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Diabetic Challenges Flashcards

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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
6 processes leading to hyperglycemic crisis
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
26
Onset DKA
Sudden
27
Cause of DKA
Absolute insulin deficiency
28
3 Characteristics of DKA
1. hyperglycemia 2. anion gap metabolic acidosis 3. ketosis
29
What type of diabetes has DKA
Type 1
30
Precipitating factors of DKA
Illness, infection, inadequate insulin dosage, insulin omission, undiagnosed type 1, poor management Increased metabolic needs/glucose breakdown
31
When do manifestations of DKA occur?
when there is no more production of insulin.
32
Symptoms of DKA are related to:
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
What is polyuria?
Frequent excessive urination resulting is osmotic diuresis
34
Why does polyuria occur in DKA?
Excess glucose in urine
35
What occurs as a result of polyuria in DKA?
Electrolyte excretion, severe water loss + dehydration
36
What is polydipsia and why does it occur in DKA?
Excessive thirst Dehydration due to osmotic diuresis
37
What occurs as a result of dehydration secondary to polyuria in DKA?
1. hemodilution 2. hypovolemia 3. poor tissue perfusion 4. hypoxia
38
What is polyphagia and why does it occur in DKA?
Excessive eating because no glucose is able to enter cells resulting in cell starvation
39
Define osmotic diuresis
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
Why does metabolic acidosis occur in DKA? What characterizes metabolic acidosis?
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
Anion Gap v Non Anion Gap Metabolic Acidosis
Anion: increased electrolytes decreasing the bicarb available, thus causing acidosis (potassium) Non Anion: caused by GI loss of bicarb
41
3 Steps of DKA Treatment
1. Restoring fluid volume 2. Preventing hypokalemia due to osmotic diuresis and treatment (though acidosis causes hyper) 3. Resolving acidosis with IV insulin
41
What are you treating in DKA?
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
DKA values BG pH Bicarb Anion Gab Ketones Precipitating Factors
BG > 14 pH < 7.35 Bicarb < 15 Anion Gap > 12 + serum/urine ketones precipitating factors (illness, infection) present
42
6 Points of Adult DKA Management
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
2 Criteria for discontinuing DKA order set
* Anion gap is less than 12 * Patient is able to tolerate oral intake
44
What does not occur in hyperosmolar hyperglycemic state?
Ketoacidosis Low or absent ketone levels
45
BG levels in DKA v HHS
Higher in HHS Blood sugar levels higher than DKA > 23 mmol/L
46
Onset of symptoms in DKA v HHS
Sudden in DKA Gradual in HHS
47
Severity of symptoms in HHS related to
the level of blood hyperosmolarity and cellular dehydration
48
Is there insulin present in HHS?
SOME insulin to prevent ketosis but not enough to decrease severe hyperglycemia
49
Causes of HHS
Client who can produce enough insulin to prevent DKA but not enough to prevent hyperglycemia, osmotic diuresis
50
7 Characteristics of HHS
o Hyperglycemia o Dehydration o Somnolence o Coma o seizures, o hemiparesia o aphasia
51
Who does HHS occur in?
Older adults with T2DM
52
Precipitating factors for HHS
Inadequate fluid intake, infection, stressors
53
Is there more or less symptoms in HHS v DKA
Fewer symptoms than DKA
54
What types of mainfestations are more common in HHS and why?
Increased serum osmolality (increased concentration of glucose and electrolytes) o = more neurological manifestations
55
Symptoms of HHS
* 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
Actions for HHS
* 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
Fluid Management for DKA
aggressive fluid resuscitation (correct dehydration and hypovolemia) potassium replacement is initiated as needed to correct electrolyte imbalances
58
Fluid Management for HHS
primary concern more cautious fluid replacement to avoid precipitating cerebral edema monitoring for signs of fluid overload
59
Insulin Administration for DKA
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
Insulin administration for HHS
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
Define diabetes as a vascular disease
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
Macrovascular complications of diabetes
* Coronary heart disease * Cerebrovascular disease * Peripheral vascular disease
63
How does nephropathy occur as a microvascular complication of diabetes?
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
How does neuropathy occur as a microvascular complication of diabetes?
o Damage to nerve fibers (sensory and motor) o Slow onset, progressive, and permanent o Foot ulcers: numbness; aren’t aware of injury
65
How does retinopathy occur as a microvascular complication of diabetes?
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
Describe Canada's Vascular Protection
* 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
What is stress-induced hyperglycemia?
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

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