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Gen Med: Ednocrine > Type 2 DM > Flashcards

Type 2 DM Flashcards

1
Q

What are the general characteristics of T2DM?

A
  1. Occurs in adults, adolescents and children
  2. Circulating endogenous insulin is sufficient to prevent ketoacidosis but is inadequate to prevent hyperglycemia
  3. Genetics and environment combine to cause beta cell loss and insulin resistance
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2
Q

What is the most important environmental factor contributing to insulin resistance?

A

Visceral obesity

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3
Q

What racial groups is T2DM more prevalent in?

A

African American, Native American, Hispanic American and Asian American populations in US compared w/ Caucasian Americans

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4
Q

What epidemiological trends are present in T2Dm?

A
  1. 39% pts with Type II DM have at least one parent w/ disease
  2. In identical twins with one affected, ~ 90% of unaffected twins eventually develop DM
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5
Q

What are the risk factors for T2DM?

A
  1. Family Hx
  2. Ethnicity
    A. African Americans, Hispanics, Native Americans, Asian Americans
  3. Obesity
  4. Fat distribution
    A. Visceral fat → insulin resistance
  5. Lifestyle factors
    A. Sedentary lifestyle, smoking, OSA
  6. Metabolic Syndrome
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6
Q

What is metabolic syndrome asst with?

A

high risk of diabetes, cardiovascular disease & stroke

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7
Q

What are the underlying causes of metabolic syndrome?

A
  1. Obesity / overweight
  2. Physical inactivity
  3. Genetics
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8
Q

Define metabolic syndrome

A

3 or more of following parameters:

  1. Abdominal obesity
  2. Triglyceride level > 150 mg/dL
  3. HDL cholesterol < 40 mg/dL in men or < 50 mg/dL in women
  4. SBP ≥ 130
  5. Waist circumference > 40 in (males) and > 35 in (females)
  6. FBS ≥ 100 mg/dL
  7. Insulin resistance or glucose intolerance
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9
Q

What are other insulin stimulating hormones?

A
  1. Incretin
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10
Q

What are the characteristics and function of incretin?

A
  1. Synthesized in ileum & colon in response to incoming nutrients
  2. Stimulate insulin secretion
  3. ↓ Glucagon secretion
  4. ↑ Beta cell survival
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11
Q

What is the most important incretin hormone?

A

GLP-1

Secretion abnormal in impaired glucose tolerance (IGT) & Type II DM

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12
Q

What are the actions of GLP-1?

A
  1. ↑ Glucose dependent insulin secretion
  2. Suppresses glucagon secretion
  3. Slows gastric emptying & promotes satiety
  4. ↑ Beta cell proliferation
  5. May improve insulin sensitivity
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13
Q

What are the sxs of T2DM?

A 
1. Asymptomatic
A. Most pts
2. Peripheral neuropathy
3. Blurred vision
4. Pruritis / skin infections
5. Candidal vaginitis
6. Acanthosis nigricans
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14
Q

Define acanthosis nigricans

A

Hyperpigmented and hyperkeratotic skin in axilla, groin, & back of neck

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15
Q

What are the urinalysis results in T2dm?

A
  1. Urinalysis
    A. Glycosuria
  2. Urine for micro-albumin
    A. Diabetic nephropathy

Baseline and annually

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16
Q

What is the FBS for impaired glucose tolerance?

A

FBS 100-126 mg/dL

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17
Q

What is the random glucose/2 hr GTT for DM?

A

Random glucose or 2 hr GTT ≥ 200 mg/dL

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18
Q

What do you do if FBS > 126 mg/dL?

A 
1. F/U with 2 hr GTT
A. Impaired (pre-diabetes) → 2 hr  GTT 140-200 mg/dL
(-) test:
B. Fasting glucose < 100 mg/dL
C. 2 hr gluc < 140 mg/dL
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19
Q

What are the lipid abnormalities with T2DM?

A

T. chol > 200 mg/dL
Trig 300-400 mg/dL
HDL < 30 mg/dL
LDL > 100 mg/dL

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20
Q

Why is an EKG performed for T2DM?

A

r/o CAD

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21
Q

Why are BUN/Cr and electrolytes tested?

A

Diabetic nephropathy

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22
Q

What are the CHO diet recommendations for a T2DM?

A

45-65% total calories

Count carbs to titrate insulin

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23
Q

What are the fat diet recommendations for a T2DM?

A

25-35% with < 7% from sat fats

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24
Q

What are the protein diet recommendations for a T2DM?

A

10-35%

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25
Q

What are the cholesterol diet recommendations for a T2DM?

A

< 200 mg/day if LDL > 100 mg/dL

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26
Q

Why is dietary fiber recommended for a T2DM?

A
  1. Slows nutrient absorption rates so glucose absorption is slower -> lowers hyperglycemia
  2. Favorable affect on cholesterol
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27
Q

What immunizations are recommended for T2DM?

A

Influenza

Pneumococcal

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28
Q

What is the HTN goal for T2DM?

A

Goal < 140/90 mmHg

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29
Q

What drugs are used to treat and prevent diabetic nephropathy?

A

ACEI or ARB

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30
Q

What is the lipid goal for T2DM?

A
  1. Goal LDL < 100 mg/dL

2. Statin therapy (*)

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31
Q

What are the treatment recommendations for CAD/PAD risk?

A
  1. Anti-platelet therapy

2. ASA or clopidogrel (Plavix)

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32
Q

What are the classes of drugs for treating hyperglycemia?

A 
1. Oral secretogogues
A. Sulfonylureas
B. Meglitinide analogs
C. D-Phenylalanine derivative
2. Biguanides
3. Thiazolidinediones (TZD’s)
4. Alpha glucosidase inhibitors
5. GLP-1 receptor agonists
6. DPP-4 inhibitors
7. Amylin analogs
8. Insulin
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33
Q

What is the moa and effects of sulfonyureas?

A
  1. Stimulate insulin release from pancreatic islet beta cells
  2. Bind to sulfonylurea receptor on beta cell
  3. ↑ insulin / ↓ pp serum glucose
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34
Q

What are the se and contraindications of sulfonyureas?

A
  1. Weight gain
  2. Hypoglycemia
    A. ↑ risk w/ certain long acting preparations
    B. Glyburide/Micronase
    3.Metabolized by liver & excreted by kidneys
    A. Contraindicated in pts with severe liver or kidney disease
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35
Q

What are the 1st generation sulfonyureas?

A
  1. Rarely used today

2. Includes Tolbutamide / Orinase, Clorpropamide / Diabenase

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36
Q

What are the 2nd generation sulfonyureas?

A
  1. Glyburide / Micronase

2. Glipizide / Glucotrol, Glucotrol XL

37
Q

What is the moa and effects of meglitinide analogs?

A
  1. MOA
    A. Stimulate insulin release from pancreatic islet beta cells
  2. Physiologic Effects
    Rapid but brief ↑ insulin -> ↓ pp serum glucose
38
Q

How are the meglitinides metabolized?

A
  1. Completely metabolized by liver
  2. Plasma half life < 1 hr
    A. Useful in pts w/ kidney disease
39
Q

What are the se of meglitinides?

A
  1. Weight gain

2. Hypoglycemia – less effect than glyburide

40
Q

What are examples of meglitinide analogs?

A
  1. “…nide” drugs

2. Repaglinide / Prandin

41
Q

What is the moa and effects of D-phenylalanine derivatives?

A
  1. MOA
    A. Stimulate insulin release from pancreatic islet beta cells
  2. Physiologic Effects
    A. Rapid but brief ↑ insulin -> ↓ pp serum glucose
42
Q

How are D-phenylalanine derivatives metabolized?

A

Completely metabolized by liver
Plasma half life 1.5 hrs
Useful in pts w/ kidney disease

43
Q

What are the se of D-phenylalanine derivatives?

A

Weight gain

Hypoglycemia – less effect than Glyburide

44
Q

What is an example of D-phenylalanine derivatives?

A

“….nide” drugs

Nateglinide / Starlix

45
Q

What is the moa and effects of biguanides?

A
  1. MOA
    A. ↑ number & affinity of insulin receptors in peripheral tissues
    B. ↓ hepatic glucose output
    C. ↓ glucose absorption from gut
    D. ↑ glucose uptake & utilization in skeletal muscle & adipose tissue
  2. Effects
    A. ↓ serum glucose
46
Q

How are biguanides metabolized?

A

Completely metabolized by kidneys

47
Q

What is first line therapy in T2DM pts?

A

Biguanides

Metformin / Glucophage

48
Q

What are the SE and contraindications of biguanides?

A 
1. SE
A. GI upset, abdominal bloating
B. DOES NOT  cause hypoglycemia
2. Contraindications
CHF
A. Renal Insufficiency
B. Hepatic Disease 
C. Metabolic (Lactic) D. Acidosis 
E. Excessive alcohol intake
49
Q

What is the moa and effects of TZDs?

A
  1. MOA
    A. Sensitize peripheral tissues to insulin  ↓ hepatic glucose production
    B. Dependent on presence of insulin for activity
  2. Effects
    A. ↓ pp serum glucose
    B. ↓ triglyceride levels
50
Q

What are the SE and contraindications for TZDs?

A 
1. SE
A. Fluid retention
B. CHF
C. Weight gain
D. DOES NOT cause hypoglycemia
2. Contraindications
A. NYHA Failure Class III & Class IV
B. Black box warning inc potential risk of MI
Limited use
51
Q

What are the TZDs?

A

“…zone” drugs
Rosiglitzone / Avandia
Pioglitazone / Actos

52
Q

What is the moa and effects of alpha glucosidase inhibitors?

A
  1. MOA
    A. Delays CHO absorption in gut
  2. Physiologic Effects
    A. Delays digestion of carbohydrates, resulting in smaller ↑ pp serum glucose
53
Q

What are the SE of Alpha glucosidase inhibitors?

A
  1. Bloating & flatulence

A. Due to undigested CHO reaching large bowel

54
Q

What are examples of alpha glucosidase inhibitors?

A
  1. Acarbose / Precose

2. Miglitol / Glyset

55
Q

What are the incretins?

A

Intestinal hormones that stimulate insulin release due to elevated GI glucose
Glucagon like peptide 1 (GLP-1)
Glucose-dependent insulinotropic polypeptide (GIP)

56
Q

What is the incretin effect in T2DM?

A

“Incretin effect” is reduced in pts with Type II DM

57
Q

What is the half life of GLP-1

A
  1. GLP-1 half life is 1-2 minutes
    A. Rapidly broken down by dipeptidyl peptidase 4 (DPP-4)
    B. As a result, GLP-1 receptor agonists were created
58
Q

What is the moa nd effects of GLP-1 agonists?

A 
1. MOA
A. Activates GLP-1 receptors
B. Physiologic Effects
C. ↑ insulin secretion 
D. Lower risk of hypoglycemia
E. ↓ glucagon secretion
F, Slows gastric emptying
G. ↓ hunger
H> Promotes weight loss
59
Q

What are the SE of the GLP-1 agonists?

A
  1. Reports of severe pancreatitis, renal impairment & ARF
  2. DO NOT use in CKD
  3. Black box warning - ↑ risk thyroid CA w/+ FH
60
Q

What are examples of the GLP-1 agonists?

A
  1. GLP-1 Receptor Agonists
    A. Liraglutide (Victoza)
    B. Exenatide (Byetta, Bydureon)
61
Q

What is the moa and effects of DPP-4 inhibitors?

A

Alternative approach to GLP-1 Agonists

1. MOA
A. Slows incretin metabolism
B. Inhibit DPP4 -> prolong action of GLP-1 & GIP
2. Physiologic effects:
A. ↑ insulin secretion 
B. Promotes ↑ glucose uptake by muscle & adipose tissue
C. ↓ glucagon secretion
D. ↓circulating glucose
62
Q

What are the SE of DPP-4 inhibitors?

A 
1. Most common
A. URI
2. Less common
A. Anaphylaxis
B. Angioedema
C. Stevens-Johnson Syndrome
63
Q

What are examples of the Dpp-4 inhibitors?

A 
1. “…gliptin” drugs
A. Sitagliptin (Januvia)
B. Saxagliptin (Onglyza)
C. Linagliptin (Tradjenta)
D. Alogliptin (Nesina)
64
Q

What is amylin and amyline analogs? Who are they used in?

A
  1. Released from beta cells with insulin

2. Used in Type I & Type II IDDM

65
Q

What is the mechanism of action of amylin analogs?

A
  1. ↓ pp glucose
  2. Delays gastric emptying
  3. Suppresses glucagon secretion
  4. Promotes satiety
66
Q

When are amylin analogs dosed?

A
  1. Injected immediately before meals

A. Hypoglycemia may occur & w/delayed gastric emptying

67
Q

What are the amylin analogs?

A

Pramlintide/Symlin

68
Q

What are the effects of Canagloflozin/Invokana?

A
  1. Inhibits Na-glucose cotransporter 2
  2. ↓ glucose reabsorption in kidney
  3. ↑ urine glucose excretion
69
Q

What are the effects of bromocriptine/cycloset?

A
  1. Resets circadian rhythm
  2. Stimulates dopamine receptors, inhibits prolactin secretion by pituitary
  3. ↓ fasting and PP hyperglycemia w/out ↑ insulin
70
Q

When should screening for complications begin in T2DM? What does this include?

A 
1. Screening for complications should begin when DM diagnosed
A. Ophthalmology referral
-Fundoscopic exam 
B. Podiatry referral
C. Urine for micro-albumin
D. Serum creatinine, BUN, lytes
E. Lipid profile
F. BP
G. EKG
71
Q

What is the leading cause of new blindness in 25-65 yo?

A
  1. Diabetic retinopathy

2. 60% of DM patients develop retinopathy after 15-20yrs of DM

72
Q

What are the sxs of diabetic retinopathy?

A
  1. Cotton wool spots (areas of ischemic retina) with resulting atrophy of axons
  2. Retinal hemorrhages
  3. Neovascularization:
    A. Several small, friable new vessels forming around the optic disc. If these rupture, the hemorrhage can lead to blindness
73
Q

How is diabetic retinopathy screened for?

A
  1. urine for micro-albumin

A. Can detect diabetic nephropathy at earliest stages

74
Q

What are the sxs of peripheral neuropathy?

A
  1. Stocking glove paresthesia
  2. Painless loss of sensation
    A. Touch, vibration, proprioception, temperature
    B. Leading to:
    Foot ulcers
    Destruction of foot architecture (Charcot Foot)
    Loss of DTR’s
    Muscle atrophy
    Foot drop
75
Q

What are the sxs of diabetic neuropathy in the cardiovascular system?

A 
1. Orthostatic hypotension
A. Loss of compensatory increase in HR
2. Exercise intolerance
3. Resting tachycardia
4. ***Silent MI***
76
Q

What are the sxs of diabetic neuropathy in the GI system?

A
  1. Dysphagia, early satiety, delayed emptying (gastroparesis), vomiting after meals
  2. Constipation, diarrhea, fecal incontinence
77
Q

What are the sxs of diabetic neuropathy in the GU system?

A
  1. Urinary incontinence/retention (neurogenic bladder)
  2. Vaginal dryness
  3. Erectile dysfunction (75% DM males by age 65)
78
Q

What are the sxs of vascular complications in T2DM?

A 
1. CAD/MI
A. Leading cause of mortality in Type II DM 
2. Stroke/TIA
3. PAD
A. Claudication 
B. Most common sx
79
Q

What are the complications to the immune system in T2DM?

A 
1. Infections
A. Mucocutaneous fungal infections
B. Bacterial foot infections (most common)
-Nonhealing ulcers
-Gangrene 
-Osteomyelitis
80
Q

What pt education needs to occur?

A
  1. Diabetic educator, dietitian, close follow up
  2. Home glucose monitoring
  3. Signs/sx’s hypoglycemia/hyperglycemia & management
  4. Early care for illness
  5. Medic alert tag
  6. Exercise
  7. Wt loss
  8. Risk of long term complications
  9. Tight glucose control in most patients
81
Q

What is Hyperglycemic Hyperosmolar State (HHS)?

A
  1. Hyperglycemic coma characterized by severe hyperglycemia in absence of significant ketosis
  2. Hyperosmolality, change in mental status & dehydration are common
  3. Most common in middle age – elderly
82
Q

What are common precipitating events for HHS?

A
  1. Infection
  2. MI
  3. CVA
  4. Recent surgery
  5. Dehydration
83
Q

What is the pathophys of HHS?

A
  1. Relative insulin deficiency reduces glucose utilization by muscle, fat and liver -> inappropriate glucagon secretion & hepatic glucose output
  2. Leads to massive glycosuria -> marked dehydration
  3. Severe hyperosmolality leads to mental confusion -> coma
84
Q

What are the sxs of HHS?

A 
1. Insidious onset over days – weeks:
A. Weakness
B. Severe dehydration
C. Polyuria
D. Polydipsia
E. Orthostatic hypotension
F. Lethargy
G. Confusion / delirium
H. Neurologic defects (reversible hemiplegia, focal seizures)
85
Q

How is HHS diagnosed?

A 
1. Serum glucose
A. >800 mg/dL
2. ↑ BUN/Cr
3. Serum Na
A. 120-125 mEq/L (mild dehydration)
B. > 140 mEq/L (severe dehydration)
4. Serum osmolality
A. > 350 mOsm/kg
5. pH
A. Normal (7.35-7.45)
6. No acidosis
A. Ketones neg
7. Normal anion gap
A. 8-10 mEq/L
8. Serum HCO3 normal
A. > 12 mEq/L
9. Hypomagnesemia
10. Hypocalcemia
11. Hypophosphatemia
86
Q

What is the workup for HHS?

A
  1. Airway, breathing, & circulation (ABC) status
    2.Mini Mental status (MMSE)
  2. BMP
  3. CBC w/diff
  4. UA & urine ketones by dipstick
  5. Plasma osmolality
  6. ABG if serum bicarbonate reduced or hypoxia suspected
    A. F/U w/venous blood gasses
  7. EKG
  8. Additional testing
    A. UC, sputum Cx , BC x 2, serum lipase/amylase, CXR
    B. Infection (pneumonia or UTI) - common precipitating event
87
Q

What are the fluid replacement guidelines in HHS?

A
  1. 0.45% NS preferred initial fluid
    A. Due to hyperosmolar body fluid of pt
    B. Slower rate than in DKA due to co-morbidities
    C. Use 0.9% NS if hypotensive or serum osmolality < 320 mOsm/L
  2. Once blood glucose reaches 250 mg/dl:
    A. D5W, D51/2 NS, D5NS
    B. Goal to maintain glycemic levels 250-300 mg/dl to prevent cerebral edema
88
Q

How is insulin and K managed in HHS?

A 
1. Insulin
A. Decrease hypergylcemia
2. K
A. Since no acidosis, less severe K depletion
B. Add 10 meq/L to initial fluid
89
Q

What is the prognosis for HHS?

A
  1. Overall mortality rate HHS is > 10x that of DKA
    A. Esp Elderly w/other co-morbidities
  2. When prompt recognition and treatment are initiated, mortality rate can be reduced

Gen Med: Ednocrine (8 decks)

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