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pharmacology exam 3 > diabetes mellitus > Flashcards

diabetes mellitus Flashcards

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1
Q

T1DM age of onset

A

Usually during childhood or young adulthood
Can occur at any age across the lifespan

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2
Q

T2DM age of onset

A

Usually adulthood
Risk for it increases with age, obesity, and lack of physical exercise

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3
Q

T1DM etiology

A

Unknown

Postulated causes include:
- Heredity
- Autoimmune response against insulin-producing beta cells
- Viral infections

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4
Q

T2DM etiology

A

Unknown, but related to weight, age, inactivity, and genetics

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5
Q

T1DM endogenous insulin

A

Secretion is markedly diminished in early disease
May be totally absent later

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6
Q

T2DM endogenous insulin

A

Levels may be low (insulin deficiency), normal, or high (insulin resistance)

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7
Q

two subtypes of T1DM

A
  • Immune-mediated
  • Non-immune mediated, or idiopathic
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8
Q

immune-mediated T1DM

A
  • Leads to the destruction of the pancreatic beta cells and absolute insulin deficiency
  • Results from the presence of various autoantibodies to islet cells, insulin, and enzymes such as glutamic acid decarboxylase-65 (GAD65)
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9
Q

nonimmune or idiopathic T1DM

A
  • Do not have autoimmune pancreatic damage, but do show a lack of insulin
  • Inherited
  • Cause is unknown
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10
Q

T1DM has a long preclinical period over months to years

A

s/s and clinical presentation are abrupt, although the autoimmunity effects and a decline in insulin secretion begin long before the s/s develop

  • The insulin-secreting beta cells of the pancreas must lose 80-90% of their function before hyperglycemia occurs
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11
Q

insulin resistance

A

a suboptimal sensitivity to insulin, especially in the liver, muscle, and adipose tissue
- result is an increased rate of endogenous glucose production secondary to increased glucagon levels

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12
Q

GI system plays a role in regulating the secretion of insulin

A

Incretin peptides secreted from endocrine cells in the intestinal tract are released in response to ingestion of food
- GLP-1 and alterations in levels of the regulatory enzyme DPP-4
- Affects the presence and duration of GLP-1 action

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13
Q

GLP-1 actions

A

Contributes to the excessive hepatic glucose production, lack of postprandial glucagon suppression, and uncontrolled eating
- deficient in people with DM and prediabetes

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14
Q

insulin resistance has been linked to three other important disorders

A

o Dyslipidemia
o HTN
o CAD

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15
Q

insulin has a direct antiplatelet effect

A

A loss of insulin results in:
- Increased adhesiveness
- Exaggerated aggregation
- Thrombus generation

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16
Q

prediabetes

A

Individuals whose glucose levels do not meet the criteria for DM but are too high to be considered normal are classified as having prediabetes
- Have impaired glucose tolerance, impaired fasting glucose, and/or elevated HbA1c between 5.7-6.4%

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17
Q

metformin for prediabetes

A

for those at high risk of developing DM
- obese and younger than 60 y/o

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17
Q

current recommendations in the treatment of prediabetes

A

continue to support intensive behavioral lifestyle interventions
1. achieving and maintaining modest weight loss
2. increasing moderate-intensity physical activity to at least 150 min per week
3. dietary changes
4. metformin to be considered for those at high risk for developing DM

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18
Q

DM diagnostic criteria

A
  1. Acute s/s of diabetes plus random or casual plasma glucose concentration < 200mg/dL
  2. Fasting plasma glucose < 126 mg/dL
  3. OGTT 2-hour postload plasma glucose >/= 200 mg/dL
  4. HbA1c > 6.5%
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19
Q

prediabetes diagnostic criteria

A
  • Fasting plasma glucose 100-125 mg/dL
  • OGTT 140-199 mg/dL 2 hr after ingestion of standard glucose load
  • HbA1c 5.7-6.4%
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20
Q

insulin pharmacodynamics

A
  • Release is stimulated by elevated blood glucose levels
  • Administration of exogenous insulin produces the same effect as the naturally occurring hormone
  • Release occurs at both a low basal rate and high-level bolus rate b/c of meals or high blood glucose levels, stress, or vagal response
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21
Q

insulin definition

A

a hormone produced in the beta cells of the islets of Langerhans in the pancreas

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22
Q

insulin lowers blood glucose levels by the following mechanisms

A
  • Stimulates storage of glucose as glycogen (glycogenesis) in muscle and liver cells
  • Inhibits glucose production in liver and muscle cells (glycogenolysis)
  • Promotes protein synthesis by increasing amino acid transport into cells
  • Enhances fat storage (lipogenesis) and prevents mobilization of fat for energy (lipolysis and ketogenesis)
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23
Q

Various insulin regimens can be used for the treatment of T1DM, including SAI or RAI boluses combined with intermediate-acting insulin (IAI) or LAI for basal coverage

Study These Flashcards
A

Can be achieved with premixed preparations such as:
 Humulin 70/30
 Novolin 70/30
 Novolog Mix 70/30

24
metformin overview
- Works primarily by decreasing hepatic glucose production by decreasing gluconeogenesis - increases peripheral glucose uptake and utilization - Improves hepatic response to blood glucose levels so the liver produces the appropriate amounts of glucose - Decreases intestinal absorption of glucose
25
only oral antidiabetic medication approved for children
metformin Only FDA approved oral drug for use in children 10 years or older
26
initial metformin therapy is indicated for
T2DM with dyslipidemia, obesity, insulin resistance, and an elevated FPG
27
sulfonylureas
increase the endogenous insulin secretion by the beta cells - may improve the binding between insulin and insulin receptors or increase the number of receptors on body cells - considered secondary agents b/c of their hypogylcemic risks and weight gain
28
alpha-glucosidase inhibitors
- do not act directly on any of the defects in metabolism seen in T2DM - competitively inhibit and delay the absorption of complex CHO from the small bowel and lower blood glucose levels after meals - activity is effective on any CHO food intake, including liquid diets taken through NG tube - have limited role in adjunct therapy except in individuals who cannot take metformin
29
thiazolidineiones (TZDs)
oral antidiabetic drugs that are best classified as insulin sensitizers - TZDs activate a nuclear receptor that regulates gene transcription -> results in increased use of available insulin by the liver, muscles cells, and adipose tissues - Additionally, TZDs reduce hepatic glucose production so that the liver produces the appropriate amount of glucagon Recommended as dual or triple therapy
30
cautious use of TZDs
should be use cautiously b/c of their potential for heart failure and edema
31
TZD medications
o Pioglitazone (Actos) o Rosiglitazone (Avandia)
32
meglitinides
The meglitinides are short-acting insulin secretagogues - Secretagogue: a substance that stimulates the secretion of other substances by the cells
33
meglitinide medications
o Repaglinide (Prandin) o Nateglinide (Starlix)
34
meglitinide MOA
- Work by closing the ATP-dependent potassium channels in the beta-cell membrane by binding at specific receptor sites - This potassium channel blockage depolarizes the beta cell and leads to an opening of calcium channels - The resultant influx of calcium increases the secretion of insulin
35
meglitinides have a very short effect
o They are only in plasma for approx. 2 hours o Insulin levels fall to baseline by 4 hours after dosing The result of their stimulation of insulin secretion o Acts like the physiological response of natural insulin o Lowers postprandial blood glucose levels
36
administration of meglitinides
administered TID, no more than 20 min before meals
37
SGLT-2 inhibitor medications
o Canagliflozin (Invokana) o dapagliflozin (Farxiga) o empagliflozin (Jardiance) o ertugliflozin (Steglatro)
38
SGLT-2 inhibitor MOA
inhibit the action of selective sodium-glucose cotransporter 2 (SGLT2) in the kidney - blocks about 90% of the reabsorption of glucose in the kidneys - promotes excretion of excess glucose in the urine
39
major side effects of SGLT-2 inhibitors
genital yeast or UTIs - related to the continuous presence of glucose in urine
40
what is GLP-1?
A naturally occurring hormone released from the gut after ingesting a meal
41
what does GLP-1 do?
- Promotes satiety - Decreases gastric emptying - Increases glucose-dependent insulin release from pancreatic beta cells - Decreases glucagon release from pancreatic alpha cells
42
GLP-1 / DPP-4 relationship
GLP-1 is rapidly inactivated by the DPP-4 enzyme
43
DPP-4 inhibitor medications
1. sitagliptin (Januvia) 2. saxagliptin (Onglyza) 3. linagliptin (Tradjenta) - does not require considerations for renal dysfunction 4. alogliptin (Nesina)
44
DPP-4 inhibitor MOA
act on the incretin hormone system to indirectly increase insulin production improve glycemic control by: - increasing insulin synthesis and secretion - reducing glucagon - slowing gastric emptying by prolonging the action of the remaining GLP-1 hormones - suppressing appetite
45
GLP-1 agonist medications
1. exenatide (Byetta) 2. liraglutide (Victoza) - FDA indication for obesity therapy and glycemic control for children 3. dulaglutide (Trulicity) 4. lixisenatide (Adlyxin)
46
GLP-1 agonist MOA
activate GLP-1 receptors -> decreasing FBG and FPG levels - increase insulin synthesis and secretion in the presence of elevated glucose levels - improve first-phase insulin release - lower glucagon - slow gastric emptying - reduce food intake
47
amylin
a pancreatic hormone that is released from the pancreas after a meal - role: to slow gastric emptying rates allows for a more gradual release of glucose into the system - prevents a sudden postprandial peak in plasma glucose - decreases the release of glucagon by the liver - satiety effect -> suppressed appetite
48
pramlintide (Symlin)
an injectable amylin hormone derivative that mimics these natural effects severe nausea is a common side effect, and the patient needs to inject the drug before meals so, it is not in widespread use
49
total daily insulin requirement is based on the patient's weight
o 0.4-1.0 units/kg/day with titration to glycemic targets o Higher doses may be indicated during acute illness o Adjustments up or down should be made in increments of 1U until sensitivity to insulin is well-understood by both provider and patient
50
initiating insulin therapy in pts w/ T2DM
start with LAI or IAI administered in single dose at bedtime or in the morning - typical starting dose: 6-10 U, or 0.1-0.25U/kg body weight/day - dose is increased by 2U every 2 days until daily FPG are consistently within the glycemic goal range
51
typical starting dose of SAI or RAI
Starting dose should be 0.3-0.5 U/kg/day - divided into the two- or three-injection regimen
52
medications shown to promote weight loss in DM
- metformin - GLP-1 agonists - GIP - DPP-4 meds - SGLT2 meds
53
meds associated with weight gain with DM
o Sulfonylureas o TZDs o Insulin
54
insulin and CAD
- Metformin has been associated with improving cardiovascular risk through its action in improving lipid levels - Two of the SGLT2 inhibitors, canagliflozin and empagliflozin, and one of the GLP-1 receptor agonists (liraglutide) are recommended for use in patients with type 2 DM and established ASCVD
55
all patients with DM and HTN should be treated with:
an ACEI or an ARB o Promote ventricular remodeling o Have been shown to significantly reduce the trajectory of diabetic nephropathy
56
current HLD guidelines with DM
All patients with DM, even those without ASCVD, will be started on statin therapy - treat all patients with DM with statins at either moderate- or high-intensity doses unless contraindicated
57
drugs approved by FDA to treat diabetic foot pain
* Duloxetine (Cymbalta) * pregabalin (Lyrica) * gabapentin * the opioid tapentadol meds used for their effect on the intrinsic pain-suppressing pathways -> Tricyclic antidepressants o nortriptyline (Aventyl, Pamelor) o desipramine (Norpramin) other meds used * venlafaxine * capsaicin cream

pharmacology exam 3 (14 decks)

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