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Clinical Med II > Exam 4 - Diabetes/Treatment > Flashcards

Exam 4 - Diabetes/Treatment Flashcards

1
Q

Which diabetes is an autoimmune etiology which causes destruction of pancreatic beta cells, leading to absolute insulin deficiency?

A

Type I DM

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2
Q

What type of antibodies are detected in Type I DM?

A
  • Glumatic acid decarboxylase (GAD-65)

- Islet cell

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3
Q

The following clinical features are associated with what disorder?

  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss
  • Nocturia
  • Blurry vision
  • DKA
A

Type I DM

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4
Q

Which type of diabetes has a gradual onset and has increasing prevalence with increasing degrees of obesity?

A

Type 2 DM

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5
Q

What is Type 2 DM characterized by?

A
  • Hyperglycemia
  • Insulin resistance
  • Relative insulin deficiency
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6
Q

What is the pathophysiological progression of Type 2 DM?

A
  • Peripheral insulin resistance/hyperinsulinemia
  • Impaired glucose tolerance (elevations in post-prandial glucose, decline in insulin secretion, increased hepatic glucose production)
  • Overt diabetes
  • Beta cell failure/”burn out”
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7
Q

What are clinical features associated with Type 2 DM?

A
  • Asymptomatic
  • Acanthosis nigricans
  • Polyuria, polydipsia
  • Nocturia
  • Blurry vision
  • Paresthesia’s
  • Chronic skin infections
  • Poor wound healing
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8
Q

When should screening for diabetes or prediabetes begin in ALL patients?

A

Age 45 years

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9
Q

When should you selectively start to screen for diabetes or prediabetes?

A

Overweight or obese (BMI > 25) adults who have one or more additional risk factors for diabetes

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10
Q

What are testing methods for diabetes?

A
  • Fasting plasma glucose
  • 2-hour oral glucose tolerance test
  • HbA1c
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11
Q

What does HbA1c measure?

A

Reflects an indirect measure of average blood glucose over approximately 3 months

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12
Q

What range is indicative of diabetes in the fasting plasma glucose, oral glucose tolerance, and HbA1c tests?

A

Fasting plasma glucose: 126 or greater

Oral glucose tolerance: 200 or greater

HbA1c: 6.5 or greater

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13
Q

What range is considered normal in the fasting plasma glucose, oral glucose tolerance, and HbA1c tests?

A

Fasting plasma glucose: < 100

Oral glucose tolerance: < 140

HbA1c: < 5.7

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14
Q

In a patient with classic symptoms, what test/result supports a diagnosis of diabetes?

A

A random plasma glucose of 200 or greater

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15
Q

Unless there is a clear clinical diagnosis, what is required for diabetes diagnosis?

A

Two abnormal test results (FPG, OGTT, HbA1c) from the same sample or in two separate test samples

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16
Q

How should we manage prediabetes?

A
  • Behavioral lifestyle intervention (exercise, weight loss, nutrition, smoking cessation)
  • Metformin* (especially in those with BMI > 35, age < 60, women with prior GDM)
  • Test at least annually for development of type 2 diabetes
  • Screen for and treat modifiable risk factors for ASCVD
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17
Q

What should you do if you screen a patient for diabetes but they do not have prediabetes or diabetes?

A

Retest patient at a minimum of 3-year intervals

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18
Q

What is the leading cause of morbidity and mortality for individuals with diabetes?

A

ASCVD (Macrovascular Complication)

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19
Q

What is ASCVD defined as?

A

CHD, cerebrovascular disease, or PAD

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20
Q

When should you screen for ASCVD in patients with DM?

A

Assess cardiovascular risk factors at least annually.

Use 10 year risk calculator

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21
Q

What are the microvascular complications of DM?

A
  • Diabetic nephropathy
  • Diabetic retinopathy
  • Diabetic neuropathy
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22
Q

When does diabetic nephropathy (diabetic kidney disease) typically develop in patients with DM?

A

Typically develops after a duration of 10 years in type 1 DM, but may be present at diagnosis of type 2 DM

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23
Q

How is diabetic nephropathy (diabetic kidney disease) clinically diagnosed?

A

Presence of albuminuria and/or reduced eGFR (in the absence of signs/symptoms of other primary causes of kidney damage)

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24
Q

How often should a diabetic patient be screened for diabetic nephropathy?

When would you consider a patient to have albuminuria?

A

At least once a year, assess urinary albumin-to-creatinine ratio (UACR) and eGFR

2-3 abnormal specimens of UACR collected within 3-6 month period

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25
When should screening for diabetic nephropathy start in a patient with type 1 DM versus type 2?
Type 1: DM with duration of 5 or more years Type 2: Time of diagnosis
26
What is the leading cause of new blindness between the ages of 20 and 74 in the United States?
Diabetic Retinopathy
27
What is the prevalence of Diabetic Retinopathy related to?
Both duration of diabetes AND the level of glycemic control
28
What is the key to controlling diabetic nephropathy?
Intensive glycemic and BP control with ACE-I or ARB
29
What is the difference between nonproliferative and proliferative diabetic retinopathy?
Proliferative diabetic retinopathy will have prominent neovascularization at the disc
30
When should you perform screening for diabetic retinopathy in a patient with type 1 DM? Type 2?
Type 1: Initial dilated and comprehensive eye exam within 5 years after the diagnosis of diabetes Type 2: Initial dilated and comprehensive eye exam at time of diagnosis ***most patients who develop retinopathy have no symptoms until the very last stages
31
What is the ADA recommendations regarding screening for diabetic retinopathy?
- If there is NO evidence of retinopathy for one or more annual eye exams and glycemia is well controlled, then screening every 1-2 years may be considered - If any level of diabetic retinopathy is present, subsequent dilated retinal examinations should be repeated at least annually
32
What does the prevalence of diabetic neuropathy vary with? What are the two main categories of diabetic neuropathy?
Varies with both severity and duration of hyperglycemia. Peripheral and Autonomic
33
What are some signs and symptoms associated with diabetic peripheral neuropathy (DPN)?
- Classic "stocking-glove" sensory loss - Pain and dysesthesias (burning/tingling) - Numbness and loss of protective sensation (LOPS) - Decreased or absent ankle reflexes
34
What are some risk factors for diabetic foot ulcers?
- Numbness and loss of protective sensation (LOPS) - PAD - Foot deformities/Charcot Arthropathy - Poor glycemic control - Visual impairment - Hx of foot ulcer - Cigarette smoking
35
When should a comprehensive foot evaluation be performed in a diabetic patient?
At least annually Type 1: Start 5 years after diagnosis Type 2: Start at time of diagnosis
36
What is an important vascular test to perform when doing a comprehensive foot examination? What about neurological exam?
Vascular: ABI Neurologic: Monofilament test
37
What is the most useful test to diagnose numbness and loss of protective sensation (LOPS)?
Monofilament test
38
What are some symptoms that should cause concern for diabetic autonomic neuropathy?
- Hypoglycemia unawareness - Gastroparesis - Sexual dysfunction (especially in males) - Abnormal pupillary responses (difficulty driving at night)
39
For many years now in the US, DM has been the leading cause of what complications? (3)
- New blindness in adults - Renal failure - Nontraumatic lower extremity amputation
40
What is the 1st line medication agent for Type 2 DM? How does it work? Adverse effects? Contraindications?
Metformin MOA: Decreases hepatic glucose production and increases insulin. sensitivity AE: GI (diarrhea), vitamin B12 deficiency (can cause megaloblatic anemia), lactic acidosis (hold before surgery or contrast dye injection until renal function has normalized) CI: Lactic acidosis, CKD (GFR < 30), hepatic disease, acute/unstable HF
41
What drugs are the TZDs? MOA? When considered? Adverse effects? Contraindications?
"glitazone" MOA: Increases insulin sensitivity Consider with early DM and high insulin resistance AE: Edema, weight gain, bone fracture risk CI: CHF (black box warning due to edema), active bladder cancer (pioglitazone)
42
What is the MOA for Sulfonylureas? When considered? Adverse effects? Contraindications?
MOA: Stimulate beta cell insulin release Considered with early stages of DM AE: Hypoglycemia CI: Sulfa allergy
43
What drugs are the DDP-4 Inhibitors? MOA? Adverse effects? Contraindications?
"gliptin" MOA: Inhibit DDP-4 which slows the breakdown of GLP-1, restoring insulin and glucagon to physiologic levels (increase insulin release, decrease glucagon) AE: Pancreatitis, edema (caution in HF) CI: Hx or acute pancreatitis, renal impairment (except linagliptin as excreted by liver instead of kidneys)
44
What drugs are the GLP-1 Agonists? MOA? Adverse effects? Contraindications?
"tide" MOA: Increases insulin secretion; slows gastric emptying leading to weight loss AE: Pancreatitis CI: Thyroid cancer; even family hx *Black box warning*, pancreatitis hx, renal impairment (specifically Exenatide)
45
Which 3 drugs FDA approved to reduce the risk of CV events (macrovascular) in Type II DM?
GLP-1 Agonist: Liraglutide (Victoza) SGLT-2 Inhibitor: Empagliflozin SGLT-2 Inhibitor: Canagliflozin
46
What drugs are the SGLT-2 Inhibitors? MOA? Adverse effects? Contraindications?
"gliflozin" MOA: Inhibit SGLT-2 cotransporter, reducing renal glucose reabsorption and promoting excretion AE: renal impairment, GU infections, diuresis (caution in elderly, hypotensive), hyperkalemia (canagliflozin), risk of LE amputation *Black Box Warning* CI: GFR < 30, DKA
47
What drug can significantly reduce the reduction of hospitalizations in patients with CHF?
SGLT-2 Inhibitor
48
What are some adverse effects of insulin?
Hypoglycemia, weight gain, hunger, nausea
49
What are the different types of premixed insulin? When would you use these?
- Insulin NPH/Insulin regular (Novolin 70/30) - Insulin lispro protamine/insulin lispro - Insulin aspart protamine/insulin aspart (Novolog 70/30) - Patients who are stable on insulin and diet is relatively the same daily. - Poor adherence to basal-bolus regimen
50
How should you start insulin treatment?
- Fix fasting glucose first | - Begin with basal insulin either based on TDD or start with 10 units QHS and then titrate
51
What type of insulin is used in insulin pumps? When should insulin pumps be considered?
Rapid acting insulin Patients who are testing and injecting multiple times per day and cannot achieve normal A1C or patients who have frequent hypoglycemia
52
Describe the Somogyi Effect and the Dawn Phenomenon?
Somogyi Effect: Morning hyperglycemia in response to undetected nocturnal hypoglycemia (common with excessive exogenous insulin) Dawn Phenomenon: Morning hyperglycemia due to elevated AM hormone levels
53
How do you treat hypoglycemia?
- Oral glucose (tabs, juice) - IV glucose - Glucagon
54
What are some symptoms of hypoglycemia?
- Sweating - Dizziness - Tachycardia - Tremors - Weakness, fatigue - Headache - Irritable
55
What is the biochemical triad associated with DKA?
- Hyperglycemia - Ketonemia - Acidemia
56
What are precipitating events of DKA?
The 4 s's: - Sepsis (infection) - Skipping insulin doses - Sickness (virus or flu) - Stress (surgery)
57
What are symptoms of DKA?
- Dehydration - Polydipsia/polyphagia - N/V - Abdominal pain - Weight loss - Shock in severe cases
58
What are some typical physical exam findings in a patient with DKA?
- Kussmaul respirations (rapid breathing due to acidosis) - "Fruity breath" or acetone breath - Tachypnea/tachycardia - Altered mental status
59
What is typically seen in the following labs during DKA? ``` Glucose UA Serum Ketones BMP CBC ```
``` Glucose: Elevated to 250 or higher UA: Glucose and ketones Serum Ketones: Positive BMP: Elevated anion gap, electrolyte imbalances CBC: Elevated WBC ```
60
What lab is needed to diagnose DKA?
ABG/arterial pH
61
What is the treatment for DKA?
- Hospitalize - IV fluids - IV insulin - Electrolyte correction
62
In what population is Non-Ketotic Hyperglycemic Hyperosmolar Syndrome (NKHS) or (HHS) more common in?
Older type 2 DM
63
What is found on labs in HHS?
- Profound hyperglycemia (> 600) - Osmotic diuresis (very dehydrated) - Not acidotic - Absent or minimal ketones in urine or blood
64
What is the etiology of HHS? What is the precipitating factor?
Insulin deficiency + increased counter regulatory hormones "I's" Illness or infection (PNA or UTI)
65
What is the clinical presentation associated with HHS?
- Altered mental status | - Polyuria, polydipsia, weakness, tachycardia, hypotension, dehydration, shock
66
What is the treatment for HHS?
Same as DKA: - Hospitalize - IV fluids - IV insulin - Electrolyte correction

Clinical Med II (17 decks)

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