Lecture 11 (Endocrine)-Exam 6

Question 1

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

Answer 1

• 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.

Question 2

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

Answer 2

• 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.

Question 3

Summary of Diabetes Mellitus
* What are the classic sxs?

Answer 3

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

Question 4

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

Answer 4

• 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

Question 5

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

Answer 5

• 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

Question 6

Type 1 DM
* What causes this disease?

Answer 6

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

Question 7

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

Answer 7

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

Question 8

⭐️

Answer 8

Question 9

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

Answer 9

• 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

Question 10

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

Answer 10

• 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.

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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)

Question 13

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

Answer 13

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

Question 14

What does the ambutatory glucose profile show?

Answer 14

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

What is first line therapy for T2D?

Answer 17

metformin and lifestyle modifications

Question 18

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?

Answer 18

• 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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

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

Question 21

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

Answer 21

• 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)

Question 22

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

Answer 22

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

Question 23

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

Answer 23

• 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

Question 24

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

Answer 24

• 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

Question 25

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

Answer 25

* 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

Question 26

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

Answer 26

* Impact on cardiovascular and renal comorbidities * Efficacy * Hypoglycemia risk * Impact on weight * Adverse effects * Cost / access * Patient preferences

Question 27

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

Answer 27

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

Question 28

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

Answer 28

* Metformin - only medication in class * Activates AMP dependent protein kinase (AMPK)

Question 29

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

Answer 29

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

Question 30

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

Answer 30

* **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

Question 31

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

Answer 31

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

Question 32

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

Answer 32

* 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

Question 33

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

Answer 33

Question 34

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

Answer 34

Question 35

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

Answer 35

* Administration with iodinated contrast agents increases risk of acute kidney injury * Decrease in kidney function – increased risk of lactic acidosis

Question 36

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

Answer 36

* 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

Question 37

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

Answer 37

Question 38

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

Answer 38

Question 39

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

Answer 39

* Effectiveness decreases with reduction in renal function * Specific agents shown to decrease atherosclerotic CV morbidity and mortality

Question 40

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

Answer 40

* Incretin is a metabolic hormone secreted by gut in response to food * Stimulates pancreas to produce more insulin

Question 41

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?

Answer 41

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

Question 42

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

Answer 42

Question 43

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

Answer 43

Question 44

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

Answer 44

* 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%

Question 45

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

Answer 45

* 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

Question 46

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

Answer 46

* GLP-1RA or SGLT2i with proven benefit * Add agent in alternative class if A1C above target or Thiazolidinedione

Question 47

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

Answer 47

First-line: SGLT2i with proven benefit

Question 48

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

Answer 48

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

Question 49

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

Answer 49

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

Question 50

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

Answer 50

* High efficacy for decreasing A1C * May require combination therapy * Should avoid hypoglycemia in high-risk patients

Question 51

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

Answer 51

* Lifestyle modifications / non pharmacotherapies * Choose medications with high to very-high glucose and weight lowering efficacy

Question 52

Answer 52

Question 53

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

Answer 53

Question 54

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

Answer 54

Question 55

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

Answer 55

Question 56

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

Answer 56

Question 57

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

Answer 57

* 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

Question 58

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

Answer 58

Question 59

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

Answer 59

Question 60

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

Answer 60

Question 61

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

Answer 61

Question 62

Answer 62

Question 63

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

Answer 63

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

Question 64

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

Answer 64

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

Question 65

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?

Answer 65

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

Question 66

Initial combination therapy * Who should get insulin?

Answer 66

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

Question 67

Initial combination therapy * Additional therapy should be added when?

Answer 67

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

Question 68

Therapy adjustments * Therapy should be constantly monitored how?

Answer 68

* A1C every three months until stable * Intermittent CGM may be beneficial in patients difficult to control

Question 69

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

Answer 69

Question 70

Answer 70

Question 71

Answer 71

Question 72

Answer 72

Question 73

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

Answer 73

* Atherosclerotic CVD leading cause of death * Smoking cessation * Blood pressure control

Question 74

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?

Answer 74

Cholesterol management * Goal based on ASCVD risk * Statin therapy Aspirin – low dose for patients with ASCVD risks (81 to 162 mg/day)

Question 75

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

Answer 75

Glipizide

Question 76

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

Answer 76

Exercise

Question 77

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

Answer 77

* Somogyi effect

Question 78

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%

Answer 78

* <6%

Question 79

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

Answer 79

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

Question 80

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

Answer 80

* 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

Question 81

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?

Answer 81

* 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”

Question 82

Insulin comparison * What are the three main classes?

Answer 82

* Rapid / short acting * Intermediate acting * Long acting

Question 83

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?

Answer 83

* 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

Question 84

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

Answer 84

* Zinc and protamine added to regular insulin * Less soluble complex * Delayed absorption and longer duration of action

Question 85

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

Answer 85

* 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

Question 86

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

Answer 86

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

Question 87

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

Answer 87

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

Question 88

Answer 88

Question 89

Answer 89

Question 90

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

Answer 90

* 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

Question 91

What is lipohypertrophy?

Answer 91

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

Question 92

What are different ways of Delivery of sq injections?

Answer 92

* Subcutaneous injections * Syringes / pens * Continuous subcutaneous insulin infusion (CSII) * Sensor augmented * Hybrid closed loop

Question 93

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

Answer 93

* 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

Question 94

Monitoring T1D: * What are typical times?

Answer 94

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

Question 95

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

Answer 95

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

Question 96

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

Answer 96

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

Question 97

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

Answer 97

* Prandial insulin or BID NPH if A1C goals not met * Begins to mimic insulin dosing for Type 1 DM

Question 98

Insulin dosing - T1D * Initial therapy? Requires what?

Answer 98

Initial therapy intensive * Requires comprehensive multidiscipline counseling and education

Question 99

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

Answer 99

Question 100

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

Answer 100

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

Question 101

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

Answer 101

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

Question 102

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?

Answer 102

Question 103

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

Answer 103

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

Question 104

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

Answer 104

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

Question 105

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

Answer 105

Question 106

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

Answer 106

* 1 unit of insulin generally disposes of 12 to 15 grams of carbohydrates * Variable, patient dependent

Question 107

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

Answer 107

Question 108

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

Answer 108

* 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)

Question 109

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

Answer 109

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

Question 110

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

Answer 110

* 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

Question 111

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

Answer 111

* 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

Question 112

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

Answer 112

* May require more insulin * Increase frequency of blood glucose testing * DO NOT discontinue insulin

Question 113

Sick day insulin * How should a patient be prepared?

Answer 113

* 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

Question 114

Answer 114

Question 115

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?

Answer 115

Question 116

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

Answer 116

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

Question 117

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

Answer 117

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

Question 118

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

Answer 118

* Frequent monitoring of blood sugar monitoring recommended * Treatment: Diet and insulin preferred

Question 119

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

Answer 119

* 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

Question 120

Answer 120

Question 121

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

Answer 121

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

Question 122

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

Answer 122

Most common causes * Sulfonylureas * Using insulin without eating * Insulinoma Drug induced: fluoroquinolones

Question 123

Hypoglycemia treatment

Answer 123

Question 124

Hypoglycemia treatment * What are the quick carbohydrate sources?

Answer 124

Question 125

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

Answer 125

Question 126

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

Answer 126

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

Question 127

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

Answer 127

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

Question 128

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

Answer 128

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.

Question 129

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

Answer 129

Question 130

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

Answer 130

Question 131

Answer 131