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Module 17 > Collapsed Diabetic & Hypoglycemia > Flashcards

Collapsed Diabetic & Hypoglycemia Flashcards

1
Q

/what could be the reasons why a diabetic patient has collapsed (4)

A
  1. diabetic ketoacidosis
  2. hypoglycemia
  3. septicemia
  4. neuropathy
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2
Q

what is the pathophysiology of diabetic ketoacidosis

A

Ketone bodies (ex. acetoacetate acid, B-hydroxybutyric acid, acetone) are derived from oxidation of non-esterified or free fatty acids (FFA) by the liver and are used as an energy source by many tissues during periods of glucose deficiency

Excessive production of ketone bodies as occurs in uncontrolled diabetes results in their accumulation in the circulation and development of the ketosis and acidosis of ketoacidosis

All dogs and cats with DKA have a relative or absolute deficiency of insulin

Insulin deficiency and insulin resistance, together with increased circulating concentrations of diabetogenic hormones —> stimulate ketogenesis

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3
Q

what are the clinical signs of DKA (8)

A

Dehydration

Tachycardia

Vomiting

Hemorrhagic diarrhea

Poor peripheral perfusion

Acidotic respiration

Collapse

Death

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4
Q

what occurs for ketone production to be enhanced

A

Enhanced mobilization of FFAs from triglycerides stored in adipose tissue

Shift in hepatic metabolism from fat synthesis to fat oxidation and ketogenesis

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5
Q

what does insulin deficiency allow in fat metabolism

A

Insulin deficiency allows lipolysis to increase and increasing the availability of FFAs to the liver

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6
Q

what occurs as ketones accumulate in the blood

A

As ketones accumulate in the blood —> the buffering system becomes overwhelmed and metabolic acidosis develops

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7
Q

what occurs as ketone bodies accumulate in the ECF

A

As ketones accumulate in the extracellular space and surpasses the renal tubular threshold for complete resorption and they spill into the urine —> osmotic diuresis caused by glycosuria and enhancing secretion of excretion of souls (ex sodium, potassium, calcium, magnesium)

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8
Q

what does insulin deficiency contribute to

A

Insulin deficiency per se also contributes to excessive renal losses of water and electrolytes —> leading to volume loss, undwrperfusion of tissues and the development of prerenal azotemia

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9
Q

what are the consequences of DKA

A

Severe acidosis

Hyperosmolality

Obligatory osmotic diuresis

Dehydration

Electrolyte derangements

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10
Q

what are the complications of DKA

A

Urinary tract infection

Pancreatitis

Gastrointestinal hemorrhage

Bacteremia/septicemia

Acute renal failure

Disseminated intravascular coagulation

Pulmonary thromboembolism

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11
Q

what can lead a diabetic patient to ketoacidosis

A

anorexia and stress

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12
Q

how do you confirm ketosis

A

urinalysis: glucosuria, ketonuria

UTI? renal casts?

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13
Q

what would be seen on biochemistry ketosis (5)

A
  1. hyperglycemia
  2. hypokalemia
  3. hypophosphatemia
  4. azotemia
  5. hepatopathy
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14
Q

what leads to hypokalemia in DKA (4)

A
  1. anorexia
  2. osmotic diuresis (glucose, ketones)
  3. ketone salts in urine
  4. insulin treatment
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15
Q

what can mask the severity of hypokalemia in DKA

A

NB: acidosis and dehydration can mask severity

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16
Q

how do you treat DKA with fluids

A

Initiation of fluid therapy should be first step in treatment of DKA and it should precede the initiation of insulin by 2 hours or longer to minimize the development of complications affiliated with insulin administration

Replacement of fluid deficiencies and maintenance of normal fluid balance are important to ensure cardiacs output, blood pressure, and blood flow to all tissues

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17
Q

what % of fluids should be given in the first hour

A

20% of requirements in first hour

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18
Q

what would the rate of 0.9% saline solution that would be suitable to treat DKA

A

60-100ml/kg/24 hours

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19
Q

what would the initial dose of soluble IM injections insulin be

A

Initial dose = 0.2 IU/kg

Subsequent doses = 0.1 IU/kg every 2-4 hours

Monitor glucose hourly

20
Q

what would the initial dose of soluble IV injections insulin be

A

0.03 units/kg/hour

Run 50ml of solution through tubing before starting

Monitor glucose hourly

21
Q

what dose of potassium would you administer to treat the hypokalemia

A

10 mmol KCl per 500 ml fluids

Do not exceed 0.5 mmol/kg/hr

If K+ concentration can be measured:

<3.0 10 mmol KCl/500ml

<2.5 15 mmol KCl/500ml

<2.0 20 mmol KCl/500ml

22
Q

what are the signs of hypophosphatemia (4)

A
  1. hemolysis
  2. severe weakness
  3. rhabdomyolysis
  4. stupor, seizures
23
Q

how would you treat hypophosphatemia

A

potassium phosphate 0.03 mmol/kg/hr

food: high protein diet

24
Q

what should you monitor in the treatment of DKA (7)

A
  1. TPR
  2. urine
  3. mm
  4. CRT
  5. PCV/TP
  6. K+
  7. PO4
25
Q

what causes unstable DM (5)

A
  1. insulin: admin, dose, type
  2. general health: infections, obesity
  3. HAC
  4. pancreatitis
  5. acromegaly
26
Q

what are the signs of acromegaly

A
  1. Increased soft tissue mass:

Inspiratory stridor — panting, exercise intolerance

Large extremities (head, limbs, gingiva)

Thickened skin

Hepatomegaly

Broad face

  1. Diabetes mellitus
  2. Neurological signs
27
Q

what is the etiology of acromegaly

A

Chronic excessive secretion of growth hormone causes overgrowth of connective tissue, bone and viscera caused by a functional adenoma of the somatotropin cells of the pituitary pars distils that secretes excess GH

Increased GH can cause catabolic and anabolic effects

Anabolic effects are caused by increased IGF-1

Causes resistance to exogenously administered insulin

28
Q

how do you diagnose acromegaly

A

Identification of conformation alterations (increased body size, large head, prognathic inferior, organomegaly)

Stable increase in body weight in a cat with insulin-resistant diabetes mellitus

Measurement of serum IGF-1 concentrations provides further evidence of acromegaly

Increased serum IGF-1

29
Q

what are the common complications of hypoglycemia

A
  1. acute or chronic insulin overdose

make sure owners know this

30
Q

how long does it take hypoglycemia to develop

A

rapid onset 6-8 hours after insulin

urine glucose negative

31
Q

what are the signs of hypoglycemia

A

Seizures

Weakness

Collapse

Ataxia

Lethargy

Blindness

Bizarre behaviour

Coma

Hunger

Hyperesthesia, trembling

Ataxia

Fitting

Collapse

32
Q

what is the hallmark sign of hypoglycemia

A

Dogs and cats usually recover from hypoglycemic seizures within a couple of minutes as a result of activation of counter-regulatory mechanisms (ex secretion of glucagon and catecholamines) that block the effects of insulin, stimulate hepatic glucose secretion

Promote an increase in the blood glucose concentration

33
Q

how would you treat a seizuring diabetic

A

Stop insulin

Feed ASAP

Sugar solution/hypostop

Not if seizuring

Subsequent dose reduction

34
Q

what are sources of infection of DM

A

urinary tract

resp

GI

skin

others

35
Q

why are diabetics more susceptible to infections (2)

A
  1. impaired neutrophil function (adhesion, chemotaxis, phagocytosis)
  2. decreased prostaglandin production (thromboxane B2, prostaglandin E)
36
Q

how would you treat infections in diabetics

A

fluid

antimicrobials

anti-pyretics

37
Q

what are other reasons for low blood glucose

A
  1. lab problems (old and wrong sample)
  2. normal variations: young dogs, toy breeds, hunting breeds
38
Q

what are metabolic diseases that can cause low blood glucose

A

Addisons disease

Insulinoma

Other tumours — large/hepatic

Severe liver failure

Xylitol poisoning

Glycogen storage disease

39
Q

what are inflammatory diseases that can cause low blood glucose

A

blood poisoning

parvovirus

40
Q

what are the signalment of insulinomas

A

Rare

Older dogs

Sexes equally affected

No confirmed breed association

Larger dogs may be predisposed

41
Q

what is the pathology of insulinomas

A

Functional tumours arising from B cells of the pancreatic islets —> malignant tumours that secrete instil independent of the typically suppressive effects of hypoglycemia

Respond to hyperglycemia by secreting insulin in excessive amounts

42
Q

what are the clinical signs of insulinomas (9)

A

History of dog that was suggestive of epilepsy but hasn’t responded to phenobarbital

  1. general weakness
  2. episodic collapse
  3. incoordinatino
  4. depressed
  5. apparent blindness
  6. muscle tremors
  7. seizures
  8. weight gain
  9. neuropathies
43
Q

what can insulinomas look like (5)

A
  1. epilepsy
  2. brain tumours
  3. congestive heart failure
  4. osteoarthritis
  5. hypoadrenocorticism
44
Q

how are insulinomas diagnosed

A

In emergency: Remember “Whipple’s triad”

Clinical signs, low glucose and response to glucose

Decreased glucose half life

Once stabilized:

Low blood glucose:

Usually <3 mmol/L

High serum insulin:

Usually >20 mU/L

Increased insulin/glucose ratio:

>4.2 U/mol

45
Q

how do you treat insulinomas

A

1. Medical:

Frequent feeding

Prednisolone (anti insulin)

Diazoxide

Others:

Diltiazem

Octerotide

Alloxan, streptozocin, other chemotherapeutics

2. Surgical:

Stabilize medically

Administer glucose before, during and after surgery

Complications

Pancreatitis

Diabetes (permanent or temporary)

Starve for 24 hours after surgery

46
Q

what is the prognosis of insulinomas

A

Median recurrence of signs = 12 months

Median life span = 18 months

With surgery = 2 years

Then steroids = 3 years

Module 17 (31 decks)

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