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SAM 4 MT 2 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

IDDM pathophysiology

A

insulin secretion ⬇️

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2
Q

NIDDM pathophysiology

A

insulin secretion ↔️ or ⬆️, but

insulin is less effective

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3
Q

Primary DM

A

(pancreatic disease)
– Autoimmune destruction of islets (dogs)
–Islets amyloidosis (cats)
–Pancreatitis, (neoplasia)

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4
Q

Secundary DM

A

– Excess of counterregulatory hormones
(GH ⬆️, glucocorticoids ⬆️)
– Obesity (reduced receptor binding of insulin)

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5
Q

What are the consequences of EC glucose excess (BG)

A
  • glucosuria -> polyuria, hypokalaemia, hyponatremia, hypophosphatemia
  • IC dehydration -> hyperglycemic coma (blood sugar over 30-40, hyperosmolar hyperglycemia)
  • glycation of proteins -> lens cataract, retinopathy, peripheral neuropathy, glomerulosclerosis
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6
Q

Blood glucose levels dog, cat

A

Dog: BG >10 mmol/l
Cat: BG >14 mmol/l

–> leads to glucosuria!

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7
Q

What are the consequences of lacking IC glucose?

A

Need another way to get energy for the cells! DM is a catabolic state!! + immunosuppr. (Protein synth)

🔺 Lipolysis (Fe!)
➡️ weight loss
➡️ hyperlipemia > fatty liver
➡️ ketonemia > ketonuria, acidosis, ketoacidotic coma
🔺GNG
➡️ protein synthesis decr > weakness, poor wound healing, susceptibility to infections incr

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8
Q

Signalment/history of DM

A 
~ Common disease
~ Middle-aged and old dogs
~ Intact females are predisposed
~ Poodle, Dachshund, Terriers, Beagle, Puli, Labrador, Retrievers,
(English cocker spaniel, Rottweiler)
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9
Q

Clinical manifestations in uncomplicated DM

A

(The first signs hasn´t caused secundary issues yet)
~ Signs may appear 1-2 months after estrus (lutheal phase - high P4 - mamm. Growth - high GH - insulin resistance)
~ History with (possible) pancreatitis +/-
~ PD/PU, weight loss, (initial polyphagia)
~ Dehydration, hepatomegaly, dull hair coat, flaking skin, cystitis,
glycos- / ketonuria and hyperglycemia
~ Chronic cases: cataracts / retinopathy, (uveitis if lens capsule ruptures - immune system can detect!), proteinuria +++, (paresis)

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10
Q

Clinical manifestations in complicated DM

A

Seen when not treated with insulin in time! See last card, and additionally:
🔺 Diabetic ketoacidosis
– Lethargy, weakness, anorexia, vomiting, coma, Kussmaul’s respiration,
odor of acetone in the breath (aromatic smell)
🔺 Hyperglycemic hyperosmolar syndrome (HHS; BG >33 mmol/l)
– Restlessness, ataxia, nystagmus, convulsions, low ketone!!
🔺 Pancreatitis (persistent high TG)
– Lethargy, vomiting / diarrhea, abdominal pain
🔺 Exocrine pancreatic insufficiency (persistent high TG)
– Poorly digested feces, sour smell, flatulence
🔺 Signs of Cushing’s syndrome, acromegaly

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11
Q

Laboratory and instrumental findings in DM

A

~ WBC⬆️, PCV⬆️
~ ALT ⬆️, ALKP (SIAP?) ⬆️, BUN / creatinine ⬆️,
K+ ⬆️ or ⬇️, amylase / lipase ⬆️, cholesterol ⬆️, lipemia
~ Metabolic acidosis
~ Progesterone ⬆️, cortisol ⬆️, GH ⬆️
~ (Fructosamine, glycosylated hemoglobin, IV glucose tolerance test)
~ Bacteriuria: sediment and culture
~ Abdominal US may give suspiscion: diffuse hepatomegaly, pancreatitis +/-, enlarged adrenal(s) +/-, nephropathy +/-, cystitis +/-, ovarian / uterine cysts +/-

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12
Q

Treatment in uncomplicated DM

A

🔺 The owner should be informed about prognosis, (lifelong) insulin therapy, dietary management, controls, costs
🔺 Oral antidiabetic drugs are ineffective ! Only work in Hu
🔺 Insulin therapy: 2x/day!
– Caninsulin AUV,
- 30% amorphous, 70% crystalline zinc insulin suspension
– 0.5 (BW >25 kg) – 1 (BW <15 kg) IU/kg/12h SC
🔺 Ovariectomy
– Reduces (risk of) insulin resistance. Always for intact female, to decr P4 source. Lutheal phase risk of severe insulin resistance!!!
Luthel phase huge decr of efficacy of treatment
➡️insulin demand ⬇️(if DM manifested within three weeks, complete recovery is possible)
(Must neuter in time, insulin deficient insulin dependant problem may develope)

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13
Q

Diet in DM

A

🔺 Amount and composition should be constant
🔺 Rich in protein, high fibre content, complex carbohydrates (fiber slows down starch digestion)
–Hill’s r/d, w/d, i/d, R.C. Weight Control Diabetic, Eukanuba Glucose Control etc.
–Home prepared: 70% meat, 25 % rice, potatoes or pasta, 5% vegetables, cereals
🔺 10-50 g/kg/24h divided into 4 equal portions
🔺 One portion few minutes before each insulin dose(to decide if give full dose or not dep on if dog eats), one portion 3-4 hours later

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14
Q

What is best to measure blood glucose, glucosuria, ketonuria

A
  • Human dipstick for glucosuria is sensitive and reliable (not ketones!! Cannot detect betahydroxybuturate, the most common one)
  • human glucometer to measure blood glucose.

(Continous interstitial glucose monitoring on neck - detection of insulin therapy problems, no stress, puncture..)

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15
Q

Fructosamine

A

Only increase in permanent hyperglycemia.

Its concentration represents the glucose average concentration in the 2-3 weeks period before sampling. Not influenced by short term hyperglycemia!

(Glycated haemoglobin - 2-3m average)

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16
Q

Important client instructions

A

🔺 Method of insulin administration must be taught in detail and tried by the owner (saline)
🔺 Reduction of insulin dose by half in case of anorexia or vomiting (OD - hypoglycemia)
🔺 Information about hypoglycemia/OD signs
– Signs: excitement, tremor, weakness, falling,
convulsions, coma (must be able to recog. NS symptoms!)
– Treatment: honey with syringe/spoon, extra meal, following insulin dose is skipped, consultation
– If there is no improvement in 15 minutes, emergency treatment is required
🔺 Diet
🔺 Daily water intake (maximum 60-70 ml/kg) - diary (glycemic control - PD disappear or not)

17
Q

Control examinations

A

~ On the first two weeks: weekly
~ After control is stable: every 3-6 months
➡️ bwt, PD/PU, hypoglycemic events?
~ Blood glucose 6 hours after morning insulin should be 4-9 mmol/l
~ Adjust insulin dose +/- 5-10%

18
Q

Hypoglycemia as a problem with insulin therapy

A

– Anorexia, vomiting, unusual physical activity,
➡️(relative) insulin overdose
– Client instructions, reduction of insulin,
IV glucose administration

19
Q

Somogyi effect as a problem with insulin therapy

A

🔺 Somogyi effect (posthypoglycemic hyperglycemia)
–BG <3 mmol/l➡️
adrenaline, glucagon, (cortisol, GH)⬆️➡️ BG⬆️⬆️
– PD/PU, hyperglycemia
- insulin lowers your blood sugar too much, it can trigger a release of hormones that send your blood sugar levels into a rebound high –> insuline resistancy that may last for 3 days. Symtoms of reccurent diabetes seen - PD/PU, blood sample - resistance vs post resistance phase of body (adrenalin, gluc) -> serial blood test needed. For the correct insulin dose
– Serial BG measurements, reduction of insulin dose

20
Q

What do you have to rule out before diagnosing problems with insulin therapy and controls

A

Insulin activity and administration problems should be ruled out

21
Q

Stress induced hyperglycemia as a problem with insulin therapy controls

A

– No complaints at home, but hyperglycemia in the examination room
– Measurement of BG at home

22
Q

Short action of insulin as a problem with insulin therapy

A

– PD/PU and hyperglycemia a few hours before insulin

– Longer acting insulin / dietary modification (should last 12h)

23
Q

Insulin resistance as a problem with insulin therapy

A

– Insulin dose >1.5 IU/kg is ineffective

– Cortisol or progesterone / GH excess should be investegated and treated (as it may cause the resistance)

24
Q

Treatment of ketoacidosis

A

🔺 Volume repletion:
– Ringer’s solution + 1 mmol KCl / 100 ml
– 20 ml/kg in the first hour, thereafter rate may be reduced by half every hour, until 2.5 ml/kg/h
🔺 Regular insulin: Actrapid HMge
– 0.25 IU/kg IM, thereafter 0.1 IU/kg repeated every hour, until BG stabilizes between 8-13 mmol/l
➡️ 0.3-0.5 IU/kg Caninsulin SC
🔺 K+ replacement: mmol KCl = (4.5 - K+) x 0.6 x BWkg ¨
🔺 Bicarbonate therapy if pH <7.1

25
Q

Dm prognosis

A

~ Uncomplicated cases have good prognosis, but
- Regular control examinations are needed
- Much depends on owner compliance
~ Complicated cases have poor prognosis

26
Q

Dm in cat - signalment

A

~ Relatively rare
~ More common in male cats
(overfed indoor cats - possibly secundary dm)

27
Q

Dm cat - clinical manifestations

A

~ Sudden onset of PD/PU
~ (Weight loss, PP)
~ Cataracts are rare
~ Neuropathy: plantigrade posture of hind legs - walk on the hocks/tarsus!

28
Q

Dm cat - Laboratory and instrumental findings

A

~ Hepatic lipidosis is more severe: TBr ñ

~ Hypokalemia is common

29
Q

Dm cat - diagnosis

A

~ Hyperthyroidism ddx:
PP and weight loss dominates, goiter. PU/PD more prominant in dm.
~ Stress hyperglycemia is frequently found in healthy cats - Challenge of diagn is perm vs stress of blood sampling. Physiol high incr of glucose during stress.
–> utine glucose at home (or: blood fructosamine)

30
Q

Dm cat treatment

A

🔺 Less problems with insulin treatment than in dogs (Caninsulin, glargin insulin – Lantus)
🔺 Diet is difficult to change in cat. Better to eat something with the insulin than nothing!
🔺 Glipizide (Minidiab 5 mg tabl.) (if owner dont want inj.)
–5 mg/cat 2-3 times a day PO
–Stimulates insulin secretion and effectiveness –Reduction in BG levels may need 1-2 months
–Many cats will require insulin therapy because of unsatisfactory control

31
Q

Cat dm prognosis

A

~ Usually good
~ Some cats will recover after a few weeks / months of insulin therapy
~ Treatment of Cushing’s syndrome or acromegaly can cure insulin resistant DM

SAM 4 MT 2 (12 decks)

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