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High Acuity > Diabetic Challenges > Flashcards

Diabetic Challenges Flashcards

1
Q

Define diabetes

A

A chronic, multisystem disease of abnormal, impaired or absent insulin production that results in chronic hyperglycemia

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2
Q

Hypoglycemia value

A

< 4.1

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3
Q

Normal fasting glucose value

A

4.1-5.9

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4
Q

Hyperglycemia value

A

> 5.9

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5
Q

Define insulin

A

Polypeptide hormone mainly secreted by β cells in the islets of Langerhans of the pancreas

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6
Q

Main functions of insulin and glucagon

A

Coordinates with glucagon to modulate blood glucose levels

Insulin = decrease BG; allows uptake of glucose into cells

Glucagon = increase BG; stimulates hepatic glucose production (gluconeogenesis and glycogenolysis)

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7
Q

How is insulin secreted?

A

daily in a two-step manner:
o Basal insulin: small amounts throughout day
o Prandial insulin: 10 minutes post eating

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8
Q

6 Roles of Insulin

A

ANABOLIC - wants to BUILD + create ATP

  1. Glucose homeostasis
  2. Glycolysis
  3. Glycogenesis
  4. Lipogenesis
  5. Protein synthesis
  6. Potassium Uptake
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9
Q

How does insulin work in the brain?

A
  • Increases hunger
  • Decreases hepatic glucose production
  • Decreases lipoprotein production
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10
Q

How does insulin work in the liver?

A
  • Decreases glucose synthesis
  • Increases glycogen synthesis
  • Increases lipid accumulation
  • Increases inflammation
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11
Q

How does insulin work in the muscle?

A
  • Increase glucose metabolism
  • Increase glycogen synthesis
  • Increase muscle mass
  • Increase mitochondrial dysfunction
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12
Q

How does insulin work in adipose?

A
  • Increase glucose metabolism
  • Increase lipogenesis
  • Decrease lipolysis
  • Increase inflammation
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13
Q

Diagnostic values of pre-diabetes

A
  • HbA1C 6.0-6.4
    OR
  • Impaired Fasting Glucose
    OR
  • Impaired Glucose Tolerance
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14
Q

Pathophysiology of Type 1 DM

A

Human leukocyte antigens (HLA) are genes in major histocompatibility complexes that help code for proteins that differentiate between self and non-self
o Do not recognize beta cells as self-cells. These cells are mutated in Type 1

Beta Cells are destroyed by immune cells leading to insulin deficiency

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15
Q

When and what manifestations occur in T1DM

A

when there is no more production of insulin
Onset of classic symptoms
 Polydipsia
 Polyuria
 Polyphagia
* Then, rapid ketoacidosis

Beta cell destruction leading to absolute insulin deficiency

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16
Q

Fasting BG for T2DM diagnosis

A

> 7

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17
Q

A1C for T2DM diagnosis

A

> 6.5

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18
Q

75 g Oral Glucose Tolerance Test (GTT) for T2DM diagnosis

A

> 11.1

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19
Q

Random Plasma Glucose for T2DM diagnosis

A

> 11.1 + classic manifestations of hyperglycemia

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20
Q

Non-modifiable and modifiable risk factors for T2DM

A

Non-modifiable risk factors:
* Age (over 65)
* Gender (adult men)
* Ethnicity

Modifiable risk factors:
* smoking
* diet
* obesity
* inactivity

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21
Q

Causes of hypoglycemic crisis

A

o Too much insulin (compared to food/activity)
o Insulin taken at the wrong time
o Wrong type of insulin
o Missing meals
o Gastroparesis; delayed gastric emptying
o Alcohol: Metabolized in liver; liver cannot participate in gluconeogenesis
o Kidney failure
 Peeing out too much glucose

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22
Q

If patient is responsive with BG < 4:

A
  1. Give 15g fast acting carbs
  2. Recheck in 15, if below 4 repeat step 1
  3. If above 4: give 15g protein and 15g cards
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23
Q

If patient is symptomatic with manifestations of hypoglycemia and you can’t obtain BGM, what do you do?

A

Treat first, check BG after

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24
Q

If patient is unresponsive with BG < 4:

A
  1. ABCs
  2. IV access: 50ml 50 % dextrose IVP
  3. No IV access: glucagon IM
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25
Q

6 processes leading to hyperglycemic crisis

A
  1. decreased glycogenesis: liver not making glycogen (storing excess glucose)
  2. Increased glycogenolysis
  3. increased gluconeogenesis
  4. increased lipolysis
  5. increased ketogenesis
  6. proteolysis

BODY THINKS IT IS STARVING: there IS sugar in the blood but there NO insulin

Inappropriate continuous glucose production into blood that can not be taken up

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26
Q

Onset DKA

A

Sudden

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27
Q

Cause of DKA

A

Absolute insulin deficiency

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28
Q

3 Characteristics of DKA

A
  1. hyperglycemia
  2. anion gap metabolic acidosis
  3. ketosis
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29
Q

What type of diabetes has DKA

A

Type 1

30
Q

Precipitating factors of DKA

A

Illness, infection, inadequate insulin dosage, insulin omission, undiagnosed type 1, poor management

Increased metabolic needs/glucose breakdown

31
Q

When do manifestations of DKA occur?

A

when there is no more production of insulin.

32
Q

Symptoms of DKA are related to:

A
  1. Acidosis
    - kussmauls resps
    - fruity odour to breath
    - tachycardia
    - palpitations
    - n/v
  2. dehydration
    - tachycardia
    - dry skin
    - poor turgor
    - dehydration
    Also
    - classic symptoms
    - stuporous
    - obtunded
    - coma
33
Q

What is polyuria?

A

Frequent excessive urination resulting is osmotic diuresis

34
Q

Why does polyuria occur in DKA?

A

Excess glucose in urine

35
Q

What occurs as a result of polyuria in DKA?

A

Electrolyte excretion, severe water loss + dehydration

36
Q

What is polydipsia and why does it occur in DKA?

A

Excessive thirst

Dehydration due to osmotic diuresis

37
Q

What occurs as a result of dehydration secondary to polyuria in DKA?

A
  1. hemodilution
  2. hypovolemia
  3. poor tissue perfusion
  4. hypoxia
38
Q

What is polyphagia and why does it occur in DKA?

A

Excessive eating because no glucose is able to enter cells resulting in cell starvation

39
Q

Define osmotic diuresis

A

When the concentration of glucose exceeds the maximum re-absorption capacity of the kidney, glucose remains in the filtrate. This causes an increase in osmotic pressure causing water and potassium to move out and into the urine.

40
Q

Why does metabolic acidosis occur in DKA?

What characterizes metabolic acidosis?

A

Metabolic starvation and hypoxia lead to ketone bodies and lactic acidosis.
o Unhealthy ways for body to create energy

Increase is systemic hydrogen ion circulation due to metabolic starvation creating ketones/lactate, thus decreasing serum bicarb

41
Q

Anion Gap v Non Anion Gap Metabolic Acidosis

A

Anion: increased electrolytes decreasing the bicarb available, thus causing acidosis (potassium)

Non Anion: caused by GI loss of bicarb

41
Q

3 Steps of DKA Treatment

A
  1. Restoring fluid volume
  2. Preventing hypokalemia due to osmotic diuresis and treatment (though acidosis causes hyper)
  3. Resolving acidosis with IV insulin
41
Q

What are you treating in DKA?

A

NOT hyperglycemia, you continue to treat until ANION GAP and ACIDOSIS is resolved

This is why dextrose is given - must continue to give insulin until anion gap closes regardless of BG

42
Q

DKA values
BG
pH
Bicarb
Anion Gab
Ketones
Precipitating Factors

A

BG > 14
pH < 7.35
Bicarb < 15
Anion Gap > 12
+ serum/urine ketones
precipitating factors (illness, infection) present

42
Q

6 Points of Adult DKA Management

A
  1. Stop all insulin sets and NPO
  2. Fluid resuscitation
  3. Insulin and Potassium Replacement
  4. Dextrose administration when BG < 14
  5. Bicarb for pH < 7
  6. Maintenance order set
43
Q

2 Criteria for discontinuing DKA order set

A
  • Anion gap is less than 12
  • Patient is able to tolerate oral intake
44
Q

What does not occur in hyperosmolar hyperglycemic state?

A

Ketoacidosis

Low or absent ketone levels

45
Q

BG levels in DKA v HHS

A

Higher in HHS

Blood sugar levels higher than DKA > 23 mmol/L

46
Q

Onset of symptoms in DKA v HHS

A

Sudden in DKA
Gradual in HHS

47
Q

Severity of symptoms in HHS related to

A

the level of blood hyperosmolarity and cellular dehydration

48
Q

Is there insulin present in HHS?

A

SOME insulin to prevent ketosis but not enough to decrease severe hyperglycemia

49
Q

Causes of HHS

A

Client who can produce enough insulin to prevent DKA but not enough to prevent hyperglycemia, osmotic diuresis

50
Q

7 Characteristics of HHS

A

o Hyperglycemia
o Dehydration
o Somnolence
o Coma
o seizures,
o hemiparesia
o aphasia

51
Q

Who does HHS occur in?

A

Older adults with T2DM

52
Q

Precipitating factors for HHS

A

Inadequate fluid intake, infection, stressors

53
Q

Is there more or less symptoms in HHS v DKA

A

Fewer symptoms than DKA

54
Q

What types of mainfestations are more common in HHS and why?

A

Increased serum osmolality (increased concentration of glucose and electrolytes)
o = more neurological manifestations

55
Q

Symptoms of HHS

A
  • Fewer symptoms than DKA
  • Blood sugar levels higher than DKA > 23 mmol/L
  • Increased serum osmolality (increased concentration of glucose and electrolytes)
    o = more neurological manifestations
  • Dehydration, polyuria
  • Somnolence (sleepy)
  • Coma
  • Seizures
  • Aphasia
  • Tachycardia
  • Palpitation
  • Warm dry skin
  • Poor skin turgor
  • Dehydrated
  • Nausea/Vomiting
56
Q

Actions for HHS

A
  • Medical emergency
  • High mortality rate
  • Treatment similar to DKA
    o Restoring fluid volume: half of estimated fluid volume deficit is replaced in first 12 hours then the rest is given over 36 hours
    o IV insulin: Humulin R to correct hyperglycemia
    o Electrolyte replacement (potassium and sodium)
57
Q

Fluid Management for DKA

A

aggressive fluid resuscitation
(correct dehydration and hypovolemia)

potassium replacement is initiated as needed to correct electrolyte imbalances

58
Q

Fluid Management for HHS

A

primary concern

more cautious fluid replacement to avoid precipitating cerebral edema

monitoring for signs of fluid overload

59
Q

Insulin Administration for DKA

A

complete deficiency

insulin is administered along with fluids

started earlier in the treatment course to halt lipolysis and ketone production

Initial insulin therapy is often given as a bolus followed by continuous infusion.

60
Q

Insulin administration for HHS

A

secondary concern (not absolute deficiency)

insulin therapy is usually delayed until fluid replacement has begun, and serum osmolality has been partially corrected

Insulin is then gradually introduced to facilitate glucose uptake by cells, promoting the resolution of hyperglycemia

61
Q

Define diabetes as a vascular disease

A

Chronic Consequences of Diabetes: Blood vessel changes lead to complications from poor tissue perfusion and tissue ischemia
Glucose is large bulky molecule that can cause damages (holes, clotting formations, etc.)

62
Q

Macrovascular complications of diabetes

A
  • Coronary heart disease
  • Cerebrovascular disease
  • Peripheral vascular disease
63
Q

How does nephropathy occur as a microvascular complication of diabetes?

A

chronic hyperglycemia causes HTN in kidney blood vessels, kidney vessels becomes leakier and narrower, leading to decreased perfusion to kidneys, kidney cell hypoxia and cell death

64
Q

How does neuropathy occur as a microvascular complication of diabetes?

A

o Damage to nerve fibers (sensory and motor)
o Slow onset, progressive, and permanent
o Foot ulcers: numbness; aren’t aware of injury

65
Q

How does retinopathy occur as a microvascular complication of diabetes?

A

o Macular edema and degeneration increased blood vessel permeability, deposits of hard exudate at retina, corneal scarring, changes in lens shapes
 Increased morbidity, decreased quality of life
 Main cause is chronic hyperglycemia

66
Q

Describe Canada’s Vascular Protection

A
  • Management of HTN, hyperglycemia, and hyperlipidemia
  • Management of modifiable risk factors
    o A1C: management of long-term glycemia – lifestyle changes
    o BP: management of HTN – lifestyle changes, medications
    o Cholesterol: plaque build-up furthers damage to vessels
    o Drugs (ACE/ARB, Statin, ASA)
    o Exercise
    o Smoking Cessation
67
Q

What is stress-induced hyperglycemia?

A

common after severe trauma and critical illness.

Neuroendocrine response to stress leads to increased cortisol

imbalance of glucose production and glucose clearance induced by increased circulating levels of stress hormones and cytokines.

increased morbidity and mortality in non diabetic patients

68
Q
A

High Acuity (20 decks)

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