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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
Q

When should screening for diabetic nephropathy start in a patient with type 1 DM versus type 2?

A

Type 1: DM with duration of 5 or more years

Type 2: Time of diagnosis

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26
Q

What is the leading cause of new blindness between the ages of 20 and 74 in the United States?

A

Diabetic Retinopathy

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27
Q

What is the prevalence of Diabetic Retinopathy related to?

A

Both duration of diabetes AND the level of glycemic control

28
Q

What is the key to controlling diabetic nephropathy?

A

Intensive glycemic and BP control with ACE-I or ARB

29
Q

What is the difference between nonproliferative and proliferative diabetic retinopathy?

A

Proliferative diabetic retinopathy will have prominent neovascularization at the disc

30
Q

When should you perform screening for diabetic retinopathy in a patient with type 1 DM?

Type 2?

A

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
Q

What is the ADA recommendations regarding screening for diabetic retinopathy?

A
  • 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
Q

What does the prevalence of diabetic neuropathy vary with?

What are the two main categories of diabetic neuropathy?

A

Varies with both severity and duration of hyperglycemia.

Peripheral and Autonomic

33
Q

What are some signs and symptoms associated with diabetic peripheral neuropathy (DPN)?

A
  • Classic “stocking-glove” sensory loss
  • Pain and dysesthesias (burning/tingling)
  • Numbness and loss of protective sensation (LOPS)
  • Decreased or absent ankle reflexes
34
Q

What are some risk factors for diabetic foot ulcers?

A
  • Numbness and loss of protective sensation (LOPS)
  • PAD
  • Foot deformities/Charcot Arthropathy
  • Poor glycemic control
  • Visual impairment
  • Hx of foot ulcer
  • Cigarette smoking
35
Q

When should a comprehensive foot evaluation be performed in a diabetic patient?

A

At least annually

Type 1: Start 5 years after diagnosis

Type 2: Start at time of diagnosis

36
Q

What is an important vascular test to perform when doing a comprehensive foot examination?

What about neurological exam?

A

Vascular: ABI

Neurologic: Monofilament test

37
Q

What is the most useful test to diagnose numbness and loss of protective sensation (LOPS)?

A

Monofilament test

38
Q

What are some symptoms that should cause concern for diabetic autonomic neuropathy?

A
  • Hypoglycemia unawareness
  • Gastroparesis
  • Sexual dysfunction (especially in males)
  • Abnormal pupillary responses (difficulty driving at night)
39
Q

For many years now in the US, DM has been the leading cause of what complications? (3)

A
  • New blindness in adults
  • Renal failure
  • Nontraumatic lower extremity amputation
40
Q

What is the 1st line medication agent for Type 2 DM?

How does it work?

Adverse effects?

Contraindications?

A

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
Q

What drugs are the TZDs?

MOA?

When considered?

Adverse effects?

Contraindications?

A

“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
Q

What is the MOA for Sulfonylureas?

When considered?

Adverse effects?

Contraindications?

A

MOA: Stimulate beta cell insulin release

Considered with early stages of DM

AE: Hypoglycemia

CI: Sulfa allergy

43
Q

What drugs are the DDP-4 Inhibitors?

MOA?

Adverse effects?

Contraindications?

A

“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
Q

What drugs are the GLP-1 Agonists?

MOA?

Adverse effects?

Contraindications?

A

“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
Q

Which 3 drugs FDA approved to reduce the risk of CV events (macrovascular) in Type II DM?

A

GLP-1 Agonist: Liraglutide (Victoza)

SGLT-2 Inhibitor: Empagliflozin

SGLT-2 Inhibitor: Canagliflozin

46
Q

What drugs are the SGLT-2 Inhibitors?

MOA?

Adverse effects?

Contraindications?

A

“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
Q

What drug can significantly reduce the reduction of hospitalizations in patients with CHF?

A

SGLT-2 Inhibitor

48
Q

What are some adverse effects of insulin?

A

Hypoglycemia, weight gain, hunger, nausea

49
Q

What are the different types of premixed insulin?

When would you use these?

A
  • 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
Q

How should you start insulin treatment?

A
  • Fix fasting glucose first

- Begin with basal insulin either based on TDD or start with 10 units QHS and then titrate

51
Q

What type of insulin is used in insulin pumps?

When should insulin pumps be considered?

A

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
Q

Describe the Somogyi Effect and the Dawn Phenomenon?

A

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
Q

How do you treat hypoglycemia?

A
  • Oral glucose (tabs, juice)
  • IV glucose
  • Glucagon
54
Q

What are some symptoms of hypoglycemia?

A
  • Sweating
  • Dizziness
  • Tachycardia
  • Tremors
  • Weakness, fatigue
  • Headache
  • Irritable
55
Q

What is the biochemical triad associated with DKA?

A
  • Hyperglycemia
  • Ketonemia
  • Acidemia
56
Q

What are precipitating events of DKA?

A

The 4 s’s:

  • Sepsis (infection)
  • Skipping insulin doses
  • Sickness (virus or flu)
  • Stress (surgery)
57
Q

What are symptoms of DKA?

A
  • Dehydration
  • Polydipsia/polyphagia
  • N/V
  • Abdominal pain
  • Weight loss
  • Shock in severe cases
58
Q

What are some typical physical exam findings in a patient with DKA?

A
  • Kussmaul respirations (rapid breathing due to acidosis)
  • “Fruity breath” or acetone breath
  • Tachypnea/tachycardia
  • Altered mental status
59
Q

What is typically seen in the following labs during DKA?

Glucose
UA
Serum Ketones
BMP
CBC
A 
Glucose: Elevated to 250 or higher
UA: Glucose and ketones
Serum Ketones: Positive
BMP: Elevated anion gap, electrolyte imbalances
CBC: Elevated WBC
60
Q

What lab is needed to diagnose DKA?

A

ABG/arterial pH

61
Q

What is the treatment for DKA?

A
  • Hospitalize
  • IV fluids
  • IV insulin
  • Electrolyte correction
62
Q

In what population is Non-Ketotic Hyperglycemic Hyperosmolar Syndrome (NKHS) or (HHS) more common in?

A

Older type 2 DM

63
Q

What is found on labs in HHS?

A
  • Profound hyperglycemia (> 600)
  • Osmotic diuresis (very dehydrated)
  • Not acidotic
  • Absent or minimal ketones in urine or blood
64
Q

What is the etiology of HHS?

What is the precipitating factor?

A

Insulin deficiency + increased counter regulatory hormones

“I’s”
Illness or infection (PNA or UTI)

65
Q

What is the clinical presentation associated with HHS?

A
  • Altered mental status

- Polyuria, polydipsia, weakness, tachycardia, hypotension, dehydration, shock

66
Q

What is the treatment for HHS?

A

Same as DKA:

  • Hospitalize
  • IV fluids
  • IV insulin
  • Electrolyte correction

Clinical Med II (17 decks)

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