Diabetes Flashcards
Diabetes Mellitus is characterized by what?
Presence of hyperglycemia…
The presence of hyperglycemia can be due to what?
1) Defective Insulin Secretion
2) Defective Insulin Action
3) Both
What are some medical complications that can arise from Diabetes Mellitus?
-CVD
-Kidney Disease
-Blindness
-Neuropathy
-Amputation
What percentage of Diabetics die from either heart disease or stroke?
80%
By how many years can unregulated Diabetes shorten one’s lifespan?
5-15yrs
Three types of Islet Cells in the Pancreas? What % of total Islet Cells do they each comprise?
1) Delta (10%)
2) Alpha (30%)
3) Beta (60%)
What do each of the three Islet Cell types produce?
Delta: Somatostatin
Alpha: Glucagon
Beta: Insulin / Amylin
Glucagon release from Alpha Cells is stimulated by what?
Low blood glucose
Insulin release from Beta Cells is stimulated by what?
High blood glucose
What actions do Insulin have on the following organs / tissues:
Liver
Adipose Tissue
Skeletal Muscles
Liver: Increase Glycogenesis (new Glycogen production) & decrease Gluconeogenesis.
Adipose Tissue / SM: Increase Glucose uptake from blood.
What actions does Glucagon have on the Liver?
Increase Glycogenolysis (Glycogen Breakdown) & increases Gluconeogenesis.
What triggers Insulin secretion?
1) Increased Blood Glucose
2) Increased Serum Amino Acids
3) Increased Serum Free Fatty Acids
4) Glucagon
5) Growth Hormone
6) Cortisol
7) GIP
What triggers Glucagon secretion?
1) Decreased Serum Glucose
2) Decreased Serum AA’s
3) E + NE
What functions do Skeletal Muscles carry out when stimulated by Insulin?
Increased Protein Synthesis & Glycogenesis
What function does Adipose Tissue carry out when stimulated by Insulin? By Glucagon?
I: Increased Lipogenesis
G: Increased Lipolysis
How do our Adipose Tissues combat excessive carbohydrate intake?
-When Glycogen stores are full, convert excess carbs to Free Fatty Acids & stores them as TG’s.
What happens to TG stores in a situation of starvation?
-Split into Glycerol + FFAs… FFAs are metabolized into Ketone Bodies, which themselves are used as an energy source.
Approximately what percentage of total bodily Glucose is utilized by the Brain?
~20%
How is T1DM characterized?
Complete lack of Insulin secretion (usually due to Beta Cell destruction)
What types of immune destructive markers are typically seen with T1DM?
1) Islet Cell Antibodies
2) Insulin Antibodies
3) Glutamic Acid Decarboxylase Antibodies
What are the peak ages of T1DM diagnoses?
13-14yrs (most cases take place before 25yrs)
At what percentage of Beta Cell destruction do we see Hyperglycemia in T1DM patients?
80-90% destruction
I’m a recently diagnosed T1DM patient (3wks ago). I’ve began receiving Insulin injections & my lab results show that my Insulin secretion has improved ever so slightly. What describes this phenomenon?
“Honeymoon Phase”… Initial improvements to Insulin secretion that occur when hyperglycemia is corrected.
Are “Honeymoon Phase” improvements in T1DM patients permanent?
NO (!!!)… This is a transient period that lasts up to a couple months post-Insulin initiation & hyperglycemic correction.
Within what concentration (in mmol / L) would somebody be diagnosed with Impaired Fasting Glucose (IFG)?
6.1 - 6.9
Within what concentration (in mmol / L) would somebody be diagnosed with Impaired Glucose Tolerance (IGT)?
2hr Plasma Glucose reading of 7.8 - 11.0
What percent Glycolated Hemoglobin (A1C) would one have to be diagnosed with Prediabetes?
6.0 - 6.4
What percentage of total Diabetes Mellitus cases are T1? T2?
T1DM: 10%
T2DM: 90%
How does T2DM manifest?
-Initial Insulin Resistance followed by a loss of one’s ability to produce Endogenous Insulin (as the body is trying to compensate for a loss of Insulin responsiveness).
Risk Factors for T2DM?
-Over 40yrs age
-1st degree relative with T2DM
-High Risk Population (ie. African, Arab, Asian, Indigenous)
-Obese
-History of Gestational Diabetes / Prediabetes / Large Infant birthweight
Other T2DM Risk Factors?
-CV / Microvascular damage
-Vascular Risk Factors (ie. Low HDL, High TG, HTN, Smoker, Obese)
-Acanthosis Nigricans / PCOS / Obstructive Sleep Apnea / HIV / Gout / Non-Alcoholic Steatohepatitis / Pancreatitis / CF / Psych Illnesses
-Certain Medications
What are some medications that may increase blood glucose?
-5-FU
-Beta Blockers
-Corticosteroids
-Statins
-Immunosuppressants
-Niacin
-Pasireotide
-Protease Inhibitors
-Thiazides / LDs
-Antipsychotics
At what organ do we see Primary Insulin Resistance?
Skeletal Muscle (as it’s the primary Glucose disposal site after a meal).
If I’m Insulin Resistant, how does my Liver respond?
Unregulated Hepatic Glucose production (because Insulin normally suppresses the process of Gluconeogenesis).
If I’m Insulin Resistant, how does my Adipose Tissue respond?
Increased Lipolysis (leading to more FFAs).
What kinds of acute symptoms might T1DM patients present with?
-Polyuria (increased urination)
-Polyphagia (increased hunger)
-Polydipsia (increased thirst)
-Weight Loss
-Fatigue
-Blurred Vision
-Infection
20-40% of T1DM patients present with what after several days of experiencing acute clinical symptoms?
Diabetic Ketoacidosis
Symptom Onset: How do they differ between T1DM & T2DM?
T1DM: Abrupt & Symptomatic
T2DM: Gradual & often Asymptomatic
Weight Presentation: How do they differ between T1DM & T2DM?
T1DM: Usually thin
T2DM: > 90% Obese
Colton is a recently diagnosed 30yr old Diabetic patient who presents with elevated C-Peptide levels & both Diabetic Retinopathy and Diabetic Nephropathy. What form of Diabetes Mellitus does he likely have?
T2DM
-Elevated C-Peptide suggests Insulin levels being secreted are high & microvascular complications at diagnosis are present with T2DM.
T or F: Gestational Diabetes is more common in Indigenous women than other ethnicities.
True… 8-18% of Indigenous Women affected (vs. 4% other).
Between what weeks of pregnancy should women be screened for Gestational Diabetes?
24-28wks (or even earlier if risk factors are present)
T or F: Screening Tests used to diagnose T1DM & T2DM differ from one another.
False… The exact same tests are used to screen & diagnose.
What initial screening tests should be used to diagnose those who might have T2DM?
FPG or A1C
Carter is a 41yr old who presents with a FPG reading of 5.6mmol / L and an A1C of 5.5%. How often should he be screened for T2DM?
Every 6-12mths
-As he is considered at risk for developing T2DM with these FPG / A1C readings.
Adam is a 41yr old who presents with a FPG reading of 5.5mmol / L and an A1C of 5.4%. How often should he be re-screened for T2DM?
Every 3yrs
-As these FPG & A1C readings are not associated with being more at risk for T2DM development.
Cole is a 41yr old who presents with an FPG reading of 7.1mmol / L & an A1C of 6.6%. How often should he be re-screened for T2DM?
Doesn’t need to… Those readings (above 7.0 mmol / L & 6.5%) suggest that he has T2DM!
An FPG above 7.0mmol / L, an A1C above 6.5%, and a 2hr PG reading [in a 75g OGTT] above what indicate a positive Diabetes diagnosis?
Above 11.1mmol / L
Which patient types would we want to avoid conducting A1C tests on for Diabetes Screening purposes?
-Gestational Diabetes
-Kids
-Suspected T1DM Pt’s
-Anemic Pt’s
-Hemoglobinopathy Pt’s
A1C vs. FPG: Which one is better at predicting Cardiovascular Disease?
A1C
FPG vs. A1C vs. 2hr PG 75g OGTT tests: Which ones are costly?
A1C & 2hr PG are costly to conduct.
Over what length of time is A1C monitored for?
Previous 3mths
What exactly is A1C looking at?
% of Hemoglobin A that is irreversibly Glycosylated
What is a normal A1C?
4 - 6%
What processes tied to Erythropoiesis may raise one’s A1C?
-Vit. B12 / Iron Deficiency
-Reduced Erythropoiesis
What processes tied to Erythropoiesis may decrease one’s A1C?
-Use of Erythropoietin
-Supplementation with Iron / Vit. B12
-Chronic Liver Disease
Johnny is an elderly patient on low dose Aspirin for cardioprotection, as well as Vitamins C & E. How might his A1C percentage show up in lab readings (relative to normal percentages)?
DECREASED
-Vit. C & E, as well as Aspirin, contribute to a reduced A1C percentage.
Catherine recently underwent a surgical procedure that saw her Spleen get taken out. She is additionally Diabetic & requires regular monitoring of her A1C. She recently went in for a check-up & her Dr. noticed a spike in her A1C. In what direction (increased or decreased) would her A1C percentage likely move towards?
INCREASED
-Splenectomies can actually raise A1C counts.
Shivani is an elderly patient from India who was recently prescribed Dapsone (an Antibiotic) to treat a recent Leprosy diagnosis. She also presents with Rheumatoid Arthritis & is a Type II Diabetic. Her Dr. notices recent changes to her A1C in a recent checkup. How might those changes present (ie. Increased or Decreased A1C)?
DECREASED
-Dapsone usage & Rheumatoid Arthritis have shown to decrease A1C.
Philip is a Type II Diabetic in Palliative Care at St. Paul’s. He has Chronic Kidney Failure due to old age, utilizes Fentanyl patches to mask excruciating back pain, and has recently been diagnosed with Hyperbilirubinemia due to a Gall Bladder blockade. If we compared his A1C from 15yrs ago to now, how might it present differently today?
INCREASED (GREATLY) !!!
-Hyperbilirubinemia, Chronic Opiate Use, & Chronic Renal Failure can all contribute to an elevated A1C.
The majority of Type I or Type II Diabetics should aim for an A1C of less than what?
< 7.0%
Kimmy is a 35yr old female patient who presents with Type II Diabetes. She has a currently measured A1C of 7.2 and no history of going Hypoglycemic since she was diagnosed 5yrs ago. She is about 35lbs overweight but is otherwise healthy in terms of clinically diagnosed conditions. What would be a realistic A1C target for her?
< 6.0 (as lifestyle modifications are a realistic goal of therapy and could even allow her to remiss to normoglycemia).
Corey is a 50yr old Type II Diabetic with an elevated A1C of 7.4. Although diagnostically rare, his mother and his brother Trevor have a history of Genetic Retinopathies. Knowing this information, what would be a realistic A1C target for Corey to try to obtain?
< 6.5 (as slightly more aggressive A1C targeting beyond 7.0 reduces the risk of CKD & Retinopathies greatly).
Gertrude is an elderly Type II Diabetic patient with Dementia and a history of recurrent fainting episodes due to going Hypoglycemic. What would be a realistic A1C target for her to achieve?
Between 7.1 - 8.5
An A1C of 5% equates to what average Blood Glucose readings?
97 mg / dL
5.4 mmol / L
An A1C of 6% equates to what average Blood Glucose readings?
126 mg / dL
7.0 mmol / L
An A1C of 7% equates to what average Blood Glucose readings?
154 mg / dL
8.6 mmol / L
An A1C of 8% equates to what average Blood Glucose readings?
183 mg / dL
10.2 mmol / L
An A1C of 9% equates to what average Blood Glucose readings?
212 mg / dL
11.8 mmol / L
An A1C of 10% equates to what average Blood Glucose readings?
240 mg / dL
13.4 mmol / L
An A1C of 11% equates to what average Blood Glucose readings?
269 mg / dL
14.9 mmol / L
An A1C of 12% equates to what average Blood Glucose readings?
298 mg / dL
16.5 mmol / L
What were the major findings of the 1993 DCCT trial for Type I Diabetics?
-Intensive targeting of an A1C of < 7.0 (via more frequented daily Insulin injections, increased Diabetes education & more frequented Dr. visits) led to a large decrease in the risk of patients experiencing Retinopathy, Neuropathy, & Microalbuminuria.
What were the major findings of the UKPDS Trials for Type II Diabetics?
-More aggressive A1C targeting of < 7.0% saw sustained relative risk reductions for suffering Microvascular-related complications even at 10yr follow-up.
-Obese patients on Metformin demonstrated decreased Macrovascular complication experiences.
What negative findings were discovered from the ACCORD Trial that caused it to be prematurely stopped at 3.5yrs?
-Further intensive targeting of an A1C of < 6% saw a substantial increase in the prevalence of all-cause death, as well as a greatly increased incidence of Hypoglycemia.
Propose a Self-Monitoring Blood Glucose strategy for somebody on solely NPH or Long-Acting Insulins.
-Once Daily before Breakfast (as these analogues are typically administered at bedtime).
Propose a Self-Monitoring Blood Glucose strategy for somebody on Premixed Insulins that are delivered prior to Breakfast & Supper (ie. BID).
-QID monitoring (ie. Prior to meals & bedtime) until Glycemic targets are met.
-Alternate BID monitoring once Glycemic targets are met.
Propose a Self-Monitoring Blood Glucose strategy for somebody on TID delivered RAA’s or Bolus Insulins & a OD NPH or LAIA.
1) QID readings (ie. Prior to meals & bed).
2) QID readings with a focus on readings Post-Prandially.
3) Intensive Management with readings being taken prior to & after meals.
How do Real-Time Continuous Glucose Monitoring scanners differ from Intermittently Scanned CGM tools such as a Libra?
-Location (RTCGM on Abdomen / Upper Butt / Back of Arm… ISCGM on Back of Arm).
-Frequency of Scans (Every 5mins for RTCGM vs. Every 15mins for ISCGM).
-When to Replace Sensor (10d for Dexcom vs. 14d for Libra).
People with Diabetes should aim to have a “Time in Range” for approximately how many hours each day?
~17hrs (as this equates to 70% of the day spent in a desired Blood Glucose range of 3.9 - 10.0 mmol / L & is approximately equal to an A1C of 7%).
How does the desired “Time in Range” differ for those who are at high risk of suffering from Hypoglycemia or are elderly?
> 50% (which equates to >/= 12hrs / day spent in the desired 3.9 - 10.0 mmol / L target range).
If a patient presents with symptoms of DKA, is Pregnant, or is a Type I Diabetic with elevated Preprandial BG readings above 14mmol / L, what would be a more appropriate test to conduct as opposed to a BG reading?
Urine / Blood Ketone Testing
Examples of popular diets that can be used as lifestyle modification tools to treat Type I or Type II Diabetes include what?
-Mediterranean Diet
-Vegan / Vegetarian Diets
-Low Carb Diets
-DASH
-Intermittent Fasting
On average, what percentage of a typical Canadian’s diet should be comprised of Carbohydrates?
45-60%
On average, what percentage of a typical Canadian’s diet should be comprised of Proteins?
10-35%
On average, what percentage of a typical Canadian’s diet should be comprised of Fats?
20-35%
For a 19-50yr old, what is the recommended DRI for Fibre intake?
W: 25g / day
M: 38g / day
For someone over the age of 50, what is the recommended DRI for Fibre intake?
W: 21g / day
M: 30g / day
Why must one subtract their Soluble Fibre from Total Carbohydrate counts?
-Because Soluble Fibre is a form of Carb that the body is unable to digest.
Why is it extremely important for Type I / Type II Diabetics to monitor their Alcohol consumption?
-Alcohol consumption can reduce Hepatic Glucose production & can mask Hypoglycemic symptoms.
How do Low-Intensity Aerobic exercises & High-Intensity Anaerobic exercises differ in terms of their effects on Blood Glucose concentrations?
Low Intensity: Reduces Blood Glucose (increases Insulin sensitivity).
High Intensity: Increases Blood Glucose (due to muscular demand increases & increased stress hormone secretion).
At what Blood Glucose levels should a Diabetic avoid exercising?
< 4mmol / L
Where was Insulin historically derived from?
Cow / Pig Pancreases
What was the 1st human Insulin analogue ever created (‘82)?
Humulin
What RAIA’s are commercially available?
Aspart (Brand Name = NovoRapid / Fiasp)
Glulisine (Brand Name = Apidra)
Lispro (Brand Name = Humalog)
Faster-Acting Aspart
What Short-Acting Insulins are commercially available?
Insulin Regular U-500 (Brand Name = Entuzity)
Insulin Regular (Brand Name = Humulin)
Onset, Peak & Duration of Action of Rapid Acting Insulin Analogues (RAIAs)?
O: 4-20mins
P: 0.5-2hrs
D: 3-5hrs
Onset, Peak & Duration of Action of Short-Acting Insulins?
O: 30mins
P: 2-3hrs
D: 6hrs
When should one take a Short Acting Insulin (ie. How long prior to a meal)?
30-45mins prior to meals.
When should one take a RAIA (ie. How long before a meal)?
0-15mins prior to meal (or within 15mins of beginning to eat).
What makes a RAIA better than a Short-Acting Insulin Analogue?
-Faster Onset of Action (4-20mins vs. 30mins)
T or F: RAIAs are more expensive than Short-Acting Insulin Analogues.
True!
How does Insulin Regular U-500 differ from Insulin Regular (ie. Humulin) in terms of its onset, peak, & duration of action?
O: 15mins (vs. 30mins)
P: 4-8hrs (vs. 2-3hrs)
D: 17-24hrs (vs. 6hrs)
How many times a day should Insulin Regular U-500 be delivered each day?
2-3x
The onset of action, peak, & duration of action of Intermediate-Acting Basal Insulin (ie. Insulin NPH) is what?
O: 1-3hrs
P: 5-8hrs
D: Up to 18hrs
The onset of action of the three Long-Acting Insulins (ie. Detemir, Glargine, Degludec) is what?
O: 90mins
The duration of action of U-100 Glargine is what?
D: 24hrs
The duration of action of U-100 Detemir is what?
D: 16-24hrs
The duration of action of U-300 Glargine is what?
D: >30hrs
The duration of action of U-100 & U-200 Degludec is what?
D: 42hrs
The onset, peak & duration of action of NPH Insulin is what?
O: 1-3hrs
P: 5-8hrs
D: Up to 18hrs
How often (per day) are NPH Insulins administered?
1-2x daily
Which Insulin appears cloudy?
NPH
What has made LAIAs more popular as of late than NPH Insulin?
-Lower risk of Hypoglycemia
-Narrowing price gap (even though LAIAs are slightly more expensive)
-Less Glucose variability
I’m on OD Lantus (ie. Glargine), dosed at 100U / mL. I’m planning on switching to either 300U / mL Glargine (Toujeo), 100U / mL Glargine (Basaglar), or Degludec (Tresiba). How would my dosing regimen change?
It doesn’t change!!!
I’m on BID Lantus (ie. Glargine), dosed at 100U / mL. Of the following options (300U / mL Toujeo, 100U / mL Basaglar, Degludec), which one(s) require dose modifications if I switch across Insulin brands?
Switch from Lantus to Degludec: Reduce overall daily dosing by 20%…
