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Gen Med: Ednocrine > Type 1 DM > Flashcards

Type 1 DM Flashcards

1
Q

What is the etiology of T1DM?

A

Immune mediated in > 90% cases

Idiopathic in < 10% cases

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2
Q

What are the characteristics of T1Dm?

A
  1. Catabolic disorder characterized by
  2. Absent or extremely low circulating insulin
  3. Increased plasma glucagon
  4. Insufficient pancreatic beta cell response
    A. Absent/low insulin secretion
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3
Q

What leads to hyperglycemia?

A
  1. Glucose acts as osmotic diuretic
    A. Leads to polyuria and polydipsia
    B. Caloric loss increases hunger (polyphagia)
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4
Q

Why is insulin required for T1Dm?

A

Reverse catabolic state
Prevent ketosis
Reduce hyperglucagonemia
Reduce blood glucose

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5
Q

What are the risk factors for Immune mediated T1Dm?

A
  1. Genetic
    A. 33% of cases
  2. Environmental factors
    A. Scandinavian & Northern European ethnicity
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6
Q

What are the risk factors for idiopathic T1DM?

A

Usually African or Asian descent

Some cases have mutated PAX-4 gene
Essential gene in development of pancreatic islet cells

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7
Q

What are teh sxs of T1DM?

A 
1. Polyuria 
A. Excessive urination
B.. Osmotic diuresis
2. Polydipsia
A. Excessive thirst
B. Hyperosmolar state
3. Polyphagia
A. Excessive appetite
4. Weakness or fatigue
A. K+ loss & protein breakdown
5. Blurred vision
A. Lens exposed to hyperosmolar state
6. Weight loss
A. Initially due to depletion of water, glycogen and trigs
B. Muscle wasting due to protein as energy source
7. Pruritis
A. Hyperglycemia & dehydration
8. Peripheral neuropathy
A. Neurotoxicity from sustained hyperglycemia
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8
Q

What are the Urinalysis results in T1Dm?

A

Glycosuria
Ketonuria
Ketones > 3 mmol/L requires hospitalization

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9
Q

What are the serum glucose results for T1DM?

A
  1. FBS 100-126 mg/dL → impaired (pre-diabetes)
  2. Random glucose or 2 hr GTT ≥ 200 mg/dL → DM
  3. If FBS ≥ 126 mg/dL, F/U with 2 hr GTT
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10
Q

What are the fasting lipid panel results for T1DM?

A

Triglycerides elevated

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11
Q

What other dx studies are used in T1DM?

A
  1. EKG
  2. BMP
    A. BUN/Cr
    B. Electrolytes
  3. HbA1c
  4. Urine Microalbumin
  5. Urinalysis
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12
Q

What are the limitations of home glucose monitors?

A
  1. Older meters calibrated against whole blood concentrations
    A. Displayed values are 10%-15% lower than plasma glucose
  2. ↑ or ↓ Hct can alter glucose value
  3. Meters & test strips calibrate glucose 60-160 mg/dL
    A. Accuracy not as good for low or high levels
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13
Q

What can cause falsely low glucose meter readings?

A
  1. critically ill pts on supplemental oxygen
    A. Various chemstrips
    B. Glucose oxidase (false readings)
    C> Glucose dehydrogenase strips preferred in these pts
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14
Q

What are the ADA carb recommendations?

A

45-65% total calories

Count carbs to titrate insulin

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15
Q

What are the ADA fat recommendations?

A

25-35% with < 7% from sat fats

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16
Q

What are the ADA protein recommendations?

A

10-35%

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17
Q

What are the ADA cholesterol recommendations?

A

< 200 mg/day if LDL > 100 mg/dL

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18
Q

Why is dietary fiber important?

A

Slows nutrient absorption rates so glucose absorption is slower -> lowers hyperglycemia
Has favorable effect on cholesterol

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19
Q

What artificial sweeteners can be used for T1Dm?

A
  1. Splenda, Sweet ‘n Low, Truvia
    A. Can be used in beverages, baking & cooking
  2. Sugar alcohols
    A. Sorbitol, Xylitol, Mannitol
    B. Not as easily absorbed as sugar so they do not raise sugar levels as much
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20
Q

What is indicated for all T1DM?

A

Insulin

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21
Q

What are the recombinant Human insulins?

A

A. Humulin R (regular) & N (NPH)

B. Novolin R (regular) & N (NPH)

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22
Q

What are the analogs of human insulin?

A

A. Rapid acting – lispro/Humalog, aspart/NovoLog, glulisine/Apida
B. Long acting – glargine/Lantus, detemir/Levemir

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23
Q

What is the function of basal insulin?

A
  1. Suppresses glucose production between meals and overnight
  2. Mimics natural pancreatic basal insulin secretory patterns
  3. Continued effect over 24 hrs
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24
Q

What is the function of bolus insulin?

A

Limits hyperglycemia after meals

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25
Q

When might an intermediate acting insulin be dosed?

A
  1. Pre-breakfast blood sugar reflects adequacy of PM or HS dose
  2. Pre-dinner blood sugar reflects adequacy of AM dose
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26
Q

When might a rapid acting insulin be dosed?

A
  1. Pre-lunch glucose level reflects adequacy of fasting AM dose
  2. HS glucose level reflects adequacy of pre-prandial (PM) supper dose
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27
Q

What are the sites of insulin injection?

A
  1. Abd (preferred), thighs, upper arms, flanks, upper buttocks
  2. Rotation of sites in specific region recommended to avoid delayed absorption
28
Q

What are the benefits of an insulin pen injector and what are some examples?

A
  1. Eliminates need for carrying various types insulin vials and syringes
  2. Lispro, Glulisine, Aspart, Regular, NPH, Detemir, Glargine
  3. Lispro Protamine/Lispro, Aspart Protamine/Aspart, NPH/Regular
29
Q

What are the advantages of insulin pumps?

A
  1. Small & easy to program
  2. Set basal rate throughout 24 hrs
  3. Adjust time over which bolus is given
  4. Allows profile tailored to pt
  5. Built in software that can assist pt in calculating boluses based on glucose reading & CHO consumed
  6. “Insulin on board” warning
30
Q

How are the basal and bolus insulins dosed with an insulin pump?

A
  1. 50% estimated insulin doses as basal
  2. Remaining insulin given as intermittent boluses prior to meals
    A. 1 unit / 15 gm CHO plus 1 unit for 50 mg/dL of blood glucose above target value of 120 mg/dL
    B. Common starting point
31
Q

What are the nocturnal effects in diabetes?

A
  1. Somogyi Effect or “posthypoglycemic hyperglycemia”

2. Dawn Phenomena

32
Q

Define Dawn Phenomena

A
  1. Rise in blood sugar in response to waning insulin & agrowth hormonesurge
    A. Due to physiologic process, NOT due to night time insulin dose
33
Q

Define Somogyi Effect or “posthypoglycemic hyperglycemia”

A
  1. Rebounding hyperglycemia in early morning that is a response to nocturnal hypoglycemia
    A. Leads to surge of counter-regulatory hormones to produce high glucose levels by 7AM
    B. Usually results from too much PM insulin (intermediate) OR too small of a bedtime snack when regular insulin is given
34
Q

What is the acceptable level of blood glucose before meals or after overnight fast?

A

80-130 mg/dL

35
Q

What is the acceptable level of blood glucose 1-3 hours post prandial?

A

< 180 mg/dL

36
Q

What is the acceptable HbA1c for adults?

A

< 7.0% in adults

37
Q

What is the acceptable HbA1c in peds?

A

<7.5% in peds

38
Q

What are the drugs that can affect blood glucose?

A 
1. Glucocorticoids
A. ↑ hepatic glucose output & peripheral insulin resistance
2. Estrogens
A. ↑ peripheral insulin resistance
3. Diuretics (thiazides)
A. Hemoconcentration effect
4. Sympathomimetics (epi, pseudoephedrine, stim.)
A. Block insulin secretion
B. ↑ hepatic glucose output
5. Nicotinic acid (Niacin) 
A. ↑ insulin resistance
6. (?) Statins
A. ↑ insulin resistance/↓ insulin production
39
Q

What are the adverse effects of insulin?

A
  1. Hypoglycemia
  2. Weight gain
  3. Local or systemic reactions
  4. Atrophy or hypertrophy of fat at injection site
40
Q

How is hypoglycemia treated in different settings?

A
  1. Glucagon
    A. Treatment at home
  2. Dextrose 50
    A. Treatment in hospital
41
Q

What can hypoglycemia result from?

A
  1. Delayed meal
  2. Unusual physical exertion w/out supplementing calories
  3. ↑ insulin dose
42
Q

What may blunt hypoglycemia sxs in T1DM?

A
  1. Most sx’s of hypoglycemia (except sweating) are blunted in pts receiving beta blockers
  2. If necessary, beta 1 selective agents should be used in diabetics
43
Q

What are the hypoglycemic sxs when glucose is below 54?

A
  1. Tachycardia
  2. Palpitations
  3. Sweating
  4. Tremulous
  5. Nausea
  6. Hunger
44
Q

What are the hypoglycemic sxs when glucose is below 50?

A
  1. Irritability
  2. Confusion
  3. Blurred vision
  4. Fatigue
  5. Headache
  6. Difficulty speaking
45
Q

How is hypoglycemia treated?

A
  1. 15 gm CHO is usually sufficient to reverse hypoglycemia
    A. Glucose tablets (3-4)
    B. Juice (1/2 c)
  2. Glucagon emergency kit (1mg)
    A. Family & friends should be instructed how to use the kit
    B. SQ or IM injection if pt unconscious or refusing oral
    C. Mobilizes glycogen from liver, ↑ glucose by 36 mg/dL in ~ 15 min
  3. Medic alert bracelet or necklace
46
Q

When should screening begin for T1DM? What screening is necessary?

A 
1. 5 years after diagnosis made 
A. Dilated eye exam
B. Podiatry exam
2. > 10 yr
A. Urine microalbumin  
B. Serum Creatinine
47
Q

What are chronic effects of T1DM?

A
  1. HTN
  2. CKD
  3. Blindness
    A. Diabetic cataracts
    B. Proliferative retinopathy
    C. Glaucoma
  4. Diabetic nephropathy
    A. Microalbuminuria
    B. Progressive nephropathy
  5. Diabetic Neuropathy
    A. Autonomic
    B. Peripheral
    C. ED
  6. Vascular disease
    A. Amputations
    B. MI
    C. CVA
48
Q

What is the pathophys of DKA?

A
  1. DKA results from shortage ofinsulin
    A. Body switches to burningfatty acids& producing acidicketone bodies
    B. Leads to ↑ in counter-regulatory hormones (glucagon, cortisol, growth hormone, epinephrine, cytokines)
    → Hepatic gluconeogenesis, glycogenolysis, lipolysis
49
Q

What are the sxs of DKA?

A
  1. Hyperglycemia & hyperosmolality
  2. Polyuria x 1+ days
    A. Osmotic diuresis (Glucose, H2O, K, Na)
  3. Polydipsia x 1+ days
  4. Marked fatigue
  5. N/V/abd pain
  6. Hypothermia
    A. Unless infection
  7. Mental status changes
    A. Confusion -> delirium -> stupor -> coma
  8. Marked dehydration
    A. Hypotension, tachycardia, poor skin turgor
    B. Avg adult total body water shortage of 6-8liters (or 100mL/kg)
  9. Kussmaul respirations
    A. Tachypnea w/air hunger
    B. Resp compensation for metabolic acidosis
  10. Fruity breath
    A. ↑ Acetone level
50
Q

What is the timeline for DKA?

A

Sx’s usually evolve over ≈ 24 hr

51
Q

What is the prognosis for DKA?

A
  1. Life threatening medical emergency
    A. Mortality rate ≈ 5% in pts < 40 yr
    B. Mortality rate > 20% in elderly
52
Q

What can cause DKA?

A
  1. Infection
  2. Stress
  3. MI
  4. CVA
  5. Cocaine abuse
  6. Poor compliance
  7. Insulin pump or insulin pen defect
    A. Pump failure
    B. Insulin leakage
53
Q

What is the workup for DKA?

A
  1. Airway, breathing, & circulation (ABC) status
  2. Mental status (MMSE)
  3. BMP
  4. CBC w/diff
  5. UA & urine ketones by dipstick
  6. Serum ketones (if urine ketones are present)
  7. Plasma osmolality
  8. ABG if serum bicarbonate reduced or hypoxia suspected
    A. F/U w/venous blood gasses
  9. EKG
  10. Additional testing
    A. UC, sputum Cx , BC x 2, serum lipase/amylase, CXR
    B. Infection (pneumonia or UTI) - common precipitating event
54
Q

What are the dx studies for DKA?

A 
1. Plasma glucose
A. > 250 mg/dL (350-900 mg/dl)
2. (+) Serum & urine ketones
A. 7-10 mmol/L
3. ↑ BUN & Cr
A. Dehydration
4. Hypo, normo or hyperkalemia
A. Total body K low (cell shift)
5. Mild hyponatremia
A. 130 mEq/L
6. ↑ Amylase
7. Hypocalcemia
8. Hypomagnesemia
9. Hypophosphatemia
A. 6-7 mg/dL
B. Total phosphate stores depleted
10. Metabolic Acidosis
A. pH < 7.30
B. pCO2 > 40 mmHg
11. Serum bicarbonate
A. < 18 mEq/L
12. High anion gap
A. Anion gap = Na - (Cl + HCO3)
B. > 15-20mEq/L(nl ≈ 3 to 10mEq/L)
55
Q

What are the treatment goals for DKA?

A
  1. Goals
    A. Restore plasma volume & tissue perfusion
    B. Reduce blood glucose & osmolality towards normal
    C. Correct acidosis
    D. Replenish electrolyte losses
    E. Identify & treat precipitating factors
  2. ICU admission
56
Q

What is the initial treatment for DKA?

A
  1. Volume replacement
    A. Normal Saline
  2. Hyperglycemia
    A. Regular Insulin
57
Q

How is fluid replaced in DKA?

A
  1. Initially, 0.9% NaCl to re-expand contracted volume (≥ 1 liter)
    A. 500-1000 mL in 1st hr, then 300-500 mL/hr over next 12 hr
    B. If serum Na > 150 mEq/L, use 0.45% NaCl
    -Avoid CHF in elderly & cerebral edema
  2. When serum glucose < 300 mg/dL, change to D5W to maintain glucose in 250-300 mg/dL range
    A. Prevents hypoglycemia
    B. Replenishes free H2O
    C. Reduces risk cerebral edema
    -Most dangerous complication
58
Q

When is regular insulin started in DKA?

A

Wait to start after K >3.3 mEq/dL

59
Q

What is the loading dose of insulin for DKA? Then what?

A
  1. Loading dose 0.15 units/kg IV bolus
  2. Then 0.1 unit/kg/h IV
    A. Replaces insulin deficit
    B. Corrects acidosis by reducing flux of fatty acids to liver and ↓ production of ketones by liver
    C. Reduces hyperglycemia
60
Q

How often is glucose monitored in DKA? What is the goal?

A
  1. Monitor glucose qh x 2 hr, then q 2-4 h

2. Goal is to ↓ glucose by 80 mg/dL/hr after initial drop from rehydration (if not, double insulin rate)

61
Q

How is K managed in DKA?

A
  1. As acidosis is corrected, K flows back into cells, resulting in hypokalemia
  2. Replace with KCL 10-30 mEq/h as soon as acidosis starts to resolve
  3. EKG can be helpful in monitoring
    A. Flattened T waves and U waves in hypokalemia
62
Q

When is phosphate replacement required in DKA?

A

Rarely

63
Q

When is NaHCO3 replacement required in DKA?

A
  1. Contraindicated unless severe acidosis
  2. Recommended if pH < 6.9 & HCO3 < 5
    A. 1 ampule (44 mEq/50 ml) should be added to 1 L 0.45% NaCl
    B. Once arterial pH reaches 7.1, NaHCO3 should be discontinued
    C. Additional HCO3 would increase risk rebound metabolic alkalosis which would shift K from serum into cells -> fatal arrhythmia & cerebral edema
64
Q

What is the overall mortality for DKA?

A

Overall mortality rate of DKA is < 5% w/ low dose insulin infusion, correction of fluid & electrolyte balance, & close monitoring of pt’s clinical & lab status

65
Q

What conditions worsen DKA prognosis?

A

Acute MI, ischemic bowel & end-stage CKD worsen prognosis

66
Q

When should cerebral edema be considered in DKA?

A
  1. Onset of H/A or deterioration in mental status during Tx should lead to consideration of cerebral edema
    A. Primarily in peds population
    B. Treat with IV Mannitol 1-2 g/kg over 15 min
67
Q

What education needs to happen for pts in DKA?

A
  1. After recovery & stabilization, pts should be instructed on how to recognize early signs/sx’s of DKA
  2. Measure urine ketones in pts w/ infection or pts w/ continued high glucose readings who are on insulin pump
  3. Contact PCP !!

Gen Med: Ednocrine (8 decks)

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