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(needs clean-up) Diabetes Mellitus: Overview and Diagnosis - Coggle Diagram
(needs clean-up) Diabetes Mellitus: Overview and Diagnosis
Definition: Hyperglycemia due to decreased insulin secretion and/or action
Relative or absolute insulin deficiency
Progressive abnormalities in carbohydrate, protein, and fat metabolism
Type 1 Etiology: Type 1
characterized by β‐cell destruction -> absolute insulin deficiency.
The damage is permanent; no remission.
In humans, autoimmune
Who gets Type 1?
Dogs
, most have permanent β‐cell destruction at the time of diagnosis.
Unlike people, only a subset of diabetic dogs have autoimmune process.
Type 2 Etiology: Type 2
characterized by peripheral insulin resistance combined with β‐cell dysfunction.
strongly associated with OBESITY,
impairs insulin signaling
causes peripheral insulin resistance.
Early treatment -> remission;
permanent β‐cell damage results if untreated
Chronic Hyperglycemia->Glucotoxicity-> β‐cell apoptosis
Islet amyloidosis
Amylin
hormone co‐secreted with insulin
helps reduce post‐prandial spikes in blood glucose
Suppresses appetite
Delays gastric emptying
primates and cats,
can aggregate into amyloid fibrils ->toxic to β‐cells.
Who gets Type 2?
Cats
peripheral insulin resistance
obesity
Each kg body weight -> 30% reduction in insulin sensitivity
potential for remission.
Other Types
On occasion, exocrine pancreatic disease can damage the endocrine pancreas (islets).
pancreatitis
neoplasia
exocrine pancreatic insufficiency.
Endocrinopathies can increase risk for diabetes and complicate management.
Endogenous or exogenous hormones can antagonize the effects of insulin.
Glucagonoma
Hypersomatotrophism.
Progesterone (e.g. Gestational)
Hyperadrenocorticism
Exogenous steroids
Pheochromocytoma
Monogenic defects in beta cells likely also exist but have not yet been discovered.
WHO and WHAT? Signalment
Breed predispositions exist, but any breed can be affected.
Dogs
Samoyeds
Terriers
Toy and Mini Poodles
Standard and Mini Schnauzers
Pugs
Keeshonds
Bichons Frise
Cats
Burmese (Australia, New Zealand, UK)
Sex
Dogs: Females 3x > males
Cats: Males 1.5x > females; neutered > intact
Both: Gestational DM in intact females
Age
Middle‐aged to older
7‐11 yo dogs
9‐13 yo cats
Juvenile uncommon
Obesity
Increases risk in cats by 3‐5x
No increased risk for dogs History
Polyuria/polydipsia
Glucosuria results in an osmotic diuresis polyuria
dehydration
polydipsia to compensate
The renal threshold for glucose estimated
180 mg/dL in dogs
280‐300 mg/dL in cats
Polyphagia
glucose entry into the satiety center is insulin‐mediated
No insulin = never feeling full.
Weight loss
decreased
glucose uptake into muscles and fat
lipid synthesis
increased lipid mobilization
may be masked by obesity.
If other signs are present, evaluate for diabetic ketoacidosis (DKA) and coexisting disease
DKA
GI signs
lethargy
altered mental state
tachypnea
Pancreatitis
GI signs
+/‐ abdominal pain
Urinary tract infection
pollakiuria
hematuria
Feline acromegaly
Corticosteroid therapy is a major risk factor in cats
Estrus in both species
Progesterone therapy
Physical Examination
largely unremarkable
+/-Hepatomegaly
hepatic glycogen and lipid accumulation.
Cataracts
Diabetic cataracts are common in DOGS
50% of DM dogs by 6 mo and 75% by 1 yr
Good glycemic regulation may reduce risk
Why not in diabetic cats?
Glucose enters the lens, metabolize to sorbitol via
aldose reductase
and then to fructose.
Sorbitol and fructose
not freely permeable
highly osmotic
cause diffusion of water into the lens
damage of lens fibers leads to cataracts
Older cats (>7 yo) have low aldose reductase activity
neuropathy in CATS
plantigrade stance.
Feline Hypersomatotrophism (HST)
Cats with DM caused by hypersomatotrophism
physical signs of excess growth hormone IGF‐1
acromegaly
Broad face
mandible protrusion
overgrowth of bone
Organomegaly
Hypertrophic Cardiomyopathy
functional pituitary adenoma -> excess growth hormone
Growth hormone causes
insulin resistance
release of insulin‐like growth factor 1 (IGF‐1).
underrecognized – affects 1 in 4 diabetic cats!!!
Diagnosis
IGF‐1 measurement
Imaging for pituitary tumor
Treatment
Insulin for DM management
dose requirements are often 10‐20x normal due to insulin resistance.
Putuitary tumor removal
radiation therapy
surgical removal
DM remission in 50‐85% of cases but response may take weeks to months.
Laboratory Findings
Hyperglycemia
Glucosuria
present on urinalysis
causes osmotic diuresis
USG is often dilute
+/‐ Pre‐renal azotemia
Hyponatremia
hypochloremia
Insulin deficiency -> Lipid mobilization
increased
cholesterol
triglycerides
ALP
+/- Ketonuria (starvation state)
+/- proteinuria (glomerular hypertrophy)
Bacteriuria
+/-pyuria
+/- hematuria
+/- lower urinary tract signs
In dogs
hyperglycemia with glucosuria is diagnostic for DM
Other causes of hyperglycemia
Epinephrine and cortisol
mild hyperglycemia
no glucosuria
Other causes of glucosuria
Proximal tubular disease (e.g. Fanconi syndrome) glucosuria
without hyperglycemia
In cats
hyperglycemia with glucosuria can be seen with DM OR stress
Stress hyperglycemia can be severe enough to raise BG > 250 -> glucosuria
If ketones are also present, DM is more likely
DM impersonators
Hyperthyroidism
PP
PU/PD
weight loss
Renal disease
PU/PD
weight loss
More testing is often needed in cats!
Fructosamine
Product of irreversible reaction between glucose and
plasma proteins (glycosylation)
Reflects mean BG of the preceding 1‐2 weeks
Important part of the diagnosis of feline DM
used to monitor response to insulin therapy
False results with low or high serum protein levels
Hyperthyroidism lowers fructosamine