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

f) 21-Oct-13 Flashcards

(68 cards)

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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
Pathophysiology differences between canine and feline diabetes
Dog: Severe loss of islets. Non-reversible Cat: Insulin resistance --> Islet hyperactivity --> Islet underactivity
26
What else can cause insulin resistance? | Which other diseases can cause diabetes?
Obesity, oestrous, pregnancy, anxiety, hypercortisolaemia (stress). Hyperadrenocorticoism, acromegaly
27
If an dog presents with suspected diabeties what must be checked before undertaking further tests?
intact? Diestrous diabetes? SPAY
28
What are a common complication of diabetes in dogs?
``` Hepatomegaly. Bilateral cataracts (85% of cases within 400Days) ```
29
What can help differentiate hyperglycemia from 'stress' hypoerglycemia?
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
What is important to remember when starting off insulin therapy?
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
What diet should be provided for a cat with diagnosed diabetes
Cat is a carnivore give LOW carbohydrate
32
Difference between corticosteroid and a glucocorticoid
Corticosteroid: Any steroid drug or molecule Glucocorticoid: Antiinflammatory enhanced potency BIND TO INTRACELLULAR RECEPTORS. Alter gene expression.
33
Glucocorticoids can alter their own metabolism. What is this known as and what is its clinical significance?
Tachyphalaxis. If given long course e.g. over 7D dose needs to be altered. Lower doses for longer periods of time = NO GOOD
34
Explain the mechanism of action
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
Why are glucocorticoids better at treating inflammation than NSAIDs?
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
What is the relative potency of mineralcorticoid to glucocorticoid ratio for the following glucocorticoids a) Dextamethasone b) Prednisalone c) Betamethasone
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
Example of a short acting and long acting glucocorticoid
short acting: Hydrocortisone | long acting: Dextamethasone/ Betamethasone
38
Duration of the action of glucocorticoid is dependent on which three factors?
- Half life of drug - ESTER'S SOLUBILITY - Dose of drug i. e. predinsalone 1-2mg/kg >24hrs
39
Example of two very soluble esters
Succinate and Phosphate e.g. hydrocortisone sodium succinate
40
Example of a moderately insoluble drug (released for days-weeks)
Acetate e.g. dextamathasone acetate. | Duration depends on SOLUBILITY
41
Fluticasone proprionate is used for
Asthmatic inflammation
42
Two steps when using glucocorticoids for treating immune-mediated disease
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
For induction of remission (for immune-mediated disease) cats are said to be more _____
Cats considered to be more 'steroid resistant'. Therefore cats need a high dose e.g. 4-5mg/kg prednisalone
44
Are gastroprotectants required when we use glucocorticoids?
e.g. sucralfate, H2 antagonists, omeprazole. | NO EFFECT!!!! UNNECESSARY
45
Examples of adverse effects for glucocorticoid therapy
Polydipsia and Polyuria, polyphagia i.e. weight gain (DO NOT FEED AD LIB).
46
Cause of hyperthyroidism
Exclusively feline disease. | Adenomatous hyperplasia with autonomous growth capacity
47
Clinical signs of hyperthyroidism
``` Average age is 10.2 years Weight loss Polydipsia Hyperactivity Cardiac changes - tachycardia/ systolic changes thyroid nodule in 70% of cases ```
48
What causes the tachycardia and cardiac changes observed in hyperthyroidism?
Hyperthyroidism results in increased catecholamine sensitivity.
49
How does hyperthyroidism cause hypertension?
IT DOESN'T. | Correcting hyperthyroidism might result in development of hypertension (can lead to blindness...)
50
Common clinical pathology of patients with hyperthyroidism
Elevated ALT (88% cases), elevated ALP, Elevated bile acids, stress leukogram.
51
Why is basal TOTAL T4 not a reliable indicator of hyperthyroidism
Decreased in any disease e.g. if heart failure as a result of hyperthyroidism causes decreased basal TOTAL t4
52
What test should be used to diagnose hyperthyroidism
T3 suppression test. measure basal t4. Give T3. | Total T4 should drop to
53
In general if an over production of hormones is suspected we run a ___ test
Suppression test. | If under production of hormones suspected e.g. addisons we run a stimulation test
54
How does hyperthyroidism affect renal function?
Hyperthyroidism increases GFR. Once corrected results in an increase in creatinine
55
What is the survival time like following treatment
Two post-treatment groups. Azotemic and normal. If develop azotemia post treatment = poorer survival time
56
Different types of treatment for hyperthyroidism
medical (carbimazole, methimazole-- SIDE EFFECTS, GIT, Pruitis, Blood dyscarasias), unilateral thyroidectomy, thyroid irradiation
57
Clinical signs of hypothyroidism
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
Clinical pathology of hypothyroidism
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
Pathophysiology of Hypoadrenoncorticoism
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
Which age/sex group/breeds is Hypoadrenocorticoism most likely?
Age: Young to middle aged dogs Sex: More common in females Breeds: Standard poodles, Rough coated collies, Leonburgers, NSDT
61
What are the two different clinical pictures
- 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
Clinical pathology of addisons disease
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
What is a stress leukogram
Neutrophillia, Lymphopenia, easinophillia
64
Diagnosis of hypoadrenocorticism. | What could interfere with this test?
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
Why is a collapsed animal with a stress leukogram unlikely to have hypoadrenocorticoism?
As has sufficient circulating cortisol for a stress response
66
What is the treatment?
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
When managing the clinical patient what do we need to be very careful of
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
How can you measure the mineralcorticoid treatment efficacy
Clinical response. Glucocorticoid evaluated by leukogram Mineralcorticoid evaluated by Na and K levels

VetMed Year 3 -Term 1 (15 decks)

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