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Renal and Endocrine Biology > REB 10. Effects of Acute and Chronic Hyperglycaemia > Flashcards

REB 10. Effects of Acute and Chronic Hyperglycaemia Flashcards

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1
Q

What are the recommended target blood glucose ranges?

A

refer so slide 3

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2
Q

What is pre-diabetes?

A

Pre-Diabetes: intermediate hyperglycaemia

  • impaired fasting glucose
  • impaired glucose tolerance
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3
Q

What is the blood glucose level in the FASTING state of those with PRE-DIABETES?

A

6.1 to 6.9 mmol/L

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4
Q

What is the blood glucose level in the 2-HOURS AFTER MEAL state of those with PRE-DIABETES?

A

7.8 to 11.0 mmol/L

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5
Q

What is the blood glucose level in the FASTING state of those with DIABETES?

A

greater than or equal to 7.0 mmol/L

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6
Q

What is the blood glucose level in the 2-HOURS AFTER MEAL state of those with DIABETES?

A

greater or equal to 11.1 mmol/L

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7
Q

What are the blood glucose levels of those with acute hyperglycaemia and the symptomatic levels (when symptoms arise)?

A

blood glucose is greater than or equal to: 8 to 15 mmol/L

symptomatic blood glucose level: greater than or equal to: 15 to 20 mmol/L (270 - 360 mg/dL)

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8
Q

What is the glycosuria threshold? What is the value in acute hyperglycaemia?

A

Glycosuria threshold is the amount of glucose the renal tubules can hold before it starts excreting glucose into the urine

the threshold is around 8 to 10 mmol/L

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9
Q

What are some causes of acute hyperglycaemia?

A

[1] Type 1 Diabetes Mellitus (decreased insulin levels)

[2] Type 2 Diabetes Mellitus (decreased insulin sensitivity of target cells)

[3] Stress Hyperglycaemia (gluceoneogenesis due to stress hormones frequently encountered during hospitalization)

[4] Other Endocrine Disorders

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10
Q

What are the symptoms of acute hyperglycaemia?

A

[1] Glycosuria (increased secretion of glucose in urine)

[2] Osmotic Diuresis (glucose in kidney tubules leads to excess water leaving in urine)

  • Polyuria (excess urine)
  • Polydipsia (increased thirst)
  • excess loss of electrolytes (Na+, K+)

[3] Polyphagia (increased appetite)

[4] Metabolism of Proteins + Fats
- weight loss + protein deficiency

[5] Episodes leave Increased HbA1c as Diagnostic Trace

  • integrated index of diabetic control
  • build up of glycated haemoglobin - reflects average level of glucose to which the cell has been exposed during its life-cycle
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11
Q

How can insulin deficiency lead to increased ventilation? (hint: there are multiple steps)

A

[1] insulin deficiency leads to decreased triglyceride synthesis + increased lipolysis

[2] increase in blood fatty acids

[3] increased liver use of fatty acids leads to release of excessive ketone bodies into the blood

[4] ketosis - body burns fat for energy and liver produces ketones

[5] metabolic acidosis (e.g. diabetic acidosis when ketone bodies build up in body)

[6] increased ventilation

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12
Q

Acute Hyperglycaemia may be due to acute illness. True of False?

A

True.

Review slide 10!

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13
Q

Diabetic Ketoacidosis occurs as a result of the transition from [1] to [2] metabolism.

A

[1] glucose

[2] lipid

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14
Q

What is the main mechanism behind why Diabetic Ketoacidosis occurs? What are some things that may arise out of it?

A
  • severe deficiency in insulin signalling as a result of decreased insulin secretion (no insulin to allow glucose into tissues)
  • elevated levels of counterregulatory hormones (glucagon, cathecholamines, cortisol, growth hormone)
  • reduced triglyceride synthesis + enhance lipolysis
  • reduced protein synthesis + enhanced proteolysis
  • elevated plasma free fatty acid (FFA) and amino acid levels and uptake into liver
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15
Q

What are some of the counterregulatory hormones that are elevated in diabetic ketoacidosis?

A

[1] glucagon
[2] catecholamines
[3] cortisol
[4] growth hormone

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16
Q

In diabetic ketoacidosis, what happens in regards to glucose production, ketosis and acidosis?

A

GLUCOSE:

  • hyperglycaemia
  • increased gluconeogensis in liver and impaired glucose utilization in peripheral tissues

KETOSIS:

  • increased ketogenesis (increased production of ketone bodies, acetoacetate, beta-hydroxybutyrate, acetone acid)
  • hyperketonaemia causes metabolic acidosis
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17
Q

What is the overall metabolic state in those with Diabetic Ketoacidosis?

A

[1] increased serum (blood level) GLUCOSE
[2] increased serum AMINO ACIDS
[3] increased serum FREE FATTY ACIDS (FFA)
[4] increased serum KETONES
[5] resultant METABOLIC ACIDOSIS

18
Q

Explain the effects of osmotic diuresis in diabetic ketoacidosis.

A
  • urinary excretion is in response to hyperglycaemia which causes additional loss of Na+ and K+
  • leads to dehydration and electrolyte loss
  • K+ lost in large quantities
  • if patients have a total body deficit the development of HYPOKALAEMIA is possible (total body potassium depletion)
19
Q

What is hypokalaemia? What is it a result of?

A

it is when there is a total body potassium depletion

it can occur during diabetic ketoacidosis as there is excessive urination and loss of both Na+ and K+ in the urine

20
Q

Where does ketogenesis occur?

A

liver

21
Q

What is ketogenesis? What occurs during ketogenesis? What are the 2 main pathways/items that are created?

A

Ketogenesis: increased fat metabolism

  • enhanced lipolysis (adipose tissue)
  • release of Free Fatty Acids (FFA) from adipose tissue
  • enhanced plasma Free Fatty Acids (FFA)
  • enhanced uptake into liver
  • beta oxidation in liver – excess acetyl coA converted to Ketone Bodies:
  • – Acetoacetate
  • – Beta-hydroxybutyrate
  • – Acetone (produced from spontaneous decarboxylation of acetoacetate and is slowly eliminated by respiration and excreted in urine)
22
Q

What are the 3 examples of ketone bodies?

A

[1] Acetoacetate
[2] Beta-Hydroxybutyrate
[3] Acetone

23
Q

How is acetone, a ketone body, created and gotten rid of in the body?

A

produced from spontaneous decarboxylation of acetoacetate

is slowly eliminated by respiration and excreted in urine)

24
Q

What is Ketonaemia and Ketonuraia? What is the difference between the two?

A

Ketonanaemia: presence of an abnormally high concentration of ketone bodies in blood

Ketonuraia: excretion of abnormally large amounts of ketone bodies in the urine

25
Q

What are some reasons that diabetic ketoacidosis (DKA) may occur?

A

[1] initiated by conditions that increase insulin requirements (infection, trauma, stress…)

[2] undiagnosed diabetes or failure of prescribed insulin administration at peak needs (insulin non-compliance)

26
Q

Is Diabetic Ketoacidosis (DKA) a life-threatening condition? Why or why not?

A

Yes, it is.

  • requires immediate treatment
  • patients can rapidly undergo shock, coma and death
27
Q

What are some symptoms of DKA?

A
  • dehydration (polyuria, very dry mouth)
  • breath that smells fruity (acetone)
  • Kussmaul Respiration (deep and laboured breathing to compensate for metabolic acidosis)
  • nausea and vomiting
  • abdominal pain (may be severe, esp. in children)
  • mental status changes (lethargy, somnolence, stupor, coma)
28
Q

What can help to make a DKA diagnosis? (general - just name)

A

DKA Biochemical Triad

29
Q

What is the DKA biochemical triad?

A

DKA Biochemical Triad: to help with DKA diagnosis

[1] Hyperglycaemia (>/= to 11mM)

[2] Ketonaemia (>/= 3mM)

  • e.g. precision Xtra meter OR
  • signficant ketonuria e.g. Ketostix

[3] Acidaemia (metabolic acidosis)
- ABG of pH < 7.3 with an anion gap of > 12 mmol/L give or take 2

30
Q

What is an anion gap?

A

Definition: difference between primary measured cation and primary measured anions in serum

  • indicator of increased concentrations of unmeasured acid anions
  • continous production of ketone bodies depletes alkali reserve – Ketoacidosis

formula: Na+ - (Cl- + HCO3-)

31
Q

How do you calculate the anion gap?

A

Na+ - (Cl- + HCO3-)

32
Q

What are the 3 main treatments for DKA? (general)

A

[1] IV Fluid Replacement
[2] IV Insulin
[3] Potassium Replacement

33
Q

What is IV Fluid Replacement and how does it work for those with DKA?

A
  1. 9% NaCl (can be up to 6 to 9L fluid deficit)
    - volume expansion and fluid replacement
    - correction of hyperglycaemia, ketosis, acidosis
    - correct electrolyte imbalance
34
Q

What is IV Insulin and how does it work for those with DKA?

A
  • correction of hyperglycaemia, ketosis, acidosis
  • reduction in ketone/increase bicarbonae blood levels
  • blood glucose requires monitoring
35
Q

What is Potassium Replacement and how does it work for those with DKA?

A
  • even if plasma K+ is normal or raised, there is TOTAL BODY POTASSIUM DEPLETION
  • insulin administration and correction of hyperosmolality moves potassium to the intracellular compartments, risk of hypokalemia
36
Q

What are the microvascular complications of chronic hyperglycaemia?

A

[1] Diabetic Nephropathy (kidney damage)
[2] Diabetic Retinopathy (eye complications)
[3] Diabetic Neuropathy (nerve damage)

37
Q

What are the macrovascular complications of chronic hyperglycaemia?

A

[1] Heart Disease
[2] Stroke
[3] Peripheral Vascular Disease

38
Q

What is the difference between microvascular and macrovascular complications?

A

Microvascular: due to damage to small blood vessels

Macrovascular: due to damage to larger blood vessels

39
Q

How are Advanced Glycation End Products (AGEs) formed?

A

in prolonged hypergylcaemia, protein glycation reactions lead to AGEs which are thought to be the major causes of different diabetic complications

40
Q

What is the process of glycation?

A

[1] non-enzymatic binding of glucose with amino group of proteins

[2] complicated molecular process involving simple and complex multistep reactions

[3] prolonged high glucose levels induces glycation of various structural and functional proteins causing molecular rearrangements that lead to the formation and accumulation of AGEs

Renal and Endocrine Biology (25 decks)

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