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Endocrinology/Nutrition > 04b: Diabetes > Flashcards

04b: Diabetes Flashcards

1
Q

Diabetes can be defined using Fasting plasma glucose (FPG) greater than (X) mg/dL on at least (Y) number of occasions.

A 
X = 126
Y = 2

(fasting = no caloric intake for at least 8h)

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2
Q

Diabetes can be defined using 2h plasma glucose, during OGTT (oral glucose tolerance test), of (X) mg/dL or greater.

A

X = 200

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3
Q

Diabetes can be defined using HbA1C greater than or equal to (X)%.

A

X = 6.5

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4
Q

HbA1c can be used to screen for/diagnose diabetes, but should not be used in which patients?

A
  1. Pregnant F
  2. Recent severe bleeding/transfusion
  3. Chronic kidney/liver disease
  4. Blood disorders (Fe-def anemia, megaloblastic anemia, SSD/thalassemia)
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5
Q

40 y.o. F patient presents with fatigue, pale skin, and mild dyspnea. Which test would you use to screen for diabetes?

A

Fasting plasma glucose or oral glucose tolerance test

NOT HbA1c since showing symptoms of anemia

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6
Q

Type I diabetes: what do you expect to see on biopsy of pancreas?

A

Insulitis (CD8 T cells infiltrate islets)

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7
Q

Pancreas biopsy showing amyloid deposits in islets is suggestive of (X) disease. Why does this amyloid deposit?

A

X = DM II

Insulin resistance causes excess insulin secretion from islets; with insulin, amylin (an amyloid protein) is also secreted and accumulates

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8
Q

Most common cause of death patients with DM is:

A

MI (Vfib)

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9
Q

Pts with DM have (X)x risk of amputations

A

X = 100

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10
Q

What’s the primary pathophysiology behind all the DM complications?

A

Accelerated atherosclerosis

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11
Q

Papillary Tip Necrosis/Necrotizing papillitis is a relatively specific renal complication of (X) disease.

A

X = DM

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12
Q

Which glomerular lesions would you expect to see in DM?

A
  1. BM thickening
  2. Mesangial sclerosis
  3. KW (Kimmelstiel-Wilson) nodules
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13
Q

KW (Kimmelstiel-Wilson) nodules are composed of (X) material and form in regions of (Y).

A 
X = pink hyaline
Y = glomerular capillary loops
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14
Q

DM: which lesions in eye develop?

A
  1. Cataract
  2. Glaucoma
  3. Retinopathy (proliferative)
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15
Q

Diabetic retinopathy can occur via which mechanisms?

A
  1. Retinal hemorrhage (sudden blindness)
  2. Retinal microaneurysms
  3. Neovascularization
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16
Q

A large (X) value along identifies 46% of subjects who will develop Metabolic Syndrome in 5y.

A

X = waist circumference (assess central fat distribution)

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17
Q

Waist circumference measured at which landmark? Taken at the end of (normal/max) (inspiration/expiration).

A

Top of Iliac crest

Normal expiration

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18
Q

T/F: BMI increase is linearly associated with decreased insulin sensitivity.

A

False - % central abdominal fat is!

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19
Q

Weight loss by 7% reduces metabolic syndrome by (X)%.

A

X = 41

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20
Q

Key relevance of metabolic syndrome is to ID patients who:

A

Need aggressive lifestyle modification focused on weight loss and increased exercise

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21
Q

Major diseases associated with metabolic syndrome:

A
  1. DM II

2. Risk of CVD

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22
Q

T/F: In metabolic syndrome, lifestyle modification has been shown to have greater risk reduction in development of diabetes than metformin.

A

True - 58% v 31% risk reduction

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23
Q

In obese patients with metabolic syndrome, NIH recommends (X)% weight reduction at rate of (Y) lb/week

A 
X = 5-10
Y = 1-2
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24
Q

Qualifications for bariatric surg:

A
  1. BMI over 40 OR

2. BMI over 35 with comorbidity

25
Q

Metabolic syndrome is an entity characterized by:

A
  1. Insulin resistance and hyperinsulinemia
  2. HT
  3. Dyslipidemia
26
Q

In general, metabolic syndrome prevalence (increases/decreases) with age.

A

Increases

27
Q

Metabolic syndrome diagnosed clinically by presence of 3 of the following:

A
  1. Fasting glucose over 100
  2. BP over 130/80
  3. Dyslipidemia (TG over 150, HDL under 40 (M)/50 (F))
  4. Increased waist circumference (based on ethnicity/sex)
28
Q

Decrease in synthesis/release of (X) hormone from adipose has been shown to predict development of DM II and CVD.

A

X = adiponectin

29
Q

Exercise has been shown to (increase/decrease) AMPK in muscle and other tissues. Which endogenous hormone (activates/inhibits) AMPK?

A

Increase

Adiponectin; activates

30
Q

Experimentally, AMPK activators were found to decrease:

A

Inflammation, oxidative/ER stress, mito dysfunction, insulin resistance

31
Q

T/F: 90-95% of diabetes patients in US are Type II.

A

True

32
Q

T/F: Majority, but not all, pre-diabetic patients eventually develop diabetes.

A

False - majority never develop diabetes!

33
Q

Pre-diabetes: most important intervention to prevent progression to diabetes is…

A

Regular exercise

34
Q

Insulin resistance has a key effect on (X) process in adipose tissue, which (increases/decreases) circulating (Y).

A

X = lipolysis (increased in insulin resistance)
Increases
Y = FFA and TGs

35
Q

How does the (increase/decrease) in FFAs cause insulin resistance?

A

Increase

Increases hepatic gluconeogenesis

36
Q

T/F: Dyslipidemia in DM II involves low HDL and high LDL.

A

False - LDL usually not affected

37
Q

List some inflammatory markers that are elevated in DM II

A
  1. CRP (also higher in obesity)

2. Cytokines (TNF-alpha, IL6)

38
Q

TNF-alpha role in DM II: (increases/decreases) (X) via activation of (Y).

A

Increases
X = FFAs and insulin resistance
Y = NF-kB transcription factor

39
Q

IL-6 role in DM II: (increases/decreases) (X) via stimulation of (Y).

A

Increases
X = FFAs
Y = lipolysis

40
Q

(X) is type II diabetes that occurs in young patients (under 25 yo). What’s the issue?

A

X = MODY (maturity onset diabetes of young)

Impaired insulin production (but no antibodies like in DM I) - AD transmission

41
Q

MODY (maturity onset diabetes of young) patients respond well to:

A

Sulfonylureas

42
Q

Requirements for DKA diagnosis.

A 
DKAA:
D: glucose over 250
K: ketonemia
A: acidosis (pH under 7.3)
A: alkalosis (bicarb under 18)
43
Q

Mild v severe DKA is dependent on level of:

A

Alkalosis (lower bicarb, worse prognosis)

44
Q

Requirements for HHS (hyperglycemic hyperosmolar state) diagnosis.

A
  1. glucose over 600 mg/dL

2. Effective serum osmolarity over 320

45
Q

Effective osmolarity differs from total osm in that (X) (is/isn’t) taken into account in the latter

A

X = BUN

is

46
Q

Which values do you need to know to calculate effective osm?

A

Serum Na and glucose

47
Q

T/F: HHS (hyperglycemic hyperosmolar state) is primarily a disorder of hyperglycemia.

A

False - disorder of dehydration

48
Q

Ketone bodies form when enzymes of (X) process become saturated

A

X = TCA cycle

49
Q

Most common medical cause of DKA is:

A

infection (esp UTI and pneumonia)

50
Q

What are two causes of euglycemic DKA (blood glucose under 250 mg/dL)?

A

Pregnancy or SGLT2 inhibitors

51
Q

T/F: Urine and plasma ketone assays measure acetoacetate.

A

True (not the predominant ketone body, so could be falsely low initially)

52
Q

T/F: Acetoacetate is the predominant ketone body.

A

False - BHB (beta-hydroxy butyrate) is

53
Q

Correcting hyperosmolarity: avoid decreasing effective osm by more than (X) in an hour

A

X = 3 mOsm/kg H2O

54
Q

Hyperglycemia: first, most important step in Rx is…

A

IV rehydration (use serum Na as guide to % saline)

55
Q

HHS/DKA Rx: when glucose reaches 300 in HHS and 200 in DKA, how does IV fluid Rx change?

A

Change to fluid containing dextrose

56
Q

T/F: Pts being treated for HHS/DKA are normokalemic.

A

True - but K still given!! (total body K low)

57
Q

T/F: In pts being treated for HHS/DKA, it’s crucial to give insulin along with or immediately after IV fluids.

A

False - no rush.. make sure K is over 3.3; check serum glucose hourly

58
Q

(X) values are the best ways to decide when DKA is resolved.

A

X = anion gap and serum bicarb

59
Q

DKA resolution criteria:

A

2/3 of:

  1. Serum HCO3 over 15
  2. Venous pH over 7.3
  3. Anion gap over 12

Endocrinology/Nutrition (10 decks)

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