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SA Medicine Endocrine > Diabetes mellitus > Flashcards

Diabetes mellitus Flashcards

1
Q

Which cells in the pancreas produce Insulin?

A
  • Beta cells
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2
Q

Which cells in the pancreas produce glucagon?

A
  • Alpha cells
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3
Q

Which cells in the pancreas produce somatostatin?

A
  • Delta cells
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4
Q

Which cells in the pancreas produce Pancreatic polypeptide?

A
  • F cells
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5
Q

Is insulin anabolic or catabolic?

A
  • anabolic
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6
Q

What does insulin help facilitate the tissue uptake of?

A
  • Glucose
  • Amino acids
  • fatty acids
  • K+, Phos, Mg+
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7
Q

Does insulin raise or lower blood glucose?

A
  • Lower
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8
Q

Does insulin inhibit or stimulate gluconeogenesis?

A
  • Inhibits* it
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9
Q

What does insulin inhibit?

A
  • Gluconeogenesis, glycogenolysis, protein catabolism, lipolysis, ketogenesis
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10
Q

Definition of diabetes mellitus

A
  • Insufficient production of insulin by beta cells of the pancreas
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11
Q

Which species get diabetes?

A
  • Dogs and cats
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12
Q

Diabetes in dogs

A
  • Absolute insulin deficiency (seen in almost all dogs)

- Insulin-dependent (IDDM)

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13
Q

Is diabetes in dogs reversible?

A

No

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14
Q

Pathogenesis of diabetes in dogs

A
  1. Genetic predisposition + autoimmune, environmental factors/predisposing conditions
  2. Beta cell degeneration and destruction
  3. Insulin dependent diabetes mellitus
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15
Q

DM in cats

A
  • Relative insulin deficiency
  • Non-insulin dependent (NIDDM) in 80%
  • Dysfunctional Beta cells (impaired insulin secretion)
  • Peripheral insulin resistance
  • Cats usually need insulin but may go into remission
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16
Q

Is DM reversible in cats?

A
  • Yes
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17
Q

Elements of DM in cats

A
  • Genetic predisposition
  • Predisposing factors
  • Amyloid deposition (Beta cell degeneration)
  • Hyperglycemia
  • Glucose toxicity
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18
Q

Predisposing factors that lead to insulin resistance in cats

A
  • Obesity (pro-inflammatory)
  • Pancreatitis (inflammation in the pancreas)
  • Glucocorticoids (BIG cause)
  • Progesterone (diestrus, megestrol acetate)
  • Infection
  • Concurrent disease
  • Stress?
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19
Q

Pathophysiology of DM in cats

A
  1. Insulin deficiency (absolute or relative)
  2. Decreased cellular glucose uptake and increased hepatic gluconeogenesis
  3. Hyperglycemia
  4. Glucosuria (renal threshold: BG >180-220 mg/dL)
  5. Polyuria (osmotic)
  6. Polydipsia
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20
Q

Sex predisposition of DM in dogs

A
  • Females are twice as common as males
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21
Q

Age predisposition of DM in dogs

A
  • Middle-aged

- 4-14 years old

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22
Q

Breed predisposition of DM in dogs

A
  • Terriers, Schnauzers, Miniature poodles, others
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23
Q

Sex predisposition of DM in cats

A
  • neutered males more common
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24
Q

Age predisposition of DM in cats

A
  • Older, >6 years
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25
Q

Breed predisposition of DM in cats

A
  • Burmese (Australia)
  • Abyssinians
  • Siamese (DKA)
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26
Q

What are the most common presentations with DM?

A
  1. “Well” Diabetic
  2. Ketoacidotic
  3. Hyperglycemic/hyperosmolar syndrome
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27
Q

What is the most common presentation of DM?

A
  1. “Well” Diabetic*****
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28
Q

Ketoacidotic presentation

A
  • Untreated or treated diabetic
  • Concurrent disease –> insulin resistant
  • Think about other conditions too
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29
Q

Classic signs of “Well diabetic”

A
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss
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30
Q

Ketoacidotic presentation

A
  • Anorexia
  • Depression
  • Dehydration
  • Vomiting
  • Look TERRIBLE
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31
Q

What are the relatively common concurrent endocrinopathies with DM in dogs?

A
  • Hyperadrenocorticism
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32
Q

What are the relatively common concurrent endocrinopathies with DM in cats?

A
  • Hyperthyroidism, acromegaly (cats)
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33
Q

PE findings on DM

A
  • Hepatomegaly
  • Dehydration
  • Cataracts (DOGS ONLY)
  • Poor coat/grooming
  • Peripheral neuropathy (cats)
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34
Q

How do you diagnose DM?

A
  • Clinical signs
  • Hyperglycemia
  • Glucosuria
  • Based on a CBC/Chem/Urinalysis
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35
Q

DfDx for DM

A
  • Stress (mostly in cats)
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36
Q

Other possibilities for initial CBC/Chem/UA in DM?

A

+/- Ketonuria (not abnormal; don’t be alarmed if they are well)

+/- fructosamine (will only show for animals that have been diabetic for awhile)

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37
Q

Stress Hyperglycemia

A
  • BG normal 80-120
  • Usually <250 mg/dL with SH but can go over 400 mg/dL
  • Normal fructosamine
  • Cause unclear
  • No clinical signs of DM
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38
Q

How do you differentiate stress hyperglycemia from DM in cats?

A
  • Recheck the BG when the cat is calm, and/or check a fructosamine level, to help rule out SH.
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39
Q

What diagnostics should be performed on all diabetics?

A
  • CBC
  • Serum biochemistry
  • Urinalysis
  • Urine culture
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40
Q

CBC results in Diabetics

A
  • Usually normal
  • Can be hemoconcentrated (often dehydrated)
  • Infection: neutrophilia, toxic change, left shift
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41
Q

Serum chemistry changes in Diabetics

A
  • Hyperglycemia
  • Hypercholesterolemia
  • Increased ALT and increased ALP (ONLY MEANS fat in the liver; be MUCH more concerned with cats than in dogs)
  • +/- amylase/lipase increase (dogs)
  • +/- azotemia (usually pre-renal)
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42
Q

Urinalysis changes in diabetics

A
  • Glucosuria!
  • +/- ketonuria
  • +/- proteinuria (bacterial infections)
  • +/- bacteriuria (not as good at putting WBCs out there)
  • +/- pyuria (MAY not because they are PU/PD)
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43
Q

Urine culture in diabetics

A
  • MANDATORY
  • They have a neutrophil dysfunction
  • Also sugar in their urine and decreased concentration
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44
Q

Radiographs and ultrasounds in diabetics

A
  • Sometimes optional
  • Abdominal and thoracic radiographs
  • Abdominal ultrasound
  • Look for the underlying/complicating disease
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45
Q

Radiographs and ultrasounds in DKA or HHS

A
  • Necessary to identify the underlying cause
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46
Q

Other tests to consider

A
  • exocrine pancreas
  • Thyroid testing
  • Hyperadrenocorticism
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47
Q

Exocrine pancreas testing in diabetics

A
  • PLI - pancreatitis
  • TLI - pancreatic insufficiency
  • Chronic pancreatitis can lead to TLI and diabetes mellitus
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48
Q

Thyroid testing in diabetics for dogs

A
  • Controversial

- Wait until regulated before testing

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49
Q

Thyroid testing in diabetics for cats

A
  • Assess at diagnosis of DM if you suspect
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50
Q

Hyperadrenocorticism testing in diabetics

A
  • DO NOT test until DM is regulated
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51
Q

Is ALP commonly elevated in canine diabetics/feline diabetics/both?

A
  • Just canine diabetics

- Very unusual in cats

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52
Q

Goals of diabetes treatment

A
  • Minimizing clinical signs
  • Minimizing the risk of hypoglycemia
  • Reducing the risk of long term complications of DM
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53
Q

What is the #1 risk of diabetes treatment?

A
  • Hypoglycemia!

- Much more dangerous than hyperglycemia

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54
Q

Signs of hypoglycemia

A
  • Muscle tremors
  • Weakness
  • Lethargy
  • Head tilt
  • Dull or dazed
  • Disorientation
  • Ataxia
  • Seizures
  • Coma
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55
Q

What are some major therapeutic considerations?

A
  • Consistency is key
  • Address predisposing conditions and maintain an ideal body condition
  • Exercise - consistent and regular
  • Diet
  • Oral hypoglycemics
  • Insulin
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56
Q

Diet and exercise with DM

A
  • Maintain ideal body condition
  • Obesity can contribute to insulin resistance
  • Consistent and regular (but not strenuous) exercise to improve glucose utilization
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57
Q

Dietary management for Diabetes in dogs

A
  • Increase fiber
  • Decrease simple sugars
  • Decrease fat
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58
Q

Point of increasing fiber for diabetes in dogs

A
  • Decreases glucose absorption

- Delays gastric emptying and intestinal absorption

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59
Q

Point of decreasing fat for diabetes in dogs

A
  • Diabetics already have derangements in fat metabolism
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60
Q

Commercial diabetes diets for dogs

A
  • W/D, OM, R/D, DCO
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61
Q

Dietary management in cats with diabetes

A
  • Increase protein
  • Decrease carbohydrates
  • Look at individual response
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62
Q

How do you decrease carbohydrates in cat diets for diabetes?

A
  • Either by increasing protein (ideal method) or increasing fiber
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63
Q

How long do you continue diabetic cat diets?

A
  • Continue even after they have gone into remission
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64
Q

Commercial cat diabetes diets

A
  • W/D
  • m/d
  • DM
  • Not great over the counter options
  • People can home cook, but harder to get them nutritionally balanced
65
Q

Fiber for thin animals with DM

A
  • Less
66
Q

DM obese animals additional dietary recommendations

A
  • Weight loss
67
Q

Raw diets in DM

A
  • Bad idea

- Immunosuppressed

68
Q

Timing of insulin relative to meals

A
  • Feed before insulin
  • Dogs»>cats
  • Schedule! Consistency!
69
Q

Oral hypoglycemics

A
  • Acarbose

- Glipizide

70
Q

Acarbose

A
  • alpha-glucosidase inhibitor
  • Slows post-prandial glucose absorption
  • Dogs
  • Side effects in 35% are diarrhea, weight loss
71
Q

Glipizide

A
  • Sulfonylurea
  • Stimulates beta cell secretion so must have functioning beta cells
  • Only for NIDDM Type 2 cats
  • Multiple side effects
72
Q

Who would get oral hypoglycemics?

A
  • Not DKAs

- Anti-insulin owners

73
Q

Response for oral hypoglycemics

A
  • 15% good response, but some become resistant

- 15% partial response

74
Q

Predisposing conditions and diabetes treatment

A
  • VERY IMPORTANT to identify and treat an predisposing conditions
75
Q

Insulin therapy origin species

A
  • Human
  • Bovine
  • Porcine
76
Q

Formulations of insulin the delay absorption

A
  • Protein binding

- Crystal size

77
Q

Starting insulin therapy for dogs

A
  1. Vetsulin (#1) - FDA approved
  2. Humulin N (longer lasting)
    - Tend to do lower doses initially to avoid hypoglycemia
    - Insulin availability varies
78
Q

Starting insulin therapy for cats

A
  1. Glargine (#1)
  2. ProZinc (FDA approved)
    - Animal size makes dosing quite difficult
79
Q

Which insulins are 40 U/mL?

A
  • Prozinc and Vetsulin
80
Q

Which insulins are 100 U/mL?

A
  • Almost every other kind
81
Q

Proper handling of insulin

A
  • Refrigerate
  • ROLL insulin gently to mix, with the exception of vetsulin, which you shake
  • Rotate site of injection
82
Q

How are insulin syringes marked?

A
  • By UNIT
  • for U40, it’s 20 units/0.5cc
  • for U100, it’s 50 units/0.5cc
83
Q

Where do you read for an insulin dose?

A
  • Top of the black rubber stopper on the plunger
84
Q

What happens if you use a U100 to give the same number of units as a U40?

A
  • Underdose
85
Q

What if you use a U40 to give the same number of units as a U100?

A
  • 2.5x overdose

- This can be FATAL

86
Q

When should you administer insulin?

A
  • After a meal (ideally)
87
Q

In the days after starting insulin therapy

A
  • Check a few BGs over the next 2 days
  • Change dose only if hypoglycemic
  • DO NOT INCREASE DOSE BASED ON SPOT CHECKS
  • Takes several days to see full effect
  • BG curve 1 week later
88
Q

When should initial glucose curve be performed?

A
  • 1 week after starting insulin or any dose adjustment
89
Q

What is the gold standard for monitoring insulin therapy?

A
  • Improvement/resolution of clinical signs
  • Blood glucose curves (gold standard)
  • Glycosylated proteins (fructosamine and glycosylated hemoglobin)
  • Urine glucose strips
90
Q

Performing a BG curve Timeline after starting insulin

A
  • 7 days after starting insulin for the first time, after changing the insulin dose, or after changing insulin type
  • It takes that long for the body to adjust to the insulin and for consistent effects to be seen
  • Don’t perform when you first start insulin, as it won’t be accurate
91
Q

BG curve day at a glance

A
  • Feed at normal time in morning at home or in hospital
  • Check BG when arrives at clinic
  • If appropriate - watch owner give insulin
  • Check BG every 2 hours for a total of 12 hours (if BID insulin)
  • Check every hour if close to or below 100
92
Q

Parts of a BG curve

A
  • Nadir

- Duration

93
Q

Nadir of a BG curve

A
  • Time and value at which BG is lowest

- Corresponds with peak insulin activity

94
Q

Duration of a BG curve

A
  • Amount of time following insulin therapy in which the BG is <250 mg/dL
  • Could also define it as your target range for that individual
95
Q

Target range for a BG curve

A
  • ~100-250 mg/dL throughout the day

- A little lower for cats on glargine

96
Q

Step 1 of interpreting a BG curve

A
  • Find blood glucose nadir and insulin duration
97
Q

What should you do if the nadir is occurring at the right time (6 hours for a 12 hours dose) but the value is too high or too low?

A

Adjust the dose

98
Q

What should you do if the nadir is occurring at the wrong time (too early or too late)?

A

Change the insulin type

99
Q

What should you do if the duration is inappropriate?

A
  • Either need to change dose or type - look at your nadir for guidance
100
Q

Reminder to look at your pictures for glucose curves!

A

DO IT

101
Q

Ideal glucose curve

A
  • Duration of 11 or 12 hours

- Nadir at 6 hrs, and not too high or too low

102
Q

What amount should you adjust an insulin dose by for dogs?

A
  • 10-25%
103
Q

What amount should you adjust an insulin dose by for cats?

A
  • Usually 1/2 unit per dose

- Will get easier with experience

104
Q

Should owners ever change insulin doses of their own accord?

A
  • No
  • NEVER, EVER, EVER without instructions to do so
  • Warn them about the risk of death
105
Q

When to repeat a BG curve?

A
  • Every 7 days until regulated
  • Then in ~1 month
  • Then every 3-6 months and include a urine culture
  • OR if clinical signs are present
106
Q

What can mess up a curve?

A
  • Forgetting to give the insulin (make sure you clarify who is giving the insulin )
  • Inappetence/anorexia (not eating in hospital can be a challenge)
  • Vomiting
  • Stress hyperglycemia (cats) - monitor with home curves, clinical signs
  • Somogyi effect
107
Q

Somogyi effect

A
  1. ) Too much insulin
  2. ) Hypoglycemia (<65 mg/dL or rapid drop)
  3. ) Diabetogenic hormones take over
  4. ) Rebound hyperglycemia (>300 mg/dL)
  5. ) Misinterpretation…NEED A BIG CURVE!
108
Q

Chronic monitoring for clinical signs for Diabetes

A
  • PU/PD

- Weight loss

109
Q

BG curve chronic monitoring

A
  • If clinical signs recur
  • Every 3-6 months
  • If stress hyperglycemia
  • Home curves
110
Q

Urine cultures for DM

A
  • Every 6 months
111
Q

Serum fructosamine monitoring

A
  • Glycated proteins synthesized during insulin-independent binding of glucose to serum protein
  • Indicates BG concentration during preceding 2-3 weeks
  • Trends are most useful
  • Measure when first regulated and then every 3-6 months
112
Q

Serum fructosamine: which patients?

A
  • MOST helpful in cats, as it is not affected by stress
113
Q

Cat remission

A
  • With insulin (and/or oral hypoglycemics) and dietary management, cats may go into remission
114
Q

Who is remission more likely in?

A
  • Cats intensively treated soon after (<6 months) diagnosis
  • Cats that recently received glucocorticoids
  • Older cats
  • Cats without peripheral neuropathy
115
Q

Estimates of remission

A
  • 80% of cats with NIDDM if treated intensively

- 30-40% might be more realistic estimate

116
Q

What’s the risk if a cat suddenly goes into remission?

A
  • Hypoglycemia
117
Q

Is relapse possible with cats that have gone into remission?

A
  • Yes
  • 25-30%
  • VERY important to keep them on a low carb diet and keep the weight off
118
Q

What is the most fatal complication of DM potentially?

A
  • Hypoglycemia
  • If they don’t eat, or if they vomit, you can skip the dose or do a 1/2 dose
  • They should call or check glucose at home
119
Q

Other complicates of DM

A
  • Insulin resistance
  • Diabetic ketoacidosis
  • Diabetic neuropathy
  • Diabetic nephropathy
  • Cataracts
120
Q

Prevention of hypoglycemia

A
  • If pet doesn’t eat or vomits food, do not give or give reduced insulin
  • Owner instructions to give Karo syrup on gums
121
Q

What to do for a huge overdose of insulin?

A
  • Hospitalization
  • IV dextrose
  • +/- other treatments as needed (should be for about 12 hours)
122
Q

What does it suggest if you’re giving a ton of insulin but still have clinical signs?

A
  • Insulin resistance
123
Q

What is the dose of insulin that’s considered insulin resistance?

A
  • > 2U/kg insulin per dose
124
Q

Simple explanation for insulin resistance

A
  • Insulin storage, expiration

- Administration (site)

125
Q

Not-so-simple explanations for insulin resistance

A
  • Somogyi effect (we think they’re resistant, but they’re actually not)
  • Stealth medications (eye drops of eardrops with steroids)
  • Concurrent disease (pancreatitis or other infections)
126
Q

Conditions associated with insulin resistance

A
  • Hyperadrenocorticism
  • Exogenous steroids
  • Glucocorticoids administered by any route
  • Hypothyroidism or hyperthyroidism
  • Pancreatitis
  • Diestrus (progresterone)
  • Obesity
  • Neoplasia
  • Acromegaly (cats&raquo_space;» dogs)
  • Infections (often occult; UTI,pyoderma, pral, pneumonia, disease)
  • Renal failure
  • Cardiac disease
  • Hepatic disease
  • Insulin antibodies (last on the list)
127
Q

What should you do if you suspect actual insulin resistance?

A
  • Look for and treat underlying illness
128
Q

Who gets cataracts for diabetes?

A
  • DOGS
129
Q

Cataracts in dogs with DM

A
  • Secondary, lens-induced uveitis
  • Surgery to remove the lens will restore vision in 75-80% of patients
  • Offer treatment options early to allow for the best chance of restoring vision
  • DO NOT IGNORE THEM
  • May need to see an ophthalmologist for surgery
130
Q

Diabetic neuropathy

A
  • Rear limb weakness
  • Plantigrade stance/walking on the hocks
  • Unknown cause
131
Q

Diabetic neuropathy: who gets it?

A
  • Cats > dogs
132
Q

Cause of diabetic neuropathy

A
  • Unknown
133
Q

Treatment for diabetic neuropathy

A
  • Improved glucoregulation

- May not fully reverse

134
Q

Diabetic nephropathy

A
  • Glomerular dysfunction
  • Proteinuria
  • Progression to failure
  • Cause unknown - multifactorial
135
Q

What is diabetic ketoacidosis?

A
  • Life threatening, acute complication of untreated diabetes mellitus
  • VERY LIFE THREATENING (though most common and most rapidly fatal complication of DM is still hypoglycemia)
136
Q

What triggers DKA?

A
  1. Marked insulin deficiency
  2. Concurrent cause of insulin resistance (e.g. infection, pancreatitis, cancer, diestrus, glucocorticoids or progesterone)
137
Q

Underlying pathogenesis of DKA

A
  • Insulin is not present to facilitate glucose uptake by cells
  • Cells are starved for energy so turn to alternative energy sources (FFAs, liver manufactures ketone bodies)
  • Contributing factors: excess glucagon, cortisol, fasting, dehydration
138
Q

What leads to the acidosis in DKA?

A
  • Ketone bodies overwhelm the body’s buffering capacity
139
Q

What leads to the dehydration in DKA?

A
  • Glucose and ketones accumulate in urine leading to osmotic diuresis
140
Q

Clinical signs/Clinical Pathologic Abnormalities of DKA PRIMARY

A
  • Diabetes + Ketonuria + “illness”
  • Hyperglycemia
  • Acidosis
141
Q

DKA CBC abnormalities

A
  • Non-regenerative anemia, left shift neutrophilia, or thrombocytosis (~50% of dogs)
  • Neutrophilia and Heinz body formation (common in cats due to ketones)
142
Q

Chemistry changes DKA

A
  • Increased ALP (almost all dogs)
  • ALT elevation
  • Cholesterol elevation
  • Azotemia (Cats > dogs)
  • Hypokalemia (often not able to take up potassium and phosphorus into cells; need insulin to take up potassium and phosphorus)
  • Hypophosphatemia (see hypokalemia)
  • Hypomagnesemia

Hyponatremia (pseudo due to expanded vascular volume?)

  • Hypochloremia
143
Q

DKA treatment?

A
  • Emergency!
  • Correct fluid deficit
  • Correct insulin deficit and reverse ketone formation
  • Correct electrolyte and acid base abnormalities
  • Supportive care
  • Identify and correct underlying disorders
144
Q

What is one of the most important aspects of resolving DKA?

A
  • Identify and correct the underlying disease
145
Q

What is something you should let owners know if their pet has DKA?

A
  • Make sure the owner is aware of the financial and time commitments of managing a diabetic prior to initiating treatment
146
Q

1st priority of DKA treatment

A
  • REHYDRATE
  • Delay insulin administration for at least 1-2 hours
  • Isotonic fluids
  • Correct deficit over 24 hours
147
Q

What are the two things that fluids help do for treating DKA?

A
  • Correct acid-base abnormalities

- May have some effect on lowering glucose levels

148
Q

Goal of insulin in DKA treatment

A
  • Decrease BG slowly over 6-12 hours
149
Q

How should you give insulin with you’re doing DKA treatment?

A
  • Short-acting and short duration (regular)

- IV CRI or intermittent IM method

150
Q

What range should you maintain BG for DKA treatment?

A
  • Moderate range (~200’s) to allow for continual administration of insulin
  • Dextrose may be added to fluids to maintain BG and allow for insulin administration
151
Q

Acidosis Treatment

A
  • Fluid therapy and resolution of ketones should correct acidosis eventually
  • +/- Bicarbonate (??) can be used to more rapidly correct acidosis if needed, but it’s controversial
152
Q

Bicarbonate opponents

A
  • Fluid therapy will correct in patient with reasonable renal function
153
Q

Bicarbonate proponents

A
  • May prevent deleterious effects of acidemia

- Acidemia is very detrimental

154
Q

How often should you be monitoring BG in DKA?

A
  • Every 1-2 hours
155
Q

What else should you be monitoring with DKA?

A
  • Potassium, phosphorus, other electrolytes, blood gases
156
Q

How often should you be monitoring electrolytes, blood gases, potassium, and phosphorus?

A
  • Every 4-6 hrs initially then less frequently with improvement
  • Insulin will drive K and Phos into cells so even if normal initially, can plummet dramatically with treatment
  • Supplement as needed
157
Q

How often should you monitor urine ketones in DKA?

A
  • Every 24 hours
158
Q

Things to be monitoring in DKA summary

A
  • BG every 1-2 hrs
  • Potassium, phosphorus, other electrolytes, blood gases every 4-6 hours
  • Urine ketones every 24 hours
159
Q

Complications of DKA treatment

A
  • Generally result from over-aggressive insulin therapy or fluids and inadequate monitoring
  • Hypoglycemia
  • Cerebral edema
  • Hypokalemic complications
  • Hypophosphatemic complications

SA Medicine Endocrine (8 decks)

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