Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y4 SA - urinary & endocrine disease > Canine diabetes mellitus > Flashcards

Canine diabetes mellitus Flashcards

1
Q

Effects on insulin on carbs

A

*Most cells - receptor mediated glucose uptake via GLUT
*Liver
– enhances uptake, phosphorylation, glycolysis
– enhances glycogen storage
– inhibits glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Effects on insulin on fat

A

*Excess glucose ->pyruvate->AcoA and FFA
*Insulin:
– Activates lipoprotein lipase
– Inhibits hormone sensitive lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Effects on insulin on protein

A

*Increased protein anabolism / synthesis
*Inhibits gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Insulin action

A
  • inhibits ketogenesis
  • stimulates glucose uptake
  • stimulates K+ uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diabetes mellitus Type 1 classification

A
  • beta–cell destruction, usually leading to absolute insulin deficiency
  • Immune-mediated (including LADA)
  • Idiopathic

i.e. insulin-deficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diabetes mellitus Type 2 classification

A
  • may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with or without insulin resistance

i.e. insulin resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Other specific types/causes of diabetes mellitus

A
  • Diseases of the exocrine pancreas
  • Endocrinopathies
    – Cushing’s syndrome, Acromegaly,
    – Phaeochromocytoma, Glucagonoma, Hyperthyroidism,
  • Genetic defects, Drug– or chemical–induced, Infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Source of the problem for type 1 DM

A

Insulin production, due to:
* Pancreatectomy
* Pancreatitis
* Auto-immunity
* Islet cell hypoplasia
* Chemical toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Source of the problem for type 2 DM

A

Affected insulin target, due to:
* Progesterone/agen
* Growth hormone
* Glucocorticoids
* Glucagon
* Catecholamines
* Thyroid
* Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aetiology of canine diabetes mellitus - type 1/insulin-deficient

A
  • Immune-mediated (probably common)
    – Antibodies in circulation against islet Ag (e.g. insulin, GAD-65, insulinoma antigen-2)
    – DLA subtypes predisposed (MHC) (Samoyed, Tibetan Terrier)
  • beta loss due to EPI / pancreatitis (probably common)
  • Congenital beta loss (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Aetiology of canine diabetes mellitus - type 2/insulin-resistant

A
  • Progesterone (e.g. metoestrus) - an acromegaly (common)
  • Hyperadrenocorticism, exogenous corticosteroids
  • IGF-1/GH excess (pituitary acromegaly extremely rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are almost all diabetic dogs? What are some exceptions to this?

A

Almost all diabetic dogs are insulin dependent (aka type 1)

Exceptions include:
* Bitches presenting in metoestrus with high levels of progesterone (inducing mammary origin growth hormone excess)
* Dogs with concurrent Cushing’s disease
* May or may not be insulin-dependent
* If not treated irreversible beta-cell damage is likely to occur and the dog will become IDDM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical presentation/signalment

A
  • DM is generally a disease seen in older dogs
    – Peak age of incidence is 7 – 9 y/o
    – Female > male cases by approx 2:1
  • Juvenille-onset DM has been reported but is rare
    – Usually develops < 1 year of age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Breed predispositions

A
  • Australian terrier
  • Standard schnauzer
  • Miniature schnauzer
  • Bichon frise
  • Spitz
  • Fox terrier
  • Miniature poodle
  • Samoyed
  • Cairn terrier
  • Keeshond
  • Maltese
  • Toy poodle
  • Lhasa apso
  • Yorkshire terrier
  • Collie (under)
  • GSD (under)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical presentation

A
  • Polyphagia but losing weight
  • Polydipsia and polyuria
  • Quickly tired/poor exercise tolerance/sleepy
  • Diabetic cataracts
  • Recurrent infection (e.g.UTI)
  • “Acetone” breath
  • Most owners therefore present due to nocturia/urinary incontinence
  • Occasionally present due to “sudden onset blindness”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathophysiology

A
  • Polyuria, polydipsia
    – Osmotic diuresis
  • Polyphagia
    – Insulin in CNS – hypothalamic satiety centre
  • Weight loss/exercise intolerance/lethargy
    – NEB
    – Reduced glucose and AA uptake
  • Recurrent infection (esp. UTI, conjunctivitis)
    – Immunological compromise
    – Local conditions favour microbial growth
  • Ketotic breath
    – Ketogenesis
  • Cataracts
    – Osmotic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Occasionally what are the first signs of illness?

A
  • acute when the dog develops diabetic ketoacidosis (DKA)
  • Dull, depressed, weak, possibly comatose
  • Often vomiting
  • Dehydrated
  • IV fluids and critical care
18
Q

Does ketonuria/ketotic breath = diabetic ketoacidosis?

A
  • not always
  • if eating and drinking: still straightforward management
19
Q

Investigation

A

Urinalysis standard part of PU/PD work-up
* Glucosuria
* Glucosuria without hyperglycaemia is not DM

Other lab findings:
* increased ALKP/ALT
* increased cholesterol, triglycerides
* Fasting hyperglycaemia
* +/- hyponatraemia
* +/- ketonuria, ketonaemia
* Fructosamine
* Urine culture

20
Q

Diagnosis

A
  • Hyperglycaemia
    – fasting hyperglycaemia
    – >12mmol/l usually
    – >5.5 – 12mmol/l more challenging
  • Glucosuria
    – Renal threshold ~ 10-12mmol/L
  • +/- Ketonuria
  • Fructosamine
    – > 400µmol/l is highly suggestive of diabetes mellitus
    – Differentiates long term high glucose from short term high glucose (e.g. stress hyperglycaemia
    – Caution (false negatives) if PU/PD history very recent
21
Q

Fructosamine

A
  • The non-enzymatic binding of glucose to albumin
  • Levels of fructosamine are dependent on the half-life of albumin and give an indication of glycaemic control over the preceding 2-3 weeks
  • ? Accuracy
  • Useful but be careful when interpreting results

When used to monitor blood glucose/diabetes management:
* Aiming for approx 400 - 450 nmol/l – excellent
* “normal” fructosamine suggests significant periods of hypoglycaemia

22
Q

Tx for the collapsed, v+, not eating diabetic

A
  • Fluid therapy
  • soluble insulin
  • +/- ICU
  • see ketoacidosis set
23
Q

Tx for the PUPD, ± ketonuria, eating and drinking diabetic

A
  • Routine management
  • intermediate insulin
24
Q

Aims of treatment

A
  • Prevent life threatening ketoacidosis
  • Abolish clinical signs
  • Restore lost condition/weight
  • Reduceriskofcomplications
25
Q

Tx considerations

A
  • Insulin
    – Type and frequency of administration
  • Diet
    – Must be carefully assessed
  • Body condition
  • Lifestyle
    – Availability for 12hourly injections
    – Availability for monitoring (e.g., hypoglycaemia)
    – Ongoing costs
  • When to spay intact female
26
Q

2 licensed insulin products for dogs

A

Caninsulin, MSD
* Intermediate acting preparation
* Lente (mixed insulin zinc suspension)
* Usually given twice daily but sometimes once
* Initial dose 0.5 iu/kg BID

ProZinc, Boehringer
* Protamine Zinc Insulin
* BID Cats, SID dogs

  • Most patients require between 0.8 – 1.2 iu/kg/dose to stabilise
  • 40IU/ml – must use companion syringes with vial product
27
Q

Insulin handling/storage

A
  • Insulin should be kept between 2-8oC
    – Fridge door often best (unless internal freezer)
  • The insulin should not be shaken, just gently rolled prior to drawing up dose
  • Insulin beyond its expiry date may be ineffectual
  • Manufacturers recommend discard bottle after 28 days in use
28
Q

Diet

A
  • essential to stick to good quality, consistent diet
  • usually feed 2x daily with BID dosing
  • feed 2x daily with SID dosing
  • dry/tinned commercial foods
  • Calculate the patients energy requirements and ensure being fed correct amount
    – [(30 x BW) + 70] x illness factor = MER (kcal)
  • food should be high in complex carbs to minimise post-prandial glucose peaks
  • food should be high in fibre
  • avoid semi-moist foods
  • if possible, O should be encouraged to feed 1 of the ‘glucomodulation’ diets
    – chappie also seem effective
29
Q

Body condition management

A
  • If the dog is thin, then the daily calorie intake must be increased accordingly
  • If the dog is overweight, then careful and monitored weight reduction will be helpful
30
Q

Life style management

A

Diabetic patients need consistent regular exercise at a similar time each day
* Owners must understand and be willing to comply
* Owners can learn to adapt food volume for particularly active days

31
Q

How to start tx

A
  • Start the insulin treatment, giving 0.5 IU/kg sc BID
  • Make sure the diet is correct and consistent
  • Ask the owner to monitor water intake
  • See the dog back in 7 days and perform a 12-hour BGC if possible
  • If control sub-optimal, increase dose by 10% and repeat cycle until stable
    – 5% change not noticeable,
    – 20% change very large and risk Somogyi
  • If repeated BGC’s not an option, use home diary and possibly fructosamine
32
Q

Blood glucose curves - what does it do in terms of monitoring?

A
  • Tells you what effect the insulin is actually having
33
Q

Can BGC be done at home?

A
  • yes if stressed
34
Q

Aims of BGC

A
  • Is insulin working at this dose?
  • What is nadir?
  • When is nadir?
  • What is duration of action for the insulin?
  • Somogyi happening?
35
Q

Disadvantage of BGC

A
  • Inconsistent curves despite consistent management (25-33% opposite management suggested in duplicate curves)
36
Q

What is somogyi?

A
  • rebounding high blood sugar that is a response to low blood sugar
37
Q

what is nadir?

A

= the lowest point on a blood glucose curve
- often considered the same as the peak of insulin activity

38
Q

Glycated haemoglobin (GHb) - what is it? what is its use?

A
  • Glucose non-enzymatically bound to haemoglobin
  • Gives an indication of the glycaemic control over preceding 2-3 months
  • Used in human medicine, value in veterinary species not clear
  • GHb stabilised diabetic 4-6%
  • GHb poorly stabilised diabetic >7%
39
Q

Urine testing for monitoring diabetes management

A
  • Insulin dosage should NEVER be adjusted on the basis of once daily urine glucose measurement
  • Somogyi possible consequence
  • Useful for documenting remission only
  • Owners can monitor but should not adjust dose on the basis of results
40
Q

Complications of diabetes management/tx

A
  • Hypoglycaemia
  • need to warm O
  • clinically uncommon
  • fatal rarely
  • hunger, food seeking, altered judgement, ataxia, weakness, collapse, convulsions
  • dextrose absorbed across gums (O can do in emergency/collapse)
  • IV glucose at clonic or glucagon injection if not debilitated

Y4 SA - urinary & endocrine disease (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions