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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
Metabolic syndrome is an entity characterized by:
1. Insulin resistance and hyperinsulinemia 2. HT 3. Dyslipidemia
26
In general, metabolic syndrome prevalence (increases/decreases) with age.
Increases
27
Metabolic syndrome diagnosed clinically by presence of 3 of the following:
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
Decrease in synthesis/release of (X) hormone from adipose has been shown to predict development of DM II and CVD.
X = adiponectin
29
Exercise has been shown to (increase/decrease) AMPK in muscle and other tissues. Which endogenous hormone (activates/inhibits) AMPK?
Increase | Adiponectin; activates
30
Experimentally, AMPK activators were found to decrease:
Inflammation, oxidative/ER stress, mito dysfunction, insulin resistance
31
T/F: 90-95% of diabetes patients in US are Type II.
True
32
T/F: Majority, but not all, pre-diabetic patients eventually develop diabetes.
False - majority never develop diabetes!
33
Pre-diabetes: most important intervention to prevent progression to diabetes is...
Regular exercise
34
Insulin resistance has a key effect on (X) process in adipose tissue, which (increases/decreases) circulating (Y).
X = lipolysis (increased in insulin resistance) Increases Y = FFA and TGs
35
How does the (increase/decrease) in FFAs cause insulin resistance?
Increase Increases hepatic gluconeogenesis
36
T/F: Dyslipidemia in DM II involves low HDL and high LDL.
False - LDL usually not affected
37
List some inflammatory markers that are elevated in DM II
1. CRP (also higher in obesity) | 2. Cytokines (TNF-alpha, IL6)
38
TNF-alpha role in DM II: (increases/decreases) (X) via activation of (Y).
Increases X = FFAs and insulin resistance Y = NF-kB transcription factor
39
IL-6 role in DM II: (increases/decreases) (X) via stimulation of (Y).
Increases X = FFAs Y = lipolysis
40
(X) is type II diabetes that occurs in young patients (under 25 yo). What's the issue?
X = MODY (maturity onset diabetes of young) Impaired insulin production (but no antibodies like in DM I) - AD transmission
41
MODY (maturity onset diabetes of young) patients respond well to:
Sulfonylureas
42
Requirements for DKA diagnosis.
``` DKAA: D: glucose over 250 K: ketonemia A: acidosis (pH under 7.3) A: alkalosis (bicarb under 18) ```
43
Mild v severe DKA is dependent on level of:
Alkalosis (lower bicarb, worse prognosis)
44
Requirements for HHS (hyperglycemic hyperosmolar state) diagnosis.
1. glucose over 600 mg/dL | 2. Effective serum osmolarity over 320
45
Effective osmolarity differs from total osm in that (X) (is/isn't) taken into account in the latter
X = BUN | is
46
Which values do you need to know to calculate effective osm?
Serum Na and glucose
47
T/F: HHS (hyperglycemic hyperosmolar state) is primarily a disorder of hyperglycemia.
False - disorder of dehydration
48
Ketone bodies form when enzymes of (X) process become saturated
X = TCA cycle
49
Most common medical cause of DKA is:
infection (esp UTI and pneumonia)
50
What are two causes of euglycemic DKA (blood glucose under 250 mg/dL)?
Pregnancy or SGLT2 inhibitors
51
T/F: Urine and plasma ketone assays measure acetoacetate.
True (not the predominant ketone body, so could be falsely low initially)
52
T/F: Acetoacetate is the predominant ketone body.
False - BHB (beta-hydroxy butyrate) is
53
Correcting hyperosmolarity: avoid decreasing effective osm by more than (X) in an hour
X = 3 mOsm/kg H2O
54
Hyperglycemia: first, most important step in Rx is...
IV rehydration (use serum Na as guide to % saline)
55
HHS/DKA Rx: when glucose reaches 300 in HHS and 200 in DKA, how does IV fluid Rx change?
Change to fluid containing dextrose
56
T/F: Pts being treated for HHS/DKA are normokalemic.
True - but K still given!! (total body K low)
57
T/F: In pts being treated for HHS/DKA, it's crucial to give insulin along with or immediately after IV fluids.
False - no rush.. make sure K is over 3.3; check serum glucose hourly
58
(X) values are the best ways to decide when DKA is resolved.
X = anion gap and serum bicarb
59
DKA resolution criteria:
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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