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VetMed Year 3 -Term 1 > f) 21-Oct-13 > Flashcards

f) 21-Oct-13 Flashcards

1
Q

How can you tell the difference between luxators and elevators

A

Luxators have thinning working ends

Elevators are slightly more spoon shaped

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2
Q

How should you hold the luxators/ elevators. How does this change when you hold the tapered fissue cutting bar?

A

Palm-Grasp. Tip of index finger placed on shaft.

Tapered fissue cutting bar is held with a MODIFIED PEN-GRASP

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3
Q

Steps when extracting a tooth

A
  1. Cut gingival attachment
  2. Insert luxator into peridontal ligament space ‘walk around’
  3. Insert elevator (spoon shaped)
  4. Use extraction forceps in rotation movement.
    If not loose enough ELEVATE MORE. Need root.
    Inspect.
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4
Q

How many roots does the upper PM4 have? What structure needs to be avoided when extracting this tooth?

A

Three roots.

Avoid the parotid duct. Parotid papilla is above distal root of maxillary PM4

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5
Q

Which important structures need to be avoided when doing dental surgery?

A

Neurovascular bundle which exits from infraoribital foramen.

Neurovascular bundle that exits from the mental foramen.

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6
Q

Pathogenesis of tooth reabsoption in cats

A

Common. Incidence increases with age.

Teeth are attacked by odontoclasts (surrounds roots). Vascular granulation tissue fills lesion.

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7
Q

Anatomic landmarks of healthy dental radiographs

A 
Lamina dura (white line around root= alveolar bone)
Peridontal ligament  (black line around root)
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8
Q

Radiographic sign of infected root?

A

Root surrounded by a lucency.

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9
Q

When performing a flap closure. What is VERY important?

A

NO TENSION. Sutures 3-4mm apart.

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10
Q

Prostaglandins and Leukotrianes are examples of

A

Eicosanoids

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11
Q

Examples of hormoens derived from tyrosine and tryptophan

A

Tyrosine: Catecholamines, thyroid hormones
Tryptophan: Seratonin, Melatonin.
Exerts actions rapid, no species variation

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12
Q

When would secondary hypofunction of an endocrine system occur?

A

Abnormal/lack of production of trophic hormones.

I.E. inactive pituatary gland results in a hypofunction of adrenal/thyroid glands

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13
Q

6 hormones released from hypothalamus

A

GnRH, TRH, GH, SS, CRH, DA

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14
Q

Which of the cell types in the anterior pitutary secretes 2 hormones?

A

Gonadotrophs secretes LH and FSH (in response to GnRH from hypothal)

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15
Q

Which hormones are released from the posterior pituatary?

A

Vasopressin (ADH) and Oxytocin (source is the paraventricular nucleus - hypothalamus)

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16
Q

What is a pituatary adenoma? Are there different types?

A

A benign epithelial tumour of glandular origin. In pars distalis. Can be functional (ACTH secreting) or non-functional.

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17
Q

Clinical signs of pituitary cysts. Which species are most commonly effected?

A

GSH, Spitz. Effects on animal are related to reduced trophic hormones NO SECRETORY CELL DIFFERENTIATION e.g. drawfism, retension of puppy coat, delay of permanent dentition

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18
Q

Adeonma of the pars intermedia in HORSES and DOGS can present as…

A

Dogs: Larger adenomas: Diabeties incipidus due to hypopituitarism
If hormonally active can cause Cushings (increased ACTH)
Horses: Different clinical signs depending on where the tumour is. Pars intermedia: MSH, CLIP, Beta-endophin
Pars distalis: ACTH = Cushings

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19
Q

Difference between central and nephrogenic diabeties incipidus

A

Central: Inadequate production of ADH from posterior pituatary. Caused by compression of pars nervosa by expanding cyst of pit tumour. Diagnosis with water dep. test.
Nephrogenic: Inability of collecting duct epithelium to utilise ADH

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20
Q

Aldoesterone is released from the ___ and is an example of a ____ hormone

A

Zona glomerulosa.

Aldosterone is an example of a mineralcorticoid

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21
Q

What causes the pot-bellied appearance associated with canine cushings?

A

Hepatomegaly and abdominal muscle weakness

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22
Q

Clinical signs associated the hypoadrenocorticism are normally associated with the lack of ____
How can addisons disease lead to bradycardia?

A

Mineralcorticoid e.g. aldosterone from zona glomerulosa.
Normally ideopathic.
Hyperkalemia can lead to bradycardia. AlsoV&D due to generalised tissue under perfusion
Addisonian crisis: Unable to respond to stressful situations as inadequate glucocorticoids

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23
Q

Actions of thyroid hormones

A

Calorigenesis (increased heat)
Increased cardiac output
Alterations to metabolism

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24
Q

How does diabetes mellitus present clinically?

A

Weight loss, increased appetite.
PD/PU
Bright and happy (doesn’t make you feel ill)
If ketoacidosis (cats) vomiting and inappetance

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25
Q

Pathophysiology differences between canine and feline diabetes

A

Dog: Severe loss of islets. Non-reversible
Cat: Insulin resistance –> Islet hyperactivity –> Islet underactivity

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26
Q

What else can cause insulin resistance?

Which other diseases can cause diabetes?

A

Obesity, oestrous, pregnancy, anxiety, hypercortisolaemia (stress).
Hyperadrenocorticoism, acromegaly

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27
Q

If an dog presents with suspected diabeties what must be checked before undertaking further tests?

A

intact? Diestrous diabetes? SPAY

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28
Q

What are a common complication of diabetes in dogs?

A 
Hepatomegaly. 
Bilateral cataracts (85% of cases within 400Days)
29
Q

What can help differentiate hyperglycemia from ‘stress’ hypoerglycemia?

A

Fructosamine - formed when glucose binds irreversible to albumin. (only use when albumin levels are constant)
Representitive for 3 weeks in dogs
10-14 days in cats

30
Q

What is important to remember when starting off insulin therapy?

A
  1. Do not alter dose for 3 days (caninsulin) as still some degree of insulin resistance
  2. Meal matching. Insulin inj then feed one hour later
31
Q

What diet should be provided for a cat with diagnosed diabetes

A

Cat is a carnivore give LOW carbohydrate

32
Q

Difference between corticosteroid and a glucocorticoid

A

Corticosteroid: Any steroid drug or molecule
Glucocorticoid: Antiinflammatory enhanced potency
BIND TO INTRACELLULAR RECEPTORS. Alter gene expression.

33
Q

Glucocorticoids can alter their own metabolism. What is this known as and what is its clinical significance?

A

Tachyphalaxis.
If given long course e.g. over 7D dose needs to be altered.
Lower doses for longer periods of time = NO GOOD

34
Q

Explain the mechanism of action

A

Intracellular receptors.
1. Acts of cell membrane phospholipids (Phospholipase A2)
2. Form arachidonic acid
COX pathway to COX-1 and COX-2
Also lipoxygenase pathoway (Leukotrienes)

35
Q

Why are glucocorticoids better at treating inflammation than NSAIDs?

A

Glucocorticoids are more effective as they act at a high level than NSAIDs . They also modify immune system. NSAIDs don’t effect i.e. they can suppress T-lymphocyte functions, reduce histamine, inhibit antigen presentation, supppres inflammatory response

36
Q

What is the relative potency of mineralcorticoid to glucocorticoid ratio for the following glucocorticoids

a) Dextamethasone
b) Prednisalone
c) Betamethasone

A

a) Dextamethasone: MC:0 GC: 30
b) Prednisalone: MC:0.25 GC: 4
c) Bethamethasone MC:0 GC: 35
i. e. if using as replacement want equal potencys. Bethamethasone would not give any mineralcorticoid replacement

37
Q

Example of a short acting and long acting glucocorticoid

A

short acting: Hydrocortisone

long acting: Dextamethasone/ Betamethasone

38
Q

Duration of the action of glucocorticoid is dependent on which three factors?

A
  • Half life of drug
  • ESTER’S SOLUBILITY
  • Dose of drug
    i. e. predinsalone 1-2mg/kg >24hrs
39
Q

Example of two very soluble esters

A

Succinate and Phosphate e.g. hydrocortisone sodium succinate

40
Q

Example of a moderately insoluble drug (released for days-weeks)

A

Acetate e.g. dextamathasone acetate.

Duration depends on SOLUBILITY

41
Q

Fluticasone proprionate is used for

A

Asthmatic inflammation

42
Q

Two steps when using glucocorticoids for treating immune-mediated disease

A
  1. Induction of remission (high dose ONCE daily) 2-3mg/kg (HARDLY EVER LOWER) for around 10 days
  2. Maintenance of remission (start on concurrent NSAIDs)
43
Q

For induction of remission (for immune-mediated disease) cats are said to be more _____

A

Cats considered to be more ‘steroid resistant’. Therefore cats need a high dose e.g. 4-5mg/kg prednisalone

44
Q

Are gastroprotectants required when we use glucocorticoids?

A

e.g. sucralfate, H2 antagonists, omeprazole.

NO EFFECT!!!! UNNECESSARY

45
Q

Examples of adverse effects for glucocorticoid therapy

A

Polydipsia and Polyuria, polyphagia i.e. weight gain (DO NOT FEED AD LIB).

46
Q

Cause of hyperthyroidism

A

Exclusively feline disease.

Adenomatous hyperplasia with autonomous growth capacity

47
Q

Clinical signs of hyperthyroidism

A 
Average age is 10.2 years
Weight loss
Polydipsia 
Hyperactivity 
Cardiac changes - tachycardia/ systolic changes
thyroid nodule in 70% of cases
48
Q

What causes the tachycardia and cardiac changes observed in hyperthyroidism?

A

Hyperthyroidism results in increased catecholamine sensitivity.

49
Q

How does hyperthyroidism cause hypertension?

A

IT DOESN’T.

Correcting hyperthyroidism might result in development of hypertension (can lead to blindness…)

50
Q

Common clinical pathology of patients with hyperthyroidism

A

Elevated ALT (88% cases), elevated ALP, Elevated bile acids, stress leukogram.

51
Q

Why is basal TOTAL T4 not a reliable indicator of hyperthyroidism

A

Decreased in any disease e.g. if heart failure as a result of hyperthyroidism causes decreased basal TOTAL t4

52
Q

What test should be used to diagnose hyperthyroidism

A

T3 suppression test. measure basal t4. Give T3.

Total T4 should drop to

53
Q

In general if an over production of hormones is suspected we run a ___ test

A

Suppression test.

If under production of hormones suspected e.g. addisons we run a stimulation test

54
Q

How does hyperthyroidism affect renal function?

A

Hyperthyroidism increases GFR. Once corrected results in an increase in creatinine

55
Q

What is the survival time like following treatment

A

Two post-treatment groups.
Azotemic and normal.
If develop azotemia post treatment = poorer survival time

56
Q

Different types of treatment for hyperthyroidism

A

medical (carbimazole, methimazole– SIDE EFFECTS, GIT, Pruitis, Blood dyscarasias),
unilateral thyroidectomy, thyroid irradiation

57
Q

Clinical signs of hypothyroidism

A

Dog disease, not very common. Normally congenital due to immune-mediated destruction of thyroid tissue.
Lethargic and disinterested, can be over weight, dermal changes- alopecia/thickened skin, infertility, muscle pain

58
Q

Clinical pathology of hypothyroidism

A

Typically a mild non-reg anaemia. 40% have elevated creatinine kinase (muscle damage).
NON-SPECIFIC!
Measure basal t4 or response test.
Treatment: Supplmentation with thyroxine tablets

59
Q

Pathophysiology of Hypoadrenoncorticoism

A

Immune-mediated disease. Affects all parts of adrenal cortex.
Reduced glucocorticoid: Mucosal damage of GIT, impaired muscle function, disrupted nutrient homestasis.
Reduced mineralcorticoid: Hypovolemia (due to impaired Na/K in DCT

60
Q

Which age/sex group/breeds is Hypoadrenocorticoism most likely?

A

Age: Young to middle aged dogs
Sex: More common in females
Breeds: Standard poodles, Rough coated collies, Leonburgers, NSDT

61
Q

What are the two different clinical pictures

A
  • Acutely collapsed compromised patient (sudden onset- hypovolemic/ dehydrated, tachycardic)
  • Variably subtle, unwell animal ‘comes and goes’ NDR= Not doing right inc weakeness, inappetence, V&D, melena
62
Q

Clinical pathology of addisons disease

A

Mild to moderate anemia, hypoproteniemic OR normoproteinemic in hypovolemic patient.
In collapsed patient LACK of a stress leukogram. YOU WOULD EXPECT STRESS!! (no cortisol)
Inappropriately dilute urine

63
Q

What is a stress leukogram

A

Neutrophillia, Lymphopenia, easinophillia

64
Q

Diagnosis of hypoadrenocorticism.

What could interfere with this test?

A

ACTH STIMULATION TEST (Synthacin). Demonstration of subnormal levels of cortisol BEFORE and AFTER.
Make sure dog is not on any prior glucocorticoid therapy- interferes with the test

65
Q

Why is a collapsed animal with a stress leukogram unlikely to have hypoadrenocorticoism?

A

As has sufficient circulating cortisol for a stress response

66
Q

What is the treatment?

A

ACUTE: If hypovolemic= fluid therapy including quick acting hormone relacement: Hydrocotisone sodium succinate
Treatment= supplmentation with glucocorticoid that has ADEQUATE mineralcorticoid AND glucocorticoid activity e.g. NOT bethamethasone or dextamethasone LONG TERM i.e. less soluble ester e.g. acetate/ acetonide

67
Q

When managing the clinical patient what do we need to be very careful of

A

Don’t want to overdose with glucocorticoid. Try to use fludrocortisone.
If need to further supplment glucocorticoid activity use least potent e.g. cortisone acetate

68
Q

How can you measure the mineralcorticoid treatment efficacy

A

Clinical response.
Glucocorticoid evaluated by leukogram
Mineralcorticoid evaluated by Na and K levels

VetMed Year 3 -Term 1 (15 decks)

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