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Pathophysiology (L3) > Diabetes > Flashcards

Diabetes Flashcards

1
Q

There are many complications associated with diabetes. What are some acute/short-term complications?

A

Hypoglycemic and hyperglycemic state of diabetic ketoacidosis
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

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2
Q

What are the different types of chronic complications associated with diabetes and list examples of each

A

Microvascular: Retinopathy, Neuropathy, Nephropathy
Macrovascular: Cerebrovascular disease, peripheral vascular disease and coronary artery disease

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3
Q

You suspect your patient is in a HYPOGLYCEMIC episode. What symptoms would you expect to see?
*Remember all symptoms related to abrupt cessation of glucose to the brain

A 
Sweating
Trembling 
Dizziness
Mood changes
Hunger
Headaches
Blurred vision
Extreme tiredness and paleness
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4
Q

You suspect your patient is in a HYPERGLYCEMIC episode. What symptoms would you expect to see?

A 
Dry mouth
Extreme thirst
Frequent urge to urinate
Drowsiness 
Frequent bed wetting
Stomach pains
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5
Q

What is the pathophysiology of hypoglycemia

A

Abrupt cessation of glucose delivery in brain results in neuroglycopenic symptoms
Caused by relative excess of insulin in blood or deficits in glucose counter-regulation feedback

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6
Q

What is the blood glucose range for hypoglycemia in a healthy patient and a patient with diabetes?

A

Healthy person: 2.5-3.3 mmol/L

Pt with diabetes: Below 4 mmol/L

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7
Q

What is the treatment for hypoglycemia?

A

15-20g of carb every 15 min if BG below 4.0mmol/L

If unconscious: IV glucose 10-25g over 1-3 min

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8
Q

When treating hypoglycemia there are three instances where glucagon is NOT effective. What are these?

A

Glucagon ineffective in pt with depleted glycogen stores
Glucagon ineffective in indiv who have consumed more than 2 standard alcoholic drinks within few hours
Glucagon ineffective in those with advanced liver disease

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9
Q

DKA and HHNKS both arise from hyperglycemia. Describe the similar pathophysiology that both of these share.

A

Insulin deficiency and inc in counterregulatory hormones

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10
Q

How does hyperglycemia affect the electrolyte balance in the body?

A

Hyperglycemia causes osmotic diuresis and large losses of electrolytes in urine
Approx. 10-15% of body weight lost in water/fluid

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11
Q

True or False: Hyperglycemia is more common in T1DM

A

True

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12
Q

True or False: HHNKS usually affects T1DM

A

False

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13
Q

True or False: HHNKS is more common than DKA

A

False

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14
Q

True or False: DKA has a lower mortality rate

A

True

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15
Q

Would you expect to see higher plasma glucose levels in HHNKS or DKA?

A

HHNKS

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16
Q

ECF volume depletion and electrolyte imbalances are common in both DKA and HHNKS. However in which of these would you see higher ECF volume depletion?

A

HHNKS has higher ECF volume depletion. This is because there are higher plasma glucose levels which results in greater osmotic diuresis. An osmolarity of greater than 320 is also seen

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17
Q

In which, DKA or HHNKS, would you see a normal pH and an abnormal pH.
What is the abnormal pH value?

A

pH is usually normal in HHNKS

DKA pH of less than 7.3

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18
Q

What are two main signs of DKA that are absent in HHNKS?

Think respiratory and breathing

A

In DKA presence of fruity breath odour cause by ketone production
Kussmaul-Kien resp due to metabolic acidosis

19
Q

In which, DKA or HHNKS, do you see absolute insulin deficiency?

A

DKA because DKA is more associated with T1DM patients

20
Q

True or False: Sodium bicarb should be used in adult and pediatric population. Explain why or why not?

A

False. Sodium bicarb should be avoided in pediatrics since it is associated with cerebral edema

21
Q

What are 4 management/treatment procedures implemented for management of DKA and HHNKS.
Note one of these is specific to DKA

A
  1. Fluid rehydration to restore normal ECFV and tissue perfusion
  2. Correction of hyperglycemia by addressing insulin deficiency
  3. Resolution of ketoacidosis
  4. Monitor and correct electrolytes
22
Q

Why is potassium added to fluid rehydration therapy even when potassium levels are normal?

A

When metabolic acidosis begins to correct K+ shifts back into cell, however there is already an overall depletion of K+ due to K+ having moved out of cell during metabolic acidosis and loss of K+ during osmotic diuresis

23
Q

Why are beta-blockers used with caution in clients with diabetes?

A

Beta blockers are used to antagonize symp system. Thus this leads to the autonomic symptoms of hypoglycemia to be hidden/masked

24
Q

Briefly explain the pathogenesis of this complication: Polyol pathway

A

Leads to intracellular accumulation of osmotically active sorbitol and fructose

25
Q

Briefly explain the pathogenesis of this complication: Advanced Glycation End products pathway

A

Irreversible binding of glucose to proteins, lipids and nucleic acids

26
Q

Briefly explain the pathogenesis of this complication: Protein Kinase C

A

Promotes synth of DAG which inc pro-inflamm gene expression and endothelial ET-1 prod

27
Q

Briefly explain the pathogenesis of this complication: Hexosamine

A

Promotes O-linked glycosylation of proteins and transcription factors

28
Q

What does the polyol pathway lead to?

A

Damages eyes, nerves and RBCs

29
Q

What does the AGE formation lead to?

A

Damages microcirculation leading to retinopathy

30
Q

What does PKC lead to?

A

Blood flow abnormalities

31
Q

What does hexosamine lead to?

A

Altered gene expression contributing to insulin resistance

32
Q

In terms of patient teaching, what should you tell the patient in order to avoid or delay complications associated with diabetes?

A

Maintain normal glycemia (A1C <7%) through healthy lifestyle and meds
Decrease other risk factors for diabetic complications
Identify and treat complications

33
Q

How does diabetes lead to macrovascular diseases?

A

Caused by atherogenesis or atherosclerosis

Hyperglycemia triggers AGEs and PKC activation which causes endothelial dysfunction

34
Q

What are the common macrovascular diseases associated to diabetes?

A

CAD
PVD
Cerebrovascular disease

35
Q

Microvascular diseases occur due to prolonged hyperglycemic states. How does it cause this?

A

Accumulation of AGEs, resultant tissue injury and pathologic conditions

36
Q

What are the two main pathologic changes in diabetic neuropathies?

A

Vessel ischemia due to thickening of walls of nutrient vessels that supply the nerve
Segmental demyelinization process affecting Schwann cells

37
Q

What is the difference between somatic and autonomic neuropathy?
Think what does it affect

A

Somatic: Involves small unmyelinated peripheral fibers and larger mylienated fibers
Sensory dysfunc occurs first and is distal, bilateral and symmetric
Autonomic: Involves symp and parasymp nervous system dysfunc

38
Q

What symptoms would you expect to see in somatic neuropathy?

A

Neuropathic pain, loss of sensation, loss of proprioception and vibration, ataxia, loss of coordination

39
Q

What symptoms would you expect to see in autonomic neuropathy?

A

Urine retention, recurrent UTI, dysfunction of enteric nerves, erectile dysfunc, dysfunc of sweating and body temp

40
Q

How does diabetes cause nephropathy?

A

Lesions of glomeruli in kidney

41
Q

There is a syndrome, Kimmelstiel-Wilson, which shares its symptoms with changes in glomerular function. What do these changes include?

A

Cap basement membrane thickening
Diffuse glomerular sclerosis
Nodular glomerulosclerosis

42
Q

What are some ways to prevent microvascular complications?

A

Good glycemic control
Prevent and treat HTN
Preventing hyperlipidemia
Preventing high levels of protein in blood and diet

43
Q

In cases of damage to the kidneys would you increase the client’s insulin dosage? Why or why not?

A

No
Normally lose insulin via urine
If kidneys are impaired that insulin is not being lost
Therefore no need for increase insulin

44
Q

When treating a hypoglycemic episode you should give:

A

6 jellybeans
3 teaspoons of sugar
Consume 15-20g of carbs

Pathophysiology (L3) (8 decks)

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