Collapsed Diabetic & Hypoglycemia Flashcards by Kayla Stauffer

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

diabetic ketoacidosis
hypoglycemia
septicemia
neuropathy

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what is the pathophysiology of diabetic ketoacidosis

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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what are the clinical signs of DKA (8)

Dehydration

Tachycardia

Vomiting

Hemorrhagic diarrhea

Poor peripheral perfusion

Acidotic respiration

Collapse

Death

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what occurs for ketone production to be enhanced

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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what does insulin deficiency allow in fat metabolism

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

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what occurs as ketones accumulate in the blood

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

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what occurs as ketone bodies accumulate in the ECF

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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what does insulin deficiency contribute to

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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what are the consequences of DKA

Severe acidosis

Hyperosmolality

Obligatory osmotic diuresis

Dehydration

Electrolyte derangements

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what are the complications of DKA

Urinary tract infection

Pancreatitis

Gastrointestinal hemorrhage

Bacteremia/septicemia

Acute renal failure

Disseminated intravascular coagulation

Pulmonary thromboembolism

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what can lead a diabetic patient to ketoacidosis

anorexia and stress

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how do you confirm ketosis

urinalysis: glucosuria, ketonuria

UTI? renal casts?

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what would be seen on biochemistry ketosis (5)

hyperglycemia
hypokalemia
hypophosphatemia
azotemia
hepatopathy

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what leads to hypokalemia in DKA (4)

anorexia
osmotic diuresis (glucose, ketones)
ketone salts in urine
insulin treatment

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what can mask the severity of hypokalemia in DKA

NB: acidosis and dehydration can mask severity

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how do you treat DKA with fluids

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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what % of fluids should be given in the first hour

20% of requirements in first hour

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

60-100ml/kg/24 hours

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what would the initial dose of soluble IM injections insulin be

Initial dose = 0.2 IU/kg

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

Monitor glucose hourly

what would the initial dose of soluble IV injections insulin be

0.03 units/kg/hour

Run 50ml of solution through tubing before starting

Monitor glucose hourly

what dose of potassium would you administer to treat the hypokalemia

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

what are the signs of hypophosphatemia (4)

hemolysis
severe weakness
rhabdomyolysis
stupor, seizures

how would you treat hypophosphatemia

potassium phosphate 0.03 mmol/kg/hr

food: high protein diet

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

TPR
urine
mm
CRT
PCV/TP
K+
PO4

what causes unstable DM (5)

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

what are the signs of acromegaly

1. Increased soft tissue mass: Inspiratory stridor — panting, exercise intolerance Large extremities (head, limbs, gingiva) Thickened skin Hepatomegaly Broad face 2. Diabetes mellitus 3. Neurological signs

what is the etiology of acromegaly

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

how do you diagnose acromegaly

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

what are the common complications of hypoglycemia

1. acute or chronic insulin overdose make sure owners know this

how long does it take hypoglycemia to develop

rapid onset 6-8 hours after insulin urine glucose negative

what are the signs of hypoglycemia

Seizures Weakness Collapse Ataxia Lethargy Blindness Bizarre behaviour Coma Hunger Hyperesthesia, trembling Ataxia Fitting Collapse

what is the hallmark sign of hypoglycemia

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

how would you treat a seizuring diabetic

Stop insulin Feed ASAP Sugar solution/hypostop Not if seizuring Subsequent dose reduction

what are sources of infection of DM

urinary tract resp GI skin others

why are diabetics more susceptible to infections (2)

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

how would you treat infections in diabetics

fluid antimicrobials anti-pyretics

what are other reasons for low blood glucose

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

what are metabolic diseases that can cause low blood glucose

Addisons disease Insulinoma Other tumours — large/hepatic Severe liver failure Xylitol poisoning Glycogen storage disease

what are inflammatory diseases that can cause low blood glucose

blood poisoning parvovirus

what are the signalment of insulinomas

Rare Older dogs Sexes equally affected No confirmed breed association Larger dogs may be predisposed

what is the pathology of insulinomas

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

what are the clinical signs of insulinomas (9)

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

what can insulinomas look like (5)

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

how are insulinomas diagnosed

**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

how do you treat insulinomas

**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

what is the prognosis of insulinomas

Median recurrence of signs = 12 months Median life span = 18 months With surgery = 2 years Then steroids = 3 years