Lecture 22-35 Diabetes Flashcards

Question

What are administration sites in which insulin can be administered and how should site rotation be utilized and why?

Answer 1

Abdomen: absorption faster and much more consistent Lateral thigh: slower and variable absorption Upper arms: slower and variable absorption and challenging to reach Superior buttocks area: slowest absorption Rotation: divide abdomen into 4 areas and inject into one area for 1 week and move clockwise ⇒ separating each injection within the area by 2-3 cm ⇒ this is done to minimize risk of lipohypertrophy and maintains a consistent insulin absorption

Answer 2

A: look for lows FIRST - BG < 4 mmol/L, sx of hypoglycemia B: start the day well C: look for consistent highs - ex. exercise, skipped doses, extra meals? D: change ONE insulin by ONE or TWO units

Answer 3

usually happens at < 3.9 mmol/L Sx: sweating, anxiety, shaking, hunger, nausea, H/A, odd dreams, weakness/dizziness, vision changes, drowsiness, unconsciousness, etc Management: manage sx, check BG and confirm a low, consume 15 grams of a simple carb, recheck BG in 15 minutes ⇒ if < 4.0 mmol/L repeat 15 grams of simple carb, if > 4.0 mmol/L consume a snack that includes a protein

Answer 4

hypoglycemia,, weight gain lipohypertrophy - thickened area of tissue that develops because fat accumulates at injection site - release from injection is delayed and unpredictable, minimize risk by rotating injection sites lipoatrophy - loss of SC fat at injection site - possibly immune-mediated inflammatory response, rare since introduction of recombinant human DNA formulations

Answer 5

is 0.4-1.0 units/kg for the total daily dose try and round the kg weight to a workable number so its easier for the patient to administer also if doing a basal+bolus regimen we can do 40%-50% of the total daily insulin dose as a basal insulin and the remaining 50-60% as a bolus split up into three different times (20% for each meal)

Answer 6

Basal: cheapest is NPH but has highest risk of hypoglycemia, degludec is the most expensive but studies suggest it has lowest risk of hypoglycemia, glargine and detemir are also expensive Bolus: regular insulin is the cheapest but has slower onset and longer duration (higher chance of hypoglycemia), while aspart, glulisine and lispro are more expensive

Answer 7

avoid hypoglycemia (ex. multiple daily insulin injections, using drugs that cause hypoglycemia) confirm a low if someone is feeling sx of hypoglycemia assess medication response assess response food during changes in normal routine (exercise, alcohol, travel, drinking) during an acute illness during pregnancy

Answer 8

should be done at least 3 times per day and include both pre and postprandial levels in individuals with T2D using once daily insulin ⇒ check at least 1x per day at variable times individuals with T2D not using insulin ⇒ frequency should be individualized depending on hyperglycemic agents, A1c level and risk of hypoglycemia, if not at A1c target structures CBG checks achieving A1c target and antihyperglycemic med not associated with hypoglycemia then daily checking isn't recommended if A1c isn't being met in all pt then can check up to 4x daily (even a nightly one) rtCGM or isCGM can be used in T1D using basal-bolus tx or continuous SC insulin infusions ⇒ increases time in range (TIR), reduces duration and incidence of hypoglycemia (time below range (TBR)

Answer 9

Before: exercise not recommended if BG too low or high ⇒ should be > 4 mmol/L and < 14 mmol/L During: individuals will respond differently, changes in regimen (intensity, aerobic vs resistance, duration, timing, etc) will create changes in BG profile After: can fluctuate up to 24 hours later ⇒ delayed hypoglycemia may occur 6-12 hours after exercise, caused by muscle cells absorbing glucose to replenish glycogen stores - important to check BG especially if exercise regimen changed, may need to consider extra snack at bedtime

Answer 10

Low: walking, golf with cart, gardening, stretching, shopping ⇒ decrease bolus dose by 25-50% Moderate: brisk walk, mowing lawn, bike ride, raking, walking golf, swimming, tennis, skiing ⇒ decrease bolus dose by 50-75% High: competitive sports, shoveling snow, aerobics, jogging, hockey, soccer, basketball ⇒ decrease bolus dose by 75-100% may need to consume a carb (15 g) every 30 mins or before exercise (if exercise occurs within an hour after meal-time insulin or after 2 hours)

Answer 11

immediate effects: some have carbs that can increase BG (beer, coolers, white wine, etc), people using insulin may consider subbing carbs in meal plan (1 beer = 1 piece of bread), adjusting insulin dose some drinks have little or no immediate effect (hard alcohol, dry wine, low carb or light beer) delayed hypoglycemia (up to 24 hours post consumption) - can happen with all types, MOA: reduced hepatic glucose production (possibly by inhibiting effects of glucagon in liver), increase risk of nocturnal hypoglycemia avoid by ⇒ eating food while drinking and have bedtime snack, check BG during night, check BG more often next day or be aware of low potential

Answer 12

have supplies in carry-on, insulin storage, insulin dosing - if traveling north-south requires no adjustment traveling east means day is shorter = reduce basal insulin dose on travel day, if within North America can decrease by 1/4 to 1/3, if to Europe then can decrease 1/3 to 1/2 traveling west will mean longer day = have extra snack and extra bolus insulin dose once you arrive at destination

Answer 13

check BG before driving, if < 4 mmol/L ⇒ tx hypoglycemia until > 5 mmol/L, wait at least 40 min before driving if BG 4-5 mmol/L ingest a carb before driving,, check BG q4h always have hypoglycemia tx within reach (glucose tabs, sugar packet, jellybeans, lifesavers, juice box) driver's medical should be conducted q2y

Answer 14

Diabetes Canada - Ramadan and Diabetes Recommendations Diabetes and Ramadan Alliance

Answer 15

body responds to illness by releasing cortisol, glucagon and other hormones ⇒ glucose release from liver increases check BG > 4 times per day or q2h if high and continuing to rise check urine or blood for ketones if BG > 14 mmol/L drink lots of fluids to avoid dehydration (include electrolytes if sig GI or urinary loss of fluid) may need more insulin than normal

Answer 16

liquid cough and cold products if used should be the "sugar free" ones decongestants (ex. pseudoephedrine) can increase BG, avoid if possible, topical products have less systemic effects than oral and only use for short period of time at recommended dose and interval avoid NSAIDs due to renal complications

Answer 17

typically evolves over days to weeks (DKA that can develop within hours to days) triggered by illness (MI, stroke, severe infection) sx similar to DKA (frequent urination, excessive thirst, dry mouth, dehydration, leg cramps, weakness, lethargy, unconsciousness) unlike DKA this will present with much higher BG (> 25 mmol/L), elevated serum osmolality and little to no ketonuria or ketonemia SGLT2i use can provide sx of DKA at BG > 13 mmol/L need tx in hospital

Answer 18

when 2 or more occur: not retaining fluids (vomiting, diarrhea), gastroenteritis with fever (> 38.5 C) for > 48 hours abdominal pain BG > 14 mmol/L or continues climbing despite corrective measures ketones - urine moderate to high (4-16 mmol/L), blood (> 3 mmol/L)

Answer 19

abdominal obesity

Answer 20

higher risk of periodontal disease retinopathy in over one third of all people with diabetes and is leading cause of vision loss in working-age adults (visual impairment/blindness 2-3 x higher in diabetes) 2-3 x more likely to have CVD ESRD up to 10 x higher every 30 seconds a lower limb or part of one is amputated due to diabetes

Answer 21

over 1 year ⇒ visit family physician 2 x more frequently, sees specialist 2-3 x more frequently, 3 x more likely to be hospitalized (if hospitalized has a 4-6 days longer stay)

Answer 22

CVD and stroke are leading (risk is 2-3 x more for CVD than non-diabetic, 48% CVD, 13% stroke) ⇒ then other causes (24%) ⇒ then cancer (15%) consequences of CVD such as mortality risk, severity, HF and other complications are sig higher compared to without diabetes life expectancy approx 6 years shorter compared to without diabetes (even pt with prediabetes are at increased risk of death)

Answer 23

Core Defects: 1. insulin resistance in muscle and liver 2. impaired insulin secretion from pancreatic beta cells Additional Defects: 3. increase in hepatic glucose production 4. decrease in GLP-1 secretion from small intestine 5. increase in lipolysis = increase in plasma free fatty acid levels 6. increase in glucagon secretion from pancreatic alpha cells 7. increase in renal glucose reabsorption by SGLT2 8. nt dysfunction and resistance to appetite-suppressive effects of insulin, GLP-1, and other nts Newer Mechs: 9. inflammation 10. vascular insulin resistance

Answer 24

professional development, CPA, diabetes practice tools and resources CANRISK tools (assess risk factors)

Answer 25

weight loss ⇒ can improve insulin sensitivity, lower blood glucose and improve lipids and BP first and ongoing step in T2D management reduces progression to diabetes by 58% in pt with impaired glucose tolerance (IGT) long term adherence is poor and most pt will require pharmacotherapy within few years of diagnosis

Answer 26

4 of the 5 agents reduce the risk of progressing from prediabetes to this Metformin: Diabetes Prevention Program (DPP) study, 31% risk reduction Acarbose: Stop NIDDM study, 25% risk reduction Pioglitazone: Actos Now for the Prevention of Diabetes (ACT Now) study, 72% risk reduction Rosiglitazone and Ramipril: Diabetes REduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) study, 62% risk reduction for pioglitazone and no real difference for ramipril

Answer 27

Muscle and Liver: insulin resistance (#1 and #2 of octet) - use thiazolidinediones (TZDs) Pancreatic beta-cell: decrease in insulin secretion - use thiazolidinediones (TZDs), GLP-1RAs, DPP4is, sulfonylureas, non-sulfonylurea secretagogues, insulin Liver: increase in hepatic glucose production - use metformin, thiazolidinediones (TZDs), GLP-1RAs, DPP4is Small intestine: decrease of incretin hormone secretion (GLP1) - use GLP1-RAs, DPP4is Adipose: increase in free fatty acids - use thiazolidinediones (TZDs) Pancreatic alpha-cell: increase in glucagon - GLP1-RAs, DPP4is Kidney: increase in glucose through SGLT2 - use SGLT2is Brain: nt dysfunction - use GLP1-RAs

Answer 28

reduce risk of micro and macrovascular complications minimize risk of hypoglycemia maintain targets for CV risk factors A1c - around 7%,, FBG and pre-meal - 4-7 mmol/L 2-hour post prandial - 5-10 mmol/L

Answer 29

A: choose initial therapy based on glycemia B: start with metformin +/- others C: individualize therapy based on person and the agent used D: reach target within 3-6 months of diagnosis

Answer 30

1.health behaviour interventions initiated at diagnosis, metformin may be used as well in conjunction with the healthy interventions 2. If glycemic targets not achieved using health behaviour alone within 3 months then antihyperglycemic tx should be added to reduce microvascular complications ⇒ metformin should be chosen over other agents due to low risk of hypoglycemia and weight gain 3.If A1c values are >1.5% above target at diagnosis initiating metformin in combo with 2nd antihyperglycemic drug should be considered to increase likelihood of target 4.pt with metabolic decompensation (ex. marked hyperglycemia, ketosis, unintentional weight loss) should get insulin with or without metformin to correct relative insulin deficiency

Answer 31

A: if A1c is <1.5% ⇒ initiate health behaviour and start metformin if not at target in 3 months OR start metformin with health behaviour B: if A1c >/= 1.5 over target ⇒ start metformin with healthy behaviour AND consider second concurrent agent if symptomatic hyperglycemia and/or metabolic decompensation (polyuria, polydipsia, weight loss, volume depletion) ⇒ start INSULIN +/- metformin

Answer 32

efficacy in lowering A1c, favourable AEs - hypoglycemia risk negligible, weight gain is minimal or neutral affordable, clinical trial evidence ⇒ UK prospective study, SPREAD-DIMCAD (not entirely shown for lowering CV effects)

Answer 33

if intolerant or contra to metformin - can have GI AEs (N/V, flatulence, ab discomfort), metallic taste, renal impairment (eGFR < 30) ⇒ alternatives: sulfonylureas (caution for hypoglycemia, start low dose and titrate), DPP4is, SGLT2is, GLP-1RAs if atherosclerotic CVD, HF, or CKD a tx regimen with SGLT2i or GLP-1RA should be considered

Answer 34

metformin is well validated for combo with DPP4is, SGLT2is, and sulfonylureas metformin is less validated with GLP-1RAs and DPP4is are less validated in combo with SGLT2is

Answer 35

regular monitoring of A1c should happen even if stable for some time timely adjustments such as dose changes, additional agents will be needed insulin is common option for tx intensification but has some negative images (may be seen as punishment for uncontrolled blood glucose, stigma, fear of hypoglycemia, weight gain)

Answer 36

high risk of CV or renal events renal fxn degree of hyperglycemia AE profile - risk of hypoglycemia, weight gain costs and coverage pt preference ability to adhere

Answer 37

despite the weak clinical trial evidence intensive glycemic control makes sense from a pathophysiology perspective

Answer 38

to determine whether insulin glargine-mediated normoglycemia can reduce CV morbidity and/or mortality in people at high risk for vascular disease with either IFG, IGT or early T2D - showed no effect on endpoints

Answer 39

to examine in overweight volunteers with T2D the long-term effects of an intensive lifestyle intervention program designed to achieve and maintain weight loss by decreased caloric intake and increased physical activity - stopped due to futility - no effect on CV endpoints

Answer 40

inclusion criteria includes people at high risk of CVOs - prior CV event or atherosclerotic disease, multiple CV risk factors placebo background glucose lowering allowed at clinician's discretion Primary Outcome: Major Adverse CV Event (MACE) - non fatal MI, nonfatal stroke, CV-related death, hospitalization for unstable angina or HF non-infeirority design

Answer 41

Age: 59-65, proportion of men: 60-70% duration of diabetes: 6-14 years baseline A1c: 8-9% "high risk" of CVD - history of vascular disease, multiple CV risk factors

Answer 42

SGLT2is: amputation, genitourinary infection, diabetic ketoacidosis, fracture DPP4is: pancreatitis,, GLP-1RAs: retinopathy, gastroparesis, suicide risk (emerging) Thiazolidinediones: HF (not recommended in pt with hx of ischemic heart disease, macular edema, distal fractures in women,, Sulfonylureas: increased risk of CV events (use gliclazide if possible as it has lowest risk)

Answer 43

when glycemic targets aren't being met on non-insulin and low risk of hypoglycemia and/or preventing weight gain are priorities adding a basal: long acting like glargine, degludec, detemir over NPH to reduce risk of hypoglycemia ⇒ picking degludec or glargine U-300 over glargine U-100 to reduce nocturnal hypoglycemia ⇒ if glycemic targets still aren't reached on insulin ⇒ can add GLP-1RA, SGLT2i, DPP4i to avoid weight gain and lower risk of hypoglycemia ⇒ if bolus is added ⇒ rapid acting preferred over short (regular insulin) for greater glycemic control ⇒ start with 1 bolus injection at 1 meal and add as needed instead of starting with bolus at every meal

Answer 44

Macrovascular: around 18% Retinopathy: around 11% Nephropathy: around 22% Neuropathy: around 11%

Answer 45

Micro: nephropathy, retinopathy, neuropathy, foot ulcerations/infections/amputations Macro: CVD, cerebrovascular disease (stroke), PVD

Answer 46

diabetes is leading cause of renal failure ⇒ up to 1/2 of people with it will develop some form of renal damage during life, people with CKD are considered at high risk for CV events Management/Reduction: development and progression can be reduced and slowed with intensive glycemic control, optimized BP control, and use of meds that disrupt RAAS - check K+ when adding or adjusting ACEis, ARBs, or direct renin inhibitors Screen: with random urine ACR and eGFR - T1D: annually starting 5 years after diagnosis T2D: annually starting at diagnosis

Answer 47

Normal: < 30 mg albumin/24 hours, ACR < 2.0 mg/mmol Microalbuminuria: 30-300 mg albumin/24 hours, ACR 2-20 mg/mmol Overt Nephropathy: > 300 mg albumin/24 hours, ACR > 20 mg/mmol Renal Failure (ESRD)

Answer 48

diabetes is leading cause of adult blindness - visual loss can also increase risk of falls, fracture, mortality Types/Sx: this process involves changes to retinal blood vessels leading to bleeding, fluid leakage, or vision distortion, includes: macular edema - diffuse or focal vascular leakage at macula, nonproliferative diabetic this: microaneurysms, intraretinal hemorrhage, vascular malformation and tortuosity capillary nonperfusion: a form of vascular closure Screening: by optometrist or ophthalmologist - T1D: annually starting 5 years after diagnosis T2D: every 1-2 years starting at diagnosis

Answer 49

affects PNS - sensorimotor nerves (Distal Symmetric Poly-this, DSP): neuropathic pain, changes to lower limb mobility, loss of sensation autonomic nerves - CV, GI, urogenital Prevalence: approx 50% of people with diabetes will develop detectable DSP within 10 years of diagnosis Screening: includes both physical assessment and history - temp, pinprick, monofilament, vibration, inspection for ulcerations, tight glycemic control will reduce risk of onset and slow progression, pharmacologic tx may be required to manage pain T1D: annually starting 5 years after diagnosis T2D: annually starting at diagnosis

Answer 50

CV: resting tachycardia (fixed, elevated HR), decreases heart variability, exercise intolerance, abnormal BP regulation - implications ⇒ increased sensitivity to CV AEs of meds GI: gastroparesis, constipation, diarrhea (esp. at night), incontinence - implications ⇒ absorption of meds may be altered, drugs that increase GI mobility (metoclopramide, domperidone, erythromycin) have limited effectiveness Urogenital: bladder dysfunction leading to overflow incontinence, ED

Answer 51

diabetes is leading cause of lower limb amputations, so important to monitor these Progression: breakdown of skin surface, ulceration, infection (multiple organisms), gangrene and osteomyelitis, amputation Screening: daily visual inspection of feet, HCPs should inspect feet at least annually Tx: (corns, calluses, ingrown toenails, warts, splinters, other wounds): referral to podiatrist/specialist, aggressive management of infections

Answer 52

reduce pain intensity: target usually 30-50% improve QoL tx should be individualized due to diversity of pain sx, causes and pt responses: neuroreceptor reuptake inhibitors (TCAs, SNRIs), anticonvulsant meds (gabapentin, pregabalin)

Answer 53

include this distress, psychological insulin resistance, persistent fear of hypoglycemic episodes wide range of psychiatric disorders like depression, schizophrenia, anxiety, sleep disorders are common in these people compared to general population all individuals with this condition should be regularly screened for presence of these things

Answer 54

A: A1c targets - /= 55 with risk factors, OR diabetes complications), Statin (if CVD, age >/= 40 for Type 2, OR diabetes complications), ASA (if CVD), SGLT2i/GLP1ra with demonstrated CV benefit (if have T2D with CVD and A1c not at target) E: Exercise goals and healthy eating - 150 min of moderate to vigorous aerobic activity per week and resistance exercise 2-3 x week, follow healthy diet pattern S: Screening for complications - cardiac ECG every 3-5 years if age > 40 OR diabetes complications, monofilament/vibration yearly or more if abnormal, kidney test eGFR and ACR yearly or more if abnormal, retinopathy yearly dilated retinal exam S: Smoking cessation - ask permission to give advice, arrange tx and provide support S: Self-management, stress, and other barriers - set personalized goals, assess for stress, mental health, and financial or other concerns that might be barriers to achieving goals

Answer 55

it confers a risk equivalent to aging approx 15 years - vascular age rather than chronological diabetes is powerful catalyst for vascular inflammation, accelerating vascular age and sig increasing risk of CV events (MI or stroke) and complications (HF, death) Managing: check BP at every clinic visit, check lipid panel every 1-3 years, follow ABCDESSS

Answer 56

reducing BG rapidly (ex. 1-1.5% drop in A1c within 6 months) in people with established T2D (ex. 8-10 years) can increase risk of all-cause and CV related mortality (ACCORD) intensive control will increase risk of hypoglycemic events - education on sx and tx of hypoglycemia is critical

Answer 57

target: <130/80 mmHg Initial Agent: microalbuminuria, CKD, or other CV risk factors in addition to HTN and diabetes ⇒ ACEi or ARB, all other choices listed: DHP CCBs, thiazide/thiazide like diuretics combo tx with 2-3 antihypertensive drugs is often required to achieve targets, when adding ACEi ⇒ DHP CCB (ex. amlodipine) is preferable to a thiazide/thiazide-like diuretic

Answer 58

pt should have lipid panel every 1-3 years, CV risk assessment every 5 years in people aged 40-75 statin tx should be used in people with diabetes for: Primary prevention - >/= 40 years old, >/= 30 years old and diabetes for >/= 15 years, microvascular disease Secondary Prevention - hx of ACVD Tx Target: LDL < 2.0 mmol/L, or 50% reduction from baseline

Answer 59

Model includes: Age, sex, HDL, total cholesterol or LDL, systolic BP, smoking, diabetes (yes/no)

Answer 60

Model includes: sex, age at diabetes diagnosis, total cholesterol, HDL, systolic BP, smoking, diabetes duration, A1c, a-fib, ethnicity

Answer 61

Studies: ramipril 10 mg qd lowers risk of major CVEs (HOPE study, Micro-HOPE: pt with diabetes >55 yrs with one other CV risk factor) perindopril 8 mg qd had similar benefit (EUROPA) telmisartan 80 mg qd similar benefit as well (ONTARGET) Benefit: unclear whether related to BP reduction or inhibition of RAAS - benefits seen in HOPE and EUROPA were independent of HTN status and BP change Recommendation: should be used in clinical CVD, age >/= 55 with additional CV risk factors or end organ damage, microvascular complications

Answer 62

people with diabetes have increased turnover, enhance aggregation, and increased thromboxane synthesis for platelets high on-treatment platelet reactivity (HTPR) (aka aspirin resistance) is more likely to occur in pt with diabetes compared to people without diabetes, using >100 mg aspirin qd may reduce likelihood of this in diabetes Primary Prevention: aspirin should NOT be routinely used, aspirin MAY be used in presence of multiple CV risk factors Secondary Prevention: low dose (81-162 mg qd) should be used with established CVD, clopidogrel 75 mg qd MAY be used in people intolerant to aspirin

Answer 63

consistent with reducing insulin requirements and managing weight (lowering or maintaining weight) mixed effects on glycemic control ⇒ A1c, blood sugar (more likely to help A1c if started promptly after diagnosis) favourable AE profile - may increase risk of GI AEs Use in Practice: use on case-by-case basis, in overweight patients - can help reduce insulin dose and lower extent of weight gain in pediatric patients - reduce insulin dose and help with weight, may have stronger efficacy in reducing A1c, may be more of benefit in younger pt

Answer 64

benefits like weight loss, better glycemic control (A1c lowering, % of time in range), reduction of insulin doses variability in research noted in these outcomes,, suggests individual pt factors play role in effectiveness (benefits seen in at least 2 parameters for most people) Use in Practice: offer benefits for glycemic control and weight management in people with this, cannot ignore risk of DKA, when using we must select patients carefully, provide monitoring techs and ask about lifestyle to ge grasp of risk factors weight benefits and risks in pt considering usage

Answer 65

usually occurs in euglycemic conditions in T1D pts can be life threatening and is more common in T1D research has linked it as a consistent AE of SGLT2i usage and is why some countries haven't approved its usage for T1D risk seems to be mitigated/influenced by existing pt factors ⇒ seems SGLT2i may exaggerate other conditions leading to DKA if pt is adherent to ketogenic diet, sick, consuming heavy alcohol, or their insulin dose has been reduced without proper titration and inadequate monitoring while on SGLT2i their risk of experiencing DKA may be heightened Summary: SGLT2i probably not main factor for DKA, they likely interact with other factors for DKA to occur

Answer 66

reduces insulin needs, improves A1c, reduces BMI, variability in effectiveness across pts AE: DKA observed but less risk compared to SGLT2i, nausea (mild), hypoglycemia (additive effect with insulin) Use in Practice: seems they are most effective in overweight individuals with detectable C-peptide levels, early initiation post diagnosis confers greatest benefits and can even eliminate insulin dependency (in youth) in recently diagnosed Summary: the earlier you start the more benefits you can expect with glycemic control, weight and insulin needs

Answer 67

nutrition therapy can reduce A1c by 1-2% and should be used for management in diabetes reduced caloric intake to achieve and maintain healthier weight should be tx goal for obese/overweight people replacing high-glycemic-index carbs with low-glycemic-index carbs in mixed meals sig benefits glycemic control consistency in spacing and intake of carbs and meal consumption (intermittent fasting) may help control glucose and weight diabetes pt should be encouraged to choose the dietary pattern best fitting them people with diabetes should receive nutrition counselling by registered dietician

Answer 68

<45% of daily energy from carbs (<130 g/day, very low is <50 g/day) aka keto diet or Atkins diet reduce carb content of diet by: increasing amount of protein and fat, using low-glycemic index foods - scale used to identify how fast and high carb food will raise glucose, glucose arbitrarily given index of 100 Advantages: helps with weight - excess calories and over-consumption of refined carbs major drivers of obesity and T2D, reduces A1c, reduces daily insulin Uncertainties: most studies are short term (3-6 months), high dropout rate, unknown long term benefits Diabetes Implications: increased risk of hypoglycemia if using insulin, sulfonylureas, meglitinides ⇒ reduce dose or discontinue increased risk of ketoacidosis if someone uses SGLT2i ⇒ usually stop in community setting metformin, GLP-1RA, DPP4i, and acarbose needs to consider risk versus benefit on pt basis blood glucose monitoring should be integral part of strategy

Answer 69

at risk for hypoglycemia - advancing age, overly intense glycemic control, comorbidities, drug intx, hypoglycemic hx or lack awareness, impaired renal fxn, low glycemic diet, taking antihyperglycemic med known to cause hypoglycemia, A1c and other blood glucose measures indicate overreaching target at risk for other antihyperglycemic AEs benefit uncertain of med or if harm is more likely than benefit - frail, dementia, limited life expectancy

Answer 70

those most likely to contribute to hypoglycemia: insulin (T2D) ⇒ highest risk with regular and NPH insulin, sulfonylureas ⇒ highest risk with glyburide and lower risk with gliclazide meglitinides (non-sulfonylurea secretagogues) ⇒ low risk renally eliminated antihyperglycemic agents when renal fxn decreases: metformin, sulfonylureas, insulin antihyperglycemic agents causing existing or potential AEs: SGLT2i ⇒ risk of ketoacidosis

Answer 71

antihyperglycemic drugs and risk of cancer: metformin ⇒ low risk insulin ⇒ long acting analogues and cancer thiazolidinediones ⇒ pioglitazone and bladder cancer drugs associated with increased risk of diabetes: atypical antipsychotics, antidepressants drugs known to increase blood glucose: beta-adrenergic agents (ex. OTC decongestants) ⇒ increases release of both insulin and glucagon but overall effect is elevation of glucose glucocorticoids (ex. dexamethasone, prednisone), protease inhibitors (ex. ritonavir, saquinavir), calcineurin inhibitors (ex. cyclosporine, tacrolimus), thiazide diuretics (not clinically important difference) beta-blockers - often used for post MI management and BP control

Answer 72

tirzepatide (Mounjaro): glucose dependent insulinotropic polypeptide (GIP) and GLP-1RA ⇒ phase 3 trials show sig reductions in blood glucose and weight, CVOT is underway right now, Health Canada approval Oct 2023 insulin icodec: once weekly insulin, similar glucose reduction and risk of hypoglycemia compared to once daily, Health Canada approval March 2024 generic forms of DPP4i and SGLT2i biosimilar insulin forms

Answer 73

made using biotech and come from living orgs or from their cells, insulin: bacteria or yeast used to produce from recombinant human DNA GLP-1RA: yeast used to produce from recombinant human DNA

Answer 74

alternative product that replicates the original reference biologic drug as closely as possible, often less expensive than reference biologic drug, shouldn't be considered interchangeable with reference biologic, switching should only occur with explicit knowledge and consent from individual living with diabetes and their HCPs

Answer 75

an HCP committed to excellence in diabetes education, who has sound knowledge in diabetes care/management and education processes, and good communication skills and who has passed the Canadian Diabetes Educator Certification Board (CDECB) exam to become one: must be HCP licensed by regulatory body in Canada, have accumulated 800 hours of diabetes education experience over previous 3 years practicing in Canada, write and successfully pass exam (held annually in May) ⇒ recertification writing exam every 5 years or choose to submit credit portfolio (250 diabetes related CE hours accumulated within 5 years)

Answer 76

when attempting to engage with our patients we should assess their Readiness, Importance, Confidence and knowledge to make a health change behaviour

Answer 77

was 16.7% in 2021, prevalence increases with maternal age, more common in low and middle income countries around 75-90% of diabetes in pregnancy is gestational diabetes presence of dysglycemia can result in adverse pregnancy outcomes ⇒ elevated glucose can affect fetus ⇒ 1st trimester: increase in fetal malformations (implications for diabetic women planning pregnancy) 2nd and 3rd trimester: increased risk of macrosomia and metabolic complications (implications for gestational diabetes screening)

Answer 78

develops during pregnancy due to hormonal changes of pregnancy, typically occurs during 2nd or 3rd trimester

Answer 79

2 approaches, Preferred: pregnant women between 24-28 weeks (if high risk of GDM based on factors screening can be offered at any stage) ⇒ 50 g GTT with PG 1 hour later ⇒ if <7.8 mmol = normal and can reassess at 24-28 weeks if done earlier if >11.1 mmol = GDM if 7.8-11.0 mmol ⇒ 75 g GTT with FPG, 1hPG, 2hPG ⇒ if 1 value is met or exceeded for FPG > 5.3 mmol, 1hPG > 10.6, 2hPG > 9.0 mmol = GDM Alternative: 75 g GTT with FPG, 1hPG, 2hPG ⇒ if 1 value is met or exceeded for FPG > 5.1 mmol, 1hPG > 10.0 mmol, 2hPG > 8.5 mmol = GDM

Answer 80

in women at high risk of GDM based on factors, nutritional counseling should be provided ⇒ eating healthy and prevention of excess weight gain to reduce risk of developing GDM ⇒ can screen for A1c in FIRST TRIMESTER

Answer 81

previous this, hx of macrosomic infant, prediabetes, polycystic ovarian syndrome, high risk population, age > 35, corticosteroid use, acanthosis nigricans, BMI >/= 30, current fetal macrosomia or polyhydramnios

Answer 82

brown or black, velvety discoloration of body folds and creases, it is a sign of insulin resistance

Answer 83

in normal pregnancy insulin resistance starts in 2nd trimester to ensure glucose supplies fetus pregnancy hormones may interfere with insulin binding = insulin resistance in mother this natural increase in resistance in context of pre-existing resistance and/or beta cell deficit can lead to GDM Hormones: placental lactogen, placental growth hormone, hCG, cortisol, prolactin, estrogen, progesterone, leptin, TNFalpha, resistin

Answer 84

trauma from LGA infant, C-section, pre-eclampsia, pregnancy induced HTN long term at higher risk for: T2D, HTN, heart disease

Answer 85

LGA and trauma from getting stuck in birth canal ⇒ shoulder dystocia, Erb's palsy/nerve injury, brain injury prematurity, neonatal hypoglycemia, immature lung fxn, jaundice, neonatal ICU admission long term higher risk for: obesity and dysglycemia, premature puberty in girls

Answer 86

receive nutrition counseling by dietician to achieve goals eat healthy diet and replace high-glycemic-index foods with low-index to reduce need for insulin initiation and decrease birthweight discuss weight gain and healthy interventions recommend weight gain according to IOM recommendations based on pregnancy BMI interventions to reduce LGA and C-section

Answer 87

BMI < 18.5 ⇒ 28-40 lbs BMI 18.5-24.9 ⇒ 25-35 lbs BMI 25.0-29.9 ⇒ 15-23 lbs BMI > 30 ⇒ 11-20 lbs

Answer 88

FPBG < 5.3 mmol 1hPBG < 7.8 2hPBG < 6.7 can perform SMBG fasting and postprandially, if targets not achieved in 1-2 weeks can initiate pharmacologic tx

Answer 89

insulin first line - may use aspart, lispro, glulisine (bolus') metformin can be used as alternative to insulin - good safety in pregnancy, evidence of less maternal weight gain, less LGA, less neonatal hypoglycemia women should be informed it crosses placenta, safety data in offspring postpartum up to 2 years, insulin necessary in 40% of those on metformin glyburide may be used in women who refuse insulin and not well controlled on metformin

Answer 90

A: encourage breastfeeding and continue for at least 3-4 months after delivery - reduces neonatal hypoglycemia, childhood obesity and diabetes, AND maternal risk of diabetes and HTN B: 75 g GTT between 6 weeks-6 months postpartum to detect prediabetes or diabetes, suggest phone calls or email reminders to improve testing rates

Answer 91

in mothers it increases risk of worsening pre-existing complications like retinopathy and nephropathy in children it increases risk of malformations if glucose is high in 1st trimester

Answer 92

use reliable birth control until adequate glycemic control, attain a preconception A1c of <7% may remain on metformin +/- glyburide until pregnancy, women on other antihyperglycemic agents should switch to insulin assess for and manage any DM complications folic acid 1 mg/day 3 months pre-conception to 12 weeks post-conception discontinue possible embryopathic meds: ACEi/ARB, statins

Answer 93

T1D: basal-bolus insulin or continuous SC insulin infusion T2D: switch to insulin (can stay on metformin +/- glyburide if on them, but should switch off other ones) should perform SMBG pre and postprandially aiming for FBG < 5.3, 1hBPG < 7.8, 2hBPG < 6.7, A1c < 6.5% (<6.1% if possible) ⇒ leads to lower late stillbirth and infant death ASA to reduce risk of pre-eclampsia starting at 12-16 weeks gestational age post-partum: can screen for postpartum thyroiditis in T1D ⇒ check TSH at 2-4 months

Answer 94

inhibits hepatic gluconeogenesis - basically tells liver to slow production of sugar when its not needed helps muscles use blood sugar more efficiently, after BG rise from eating this med helps muscles absorb sugar more effectively and use it for energy

Answer 95

mimic effects of this and work by ⇒ reducing glucagon secretion which lowers BG levels delays gastric emptying which slows down the rate of stomach emptying which helps counteract spikes in glucose levels suppresses appetite by working in areas of brain controlling satiety

Lecture 22-35 Diabetes Flashcards

(119 cards)