Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology III > Type II DM > Flashcards

Type II DM Flashcards

1
Q

What is the pathology/presentation of DM type II?

A

Insulin resistance
Relative insulin deficiency
Gradual onset
Patient often obese or history of obesity
Often asymptomatic
Mico/macrovascular complications often present at diagnosis

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

What are the other physiologic issues in Type II DM?

A

Reduced circulating levels of Glucagon-like peptide (GLP-1)
GLP-1 released from distal ileum and colon in response to food containing carbs and fats
Loss of first-phase insulin response
Loss of Amylin
Amylin and insulin secreted from beta-cells
Absent in Type I; same fate as insulin in Type 2

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

How is type II diabetes diagnosed?

A 
FPG >/= 126mg/dL (preferred test)
                  OR
Symptoms of diabetes + casual plasma glucose >/= 200 mg/dL
                  OR
Oral glucose tolerance test  (OGTT): 
   2hr-postload glucose >/= 200 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the definition of Pre-Diabetes?

A

Impaired fasting glucose (IFG) = FPG 100-125 mg/dL
Impaired glucose tolerance (IGT) = 2-hr post-load glucose 140-199 mg/dL
IFG and IGT indicate a risk factor for diabetes and cardiovascular disease

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

Who should be screened for diabetes and how should it be done?

A

-Screening identifies asymptomatic patients who might have diabetes
-Consider in patients of any age if their BMI ≥ 25 kg/m2 and they have an additional risk factor for diabetes
-If no risk factors are present, begin at age 45
FPG (fasting plasma glucose) should be done initially
-Repeat screening every 3 years

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

When should you screen children for type II DM?

A

Overweight: BMI >85th percentile for age and sex, wt for height >85th percentile, or weight >120% of ideal for height
Plus 2 of the following
FH of type 2 diabetes in 1st or 2nd degree relative
Native American, African American, Latino, Asian American, Pacific Islander
Signs of insulin resistance ( acanthosis nigricans, hypertension, dyslipidemia, or PCOS)
Maternal history of diabetes or gestational diabetes

Start testing at age 10 or onset of puberty
Test FPG every 2 years

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

What are the three major metabolic abnormalities that contribute to hyperglyceemia in NIDDM?

A

Defective glucose-induced insulin secretion
Increased hepatic glucose output
Inability of insulin to stimulate glucose uptake in peripheral target tissues.
These abnormalities involve the cellular glucose transport in cells, liver, adipose tissue and skeletal muscle.
Also reduced sensitivity of fat and muscle cells to the effects of insulin (insulin resistance).

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

What are the other causes of insulin resistance?

A 
Cushing’s Syndrome (excessive corticosteroids)
Acromegaly (excessive growth hormone)
Polycystic ovarian syndrome
Hyperandrogenism
Hirsutism
Menstrual irregularities
Obesity 
infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the microvascular complications of DM?

A

Retinopathy-occurs when microvasculature that supplies the retina becomes damaged
Nephropathy-most common complication reported in type II, pain, tingling, or numbness in the extremeties
Neuropathy

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

What are the macrovascular complications of DM?

A

Atherosclerotic Cardiovascular diagnosis

Dyslipidemia

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

What is the A1C goal for adults in general?

A

A1C goal for adults in general is < 7.0%

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

What is used for diabetes prevention in patients with IGT or IFG?

A 
Weight loss (7% of body weight) and ↑ physical activity (150 min/week)	
Helps patients from progressing from pre-DM to DM. 
14 g dietary fiber/1000 kcal
Drugs studied for prevention
Metformin
Rosiglitazone
Acarbose
Troglitazone
Orlistat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is gestational diabetes mellitus (GDM)?

A

Glucose intolerance with onset or first detection during pregnancy
Associated with maternal morbidity
Fetal macrosomia
Higher rate of pre-eclampsia
Mother is then at risk for developing type 2 diabetes later on

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

Who is at very high risk for GDM?

A 
Severe obesity
Prior history of GDM or delivery of large-for-gestational age infant
Presence of glycosuria
Diagnosis of polycystic ovarian syndrome
Strong family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When should women be screened for GDM?

A

Women at very high risk should be screened as soon as possible after confirmation of pregnancy
All other women should be screened at 24-28 weeks of gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What diagnosis a woman with GDM?

A 
Fasting ≥ 95 mg/dL
 1h ≥ 180 mg/dL
 2h ≥155 mg/dL
 3 h ≥ 140 mg/dL
 Women with GDM should be screened for type 2 diabetes 6-12 weeks postpartum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the clinical management of diabetes?

A

Diet and exercise are the cornerstone of management of diabetes regardless of severity of symptoms.
>7% weight loss
150 min/wk exercise
14 g dietary fiber/1000 kcal
Therapeutic management must be highly individualized.

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

What is the goal of diabetes management?

A

Goal: To improve symptoms of hyperglycemia, reduce onset & progression of microvascular and macrovascular complications, reduce mortality & improve QOL.

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

What is the treatment of DM?

A 
Improve sugars but aggressive management of traditional cardiovascular risk factors is required as well.
Smoking cessation
Lipid management
Blood Pressure control
Antiplatelet therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When should a patient with DM monitor blood glucose levels?

A

Self monitoring of blood glucose (SMBG)
At least 3 times/day if on insulin injections
If on orals, just use SMBG to help them achieve their glycemic goals
Use the data to make decisions on what therapy to add

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

When should a patients A1C be monitored?

A

At least twice a year in patients at goal

Every 3 months in patients whose therapy has changed or aren’t meeting treatment goals

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

Secretagogues Sulfonylureas- MOA

A

Direct stimulation of insulin release from viable pancreatic beta-cells thus reducing blood glucose levels (↑ insulin secretion)
Blocks ATP-sensitive K+ channels, resulting in depolarization and Ca++ influx->release of insulin
At higher doses these drugs also decrease hepatic glucose production
Decreased levels of glucagon
Derivatives of sulfonamides, but no antibacterial activity

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

Secretagogues Sulfonylureas- Efficacy

A

↓ A1C 1.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the drug names of the sulfonylureas?

A

Glyburide, Glipizide, Glimepiride (Amaryl®)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Glyburide, Glipizide, Glimepiride (Amaryl®)- clinical uses
Mild to moderate Type 2 diabetes Ineffective in Type I diabetics and severe diabetics as the number of viable beta cells is very small. Not used in gestational diabetes (not good for the baby)
26
Glyburide, Glipizide, Glimepiride (Amaryl®)- ADRs
``` HYPOGLYCEMIA --Elderly, hepatic/renal impairment; combo therapy WEIGHT GAIN Muscular weakness Dizziness Confusion Skin rash Photosensitivity Blood dyscrasias Cholestatic jaundice ```
27
Glyburide
Sulfonylureas Administer with breakfast or first main meal Greater risk of hypoglycemia than other sulfonylureas: longer half-life Not recommended if CrCl < 50 ml/min (use a different sulfonylurea) 2009 guidelines do not recommend glyburide as a first line sulfonylurea
28
Glipizide
Sulfonylureas Administer 30 min before first main meal Not recommended if CrCl < 10 ml/min
29
Glimepiride
Administer with first main meal Not recommended if CrCl < 22 ml/min Response of sulfonylureas plateaus after half the max dose Reduced GI absorption if blood glucose > 250 mg/dL
30
When should sulfonylureas be administered?
With a meal. Associated with a meal time dose.
31
Glyburide, Glipizide, Glimepiride (Amaryl®) (sulfonylureas)- Monitoring
FPG in two weeks | A1C in 3 months
32
Glyburide, Glipizide, Glimepiride (Amaryl®) (sulfonylureas)- Contraindications/cautions
Cross-sensitivity to sulfa Higher risk w/hypoglycemia in patients w/renal or hepatic disease. Avoid w/ETOH Cross placenta and decrease fetal insulin->contraindicated in pregnancy
33
Glyburide, Glipizide, Glimepiride (Amaryl®) (sulfonylureas)- Drug interactions
``` may potentiate hypoglycemia via reduced hepatic metabolism, decreased urinary excretion or displacement from plasma proteins Sulfonamide antibacterials Propranolol Salicylates Phenylbutazone ETOH ```
34
Meglitinides- MOA
Short-acting secretagogues Stimulate insulin release from pancreatic beta-cells Shorter half life than sulfonylureas Rapid release of insulin that only lasts 1-2 hours Taken with meals- targets postprandial glucose levels
35
Meglitinides-- efficacy
↓ A1C by 1.5%
36
Meglitinides- adverse effects
Hypoglycemia- less than with sulfonylureas | Weight gain
37
Meglitinides- Monitoring parameters
FPG at 2 weeks Postprandial glucose at initiation A1C at 3 months
38
What are the biguanides?
Metformin (Glucophage)
39
Metformin (Glucophage®)- MOA
Does not affect insulin secretion but requires the presence of insulin to be effective. Decrease production of hepatic glucose production. Decrease intestinal glucose absorption. Incease peripheral glucose uptake. Increase insulin sensitivity at sights of insulin uptake
40
Metformin (Glucophage®)- Efficacy
↓ A1C by 1.5%
41
Metformin (Glucophage®)- clinical uses
Works best in patients w/significant hyperglycemia Often considered first-line therapy in the treatment of mild to moderate Type 2 overweight diabetics who demonstrate insulin resistance
42
Metformin (Glucophage®)- ADRs
GI symptoms (up to 50%)—less when taken w/food. Diarrhea, abdominal bloating, nausea Titrate dose at weekly intervals to minimize AEs Give with meals HAS THE ABILITY TO CAUSE LACTIC ACIDOSIS—very rare, but a greater potential w/: renal failure- biggest one. CHF Hypoxemia ETOH use
43
Metformin (Glucophage®)- Monitoring
SCr at baseline FPG at 2 weeks A1C at 3 months Hypoglycemia is rare
44
How is lactic acidosis developed with metformin?
Increase production of lactate in the intestine leads to increased portal lactate which equals decreased liver pH leading to decreased lactate metabolism and lactate accumulation in the blood.
45
Metformin (Glucophage®)- Contraindications
Renal impairment SCr >1.5 for men SCr >1.4 for women Acute or chronic metabolic acidosis- not DOC because risk of worsening this
46
Metformin (Glucophage®)- Precautions
Radiocontrast studies-- Hold metformin for 48 hours. Important to remember Age>80 unless normal GFR Hypoxic states Liver dysfunction Alcoholism Heart failure requiring pharmacologic therapy
47
What are the benefits or metformin?
No weight gain No hypoglycemia as monotherapy Inexpensive Approved for use as monotherapy and in combination with other therapy
48
What are the thiazolidinediones (TZDs) insulin sensitizers?
Rosiglitazone (Avandia) and Pioglitazone (Actos)
49
Rosiglitazone (Avandia) and Pioglitazone (Actos)- Efficacy
↓ A1C by 0.5-1.4%
50
Rosiglitazone (Avandia) and Pioglitazone (Actos)- MOA
PPAR-gamma receptor activators (Peroxisome proliferator-activated receptors) which regulate glucose metabolism resulting in increased insulin sensitivity in adipose, liver and skeletal muscle Biologic effect may not be seen for 4 weeks Insulin required for action…doesn’t promote insulin release from pancreas due to acting at the tissues. Don’t give exogenous insulin with Avandiaedema
51
Rosiglitazone (Avandia) and Pioglitazone (Actos) (TZDs)- Cardiovascular effects
Pioglitazone: Increased HDL; Decreased triglycerides Rosiglitazone: Increased LDL and HDL Change in LDL more buoyant and less atherogenic lipoproteins Inhibit vascular smooth muscle proliferation in coronary and carotid vessels
52
Rosiglitazone (Avandia) and Pioglitazone (Actos) (TZDs)- Adverse effects
``` Fluid retention and peripheral edema Weight gain Fluid retention is major contributor Redistribution of adipose tissue New-onset heart failure <1% 2-3% when combined with insulin ```
53
Rosiglitazone (Avandia) and Pioglitazone (Actos) (TZDs)- Contraindications
``` Alcohol abuse Elevated liver enzymes Hepatotoxicity d/c liver enzymes rise 2-3 times the upper limit of normal Hepatic disease HF NYHA class III or IV ```
54
When are TZDs used in heart failure?
``` Use of TZDs in patients with NYHA class I or II HF May be used with initiation of treatment at lowest dosage (rosiglitazone 2mg daily or pioglitazone 15 mg daily) Observe for weight gain, edema or exacerbation of HF Do not use TZDs in patients with NYHA class III or IV HF ```
55
What are the alpha-glucosidase inhibitors?
Acarbose (Precose®) | Miglitol (Glyset®)
56
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)- MOA
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)-Delays intestinal carbohydrate absorption Inhibits alpha-glucosidase found in the small intestinal brush border Prevent glucose absorption and decreases post-prandial glucose levels
57
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)- Efficacy
↓ A1C 0.5-0.8%
58
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)- Adverse effects
Not well tolerated In clinical trials 25-45% discontinuation GI disturbances Loose stools Flatulence Abd. Cramping Minimize these effects by starting low, going slow Can also be minimized by curtailment of carbohydrate consumption. Usually transient effects Does NOT cause wt. gain Hypoglycemia does not occur
59
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)- Contraindications
Chronic intestinal disease | Cirrhosis
60
Acarbose (Precose®), Miglitol (Glyset®) (Alpha-glucosidase inhibitors)- monitoring
Post prandial glucose at initiation | A1C in 3 months
61
What are the Dipeptidyl peptidase-4 (DPP-4) inhibitor s?
Sitagliptin (Januvia®) | Saxagliptin (Onglyza)
62
Sitagliptin (Januvia®), Saxagliptin (Onglyza) (DPP-4 inhibitors)- MOA
Prevent degradation of endogenous glucagon-like peptide-1 (GLP-1) and insulinotropic polypeptide (GIP) Incretin hormones released in response to meal Increase insulin synthesis and release from beta cells Intracellular signaling GLP-1 also lowers glucagon secretion from pancreatic alpha cells Results in increased insulin release and decreased glucagon levels in circulation in glucose-dependent manner
63
Sitagliptin (Januvia®), Saxagliptin (Onglyza) (DPP-4 inhibitors)- efficacy
↓ A1C 0.5-0.7% Dose adjusted for CrCl Approved for monotherapy or combination therapy Weight neutral
64
Sitagliptin (Januvia®), Saxagliptin (Onglyza) (DPP-4 inhibitors)- Adverse effects
Well tolerated Similar to placebo Few post-marketing
65
Sitagliptin (Januvia®), Saxagliptin (Onglyza) (DPP-4 inhibitors)- Contraindications
Haven't been identified yet
66
Sitagliptin (Januvia®), Saxagliptin (Onglyza) (DPP-4 inhibitors)- monitoring
Renal function | A1C in 3 months.
67
Colesevelam (WelChol)- MOA
Bile acid sequestrant: received FDA indication in January 2008 for Type 2 diabetes as an adjunct to diet and exercise Previously only approved for LDL reduction
68
Colesevelam (WelChol)- Efficacy
↓ A1C 0.4-0.8% | Not indicated as monotherapy
69
Colesevelam (WelChol)- Adverse effects
Constipation/nausea/indigestion | Increased triglycerides
70
Colesevelam (WelChol)- Contraindications
Bowel obstruction History of hypertriglyceridemia-induced pancreatitis Triglycerides >500 mg/dL
71
What are the oral therapies?
-Secretagogues sulfonylureas- Glyburide, Glipizide, Glimepiride (Amaryl®) -Meglitinides- Repanglinide (Prandin) and Nateglinide (Starlix) -Biguanides- Metformin -Thiazolidinediones (TZDs) Insulin Sensitizers - Rosiglitazone (Avandia) and Pioglitazone (Actos) -Alpha-Glucosidase Inhibitors-Acarbose (Precose®) Miglitol (Glyset®) - Dipeptidyl peptidase-4 (DPP-4) inhibitor - Sitagliptin (Januvia®), Saxagliptin (Onglyza) -Colesevelam (WelChol)
72
What are the non-oral therapies?
Glucagon-like peptide 1 (GLP-1) agonists-Exenatide (Byetta) | Pramlintide (Symlin)
73
Repaglinide (Prandin)
``` Meglitinides- Short-Acting Secretagogues Approved for monotherapy or in combination w/metformin. Taken before meals 3 X/day Allergy to sulfas not an issue ADR hypoglycemia ```
74
Nateglinide (Starlix)
Meglitinides- Short-Acting Secretagogues Phenylalanine derivative Faster onset of action and shorter duration of action than repaglinide; less A1C reduction than repaglinide Approved for monotherapy an combination w/metformin. Taken 3X/d before meals
75
Exenatide (Byetta)- MOA
``` Glucagon-like Peptide 1 (GLP-1) agonists GLP-1 analog Incretin mimetic Resistant to degradation by DPP-4 Suppresses high glucagon levels Delays gastric emptying (can affect absorption of other meds) ```
76
Exenatide (Byetta)- Efficacy
↓ A1C 0.5-1%
77
Exenatide (Byetta)- indications
FDA approved for type 2 diabetes in patients on metformin, sulfonylurea, TZD, or a combination who are not at goal Not yet approved for use with basal insulin
78
Exenatide (Byetta)- Adverse effects
N/V/D (30-45%0 Modest weight loss Hypoglycemia wspecially in combination with sulfonylureas Anti-exenatide antibodies
79
Exenatide (Byetta)- Monitoring
Renal function | A1C in 3 months
80
Exenatide (Byetta)- Contraindications
Type I DM
81
Exenatide (Byetta)- Precautions
ClCr <30 ml/min Gastroparesis Hypoglycemia
82
Pramlintide (Symlin)- indications
FDA approved for Type 1 or 2 diabetes in patients on optimal insulin therapy who are still not at goal With or without metformin and/or sulfonylurea therapy
83
Pramlintide (Symlin)- Efficacy
↓ A1C ~0.1-0.4% in type 1; 0.3-0.7% in type 2
84
When is pramlintide administered?
In conjunction with mealtime insulin
85
What is the treatment of CHD is a patient with DM?
Should receive at least a daily aspirin unless contraindicated (81mg baby aspirin)
86
What is the treatment of Hyperlipidemia in a patient with DM?
Statin
87
What is the treatment of hypertension in a patient with DM?
ACEI or ARB 1st line in combination with a thiazide diuretic
88
What should you use to lower LDL in a patient with DM?
1st choice: Statin Statin should be added (along with lifestyle intervention) regardless of lipid levels in diabetic patients with: Overt CVD Without CVD who are over the age of 40 and have one or more other CVD risk factors In pts whose LDL goal can’t be achieved, a 30-40% reduction is acceptable 2nd choice: BAR- bile acid resin, niacin, or fibrate (non of these are first line)
89
What is hyperosmolar hyperglycemic state?
Hyperosmolar hyperglycemic state (HHS) is a life threatening condition similar to DKA Extreme hyperglycemia and fluid deficits Arises from inadequate insulin but occurs primarily in older type II patients HHS lacks lipolysis, ketonemia, and acidosis (this is the difference of why its not DKA) Illness often precipitates (usually have some sort of illness) Patients with hyperglycemia and dehydration lasting several days to weeks are at greatest risk of developing HHS.
90
How is HHS diagnosed?
Plasma glucose > 600mg/dL | Serum osmolality of > 320 mOsm/kg
91
How is HHS treated?
Rehydration Correction of electrolyte imbalances Continuous insulin infusion Reduce blood glucose levels gradually to avoid cerebral edema

Pharmacology III (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions