Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3152 > diabetes > Flashcards

diabetes Flashcards

1
Q

When to screen for DM in the adult population?

A
  1. adults age >= 40 years old
  2. adults < 40 years old with >=1 of these risk factors for diabetes:
    - obesity/overweight
    - first degree relative with DM
    - high risk race / ethnicity
    - women who have delivered a baby that was >= 4 kg, or who have history of gestational diabetes
    - HTN >= 140/90
    - HDL-C < 1 mmol/L (male), <1.3 mmol/L (female) and/or TG >= 2.2 mmol/L
    - women with PCOS
    - history of CVD
    - impaired glucose tolerance (IGT) or Impaired fasting glucose (IFG) on previous testing (pre-DM)

to screen annually for those who have IGT/IFG (pre-DM), if not once every 3 years for those with normal glucose tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the recommended tests for DM screening in the adult population?

A
  1. fasting plasma glucose (FPG)
    - fasting = no calorie intake for >= 8 hours
  2. hbA1c
    - avg amount of glucose in blood over the past 3 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the criteria for the diagnosis of type 2 DM

A

Hba1c =< 6.0%
» no diabetes

Hba1c between 6.1 to 6.9%
+ FPG =< 6.0 mmol/L OR 2hOGTT =< 7.7 mmol/L
» no diabetes

Hba1c between 6.1 to 6.9%
+ FPG between 6.1 to 6.9 mmol/L OR 2hOGTT between 7.8 to 11.0 mmol/L
» pre-diabetes

Hba1c between 6.1 to 6.9 %
+ FPG >= 7.0 mmol/L OR 2hOGTT >= 11.1 mmol/L
» diabetes

Hba1c >= 7%
» diabetes

note: for doctors who prefer to use FPG or OGTT for screening and diagnosis (instead of Hba1c), they may continue to do so, but would require abnormal results from at least two different tests to confirm diagnosis of diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the recommended management for adults with pre-DM?

A
  1. lifestyle intervention
    - recommended pre-DM patients
    - healthy diet
    - increased physical activity
  2. metformin
    - considered for pre-DM patients, whose glycemic index does not improve despite lifestyle modifications, or if they are unable to adopt lifestyle modifications; especially if these patients are <60 years of age, have BMI >= 23 kg/m^2 or are women with history of gestational diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the staging for type 1 DM and the characteristics of each stage

A

stage 1: positive autoantibodies, normoglycemia, presymptomatic

stage 2: positive autoantibodies, dysglycemia, presymptomatic

stage 3: positive autoantibodies, new onset hyperglycemia, presymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

compare and contrast type 1 DM and type 2 DM?

A

type 1 DM: positive autoantibodies, c-peptide absent, onset abrupt, age of onset usually < 30 years, appearance is often thin, ketosis is frequent

type 2 DM: negative autoantibodies, c-peptide present, onset gradual, onset usually > 40 years, appearance often overweight, ketosis is not common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the signs and symptoms of hyperglycemia

A

polydispia (thirst), polyuria (frequent urination), polyphagia (hunger), blurred vision, drowsiness, dry skin, decreased healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe the signs and symptoms of hypoglycemia

A

tachycardia, tremors, sweating, dizziness, anxiety, irritability, impaired vision, weakness/fatigue, headache, hunger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

at high hbA1c levels, does basal hyperglycemia or post-prandial hyperglycemia contribute more to hbA1c?

A

basal hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the complications of DM?

A

microvascular: retinopathy , neuropathy, nephropathy (increased risk of albuminuria)

macrovascular: cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the monitoring for the cardiovascular risk factors and the complications of DM?

A

HbA1lc:
> measure every 3 months if unstable; every 6 months if stable

Lipid panel:
> measure every 3-6 months if uncontrolled; annually if controlled

BP:
> measure at every visit

For retinopathy: retinal fundal photography (eye exam)
- when to start?
> type 1 DM: recommended to screen within 5 years of diagnosis
> type 2 DM: recommended to screen at time of diagnosis
- how often to screen?
> screen every 6 months if unstable; annually if stable

For nephropathy: serum Cr / eGFR AND urine albumin/creatinine ratio (uACR) or urine protein/creatinine ratio (uPCR)
- when to start?
> type 1 DM: recommended to screen beginning five years after diagnosis
> type 2 DM: recommended to screen at time of diagnosis
- how often to screen?
> screen every 6 months if albuminuria is present; annually if stable

For neuropathy: diabetic foot examination
- how often to examine?
> foot inspection daily by the patient
> foot assessment annually by podiatrist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe diabetic foot assessment and the counselling points for patients?

A

diabetic foot assessment:
- examination includes: inspection of the skin, assessment of foot deformities, neurological assessment (10g monofilament testing + either pinprick or temperature or vibration test), vascular assessment (incl. pulses in legs and feet)
- advice patients to maintain optimal glycemic control
- encourage smokers to quit smoking
- educate on good foot care and appropriate foot wear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the treatment goals for glucose in DM, according to the MOH 2014 guidelines?

A

Hba1c: < 7%
FPG: 4.0-7.0 mmol/L (in practice usually aim for 5.0-7.0 mmol/L in order to prevent hypotension)
PPG: < 10.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

list the oral glucose lowering agents used in the management of diabetes?

A
  1. metformin
  2. thiazolidinediones (TZDs)
  3. sulfonylureas / meglitinides
  4. DPP4-i
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

list the injectables used in the management of diabetes?

A
  1. insulin
  2. GLP-1 agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe the use of metformin in the management of diabetes, including the indications, MOA, dosing regimen, onset, elimination route, DDI, S/E and pregnancy recommendation

A

Metformin:
Indication: monotherapy/ in combination for T2DM

MOA: decreases hepatic glucose output (main), increases glucose uptake and utilization in muscle/peripheral tissues (secondary)

Dosing:
- immediate release (available in 250 / 500 / 850 / 1000 mg tablets):
> start with 500 / 850 mg OD
> increase by 500 / 850 mg OD every 1-2 weeks, in divided doses
> max dose is 2500 / 2550 mg per day

  • extended release (available in 500 / 750 / 1000 mg tablets):
    > start with 500 mg OD
    > increase by 500 mg every week
    > max dose is 2000 mg OD, may divide into BD dosing if glycemic control is not achieved with OD dosing, and if dose > 2000 mg is needed, to switch to immediate release

Onset: days, max effect takes 2 weeks

Elimination: renal, excreted unchanged in urine

DDI: alcohol (increased risk of lactic acidosis), iodinated contrast material (metformin accumulation; temporarily withhold for at least 48h after iodinated contrast administration and restart when renal function is stable), OCT 2 inducers / inhibitors (e.g. cimetidine, dolutegravir, ranolazine may lead to metformin accumulation)

S/E: GI disturbances, e.g. N/V/D (take with food to minimize), loss of appetite, metallic taste, may decrease serum b12 concentrations in the long term (consider periodic measurement esp. in patients with anemia / peripheral neuropathy), lactic acidosis (rare but fatal)

CI: severe renal impairment (eGFR < 30 mL/min), hypoxic states / risk for hypoxemia due to increased risk for lactic acidosis (e.g. acute decompensated HF, HF, sepsis, respiratory failure, liver impairment, alcoholism, >= 80 yo)

Pregnancy: safe to use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe the signs and symptoms of lactic acidosis (rare but fatal S/E of metformin, as metformin blocks aerobic respiration and increases anaerobic respiration, thus increasing

A

N/V, abdominal pain, shallow/laboured breathing, mental confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the place in therapy of metformin, in DM management?

A

lowers Hba1c by 1.5 to 2.0 %, promotes weight loss, negligible hypoglycemia, can prevent and delay T2DM, can be used for pregnant patients with DM,

*possible reduction in cardiovascular events patients with T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe the use of thiazolidinediones (TZDs) in the management of diabetes, including the indications, MOA, dosing regimen, onset, elimination route, DDI, S/E and pregnancy recommendation

A

indication: alternative monotherapy for patients who cannot take metformin / combination in T2DM

MOA: peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, promotes glucose uptake and utilization into skeletal muscle tissues and adipose tissues

dosing:
- pioglitazone (available in 15 / 30 mg tablets)
> start with 15 mg or 30 mg OD; can increase by 15 mg, up to a max of 45 mg OD, for inadequate response

onset: up to one month for maximum effect

elimination: liver

DDI: CYP3A4 and CYP2C8 inducers / inhibitors

S/E: hepatotoxicity (do not initiate / discontinue if ALT > 3x ULN; if ALT > 1.5x ULN to repeat LFTs weekly until normal), fluid retention (monitor s/sx of heart failure), weight gain, increased risk of fracture, increased risk of bladder cancer (FDA black box)

CI: active liver disease, symptomatic HF / history of HF, active bladder cancer / history of bladder cancer

pregnancy: not recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe the place in therapy of TZDs, in DM management?

A

decrease Hba1c by 0.5 to 1.4%, potential reduction in stroke risk but increased risk of heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

describe the use of sulfonylureas in the management of diabetes, including the indications, MOA, dosing regimen, onset, elimination route, DDI, S/E and pregnancy recommendation

A

indication: alternative monotherapy for patients who cannot take metformin / combination in T2DM

MOA: binds to and blocks the K+ channel on pancreatic beta cells, stimulating opening of voltage gated Ca2+ ions allowing Ca2+ influx, stimulating insulin secretion

dosing:
- Glipizide is the choice of SU for renal impairement, as it is 90% eliminated by the liver, dose is 5 mg BD (max of 40mg/day), take 15 to 30 min before a meal
- Glimepiride is a newer generation Su that is dosed 1-4mg OD (max of 8mg/day), take 15 to 30 min before a meal

onset: 15 to 30 min

elimination: various

DDI: beta blockers (may mask the symptoms of hypoglycemia), alcohol (1st gen&raquo_space; 2nd/3rd gen; SU and alcohol taken together might cause a disulfiram-like reaction, with symptoms of flushing and tremor), CYP2C9 inhibitors (e.g. amiodarone, 5-FU, fluoxetine; increase the concentration of glimepiride and glipizide)

S/E: hypoglycemia (very common, esp. in elderly), weight gain (2-5kg)

CI: hypersensitivity to any SUs / sulphonamides

pregnancy: not recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

describe the place in therapy of SUs, in DM management?

A

decrease HbA1c by 1.5% (but require the presence of functioning beta cells to work), use with caution with patients with irregular eating schedule (due to hypoglycemia), exercise and diet management to minimzie weight gain, SUs are a cost effective therapy at the initial stage of diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe the use of DPP-4i in the management of diabetes, including indication, MOA, dosing regimen, onset, elimination, DDI, S/E and pregnancy recommendations

A

indication: second / third line agents in T2DM treatment, usually used in dual / triple combination therapy

MOA: inhibits the breakdown of GLP-1 by the dipeptidyl peptidase 4 enzyme, thus potentiating its effects such as promoting satiety, delaying gastric emptying, increasing insulin secretion and inhibition of glucagon secretion, improving beta cell function

Dosing:
Sitagliptin: 100mg OD
- eGFR >=30 to < 45: 50mg OD
- eGFR < 30: 25mg OD
- take regardless of meals
- weight neutral
- DDI: increases the concentration of digoxin (minimal)

Vildagliptin: 50mg BD if given with metformin or TZD; 50mg OD if given with SU
- CrCL < 50 mL/min: max 50mg OD, but usually avoid use
- use with caution if >= 75 years old, or LFT > 3 x ULN
- take regardless of meals
- weight neutral
- DDI: none reported

Linagliptin: 5mg OD
- no dose adjustment required
- take regardless of meals
- weight neutral
- DDI: avoid with CYP3A4 inducers (decrease concentration of linagliptin)

S/E: severe joint pain that can be disabling (FDA warning), headache, acute pancreatitis, hypersensitivity reaction, bullous pemphigoid and skin rash (serious but rare)

increase risk of congestive failure (for Saxagliptin and Aglogliptin, which are not approved in Singapore)

CI: patients with hx of acute pancreatitis, patients with hypersensitivity to DPP-4i

pregnancy: not recommended

24
Q

describe the place in therapy of DPP-4i, in DM management?

A

decrease HbA1c by 0.5 to 0.8 % (based on monotherapy);

advantages compared to GLP-1: DPP-4i has lower GI side effects, is cheaper, and is mostly oral formulation (GLP-1 mostly SC other than new PO Semaglutide)

disadvantages compared to GLP-1: weight neutral, smaller HbA1c reduction, no benefits for ASCVD, HF and/or CKD

25
Q

describe the use of SGLT2i in the management of diabetes, including indication, MOA, dosing regimen, onset, elimination, DDI, S/E and pregnancy recommendations

A

indication: second / third line agents in T2DM treatment, usually used in dual / triple combination therapy

MOA: blocks the reabsorption of glucose at the SGLT2 transporters in the proximal renal tubule, resulting in increased glucosuria (renal glucose excretion)

dosing:

Canaglifozin (Invokana): 100mg OM, taken on empty stomach before breakfast; can titrate up to 300mg OM if eGFR > 60 mL/min and need further blood glucose control
- in patients without CVD/CKD: discontinue / do not initiate if eGFR < 30 mL/min
- in patients with CVD/CKD: may continue at 100mg OM until dialysis starts

Empaglifozin (Jardiance): 10mg OM, regardless of food; can titrate up to 25mg OM
- in patients without CVD/CKD: discontinue / do not initiate if eGFR < 45 mL/min
- in patients with CVD/CKD: do not initiate when eGFR < 20mL/min, else, may continue until dialysis starts

Dapaglifozin (Farxiga/Forxiga): 5mg OM, regardless of food; can titrate up to 10mg OM
- in patients without CVD/CKD: discontinue / do not initiate if eGFR < 45 mL/min
- in patients with CVD/CKD: do not initiate if eGFR < 25 mL/min, else, may continue until dialysis starts

DDI: -

S/E: hypotension, increased urinary urgency (polyuria), hypoglycemia (uncommon), nephrotoxicity, increased LDL levels, genital mycotic infection/UTI, increased risk fo diabetic keto-acidosis (esp euglycemic DKA; FDA warning) , Fournier’s gangrene (necrotizing fasciitis of the perineum; FDA warning)

canaglifozin specific: lower limb amputation, hyperkalemia, fractures

CI: end stage renal disease / dialysis

pregnancy: not recommended for use

26
Q

Describe the risk factors for diabetic ketoacidosis (happens for type I DM patients, and as a S/E for SGLT2 inhibitors)

A

stress, alcohol abuse, malnutrition, surgery, acute illness, dehydration
- to hold off SGLT2i until recovered

27
Q

describe the place in therapy of SGLT2i, in DM management?

A

reduce HbA1c by 0.8-1.0%, neutral for hypoglycemia, slight weight loss benefits,

*has benefits for ASCVD (Canaglifozin, Empagliflozin), HF (class benefit) and CKD (class benefit), but cost remain a limitation

28
Q

describe the use of a-glucosidase inhibitors in the management of diabetes, including indication, MOA, dosing regimen, onset, elimination, DDI, S/E and pregnancy recommendations

A

Indication: add on for management of T2DM; patients who are on T1DM insulin therapy but require additional control in PPG level (off label)

MOA: competitively inhibits alpha glucosidase enzyme found in the intestinal brush borders, which is required for the break down of complex carbohydrates, thus delaying glucose absorption and decreasing PPG levels; acts locally only

Dosing:
Acarbose: start with 25mg BD-TDS with each meal; increase by 25mg/day every 2-4 weeks to a maximum of 150mg/day (for =<60kg) or 300mg/day (for > 60kg)

Onset: rapid with each meal, hence to take with meal

Elimination: feces, as unabsorbed drug

DDI: intestinal adsorbents and digestive enzyme preparations may decrease effects of a-glucosidase inhibitors

S/E: GI effects, incl. flatulence (main), abdominal pain, diarrhoea; increase in LFTs (risk increased at dose > 100 mg TDS)

CI: GI diseases (e.g. obstruction, IBD), liver cirrhosis

pregnancy: not recommended

29
Q

describe the place in therapy of a-glucosidase inhibitors in DM management?

A

reduce HbA1c by 0.5 to 0.8%, mainly used to control post prandial glucose, useful in carbohydrate rich diet (may consider taking with the largest meal of the day or with the meal that consists of the most carbs), flatulence is the top reason for drug discontinuation

30
Q

describe the rule of thumb for the stability of insulin

A

unopened vial: if refrigerated, good until exp date; if unrefrigerated, good for 28 days
opened vial: good for 28 days regardless or refrigeration

*exception: opened insulin detemir good for 42 days

31
Q

describe the place in therapy of insulin, in the management of DM?

A

most effective blood glucose lowering agent, can reduce HbA1c up to 2.5%, can be used in both type I and type II DM patients, drug of choice in pregnant patients with DM

MOA: increase glucose uptake and utilization in muscle and adipose tissue, inhibit gluconeogenesis and glycogenolysis (responsible for hepatic output of glucose), inhibit lipolysis and stimulate lipogenesis, inhibit proteolysis and stimulate proteogenesis

exogenous insulin cleared by kidney; endogenous insulin cleared by liver

32
Q

list the different types of insulin available

A
  1. ultra short acting insulin (aspart/Fiasp, lispro-aabc/lyumjev)
  2. rapid acting insulin (aspart/Novorapid, lispro/Humalog, glulisine/Apidra)
  3. short acting insulin (regular/Actrapid)
  4. intermediate acting insulin (NPH/Insulatard, protamine)
  5. long acting insulin (detemir/levemir, glargine U-100/Lantus)
  6. ultra long acting insulin (degludec, glargine U-300/Toujeo)
  7. others: pre-mixed insulin (Novomix30, Humalog Mix 75/25, Humalog Mix 50/50, Mixtard 30/70 - 30% regular insulin and 70% NPH)
33
Q

Describe the profile of ultra short acting insulin?

A

Aspart/Fiasp, Lispro-aabc/Lyumjev:
- dose at first bite / at the start of the meal or within 20 minutes after starting a meal
- for aspart/Fiasp, contains additional vitamin B3 (increases speed of initial absorption) and L-arginine (stabilizes the formulation)
- for Lispro-aabc/Lyumjev, contains additional Treprostinil (increases initial absorption rate due to vasodilation) and Citrate (increases intial absorption rate due to increased vascular permeability)

34
Q

Describe the profile of rapid acting insulin?

A

Aspart/Novorapid, Lispro/Humalog, Glulisine/Apidra:
target PPG, onset is 5-15 min (take 15 min before meal), peak effect is 1-2 hours, duration of action is 3-5 hours

35
Q

Describe the profile of short acting insulin?

A

Regular/Actrapid:
target PPG, onset is 30-60 mins (take 30 mins before meal), peak effect is 2-4 hours, duration of action is 6-8 hours

36
Q

Describe the profile of intermediate acting insulin?

A

NPH/Insulatard:
target FPG, onset is 1-2 hours, peak effect is 6-12 hours, duration of action is 10-16 hours (dose BD for 24hr coverage)
- inject regardless of meal, at the same time everyday (BD)
*NPH is used to manage steroid induced hyperglycemia, due to best profile match

37
Q

Describe the profile of long acting insulin?

A

Detemir/Levemir:
target FPG, onset is 0.8-2 hours, peak is a hill, duration of action is 12 hours for 0.2 units/kg and 24 hours for 0.4 units/kg (dose BD to provide better coverage of 24h)

Glargine U-100/Lantus:
target FPG, onset is 1.5 hours, peakless, duration of action is 24 hours (dose OD to provide 24h coverage)

  • inject regardless of meal, at the same time everyday (BD/OD)
38
Q

Describe the profile of ultra long acting insulin?

A

Degludec:
- peakless, duration of action is 24h
- inject SC OD at any time of the day

Glargine U-300/Toujeo:
- peakless, duration of action is 36h
- inject SC OD at the same time everyday

39
Q

Which mixes of insulin are stable?

A

NPH + short acting insulin (regular)
NPH + rapid acting insulin (aspart/Novorapid, lispro/Humalog, glulisine/Apidra)

40
Q

Which mixes of insulin are unstable?

A

Glargine + other insulins (incompatible pH)
Detemir + other insulins (not recommended by manufacturer)
Glulisine + any other insulin other than NPH (not compatible)

41
Q

what are the considerations about oral therapies when injectable insulin is started?

A

metformin: continue
TZD: discontinue or reduce dose
SU: discontinue if bolus insulin initiated / on pre-mix regimen; discontinue or reduce dose by 50% if basal insulin initiated (if patient at high risk of hypoglycemia)
SGLT2i: continue
DPP-4i: discontinue if GLP-1 agonists initiated

42
Q

in which cases must we decrease dose when doing insulin dosing conversion?

A
  1. when switching from NPH BD to glargine/detemir OD -> to decrease dose by 20% then slowly titrate back up (reason: very large dose, cannot give to patient at once)
  2. when switching from glargine U-300 to other alternative basal insulin analogs -> to decrease dose by 20% (reason: in clinical trials, patients taking U-300 seemed to require larger doses to achieve the same glycemic goals as compared to glargine U-100)
43
Q

Describe the S/E of insulin and management?

A

main adverse effect: hypoglycemia (BG < 4.0 mmol/L or < 70mg/dL)
> to counsel patient:
- signs and symptoms: blurry vision, sweating, tremor, hunger, confusion, anxiety, shaking, rapid heart beat, dizziness, headache, weakness, fatigue, irrtability
- nocturnal ones: nightmares, restless sleep, profuse sweating, morning headache
- 15-15-15 rule: 15g of fast acting carbohydrates, 15 min waiting and recheck, if still low to take another 15g of fast acting carbohydrates
- commonly found fast acting carbohydrates: 1/2 cup fruit juice / regular soft drinks, 2tbsp raisins, 1tbsp/3 cubes of sugar, 5-6 hard candies, 1tbsp honey

other adverse effect: weight gain (more than SU)
> to counsel patient:
- benefits of glycemic control outweigh weight gain
- diet, exercise to lose weight

other adverse effect: lipoatrophy (rare nowadays), local allergic reaction incl. burning, pain, itching at injection site (rare nowadays), lipohypertrophy (rotate injection sites), systemic allergic reaction (rare), insulin resistance (rare)

44
Q

describe the use of GLP-1 agonists in the management of diabetes, including indication, MOA, dosing regimen, onset, elimination, DDI, S/E and pregnancy recommendations

A

indication: recommended over insulin as first line injectable when greater glucose lowering is needed (unless patient is symptomatic)

MOA: mimics endogenous GLP-1 (but with longer t1/2!), thus promoting satiety, delaying gastric emptying, increasing insulin secretion from beta cells and inhibiting glucagon secretion, improves beta cell function

dosing:
Liraglutide:
- SC injection once daily, regardless of meals
- Initiate at 0.6mg, then titrate up to 1.2mg after 1 week; can increase to 1.8mg
- no renal dosing adjustment

Dulaglutide:
- SC injection once weekly, regardless of meals
- Initiate at 0.75mg, then titrate up to 1.5mg after 4 weeks; can increase to 3mg and 4.5mg
- no renal dosing adjustment

Lixisenatide:
- SC injection once daily, before first meal of the day
- Initiate at 10mcg, then titrate up to 20mcg after 2 weeks
- Lixisenatide is contraindicated when eGFR < 15

Semaglutide (Ozempic):
- SC injection once weekly, regardless of meal
- Initiate at 0.25mg, then titrate to 0.5mg after 4 weeks; can increase to 1mg
- no renal dosing adjustment

Semaglutide (Rybelsus):
- PO once daily, 30 mins before the first meal of the day, with no more than 120mL of water (for adequate absorption)
- Initiate at 3mg, then titrate to 7mg after 30 days; can increase to 14mg
- no renal dosing adjustment

S/E: headache, acute pancreatitis, N/V (common), acute cholecystitis, injection site reactions, risk of thyroid C-cell tumours (FDA black box warning, shown in animals but human prevalence unknown; to counsel patients on the risk and symptoms of thyroid cancers)

CI: patients with hx of acute pancreatitis, patients with thyroid cancer / family history of thyroid cancer

45
Q

describe the place in therapy of GLP-1 agonists, in the management of DM?

A

reduce HbA1c by 1.2%, causes weight loss, does not cause hypoglycemia, most agents have benefits for ASCVD (Liraglutide, Dulaglutide, SC Semaglutide), minimal benefits for reducing macroalbuminuria (SC agents only)

46
Q

describe the principles of insulin dosing?

A

Act on FPG first:
- usually initiate insulin NPH, 10 units at bedtime OR 0.1-0.2 units/kg per day
- if HbA1c is uncontrolled, increase insulin dose by 2 units every 3 days, until FPG is at goal (4.0/5.0 - 7.0 mmol/L); if FPG is consistently > 10 mmol/L, may increase insulin dose by 4 units every 3 days
- can titrate insulin to a max of 0.5 units/kg per day (max total daily dose for basal insulin)
- if there is no clear reason for hypoglycemia, decrease insulin dose by 10-20%

If HbA1c still above goal, and patient already at max total daily dose for basal insulin of 0.5 units/kg/day, or FPG already at goal:
- add prandial coverage (rapid/short acting insulin) starting with 1 dose at the largest meal, and this dose would be either 4 units or equivalent to 10% of the total daily dose
- if HbA1c < 8%, to also decrease the basal those by 4 units or 10%
OR
- if on bedtime NPH, to consider splitting into two doses, 2/3 in the morning and 1/3 in the evening

47
Q

which agents should we consider to add (add on to metformin), if the patients have hx of ASCVD/HK/CKD, independently of HbA1c?

A

ASCVD: GLP-1 agonist > SGLT2i
HF: SGLT2i
CKD: SGLT2i > GLP-1 agonist

48
Q

when should we consider insulin over GLP-1 agonist, when the patient needs greater glucose lowering than can be obtained with oral agents?

A

when patient:
- has ongoing catabolism (weight loss)
- symptoms of hyperglycemia
- HbA1c > 10 %
- BG > 16.7 mmol/L

49
Q

What are the ASCVD conditions?

A

stable angina, acute coronary syndromes, cerebrovascular accident, transient ischemic attack (myocardial infarction), carotid artery disease, peripheral artery disease

50
Q

What are the risk factors for ASCVD?

A

LDL >= 2.6mmol/L, hypertension, smoking, chronic kidney disease, albuminuria, family history of premature ASCVD, obesity

51
Q

Outline the lipid management in diabetes

A

LIPID MANAGEMENT IN DIABETES
- if have DM + ASCVD > target 1.4 mmol/L using high intensity statins (secondary prevention)
- if have DM + age 40-75 years old, without any cardiovascular disease > target 1.8 mmol/L using moderate intensity statins (primary prevention)
- if have DM and additional ASCVD risk factors, consider high intensity statin

52
Q

Outline the blood pressure management in diabetes

A

BLOOD PRESSURE MANAGEMENT IN DIABETES
- blood pressure target is <130/80 mmHg
- ACEi/ARB is the preferred first line agent for the treatment of hypertension, with or without CKD
- ACEi/ARB are not recommended for primary prevention for those who have normal blood pressure (<140/90 mmHg)

53
Q

Outline the treatment for chronic kidney disease (albuminuria) in diabetes

A

CHRONIC KIDNEY DISEASE IN DIABETES
- ACEi/ARB is the preferred first line agent and should be started for those with micro/macro albuminuria (it slows CKD progression); titrate to max dose
- SGLT2i should be added on for those with T2DM DKD (CKD associated with DM) and eGFR > 20-25 mL/min/1.73m^2
- Finesterone (MRA) is indicated for those with T2DM DKD (CKD associated with DM) and eGFR > 25mL/min/1.73 m^2
- all the above refer to secondary prevention (patient already has some form of CKD either in the form of micro/macroalbuminuria/DKD), and are not recommended for primary prevention; main primary prevention of CKD in DM patients are blood sugar and blood pressure control

54
Q

Describe the use of finerenone in the management of T2DM DKD including the indication, MOA, dosing regimen, onset, elimination, DDI, S/E and pregnancy recommendations

A

Finerenone:
indication: indicated to slow CKD progression, reduce the risk of kidney failure, heart attack, heart failure, hospitalization and cardiovascular death (beneficial effects in ASCVD, HF and CKD) in adult patients with CKD associated with T2DM

MOA: non-steroidal mineralocorticoid receptor antagonist, hence inhibits the reabsorption of sodium and water at the renal tubules

S/E: hyperkalemia, hypotension, lesser risk of gynecomastia as compared to spironolactone

CI: eGFR < 25

55
Q

Outline the use of anti-platelet therapy in diabetes

A

USE OF ANTI-PLATELET THERAPY IN DIABETES
- if have DM + ASCVD > aspirin is indicated (secondary prevention)(if allergic to aspirin, use clopidogrel 75mg/day)
- if have DM and high risk of ASCVD, e.g. between 50 to 70 years old AND have at least one additional ASCVD risk factor > aspirin can be started for primary prevention (studies show that it has benefits in preventing ASCVD)
- if have DM but low risk for ASCVD, e.g. < 50 years old AND no other additional ASCVD risk factors > aspirin not recommended for primary prevention (no benefit)
- Do not start aspirin for patients > 70 years old as risk > benefit
- for the intermediate range, e.g. < 50 years old but have ASCVD risk factors or >= 50 years old but have no risk factors, to exercise clinical judgement

3152 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions