
Q

Stages of peridontal disease

A

5 stages of peridontal disease
Stage 0: Healthy
Stage 1: hyperaemia, oedema, gingivitis. no attachement loss. Reversible
Stage 2-4. Decreasing o2 favours anaerobic bacteria.

75
Q

What are some systemic associated with peridontal disease

A
  • Myocardial disease
  • Renal disease
  • Hepatitis
76
Q

Potential complications of Peridontal disease

A

Oronasal fistula. Symptoms; nasal discharge, sneezing after eating or drinking.
Jawbone necrosis
ASPIRATION PNEUMONIA

77
Q

Treatment of stomatitis

A

REFER EARLY. Not cheap.
Extensive pain relief and extractions,
Corticosterioids should be a last resort.

VetMed Year 3 -Term 1 (15 decks)

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