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DM Management Flashcards

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1
Q

What is the typical glycemic target/goal for px with DM?

A

<7% HbA1C w/o significant hypoglycemia (for non-pregnant

may increase depending on life expectancy, harms of treatment>benefit

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2
Q

What are 3 main considerations when personalising T2DM management?

A

1) Glycemic control
2) Reduction of cardiorenal risk (eg. comorbidities and contraindications)
3) Medication-related factors influencing adherence
4) Px preferences, needs and values (eg. weight, access to treatment)

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3
Q

What is the definition of hypoglycemia?

A

Plasma glucose conc. low enough to cause symptoms/signs
- impairment of brain function (eg. seizures, unconsciousness, brain death)
- MI, fatal arrythmias

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4
Q

What is Whipple triad?

A

Method to clinically diagnose symptomatic hypoglycemia:
1) Symptoms, signs, or both consistent w hypoglycemia
2) low reliably measured plasma glucose conc.
3) resolution of symptoms and signs after plasma glucose conc. is raised

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5
Q

What are 6 symptoms and signs of hypoglycemia?

A

Neuroglycopenic:
1) Confusion/slowed thinking
2) Incoordination
3) Speech difficulty
4) Vision changes
5) Hemiparesis
6) Seizures

Autonomic:
1) Hunger
2) Palpitations
3) Shaking
4) Sweats
5) Tremors
6) Pallor

Non-specific:
1) Irritability
2) Malaise
3) Headache
4) Nausea
5) Nervousness

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6
Q

What are the physiological responses to hypoglycemia?

A

1) ↓Insulin from ß-cells
2) ↑Glucagon from α-cells
3) ↑Epinephrine from Adrenal medulla
4) ↑Neurogenic symptoms (eg. hunger) from SNS

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7
Q

What are the implications of hypoglycemia?

A

ST:
1) Acute symptoms
2) Cognitive impairment
3) Mood change
4) Work, Social life and driving impairment
5) Hypothermia
6) Acute morbidity (eg. accidents, coma, CVS/NeuroCVS events)

LT:
1) Weight gain
2) Employment and driving restriction
3) Worsening of DM/vascular complications
4) Cognitive decline
5) Acquired hypoglycemia-induced syndromes

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8
Q

What are 4 causes of hypoglycemia?

A

Too much insulin:
1) Insulin/sulphonylurea dose too high/ill-timed
2) Medication error

Too little carb intake:
1) Poor oral intake
2) Px kept NBM/missed meals

Others:
1) Disease factors (↓insulin clearance from liver clearance, renal impairment)
2) ↑insulin sensitivity (eg. weight loss)
3) ↑glucose utilisation (eg. exercise)

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9
Q

What are 5 ways to prevent hypoglycemia in DM px?

A

1) Px education
2) Dietary intervention
3) Exercise management
4) Glucose monitoring
5) Medication adjustment
6) Clinical surveillance

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10
Q

When is insulin therapy indicated?

A

1) T1DM
2)T2DM
- w severe hyperglycemia
- glycemic target were not reached w 2 or more hypoglycemic agent (HAs)

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11
Q

What are 3 examples of rapid-acting insulin analogues?

A

1) Lispro
2) Aspart
3) Glulisine

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12
Q

How do rapid-acting insulin analogues act rapidly?

A

Substitution/addition of amino acids to weaken propensity for insulin to self-associate → less dimer formation → rapid absorption of monomers from subcut tissue @ time of injection

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13
Q

Rapid-acting insulin such as Lispro, Aspart, Glulisine have a (short/long) duration of action and have a (higher/lower) incidence of hypoglycemia.

A

Rapid:
- short duration
- lower incidence

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14
Q

Rapid-acting insulin such as Lispro, Aspart, Glulisine attain (higher/similar/lower) concentrations after subcut injection compared to conventional human insulin and reduce post-prandial glucose to a (greater/similar/lower) extent.

A

Rapid:
- high conc. and greater post-prandial reduction than endogenous insulin

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15
Q

What is an example of short-acting insulin?

A

Regular human insulin

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16
Q

When is regular human (short-acting) insulin administered?

A

at least 20-30mins prior to meals

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17
Q

Can regular insulin be administered IV vs subcutaneously?

A

Yes esp during a hyperglycaemic crisis

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18
Q

Regular (short-acting) insulin is associated with (greater/lower) hypoglycemia risk than rapid-acting insulin.

A

Regular > risk than rapid

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19
Q

What is an example of intermediate-acting insulin?

A

Neutral Protamine Hagedorn (NPH)
- cloudy

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20
Q

Why does NPH (intermediate-acting) have a high risk of hypoglycemia?

A

1) High intra/inter px variability of NPH action
2) Long peak effect (NPH acts as basal and prandial so px HAVE to eat when insulin is peaking)

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21
Q

NPH typically requires ____ a day dosing.

A

Twice

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22
Q

What are 2 examples of long acting insulin analogues?

A

1) Glargine
2) Detemir

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23
Q

Insulin glargine and detemir (long-acting) have virtually no plasma peak and act for 18-24 hours. Hence, it can be administered ______ daily.

A

once daily as background insulin

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24
Q

Why are insulin glargine and detemir long acting?

A

Glargine: forms aggregates at physiological pH and slowly release insulin

Detemir: self-association and binding to albumin

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25
Long acting insulin such as glargine and detemir have (higher/lower) intra-subject variation and (higher/lower) risk of hypoglycemia than NPH
Long acting: lower variation, lower risk than intermediate (NPH)
26
Long-acting insulins (can/cannot) be mixed in the same syringe with other insulins.
Cannot - could change how the insulin works
27
What are 3 ways to mix insulins?
Just prior to administration: 1) Regular + NPH 2) Rapid + NPH 3) Aspart (Rapid) + Degludec
28
Which insulins CANNOT be mixed?
1) Glargine w anything (incompatible pH) 2) Glulisine w anything (except NPH) 3) Detemir w anything (not recommended by manufacturer)
29
What are 3 methods of insulin administration?
1) Subcutaneous (default) 2) IV (emergency) 3) Nasal (AVOID IM and areas with bruises, scar, joints, groin, navel)
30
What are 5 factors influencing PK of insulin?
1) Injection site (abdo faster than arm, buttock, thighs) 2) Depth of injection (muscles faster than subcut faster than superficial) 3) Larger volumes delay absorption 4) Exercise (specific muscle group → faster abs) 5) Massage of injection site/Heat (faster)
31
What is a key cause of drug-induced hyperglycemia?
Steroids (glucocorticoids)
32
What are 4 risk factors of hypoglycemia?
1) Advanced age 2) Renal impairment 3) Intensive insulin regiment 4) poor oral intake/prolonged fasting w high activity levels
33
How is hypoglycemia managed?
1) Consume glucose tablets or drinking fruit juice 2) If severe: glucagon
34
What are 2 AEs of insulin treatment?
1) Hypoglycemia 2) Lipodystrophy (lipoatrophy or lipohypertrophy)
35
What are 3 ways to diagnose DM?
1) Casual plasma glucose >11.1mmol/L 2) Fasting plasma glucose >7.0mmol/L 3) 75g of glucose and measure after 2 hours >11.1mmol/L
36
What are the caveats of using HbA1C to diagnose DM?
1) Haemoglobinopathies 2) Anything that increases/decreases RBC turnover
37
What are 5 classes of hypoglycemic agents other than insulin used for DM management?
1) Insulin sensitizers a) Biguanide - Metformin b) Thiazolidinedione - Pioglitazone 2) Insulin secretagogues a) Sulfonylureas - Glibenclamide, Glipizide, Gliclazide b) Meglitinides - Repaglinide 3) α-glucosidase inhibitors a) Acarbose 4) Incretin based therapy a) DPP4 inhibitors - Sitagliptin, Linagliptin b) GLP-1 receptor agonist - Semaglutide, Liraglutide 5) SGLT2 inhibitor a) Dapagliflozin b) Empagliflozin
38
What is the first line monotherapy for T2DM?
Metformin
39
What is the moa of biguanides/metformin?
1) ↓hepatic glucose production 2) ↑density of insulin receptors @ tissues 3) ↓intestinal glucose absorption 4) ↑muscular glucose absorption (GLUT4)
40
How does metformin affect (i) glucose tolerance, (ii) basal plasma glucose (iii) postprandial plasma glucose?
↑ glucose tolerance ↓basal & postprandial plasma glucose
41
Metformin PK: A D M E T1/2: DOA:
Metformin PK: A: Oral, 1-3x w meals D: rapid, minimal binding to serum proteins M: NA E: urine T1/2: 1.5/3h DOA: 8-12h
42
What are 2 AEs of metformin?
1) GI issues - diarrhoea, vomiting, indigestion - take w meals 2) ↑B12 malabsorption - metformin affects gut flora - worsen peripheral neuropathy 3) ↑risk of lactic acidosis - CI in renal problems, acute or chronic metabolic acidosis
43
True or false: px with metformin Rx should be monitored for hypoglycemia.
False. Metformin doesn't cause hyperinsulinemia or hypoglycemia - just ↑ sensitivity to insulin
44
What is the moa of thiazolidinediones (eg. Pioglitazone)?
Activation of PPAR-y nuclear transcription factor → i) regulate glucose metabolism ii) adipogenesis iii) ↑insulin sensitivity @ adipose, liver, skeletal muscles iv) ↑GLUT1 and 4 → ↑tissue insulin sensitivity
45
What are 3 AEs of Pioglitazone?
1) Weight gain 2) Peripheral edema 3) ↑HF risk 4) Fractures 5) CYP450 inducer
46
Pioglitazone PK: A D M E
Pioglitazone PK: A: Oral (once daily w or w/o food) D: binds extensively to proteins M: hepatic E: fecal
47
When is pioglitazone contraindicated?
1) px with symptoms of angina or HF 2) postmenopausal women 3) px w hepatic impairments 4) obese px
48
What are 4 examples of sulfonylureas?
1st gen: 1) Tolbutamide 2nd gen: 2) Glipixide 3) Gliclaxide 4) Glibenclamide
49
True or false: Sulfonylureas and Meglitinides increase insulin secretion dependent on functioning ß cells
True
50
Describe the moa of sulfonylureas.
Binds to SU receptor proteins (subunits of K ATP channels) → inhibit K+ efflux → hyperpolarisation → open voltage-gated Ca2+ channels → trigger Ca2+ dependent exocytosis of insulin from ß cells
51
Sulfonylureas (Glipizide, Glibenclamide, Gliclazide) PK: A D M E Onset DOA
Sulfonylureas (Glipizide, Glibenclamide, Gliclazide) PK: A: Oral (1/2 daily, 30min before meals) D: - M: Hepatic E: All urine (glibenclamide also 50% fecal) Onset/DOA: Glipizide: 0.5h / 14-16h Glibenclamide: 1.5h / 24h Gliclazide: 4-6h / 10-24h
52
What are 2 AEs of Sulfonylureas?
1) Weight gain 2) Hypogly (esp elderly and renal/hepatic impairment)
53
When are sulfonylureas contraindicated?
1) Sulfa allergy 2) px with renal and hepatic impairment
54
What is the moa of meglitinides (eg. Repaglinide)?
Bind and close Katp channels on ß cells in a *glucose dependent* manner stimulating insulin release - SUR1 binding site (vs SU binding receptor)
55
Repaglinide PK: A D M E
Repaglinide PK: A: Oral (before each meal) D: F=56% M: hepatic E: 90% fecal, 8% renal
56
Why is repaglinide useful to control post-prandial glucose levels?
Rapid onset and short DOA
57
What are 2 AEs of repaglinide
1) Hypogly (but low since insulin release is glucose-dependent) 2) mild weight gain
58
In which px should caution be exercised when Rx repaglinide?
px w hepatic impairment
58
What is the moa of α-glucosidase inhibitors (eg. acarbose)?
Reversibly inhibit membrane-bound α-glucosidase in intestinal brush border → slow down post-prandial hyperglycemia
59
Acarbose PK: A D M E
Acarbose PK: A: Oral (w first bite of each meal) D: not absorbed M: intestinal bacteria and digestive enzymes E: fecal
60
What are 2 AEs of acarbose?
Higher glucose load in colon: 1) Gaseous distention 2) Flatulence
61
What are incretins?
Metabolic hormones released after eating - augment the secretion of insulin in a glucose-dependent manner 1) Glucose-dependent insulinotropic polypeptide (GIP) 2) Glucagon-like peptide-1 (GLP-1) - both short half-life because of their rapid inactivation by dipeptidyl peptidase-4 (DPP-4)
62
When is acarbose contraindicated?
1) px with GI diseases (eg. IBD) 2) px w severe renal and hepatic disease
63
What are 2 examples of DPP4 inhibitors?
1) Sitagliptin 2) Linagliptin
64
What is the moa of DPP4 inhibitors (eg. Sitagliptin, Linagliptin)?
Inhibit DPP4 → ↓degradation of incretins → prolonged action of: GLP-1 → ↑satiety + delayed gastric emptying → ↓body weight GIP → ↑ß cell mass + ↑insulin secretion ∴↑glucose-stimulated insulin release + suppress α-cell glucagon release + ↓hepatic glucose production
65
Sitagliptin + Linagliptin PK: A D M E
Sitagliptin + Linagliptin PK: A: Oral (once daily) D: Sita>Lina M: Sita Low hepatic > Lina minimal metabolism E: Sita 80% renal, Lina 80% fecal, 5% urine
66
True or false: dose adjustment is needed for DM px with chronic kidney w DDP4 inhibtors
False. Only Sitagliptin need, Linagliptin is excreted 80% fecal
67
What are 3 AEs of DDP4 inhibitors (eg. Sitagliptin, Linagliptin)?
1) Nasopharyngitis 2) Headache 3) ↑risk of pancreatitis
68
When should extra care be taken with Rx DDP4 inhibitors?
1) Financial concerns (both very ex) 2) px w CKD (For Slitagliptin) 3) px with Hx of pancreatitis
69
What are 2 examples of GLP1 receptor agonists?
1) Liraglutide 2) Semaglutide
70
What is the moa of GLP-1 receptor agonists (eg. Liraglutide, Semaglutide)?
Activate GLP-1 receptor i) ↑insulin release in presence of ↑[glucose] (glucose dependent) ii) delay gastric emptying → slower absorption of glucose from GIT iii) ↑satiety and ↓appetite → weight loss
71
Semaglutide, Liraglutide, Dulaglutide PK: A D M E
Semaglutide, Liraglutide, Dulaglutide PK: A: i) Sema (SQ: 1/wk, Oral: 1/day) ii) Lira (SQ: 1/wk, Oral: 1/day) iii) Dula (SQ: 1/wk) M: all Proteolytic
72
What are 4 AEs of GLP-1 receptor agonists (eg. Liraglutide, Semaglutide)?
1) GI (eg. nausea, vomiting, diarrhea) 2) Nasopharyngitis 3) ↑risk of pancreatitis 4) caution in px with Hx of suicidal attempts or active suicidal ideation
73
In which px should caution be taken with Rx GLP-1 receptor agonists (eg. Liraglutide, Semaglutide)?
1) Financial problems (very expensive) 2) px w Hx of pancreatits 3) px w Hx of suicidal attempts or active suicidal ideation
74
What are 2 examples of SGLT2 inhibtors?
1) Empagliflozin 2) Dapagliflozin
75
How do SGLT2 inhibitors (eg. Empagliflozin, Dapagliflozin) help in T2DM management?
Inhibit SGLT2 → ↓reabsoprtion of glucose → ↓renal threshold for glucose → ↑urinary glucose excretion
76
SGLT2 inhibitors (eg. Empagliflozin, Dapagliflozin) PK: A D M E
SGLT2 inhibitors (eg. Empagliflozin, Dapagliflozin) PK: A: Oral (once daily in the morning) D: High plasma protein binding E: urine and feces
77
What are 4 AEs of SGLT2 inhibitors?
1) Genitourinary infections (esp vulvovaginal candidiasis) 2) Hypotension (esp w other diuretics, antihypertensives) 3) DKA, specifically euglycemic DKA 4) ↑risk of lower limb amputation (use w caution with px w vascular disease)
78
Which of the drugs used in DM management risk hypoglycemia?
1) Sulfonylureas (Glipizide, Glibenclamide, Gliclazide) 2) Insulins
79
Which of the drugs used in DM management risk weight changes?
Neutral: 1) Metformin 2) DPP4 inhibitors (Sitagliptin, Linagliptin) Gain: 1) Thiazolidinediones (Pioglitazone) 2) Sulfonylureas (Glipizide, Glibenclamide, Gliclazide) 3) Insulins Loss: 1) SGLT2 inhibitors (Dapagliflozin, Empagliflozin) 2) GLP1 receptor agonists (Semaglutide, Liraglutide)
80
Which of the drugs used in DM management are cardiorenal protective?
1) SGLT2 inhibitors (Dapagliflozin, Empagliflozin) 2) GLP-1 receptor agonists (Semaglutide, Liraglutide)

Endocrine System (9 decks)

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