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Endocrinology - 2nd year > DM and DKA > Flashcards

DM and DKA Flashcards

1
Q

Factors affecting absorption of insulin?

A
  1. pH (stable at 7.4)
  2. Crystal size
  3. Zinc binding
  4. Protein (protamine) binding
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2
Q

What is type I diabetes? What species is it seen most commonly in?

A

Insulin-dependent (juvenile)
It is when the islet cells of the pancreas do not produce sufficient insulin.
Occurs most commonly in dogs.

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3
Q

What is type II diabetes? What species is it seen most commonly in?

A

Non-insulin dependent (adult)
Enough insulin is made by pancreas, but it is being antagonized by something else.
Occurs most commonly in cats.

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4
Q

Ways to get secondary diabetes?

A 
Pancreatic disease
Hormonal
Drug-induced (steroids)
Insulin receptor abnormalities
specific genetic syndroms
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5
Q

Cushing’s relationship with diabetes? Variation with species?

A

An animal with cushings can become diabetic; this is more commonly seen in cats than dogs.

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6
Q

What is an example of an animal getting drug-induced secondary diabetes?

A

A cat being treated with long-term steroids for asthma.

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7
Q

What should you do soon after diagnosis of diabetes mellitus in the case of an intact female dog?

A

OHE (Spay) to avoid insulin resistance from diestrus.

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8
Q

How does diestrus lead to insulin resistance?

A

During diestrus, there is an increased level of progesterone.
This stimulates GH release which increases peripheral insulin resistance.

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9
Q

Clinical signs of a “not very sick” DM case?

A

PD/PU and weight loss

can sometimes see polyphagia and hepatomegaly also

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10
Q

Clinical signs of a “sick” DM case?

A 
Dehydration
vomiting 
depression
anorexia
tachypnea
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11
Q

Progression of DM

A

Hypoinsulinemia –> hyperglycemia –> increased water intake to compensate –> PD/PU
As hyperglycemia kidney threshold is reached and glucose starts to spill into the urine, it drags water (and electrolytes) out with it also –> increases PD/PU
Since cannot use the glucose present in the blood, will eventually switch to ketogenic metabolism –> can progress to DKA

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12
Q

DKA pathogenesis

A

Stored fats in body acted on by peripheral tissue lipase –> FAs and glycerol released into the blood –> liver –> ketogenic pathway –> ketoacids made –> try to balance with bicarb –> metabolic acidosis

DKA is also associated with acetone being made in the lungs as a byproduct of acetoacetate metabolism. Acetone can cause + ketones.

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13
Q

Diagnosis of DM

A

PD/PU
Glycosuria
Persisting hyperglycemia** > 150mg

Can have elevated liver enzymes (ALP/ALT/AST) due to hepatic lipidosis

**Cats can have transient hyperglycemia due to stress so must have consistently high value. (Not the case for dogs; high is high for them)

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14
Q

Transient DM?

A

DM can occur secondary to high progesterone in the case of a hydrometra or pyometra. In this case, the DM may resolve after surgical resection of the infected uterus.

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15
Q

Never diagnose DM solely on the presence of ______; always check ______ also.

A

Glucosuria

Blood glucose

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16
Q

Intermediate-acting insulins

A

NPH and Lente-Vetsulin

should be given SQ BID

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17
Q

Rapid acting insulin

A

Regular-type

Can be given IV, IM, or SQ

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18
Q

Most human intermediate and long acting insulins have __a__ peak and __b__ duration of action in dogs and cats. Therefore ALWAYS GIVE ___c__.

A

a. earlier
b. shorter
c. MAINTENANCE DOSES SQ DIVIDED BID - begin at 0.5 U/kg divided BID.

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19
Q

What insulin to give to dogs?

A

Intermediate or long acting

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20
Q

What insulin to give to cats?

A

Only ultra long acting!

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21
Q

Ultra-long-acting insulins

A

PZI
glargine
Should be given SQ BID

  • this insulin type does not peak in humans but DOES peak in CATS
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22
Q

Standard Starting Dose for Not-So-Sick Patient!

A

NPH - dogs
PZI, Glargine - cats
0.5 U/kg SQ/BID

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23
Q

Topics covered when talking to owner of animal dx’d with DM

A
  1. What is DM?
  2. Rationale for treatment
  3. Insulin syringe (specifically calibrated)
  4. Injection technique
  5. Urine testing/monitoring (dipstick - check for glucose and ketones)
  6. Diet (low carb, high protein)
  7. Recognizing hypoglycemia
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24
Q

Insulin overdose - what happens?

A

Hypoglycemia!!

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25
Q

Brain insurance drugs against insulin overdose?

A 
Karo syrup (PO)
Glucagon (IM)
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26
Q

Recommended treatment schedule for regulated, nonketotoacidotic diabetic

A

8 am: collect urine sample and determine amount glycosuria
8:15 am: give adjusted NPH/PZI dose
8:30 am: feed half daily food requirement.
6 pm: feed other half daily food requirement and administer other insulin dose.

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27
Q

Somogyi reaction

A

Posthypoglycemic hyperglycemia

Pattern:
Animal is dosed with insulin and becomes hypoglycemic in the early morning or late afternoon. By next morning, they are hyperglycemic with excess glycosuria.

Usually happens when animal is only receiving one dose insulin/day. If this happens, reduce the dose by 25-50% and split in half for BID. Can also consider switching to longer acting insulin.

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28
Q

In what situation can you use oral hypoglycemic drugs?

A

Only for type 2 DM in cats!

Not perfect, variable efficacy, may eventually need injectable insulin over time.

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29
Q

Causes of insulin resistance in the dog?

A 
estrus and diestrus
progestagen treatment 
acromegaly
hypercortisolism 
bacterial infection
30
Q

Cause of insulin resistance in the cat?

A

Obesity

31
Q

When does DKA occur?

A

When an animal has DM and cannot compensate; makes XS ketones.

32
Q

Hepatic Lipidosis (Fatty liver) phatogenesis?

A

Low insulin –> switch to peripheral breakdown of lipids by lipase –> FA and Glycerol –> FAs accumulate in the liver

Can cause elevation in liver enzymes

33
Q

DKA - significant test values?

A 
1. Metabolic acidosis 
(low TCO2) 
2. High anion gap 
3. High serum ketones
4. Ketones on UA
5. High blood glucose
6. Glucose on UA
7. High osmolality (Sosm)
34
Q

If blood glucose is incredibly high and only have +1/+2 glycosuria, this is a sign of _____.

A

Poor renal perfusion

35
Q

What is common with hyperosmolar diabetics?

A

Acute renal injury, usually ketones negative

36
Q

Bi-hormonal disorder concept?

A

Hyperinsulinemia effects are compounded with the effects of concurrent hyperglucagonemia. They work together to promote hyperglycemia and ketogenesis

37
Q

Muscle wasting with DM pathogenesis

A

Proteins from muscle breakdown as alternative energy source –> liver –> gluconeogenesis and muscle wasting

38
Q

Sepsis and shock _____ FA metabolism

A

increase; due to hypoxia and increases in NADH2

39
Q

Nitroprusside test tests for what ketones?

A

Acetoacetate - strongest
Acetone - weak

Use this test when can’t get urine sample

*betahydroxybutyrate is the most common ketone but cannot be tested for!

40
Q

DKA treament principles

A
  1. Rehydrate
  2. Correct severe acidosis - use bicarb when pH <7.1
  3. Use regular insulin (rapid-acting insulin easier to titrate to patient’s response v. long-acting insulin)
  4. Correct electrolye imbalances (Focus on K and Na, sometimes Mg and P)
  5. Feed when they are able to hold food down
41
Q

DKA DON’Ts

A
  1. Don’t overtreat
  2. Don’t over bleed
  3. Don’t make hypokalemic
42
Q

Use ____ fluids to correct dehydration with DM

A

Isotonic! (LRS, Normosol)

Helps with dehydration and hypovolemia. NaCl can be too acidic. Check urine output.

43
Q

Regular insulin is not absorbed well SQ is animal is ____.

A

Dehydrated/In shock

44
Q

If patient is mildly sick (still eating and drinking, not vomiting), how do you administer regular insulin?

A

SQ

45
Q

If patient is moderately sick (not eating, some dehydration, vomiting), how do you administer regular insulin?

A

SQ, IM, CRI

46
Q

If patient is markedly sick (recumbent, hypovolemic), how do you administer regular insulin?

A

CRI, maybe IM

requires close blood test monitoring

47
Q

When regular insulin is given SQ, the ____ levels decline before the _____.

A

Glucose; ketones

48
Q

What happens when you decline glucose too rapidly?

A

Cerebral osmotic dysequilibrium!

Initially high glucose –> brain makes osmolytes to maintain water gradient (avoid losing water) –> drop glucose too fast –> brain is now hyperosmolar –> water goes into brain –> acute cerebral edema/ sudden death

49
Q

The rate of blood glucose decline should not exceed ______.

A

75-100mg/dl/hr

50
Q

What to do if blood glucose is dropping too fast?

A

Add dextrose to IV

51
Q

_____ supplementation is essential with DKA treatment!

A

K+

52
Q

Causes of hypokalemia during DKA treatment

A
  1. dilution
  2. renal tubular losses
  3. GI losses with vomiting
  4. insulin-induced cellular influx of K+ (EXC –> INC)
53
Q

If animal presents acutely for DKA, but also severly hypokalemic, what should you do?

A

Give fluids containing K+ first.
Delay giving insulin until hypoK has been resolved because will only worsen it.
Just by giving fluids, can dilute blood and induce diuresis which will help lower blood glucose.

54
Q

Hypophosphotemia treatment?

A

KPhos

55
Q

What happens if you increase P too fast/too much?

A

Lowered Ca!

Because Ca and P will bind and precipitate into the tissues.

56
Q

Diabetic nonketotic hyperosmolar syndrome (NKHDS)

A

Renal dysfunction!!
Should not have blood glucose >800 if also has glycosuria.
USG is also really low
Negative for ketones

57
Q

NKHDS pathogenesis

A

insulinized liver –> deters ketone production

peripheral insulin depletion –> decreased glucose utilization and increased gluconeogenesis

58
Q

NKHDS features

A
  1. extreme dehydration
  2. brain dysfunction
  3. marked hyperglycemia
  4. absent KA
  5. decreased renal function
59
Q

Diabetic cataract species preferences?

A

More common in dogs than cats!

60
Q

Diabetic cataract pathogenesis?

A

Sugars accumulate in the lens —> sucks water into the eye —> laminar separation of the lens and cataract formation

61
Q

Diabetic neuropathy species preferences?

A

In dogs and cats

Associated with diabetic dysregulation

62
Q

Diabetic neuropathy pathogenesis?

A

Sugars accumulate in vascular walls –> vascular dysfunction –> adverse myelin dysfunction –> neuro effects

63
Q

What is plantar posturing indicative of?

A

Diabetic neuropathy;

diabetic dysregulation

64
Q

Diabetic vasculopathy

A

thickened capillary epithelium compromises circulation.

irreversible once reach diabetic kidney disease

65
Q

Why are diabetics predisposed to infection?

A

Neutrophils cannot kill bacteria in a dysregulated diabetic

66
Q

DKA clinicopathologic abnormalities

A 
azotemia
low bicarb
elevated liver enzymes
hypoK
hypoNa
hypoP
anemia
67
Q

Hormones affecting DKA

A 
Low insulin
High glucagon
Epinephrine
GH
Cortisol

***All contribute to ketogenesis and hyperglycemia

68
Q

Treat hypoK with ___.

A

KCl (unless concurrently HypoP, then give KPhos)

69
Q

Acute diabetes complications

A 
Hypoglycemia
HypoK
cerebral edema
paradoxical CSF acidosis (with bicarb rx) 
Sepsis and acute pancreatitis (chronic complications)
transient insulin response 
somogyi reaction 
EPI 
high insulin dose-requiring cat
highly insulin-sensitive cat
diestrus
diabetic dog with cushing's
acromegaly
infections
faulty insulin absorption (SQ)
70
Q

Diabetic phenomena

A 
Persistent ketonuria despite clinical improvement
Exercise associated hypoglycemia
insulin absorption variability 
early morning hyperglycemia
somogyi reaction 
fever after hypoglycemia
altered CNS function with KA and hyperosmolar diabetic 
cerebral edema 
hyperosmolar hyperglycemia without KA
progressive hyperglycemia
glucose toxicity 
life-threatening hypoK
metabolic alkalosis with DKA (because XS vomiting)

Endocrinology - 2nd year (8 decks)

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