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Endocrine > Endocrine pancreatic disorders > Flashcards

Endocrine pancreatic disorders Flashcards

1
Q

Describe DM in pancreatitis

A
  • may develop omparied insulin secretion
  • generally reversible
  • resolves as inflammation subsides
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2
Q

Define Diabetes mellitus (DM)

A

a manifestation of various pathophysiological proceses

- clinically significan glucose intolerance d/t absolute or relative lack of insulin (can fluctuate)

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3
Q

T/F: any condition –> chronic insuline resistance (IR) results in hyperinsulinism that may lead to ‘iselt exhaustion in susceptible individuals

A

True - may be variably reversible depending on the length of time the islets have been exposed to this increased secretory demand and the presence of inherent individual susceptibility to the damaging effects of chronic insulin “hypersecretion”.

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4
Q

CS - DM

A 
-•	Mostly various combinations of PD/PU, polyphagia and weight loss (especially dogs).
•	Varying degree of muscle wasting
•	hepatomegaly 
•	cataracts (almost exclusively dogs)
- signs of ketoacidosis (sometimes)
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5
Q

CS - ketoacidosis

A

dehydration, depression, inappetance, vomiting and diarrhoea. They will also have a ketotic breath (not all humans can detect this)

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6
Q

Dx - DM

A
  • Moderately elevated ALP (most)
  • mildly elevated ALT (most)
  • both of above as a result of the secondary hepatic lipidosis that occurs as a result of reduced insulin activity.
  • Other biochemical abnormalities: hypercholesterolaemia, hypertriglyceridaemia, and depending on renal perfusion, azotaemia.
  • Confirmed in dogs with fasting hyperglycaemia of greater than around 14mmol/L. In the cat elevations in blood glucose of this magnitude or higher can be a result of stress due to any illness and further corroborating evidence should be obtained.
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7
Q

Should you treat all dogs/cats with glucosuria?

A

No - hyperglycaemia should be confirmed (to confirm DM) before tx is considered.

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8
Q

What should you do if you doubt the significance of hyperglycaemia?

A

 determine the glycosylated haemoglobin or plasma fructosamine level. Both estimate the proportion of haemoglobin and albumin respectively that has glucose bound to it in a non-enzymatic irreversible way. As the process is both non-enzymatic and irreversible the proportion of the relatively constant protein that is “glycated” is an estimate of the “average” blood glucose concentration over a preceding period (variable depending on whether dog or cat)

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9
Q

What does canine fructoasmine concentration determine?

A

blood glucose levels over last 2-4 weeks

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10
Q

What does feline [fructosamine] reflect?

A

more variable than dogs - blood glucose over previous 5-10 days.

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11
Q

Why is plasma fructosamine useful?

A

to differentiate short-term and persistent hyperglycaemia

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12
Q

What are the most effect methods of evaluating effective management of diabetic patients?

A

 Glycosylated haemoglobin and fructosamine estimations

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13
Q

Tx - uncomplicated DM

A
  • correct underlying cause of DM
  • some obese diabetics may initially require insulin injections until weight normalises
  • dogs: insulin
  • cats: insulin or oral hypoglycaemics
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14
Q

Why are oral hypoglycaemic agents attractive tx for cats?

A

unlikely to produce clinically significant hypoglycaemia (vs insulin injections)

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15
Q

Efficacy - oral hypoglycaemic agents

A

10-20% cats respond

  • traditionally most effective in animals with some insulin secreting capacity
  • may be effective where no significant insulin levels at presentation
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16
Q

Consequences - oral hypoglycaemic agents

A

possible accelerated islet cell exhaustion (thus a controversial tx)

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17
Q

Action method - oral hypoglycaemic agents

A

increasing the rate and amount of insulin released and/or increasing peripheral insulin sensitivity.

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18
Q

Examples - oral hypoglycaemic agents

A

Glipizide or glibenclamide usually

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19
Q

When will you know if oral hypoglycaemic agents are effective?

A

If effective, will have significantly lowered fasting hyperglycaemia within 5-7 days. Evaluate regularly (min q2-3 days) since often ineffective.

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20
Q

What are the 4 main differences b/w insulins?

A
  • insulin source
  • solubility
  • physical structure,
  • degree of purification
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21
Q

What are the possible insulin sources?

A
  • bovine, porcine or human (from recombinant DNA)
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22
Q

How are insulins made insoluble?

A
  • either through complexing with zinc or protamine-zinc (lente, isophane or protamine zinc insulin) OR:
  • modification of the amino acid sequence to cause a marked reduction in solubility when the modified insulin molecule is exposed to a neutral pH environment (glargine or determir insulin).
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23
Q

Other names - soluble insulin

A
  • USA: ‘crystalline insulin’

- UK: ‘neutral insulin’

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24
Q

Describe insulin complexed with zinc

A

can form conglomerates (various shapes, amorphous material with high surface area:volume ratio to large crystals with a low surface area:volume ratio). By altering these components the duration of action can be modified by altering absorption rates.

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25
Q

How can the lente group of insulins be differentiated?

A

By physical structure which specifically affects rate of absorption:
• semilente (all amorphous) - short acting
• lente (30% amorphous, 70% crystalline) intermediate acting
• ultralente (all crystalline) long acting

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26
Q

Why do synthetic insulin analogues (glargine) have delayed absorption?

A

their solubility is markedly pH dependent. Glargine is soluble in acidic solutions but binds to tissue sites when it is injected into the pH-neutral environment of the subcutaneous tissues

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27
Q

Does insulin tend to last longer in dogs or cats?

A

Dogs

28
Q

Benefit - highly purified insulin (monocomponent)?

A

reduce the incidence of insulin antibody formation. Nowadays insulin contains no significant peptide contaminants so the purity of the insulin preparation has become a relatively unimportant issue.

29
Q

T/F: chronic insulin injections are likely to produce ciruclating insulin antibodies in the patient

A

True - These antibodies can substantially interfere with the measurement of circulating insulin levels but do not result in any significant reduction in insulin activity.

30
Q

What insulins are currently UK licensed?

A
  • lente insulin of porcine origin, 40 IU/ml (Caninsulin®), lente insulin of porcine/bovine (Insuvet lente®) or protamine zinc insulin of porcine/bovine origin (Insuvet PZI®).
  • Additionally the synthetic insulin analogues, insulin glargine and insulin determir, have been recommended for use as a twice daily exogenous insulin in cats.
31
Q

Which insulin is 1st choice in cats?

A
  • protamine zinc insulin (PZI) as a first-choice for cats as it lasts a little longer than lente
32
Q

Peak effect - lente insulins (caninsulin)

A

peak effect 1-4 hours after administration, last for approximately 12-14 hours.

33
Q

Peak effect - protamine zinc insulin and insulin glargine

A

last for around 12-14 hours but have a less pronounced period of peak effect

34
Q

What injection sites for insulin should be avoided?

A
  • Areas that are subject to variations in movement and stretching
  • thigh and arm
  • IDEAL = abdominal walls (left/right)
35
Q

T/F: • Any dog with an absolute or relative insulin deficiency will have some degree of insulin resistance and this needs to be overcome before a true indication of the animal’s insulin requirements can be determined.

A

True400

36
Q

What should the ideal dose give?

A
  • good clinical picture

- blood [glucose] of 6-10mmol/L at lowest point OR fructosamine of 350-400mol/L

37
Q

Guidelines - insulin in cats

A
  • ensure cat truly requires insulin
  • low glycaemic indx food (low carbodhydrate, relatively high protein
  • home glucose monitoring (avoid severe anxiety induced hyperglycaemia)
38
Q

What disorder should you check every suspect diabetic cat for?

A

hypersomatotrophism/ acromegaly (causes insulin resistance)

39
Q

What is ‘sudden stablilisation’?

A
  • As the endogenous insulin resistance starts to diminish diabetics often seem to suddenly stabilise
  • Also once the islets have been “unloaded” there may be a return of insulin secreting capacity which can result in the animal no longer requiring insulin for some time
40
Q

What is important about food and short duration insulins?

A

all offered food is consumed within short space of time.

41
Q

How much to feed an animal on insulin

A

50-70 kcals/kg. • If underweight, increase intake. If overweight, decrease caloric intake.

42
Q

What supplementation may aid diabetic control?

A
  • high fibre vegetables or soluble fibre
  • as may decrease rate of postprandial glucose elevation and also the daily insulin requirement
  • not much evidence though
43
Q

Effect of exercise on insulin

A
  • lowers insulin requirements (consistent, encouraged)

- overexercise tends not to be a be a problem as patients tend to be older and overweight to start with

44
Q

What happens when glucose deficiency occurs d/t decreased insulin-mediated uptake?

A

the liver will start oxidation of non‐esterified fatty acids (NEFAs) as an alternative source of energy. Oxidation of free fatty acids (FFA)  aceto‐acetate, beta‐hydroxybutyrate and acetone (the ketone bodies).

45
Q

Conditions for increased ketogenesis

A

mobilisation of FFA from triglycerides in adipose tissues (more in obese animals!), fat synthesis in the liver and fat oxidation

46
Q

Dx - DKA

A
  • already DM
  • concurrent ketonuria/ ketonaemia
  • DK vs DKA depends on blood pH
47
Q

Causes - DKA episode

A
  • DM CS ignored so not diagnosed
  • bout of pancreatitis
  • insulin stored inappropriately
  • steroids
  • concurrent dz
48
Q

Tx - DK

A
  • not as aggressive as DKA
  • adapt normal SC insulin injection
  • reslove underlying issues
49
Q

Tx - DKA

A
  • aggressive approach
  • long term hospitalisation
  • IVFT
  • hourly IM soluble insulin injecitons or IV insulin
50
Q

How do fluids help in DKA?

A
  • very dehydrated
  • promotes ketone excretion
  • often corrects acidosis
  • can lower blood glucose
  • use 0.9% saline initially, 60-100ml/kg/24 hours
51
Q

What supplementation to IVFT is essential in DKA?

A
  • POTASSIUM: especially once insulin given as this further lowers K
  • PHOSPHATE (since HA might ensue if levels fall too much)
52
Q

What does succes of an insulin protocol depend on?

A
  1. appropriate monitoring;
  2. only inducing gradual changes;
  3. reducing the amount administered or completely delaying start of insulin when dealing with a hypokalaemic patient.
53
Q

Advantages - IV insulin protocol

A
  1. more reliable control over serum insulin levels;
  2. more predictable bioavailability;
  3. less labour-intense and
  4. corrections can be made quickly if BG drops too quickly.
54
Q

Aim - DKA management

A

use insulin primarily to reverse the ketogenesis (not lower the BG). Once ketogenesis reverse, patient feels better, starts eating and then switch to SC regular insulin.

55
Q

Outline bicarbonate tx in DKA management

A
  • least necessary part of tx
  • avoid where possible
  • can cause deterioration if not indicated
56
Q

Adverse effects - bicarbonate tx in DKA

A

worsening of hypokalaemia, paradoxical cerebral acidosis and delaying the decrease in blood lactate and ketone body levels.

57
Q

Parameters to monitor when initiating DKA tx

A

 BG, hydration, respiration, pulse, electrolytes, CO2/acid/base, urine output, body weight (fluid overload), PCV (haemolysis), temperature (sepsis, shock, infection) and systolic blood pressure.

58
Q

Outline insulin-secretin islet neoplasia (insulinoma)

A
  • uncommon (dogs, cats)

- recognised as result of metabolic consequences of unregulated insulin production

59
Q

Outline insulinomas

A
  • mostly functional
  • 80% tumours solitary
  • mostly found in a limb of the pancreas
  • invariably malignant (45-65%)
  • usually have metastasised (liver) by time of dx
  • increased levels of somatotrophs documented
60
Q

How does glucose control insulin secretion?

A

by modifying intracellular energy levels resulting in exocytosis of insulin-containing secretory granules. Normally insulin secretion will be substantially inhibited when the blood glucose concentration falls to below ~4mmol/L. Insulin secretion not diminished from an insulinoma though

61
Q

Counterregulatory mechanisms to insulin in a period of hypoglycaemia

A
  • glucagon
  • growth hormone,
  • cortisol
  • catecholamines.
62
Q

Signalment - insulinoma

A
  • middle aged
  • larger breed dogs
  • no gender bias
63
Q

CS - hypoglycaemia

A

 CS dominated by hypoglycemia effects on the CNS and specifically the cerebral cortex or by the clinical consequences of elevated levels of catecholamines.
o Cerebral cortical dysfunction: diminished mentation, weakness, behavioural changes, disorientation, ataxia, visual disturbances and ultimately coma and death.
o Clinical signs related to excess catecholamine release: hunger and anxiety.

64
Q

Dx - insulinoma

A

 Hematologic, biochemical and urinalysis findings generally variable and non-specific.
 +/- hypoglycaemia
- Dx based on inappropriately high insulin at time of hypoglycaemia
- abdominal ultrasound: may reveal a focal structural pancreatic abnormality but

65
Q

Tx - insulinoma

A
  • sx (1st line, permanent)

- medical tx

66
Q

Outline medical tx of insulinoma

A
  • prednisolone (inducing insulin resistance)
  • diazoxide (inhibiting insulin secretion)
  • streptozotocin/ streptozocin (chemotherapeuticum with beta-cell toxicity)
  • pasireotide (somatostatin analogue)
  • diet (low carbohydrate and mostly complex, high protein)

Endocrine (11 decks)

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