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Pharm II > Lecture 11 (Endocrine)-Exam 6 > Flashcards

Lecture 11 (Endocrine)-Exam 6 Flashcards

1
Q

Summary of Diabetes Mellitus
* The term diabetes mellitus describes what?
* It is associated withwhat?

A
  • The term diabetes mellitus describes diseases of abnormal carbohydrate metabolism that are characterized by hyperglycemia.
  • It is associated with a relative or absolute impairment in insulin secretion, along with varying degrees of peripheral resistance to the action of insulin.
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2
Q

Summary of Diabetes Mellitus
* What is type one vs type two?

A
  • Type 1- Early onset, autoimmune destruction of the pancreatic beta cells leading to absence of insulin, DKA may be initial presentation in 25% with new Dx
  • Type 2-Most common (>90%), usually later onset, associated with overweight, obesity, + FH. Hyperglycemia usually due to progressive loss of insulin secretion from the beta cell with a background of insulin resistance, resulting in relative insulin deficiency.
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3
Q

Summary of Diabetes Mellitus
* What are the classic sxs?

A

Classic symptoms of hyperglycemia include polyuria, polydipsia, nocturia, blurred vision, and weight loss.

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4
Q

Normal insulin regulation
* What is the response to increased blood gluce from food intake?

A
  • Food intake increases glucose in the blood
  • Stimulates pancreas beta cells to release insulin
  • Insulin stimulates glucose uptake by the cells
  • Cells use glucose for energy – ATP production
  • Excess glucose stored as glycogen in the liver
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5
Q

Normal insulin regulation
* What is the response to low blood glucose?

A
  • Low blood glucose stimulates alpha cells of the pancreas islet cells to secrete glucagon
  • Glucagon stimulates the liver to convert stored glycogen to glucose
  • Glucose released into the blood for use as energy
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6
Q

Type 1 DM
* What causes this disease?

A

Immune mediated destruction of beta cells
* T-cells attack beta cells
* Eliminating insulin production

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7
Q

Type 2 DM
* What are the causes?(2)
* What is the result?(2)

A

Insulin resistance
* Tissue cells have trouble responding to insulin -> decreased glucose uptake from the blood

Gradual insulin deficiency
* Secondary to prolonged beta cell hyperstimulation

Result:
* Increased blood glucose
* Starved tissue cells

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8
Q

⭐️

A
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9
Q

AIC Goals
* Glycated hemoglobin (A1C) goals in patients with diabetes should be tailored to what?
* What is a reasonable goal? ⭐️

A
  • Glycated hemoglobin (A1C) goals in patients with diabetes should be tailored to the individual, balancing the improvement in microvascular complications with the risk of hypoglycemia.
  • A reasonable goal of an A1C value of ≤7.0 percent for most patients
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10
Q

AIC Goals
* Glycemic targets are generally set somewhat higher for who?
* What is the goal for T1D and pregnancy?

A
  • Glycemic targets are generally set somewhat higher (eg, <8 percent) for older adult patients and those with comorbidities or a limited life expectancy and little likelihood of benefit from intensive therapy.
  • More stringent control (A1C <6 percent) may be indicated for individual patients with type 1 diabetes and during pregnancy.
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11
Q

Monitoring AIC
* What is the monitoring if A1C is met or not met?

A
  • Every 6 months if A1C goal met
  • Every 3 months if A1C goal not met; or with therapy change
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12
Q

Continuous glucose monitoring
* MC used for patients on what?
* MC for patients with what? What are the two ways?

A

MC used for patients on insulin therapy

MC for patients with type 1 DM
* Continuous – every day
* Intermittent continuous – 10 to14 day snapshot (common with T2D to get a look in blood sugar levels)

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13
Q

Continuous glucose monitoring
* Looking for what? TIR of 70% approximately equal to what?
* What is also evaluated?

A

Looking for time in range (TIR)
* TIR of 70% approximately equal to an AIC of 7%

Time above range and time below range also evaluated

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14
Q

What does the ambutatory glucose profile show?

A
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15
Q

PharmacoTherapy: T1D
* What is recommended for most patients?
* Management should be directed by who?

A
  • Intensive insulin therapy is recommended for most patients
  • Management should be directed by Endocrinologist
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16
Q

PharmacoTherapy: T2D
* Care directed by who? Who else do they need to see?

A
  • Care directed by primary care providers and their health care teams / specialists
  • Ophthalmology
  • Podiatry
  • Nutrition
  • Endocrinology
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17
Q

What is first line therapy for T2D?

A

metformin and lifestyle modifications

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18
Q

Lifestyle modifications – ALL patients
* What is the primary goal along with what?
* Overweight or obese patients: Some benefits seen with what? Greater benefits with what?

A
  • Primary goal along with glycemic control
  • Overweight or obese patients
    * Some benefits seen with weight decreases of 3 to 7%
    * Greater benefits with sustained loss of ≥ 10%

Weight management – successful in small percent of patients

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19
Q

Lifestyle modifications – ALL patients
* improves what?
* Decreases what?
* Partial correction of what?

A
  • Improves glycemic control
  • Decreased cardiovascular risks - tobacco cessation
  • Partial correction of insulin resistance and impaired insulin secretion
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20
Q

Lifestyle modifications-All Patients
* Intense what? High frequency what? What happens with calorie?

A

Intense nutrition education
* High frequency counseling
* Calorie deficit 500-750 kcal/day

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21
Q

Lifestyle modifications-All Patients: Physical activity
* Similar effects as what?
* How much a week?
* Not more than what? (2)
* Improvement with what?

A
  • Similar effects as weight loss
  • 150 min moderately intense aerobic activity / week
  • No more than 2 days without activity
  • No more than 30 minutes without movement
  • Improvement in macrovascular outcomes – cardiovascular disease, MI, stroke ( no micro)
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22
Q

Obesity Pharmacotherapy
* Consider for patients with what?
* used along with what?

A
  • Considered for patients with diabetes and obesity / overweight
  • Used along with lifestyle changes
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23
Q

Obesity Pharmacotherapy
* What are the preferred agents?
* What does it do?

A
  • Glucagon-like peptide 1 receptor agonists (semaglutide / liraglutide)OR
  • Dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 receptor agonist (tirzepatide)

Lower blood glucose levels and reduce weight

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24
Q

Metabolic surgery:
* Considered as what?
* Strong evidence to support what?

A
  • Considered as a weight and glycemic management approach for patients with a BMI of ≥ 30 kg/m2
  • Strong evidence to support superior glycemic control and reduction of cardiovascular risk in patients with T2DM and obesity
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25
Q

Metabolic surgery
* MC procedures in the US are what?
* What has fallen out of favor?

A
  • MC procedures in the US are the vertical sleeve gastrectomy and Roux-en-Y gastric bypass
  • Medical devices such as gastric banding have fallen out of favor
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26
Q

Type 2 DM pharmacotherapy: patient centered
* Initial and add on therapies based on what? (7)

A
  • Impact on cardiovascular and renal comorbidities
  • Efficacy
  • Hypoglycemia risk
  • Impact on weight
  • Adverse effects
  • Cost / access
  • Patient preferences
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27
Q

Type 2 DM pharmacotherapy: patient centered
* When should pharmcotherapy be started

A

Pharmacotherapy should be started at the time T2DM is diagnosed unless specifically contraindicated

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28
Q

Biguanides
* What is the only medication in this class?
* What does it activate?

A
  • Metformin - only medication in class
  • Activates AMP dependent protein kinase (AMPK)
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29
Q

Biguanides
* What does it decrease in the liver?
* Moves what? What does that increase? (2)
* What does it decrease in the GI tract?

A

Decreases gluconeogenesis in the liver
* Decreases glucose production

Moves the glucose transporter protein GLUT4 from inside the cell to the plasma membrane
* Increasing glucose uptake into cells
* Increasing insulin sensitivity

Decreases glucose absorption for the GI tract

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30
Q

Metformin
* Historically what?
* Only medication recommended to prevent what?
* Safe and what?
* Does not cause what?

A
  • Historically, first-line therapy for most patients with T2DM with no specific contraindications
  • Only medication recommended to prevent onset of T2DM
  • Safe and well tolerated
  • Does NOT cause hypoglycemia
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31
Q

Metformin
* May reduce what?
* No effect on what?
* Excellent what?
* Easy what?
* Priced?

A
  • May reduce major adverse cardiovascular events (MACE)
  • No effect on diabetic kidney disease
  • Excellent long-term effectiveness
  • Easy regimen
  • Moderately priced
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32
Q

Metformin
* How is it dosed?
* Take with what?
* What is the inital dose?
* What is the usual dose?

A
  • Slow titration necessary to improve GI tolerance
  • Taking with food improves GI tolerance
  • Initial dose: 500 mg PO daily or BID, OR 875 mg daily, titrate every 7 days by 500mg or 875mg increments to maximum tolerated dose
  • Usual dose: 875mg or 1000mg PO BID
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33
Q

Biguanides:
* How much does it decrease the A1C?
* What is the MOA?
* What are the effects?

A
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34
Q

Biguanides:
* Weight change?
* What are the SE?
* What is the BBW?

A
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35
Q

Metformin
* What increases risk of acute kidney injury?
* Decrease in kidney function causes what?

A
  • Administration with iodinated contrast agents increases risk of acute kidney injury
  • Decrease in kidney function – increased risk of lactic acidosis
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36
Q

Metformin
* Most guidelines recommend holding metformin when?
* Serum creatinine reassessed when?
* Resume metformin when?

A
  • Most guidelines recommend holding metformin at the time of contrast administration; especially patients with reduced GFR (CrCl < 45 ml/min/1.73m2)
  • Serum creatinine reassessed in 48 hours after contrast administration
  • Resume metformin if serum creatinine acceptable
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37
Q

Sodium-glucose co-transport 2 inhibitors
* How much does it decrease A1C?
* What is the MOA?
* What are the effects?

A
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38
Q

Sodium-glucose co-transport 2 inhibitors
* What is the weight effect?
* What are the SE?

A
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39
Q

Sodium-glucose co-transport 2 inhibitors
* Effectiveness decreases with what?
* Specific agents shown to decrease what?

A
  • Effectiveness decreases with reduction in renal function
  • Specific agents shown to decrease atherosclerotic CV morbidity and mortality
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40
Q

Incretin mimetics (GLP-1 agonists)
* What is incretin? What does it stimulate?

A
  • Incretin is a metabolic hormone secreted by gut in response to food
  • Stimulates pancreas to produce more insulin
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41
Q

Incretin mimetics (GLP-1 agonists)
* Two endogenous incretins is rapidly inactivated by what?
* What are the two molecules triggered after food?
* Synthetic GLP-1RA is resistant to what?

A

Two endogenous incretins – rapidly inactivated by dipeptidylpeptidase-4 (DPP4)
* Glucose-like peptide -1 (GLP-1)
* Glucose-dependent insulinotropic polypeptide (GIP)

Synthetic GLP-1RA – resistant to DPP-4

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42
Q

Incretin mimetics (GLP-1 agonists)
* How much does the A1C decrease?
* What is the MOA?
* What are the effects?

A
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43
Q

Incretin mimetics (GLP-1 agonists)
* Weight loss?
* What are the SE?

A
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44
Q

Tirzepatide (Mounjaro)
* First what?
* Activated both what?
* Increased what?
* Decreased what?

A
  • First dual GIP and GLP-1 receptor agonists
  • Activates both incretin receptors
  • Increased weight loss compared to GLP-1 RA
  • Decreased weight 9.6 to 11.6%
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45
Q

Tirzepatide (Mounjaro)
* Decrease what?
* Limited data on what?
* SE similar to what?
* Once what?

A
  • Decreased A1C by 1.55 to 1.57%
  • Limited data on cardiovascular or renal effects
  • Adverse effects similar to GLP-1 RA
  • Once weekly SQ injection
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46
Q

Goal: Cardiorenal risk reduction
* What do you give for ASCVD or high risk for ASCVD?

A
  • GLP-1RA or SGLT2i with proven benefit
  • Add agent in alternative class if A1C above target or Thiazolidinedione
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47
Q

Goal: Cardiorenal risk reduction
* What do you give for heart failure?

A

First-line: SGLT2i with proven benefit

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48
Q

Goal: Cardiorenal risk reduction
* What is first line (what does patient have to have?) and second line (what should be added)?

A

First-line: SGLT2i with proven benefit
* Patients should have an eGFR ≥ 20 ml/min/1.73m2

Second-line: GLP-1RA with CVD benefit if SGLT2i not tolerated or contraindicated
* GLP-1RA should be added for patients not at A1C goal on a SGLT2i

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49
Q

Goal: Glycemic and weight management
* What is first line for glycemic management?

A

First-line: metformin or other agents with high likelihood of achieving glycemic goals

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50
Q

Glycemic management
* High efficacy for what?
* May require what?
* Should avoid what?

A
  • High efficacy for decreasing A1C
  • May require combination therapy
  • Should avoid hypoglycemia in high-risk patients
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51
Q

Weight management
* What do you do first?
* Choice medication with what?

A
  • Lifestyle modifications / non pharmacotherapies
  • Choose medications with high to very-high glucose and weight lowering efficacy
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52
Q
A
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53
Q

DPP-4 Inhibitors
* How much does it lower the A1C?
* What is the MOA?
* What are the effects?

A
54
Q

DPP-4 Inhibitors
* How does it effect weight?
* What are the SE?

A
55
Q

Thiazolidinediones
* How much does it decrease A1C?
* What is the MOA?
* What are the Effects?

A
56
Q

Thiazolidinediones
* What is the weight effect?
* What are the SE? (4) BBW? CI?

A
57
Q

Hypoglycemics
* Glucose enters where?
* What happens to the glucose?
* Accumulation of ATP inhibits what?
* What does that block?
* What is triggered?
* Increased what?

A
  • Glucose enters pancreatic beta cells through glucose transporter 2 (GLUT2)
  • Intracellular glucose it is metabolized to ATP
  • Accumulation of ATP inhibits ATP sensitive K+ channels
  • Blocks K+ influx which causes cell membrane depolarization
  • Triggers activation of voltage-gated calcium channel and Ca++ influx
  • Increased intracellular Ca++ causes insulin containing vesicles to fuse to the cell wall and release insulin
58
Q

Hypoglycemics: Sulfonylureas
* How much does it decrease A1C?
* MOA?
* What is the Effect?

A
59
Q

Hypoglycemics: Sulfonylureas
* What is the weight effect?
* What are the SE?

A
60
Q

Hypoglycemics: Glinides
* How much does it decrease A1C?
* MOA?
* What is the Effect?

A
61
Q

Hypoglycemics: Glinides
* What is the weight effect?
* What are the SE?

A
62
Q
A
63
Q

Initial combination therapy
* When should dual combo therapy be started? Example of combo

A

Dual combination therapy should be considered for A1C > 1.5% above goal
* Ex: metformin + SGLT2i or other combo for A1C > 8.5%

64
Q

Initial combination therapy
* What should be considered as part of any combination regimen for severe hyperglycemia?

A

Insulin, GLP-1 RA, sulfonylurea, dual GIP and GLP-1 RA should be considered as part of any combination regimen for severe hyperglycemia

65
Q

Initial combination therapy
* GLP-1RA, SU, dual GIP/GLP-1 RA for who?
* GLP-1 RA and dual GIP/GLP-1 RA have decreased risk of what?

A

GLP-1RA, SU, dual GIP/GLP-1 RA – random blood glucose level ≥ 300 mg/dL or A1C > 10% without symptoms of hyperglycemia (polyuria, polydipsia, weight loss)
* GLP-1 RA and dual GIP/GLP-1 RA have decreased risk of hypoglycemia and favorable weight benefit
* May be cost prohibited

66
Q

Initial combination therapy
* Who should get insulin?

A

Insulin - random blood glucose level ≥ 300 mg/dL or A1C > 10% with symptoms of hyperglycemia

67
Q

Initial combination therapy
* Additional therapy should be added when?

A

Additional therapy should be added if A1C goal not obtained in 3 months

68
Q

Therapy adjustments
* Therapy should be constantly monitored how?

A
  • A1C every three months until stable
  • Intermittent CGM may be beneficial in patients difficult to control
69
Q

Therapy adjustments
* Escalation or de-escalation of therapy may be indicated when?(5)

A
70
Q
A
71
Q
A
72
Q
A
73
Q

Adjunct therapies / interventions: Decrease CV risk factors
* What is the leading cause of death?
* What should be stopped?
* What should be under control?

A
  • Atherosclerotic CVD leading cause of death
  • Smoking cessation
  • Blood pressure control
74
Q

Adjunct therapies / interventions: Decrease CV risk factors
* What should you manage? Goal based on what? What therapy?
* Would should be started for patients with ASCVD risks?

A

Cholesterol management
* Goal based on ASCVD risk
* Statin therapy

Aspirin – low dose for patients with ASCVD risks (81 to 162 mg/day)

75
Q

Which of the following oral hypoglycemic agents when used as monotherapy is most likely to cause hypoglycemia?
* Glipizide
* Metformin
* Pioglitazone
* Acarbose
* Canagliflozin

A

Glipizide

76
Q

Which of the following strategies promotes improved carbohydrate metabolism and is recommended for all Type 2 diabetic patients?
* Vegan diet
* Metformin
* Exercise
* Smoking cessation
* Glipizide

A

Exercise

77
Q

A 7-year-old child with a history of type 1 diabetes mellitus for 3 years presents for routine follow-up. The mother states that the child has been having nightmares and night sweats. Additionally, his average morning glucose readings have risen from an average of 100 mg/dL to 145 mg/dL over the past week. This child is most likely experiencing?
* Night terrors
* Somogyi effect
* Dawn phenomenon
* Growth spurt
* Honeymoon phase

A
  • Somogyi effect
78
Q

As part of the long-term management of a patient with type 1 diabetes mellitus, the glycosylated hemoglobin (HgbA1C) level should be ideally maintained at?
* < 6%
* <6.5
* <7%
* <7.5%
* <8%

A
  • <6%
79
Q

DM Type 1
* Destruction of what?
* No what? Must be what?
* Human insulin reproduced using what?

A
  • Destruction of insulin-producing pancreatic beta cells
  • No insulin production – must be replaced with exogenous insulin
  • Human insulin reproduced using recombinant DNA technology
80
Q

DM Type 1
* Amino acid sequence can also be what?
* Degraded where?

A
  • Amino acid sequence can also be altered to make analogs with variable onsets and durations of action
  • Degraded in GI tract – requires SC or IV or inhaled administration
81
Q

Insulin – history lesson
* When and who it is discovered from?
* When and how was it given to a dying boy?
* Eli lilly begin what?
* When was the first genetically engineered?

A
  • 1921 - first discovered from a dog pancreas
  • 1922 – refined insulin product from cow given to 14-year-old dying boy
  • 1922-1923 – Eli Lilly began mass production – cow and pig based
  • 1978 – first genetically engineered human insulin “Humulin”
82
Q

Insulin comparison
* What are the three main classes?

A
  • Rapid / short acting
  • Intermediate acting
  • Long acting
83
Q

Insulin comparison
* Regular insulin likes to do what?
* Six insulin subunits too large to do what?
* Rapid acting analogs have what? What do they not do? Faster what?

A
  • Regular insulin likes to group together in hexamers
  • Six insulin subunits too large to move from the subcutaneous tissue to the blood stream
  • Rapid acting analogs have altered amino acid sequences
    * Do not aggregate as hexamers
    * Faster absorption
84
Q

Insulin comparison: Intermediate acting?
* What is added to regular insulin?
* Less what?
* Delayed what?

A
  • Zinc and protamine added to regular insulin
  • Less soluble complex
  • Delayed absorption and longer duration of action
85
Q

Insulin comparison: Long acting
* Modification of insulin molecule to what?
* Detemir-
* Binds to what?
* Still has what?
* Duration?

A
  • Modifications of insulin molecule to prolong duration of absorption
  • Detemir – addition of fatty acid side chain
    * Binds to albumin and slows release into the blood stream
    * Still has peak effect
    * Shortest duration
86
Q

Insulin comparison: long acting
* Glargine-
* Forms what?
* Slowly does what?
* No what?

A

Glargine – low solubility at neutral pH
* Forms precipitate in subcutaneous tissue
* Slowly releases insulin into blood stream
* No peak

87
Q

Insulin comparison: long acting
* Degludec-
* Forms what?
* No what?
* Duration?

A

Degludec – forms long chains of hexamers in subcutaneous tissue
* Forms depot from which insulin is slowing and continuously released
* No peak
* Longest duration of action

88
Q
A
89
Q
A
90
Q

Administration of insulin
* Proper administration optimies what?
* Inject where? What should you do to prevent liphypertrophy?
* _ Technique
* What delivery?
* Caregivers should regularly inspect what?

A
  • Proper administration optimizes glucose control and safety
  • Injection into appropriate sites
  • Injection site rotation – prevent lipohypertrophy
  • Aseptic technique
  • Subcutaneous delivery – not IM
  • Caregivers should regularly inspect injection sites for complications
91
Q

What is lipohypertrophy?

A

subcutaneous fat accumulation in response to adipogenic actions of insulin; development decreases insulin absorption at the site

92
Q

What are different ways of Delivery of sq injections?

A
  • Subcutaneous injections
  • Syringes / pens
  • Continuous subcutaneous insulin infusion (CSII)
  • Sensor augmented
  • Hybrid closed loop
93
Q

Monitoring T2D:
* Frequency dependent of what?
* Used most with what?
* What may not regularly monitor?

A
  • Frequency dependent of tightness of control / use of insulin
  • Used most with insulin initiation or changes to therapy
  • Patients with A1C at goal on a basal insulin may not regularly monitor
94
Q

Monitoring T1D:
* What are typical times?

A

Typical times – before meals, bedtime, or exercise; hypoglycemia possible

95
Q

Capillary glucose monitors vs continuous monitors
* Continuous monitoring: improve and reduce what? Various types?

A

Continuous monitors
* Improve A1C levels / reduce hypoglycemia
* Various types – real time, intermittently scanned, professional

96
Q

Type 2 DM-Insulin dosing
* Initial what? What are the options?

A

Initial once daily therapy
* Bedtime NPH or
* Long-acting insulin

97
Q

Type 2 DM
* What do you give if A1C goals not met?
* Begins to mimic what?

A
  • Prandial insulin or BID NPH if A1C goals not met
  • Begins to mimic insulin dosing for Type 1 DM
98
Q

Insulin dosing - T1D
* Initial therapy? Requires what?

A

Initial therapy intensive
* Requires comprehensive multidiscipline counseling and education

99
Q

Type 1 DM
* What type of insulin?
* What counting?
* What type of correction?
* Multiple what? How?

A
100
Q

Initial insulin dosing Type 2 DM
* Initial therapy to augment what? What are the types?

A

Initial therapy to augment oral regimens (* DC sulfonylureas)
* (insulin) NPH-> bedtime dosing recommended, glargine, detemir, degludec

101
Q

Initial insulin dosing Type 2 DM
* What should be the dose?
* Titrate dose based on what?
* Increase by what?
* What is Usual target FBG?

A

10 units/day or 0.1 to 0.2 units/kg/day given once daily
* Titrate dose based on fasting blood glucose
* Fasting = just prior to meal
* Increase by 2 to 4 units every 3 days unit target FBG met
* Usual target FBG: 80 to 130 mg/dL or individualized number

102
Q

Initial insulin dosing Type 2 DM
* Dose reduction may be necessary for what?
* If FBG not controlled with 0.7 to 1 units/kg basal insulin and/or A1C not improved at 3 months, what needs to be added? May alternately increase what?

A
103
Q

Insulin dosing – Type 1 DM
* Tight glucose control improves what?

A

Tight glucose control improves A1C and long-term microvascular and macrovascular outcomes
* Microvascular – neuropathy, nephropathy, retinopathy
* Macrovascular – MI, stroke, CAD

104
Q

Insulin dosing – Type 1 DM
* what does the Study spanning over 11 years in patients with T1DM show?
* Insulin increases the risk of what?

A

Study:
* 42% reduction in risk of cardiovascular disease
* 57% reduction of MI, stroke, or death from cardiovascular disease

Increases risk of hypoglycemia

105
Q

First calculate total daily and total basal insulin dose
* how do you do that? Example of 80kg patient?

A
106
Q

Insulin Dosing Type 1 DM
* How do you calciulate carbohydrate coverage ratio?

A
  • 1 unit of insulin generally disposes of 12 to 15 grams of carbohydrates
  • Variable, patient dependent
107
Q

Insulin Dosing Type 1 DM
* How do you calculate for initial carbohydrate overage ratio?

A
108
Q

Insulin Dosing type 1 DM
* How do you Calculate high blood sugar correction factor (sliding scale)?

A
  • Correction factor = 1800 ÷ total daily insulin dose = blood sugar reduction (mg/dL) estimation from 1 unit insulin
  • Example: 1800 ÷ 40 units = 45 (round to 50 units for ease of calculation)
109
Q

Each 1 unit of insulin will reduce blood glucose by what?

A

Each 1 unit of insulin will reduce blood glucose by 50 mg/dL (Given as ultra rapid insulin)

110
Q

Based off of Correction factor of 45 (round to 50 units for ease of calculation), how does the sliding scale work?

A
  • FBG > 150 to 200 – give 1 unit
  • FBG 201 to 250 – give 2 units
  • FBG 251 to 300 – give 3 units
  • FBC 301 to 350 – give 4 units
  • FBG > 350 give 5 units
111
Q

Insulin Dosing type 1
* Put all the calculation we previously did together?

A
  • Basal dose: 20 units – long-acting insulin or pump (e.g., insulin glargine)
  • Carb ratio: 1 unit / 12 grams carbs; rapid acting (e.g., insulin lispro)
  • Correction per sliding scale (1 unit per every 50 above 150): rapid acting
  • BG levels monitoring continuously or pre-meals and at bedtime
112
Q

Sick day insulin
* May require more what?
* Increase frequency of what?
* DO NOT do what?

A
  • May require more insulin
  • Increase frequency of blood glucose testing
  • DO NOT discontinue insulin
113
Q

Sick day insulin
* How should a patient be prepared?

A
  • Know how to contact provider
  • Check urine for ketones if dehydration suspected
  • Have quick acting carbohydrate source / glucagon available
  • Attempt to intake sugar-free fluids
114
Q
A
115
Q

Caring for elderly patient with dM
* Patients > 65 years - goals dependent on what?
* A1C goal for Healthy older adults with life expectancy > 10 years?
* A1C goal for Older adults with significant comorbidities (frail, life expectancy < 10 years)?
* A1C goal for Older adults with poor health?

A
116
Q

Caring for elderly patient with dM
* What should you avoid and why?

A

Avoidance of hypoglycemia
* Increased risk of falls, missed diagnosed as stroke, cognitive decline

117
Q

Caring for the Pregnant Diabetic Patient
* Tight glycemic control to what?
* Poor control in early pregnancy =
* Poor control in late pregnancy =

A

Tight glycemic control to normal HbA1c (< 6 to < 6.5) – while preventing hypoglycemia
* Poor control in early pregnancy = increased risk of spontaneous abortion and congenital malformations (cardiac)
* Poor control in late pregnancy = increased risk of pre-term labor, preeclampsia, stillbirth

118
Q

Caring for the Pregnant Diabetic Patient
* Frequent what?
* What is the txt?

A
  • Frequent monitoring of blood sugar monitoring recommended
  • Treatment: Diet and insulin preferred
119
Q

Caring for the hospitalized patient with DM
* What will be adjusted?
* What does surgery cause?
* Always check what?
* Avoid what?

A
  • Outpatient regimens will have to be adjusted
  • Surgery typically results in hyperglycemia
  • Always check renal function prior to restarting outpatient metformin
  • Avoid NSAIDs (other than ASA) in diabetics
120
Q
A
121
Q

Hypoglycemia
* What is the blood glucose level?
* What do you need to education on?
* What is the risk reduction?

A
  • Blood glucose level < 70 mg/dL
  • Education – symptoms of hypoglycemia
  • Risk reduction – adjusting medication / insulin regimen to reduce risk
122
Q

Hypoglycemia
* What are the MCC (3)
* Drug induced? (1)

A

Most common causes
* Sulfonylureas
* Using insulin without eating
* Insulinoma

Drug induced: fluoroquinolones

123
Q

Hypoglycemia treatment

A
124
Q

Hypoglycemia treatment
* What are the quick carbohydrate sources?

A
125
Q

Glucagon
* What is the MOA?
* What are the SE?

A
126
Q

What are two of the most serious acute complications of diabetes?

A

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, aka hyperosmotic hyperglycemic nonketotic state or hyperosmolar nonketotic state [HHNK/HONK]) are two of the most serious acute complications of diabetes

127
Q

DKA is characterized by what? HHS?
* Which one affects T1D and T2D?

A

DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia with volume depletion but no ketoacidosis
* DKA – primarily affects DM1
* HHS – primarily affects DM2

128
Q

For both DKA and HHS-The most common events are what?
* Compromised water intake due to what?

A

For both DKA and HHS-The most common events are infection (often pneumonia or urinary tract infection) and discontinuation of or inadequate insulin therapy.
* Compromised water intake due to underlying medical conditions, particularly in older patients, can promote the development of severe dehydration and HHS.

129
Q

DKA treatment summary
* First what?
* Obtain what?
* Give what? Dose?
* Add dextrose when?

A
130
Q

DKA treatment summary
* Replete what?
* Give what until DKA resolves? Start after what?
* Monitor what?
* What should be done every 2 hours?

A
131
Q
A

Pharm II (14 decks)

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