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REM II > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what are the main health consequences of being overwt or obese in childhood?

A 
HTN
T2DM
increased cholesterol
fatty liver
negative psychological outcomes
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2
Q

what are the main health consequences of being overwt or obese in childhood?

A 
HTN
T2DM
increased cholesterol
fatty liver
negative psychological outcomes
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3
Q

What is the only hunger hormone?

A

ghrelin

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4
Q

how do you calculate BMI

A

body wt (kg)/ ht (m)squared

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5
Q

what is underweight in adults? children?

A
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6
Q

what is obese in adults? children?

A

> 30 (morbid is >40)

>95th percentile

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7
Q

what is obese in adults? children?

A

> 30 (morbid is >40)

>95th percentile

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8
Q

What is the only hunger hormone?

A

ghrelin

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9
Q

how do you calculate BMI

A

body wt (kg)/ ht (m)squared

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10
Q

what is underweight in adults? children?

A
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11
Q

what is overweight in adults? children?

A

> 25-29

85th-95th percentile

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12
Q

what is obese in adults? children?

A

> 30 (morbid is >40)

>95th percentile

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13
Q

what are health consequences of being overwt/obese?

A 
inflammation
atherosclerosis 
HTN
dyslipidemia
T2DM
thrombosis -> stroke
depression
GERD (other GI dz)
gout
etc
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14
Q

what conditions are used to diagnose metabolic syndrome? how many need to be present?

A 
3/5
abd obesity- >40 M, >35 W
Hyperglycemia- >100FBG (or drug tx)
hypertriglyceridemia- >150 (or drug tx) 
low HDL-130/85 (or drug tx)
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15
Q

what are the therapeutic goals for metabolic syndrome?

A

treat underlying causes- lifestyle changes (exercise, diet)

treat cardiovascular risk factors

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16
Q

Where are the GLUT 2 transporters found? what do they signal?

A

found in pancreatic beta cells

signal insulin release

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17
Q

what is the MOA for insulin release?

A

glucose binds GLUT2 -> inc ATP intracellularly -> K channels closing -> Ca going into the cell -> depolarization -> insulin release

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18
Q

Where is GLUT 4 found?

A

Muscle and adipose

insulin binds and upregulats them on cell surfaces

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19
Q

what are the actions of insulin?

A

through the IP3 pathway

it stimulates glycogen, fat, and protein synthesis to get rid of glucose in the blood

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20
Q

what is the function of glucagon?

A

produce in alpha cells

stimulates glycogenolysis, fat catabolism, and gluconeogenesis

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21
Q

when is glucagon secreted?

A

very low carb and high protein meals

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22
Q

what are the 4 anti insulin hormones?

A

glucagon
epi/norepi
GH
ACTH

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23
Q

where is the GLUT 3 transporter?

A

brain

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24
Q

what are the different hormones released from the pancreas?

A 
insulin
glucagon
somatostatin
pancreatic polypeptide
ghrelin
25
what is the pathogenesis of T2DM?
high circulating FAs block the secondary messenger system inside cell once insulin binds this blocks glucose from entering cell this increases glucose in blood this further stimulates insulin release
26
how does DKA develop?
acute insulin deficiency -> inc lipolysis -> inc ketogenesis
27
what are the symptoms of DKA?
N/V, stomach pain, fruity breath, polyuria, polydipsia, weakness, fatigue, confusion, heavy deep breathing
28
What is the function of PPARgamma
``` inhibits pro inflammatory cytokines activates adiponectin dec insulin resistance leptin levels dec highly expressed in adipose ```
29
what do thialzolidinediones do?
activate PPAR gamma
30
what are the FPG, OGTT, and HbA1C of pre diabetes
FPG- 100-125 OGTT- 140-199 A1C- 5.7-6.4
31
what is normal A1C?
32
what are the FPG, OGTT, and HbA1C of diabetes?
FPG- >126 OGTT- >200 A1c- >6.5
33
how often do you check A1C?
every 3 mo
34
what would the BG be if A1C is 7? what is the increase in BG for every 1 pt inc in A1C
7=150 | raises 30 pts for every 1 pt
35
when can you diagnose diabetes with one test?
if they have symptoms and random plasma glucose is >200 | everything else needs repeating
36
which diabetes shows acanthosis nigricans?
Type 2 DM
37
In which diabetics do HHS and DKA present?
HHS- type 2 | DKA- type 1
38
what is acanthosis nigricans
skin condition characterized by dark, thick, velvety skin in body folds and creases mostly neck and axilla associated with inc insulin and malignancy
39
what is the genetic etiology of gestational diabetes
MODY
40
what endocrinopathies are related to secondary etiologies of T2DM?
``` cushings acromegaly pheo glucagonoma somatostatinoma hyperthyroid ```
41
What are the microvascular complications of diabetes
retinopathy neuropathy nephropathy
42
what is the key feature of proliferative retinopathy?
neovascularization | no reversible
43
how often do you check for retinopathy?
every year
44
what does diabetic neuropathy lead to?
foot ulcers | muscle and joint disease
45
how often do you check for neuropathy?
annual comprehensive exam with monofilament | visual inspection every visit
46
what happens with diabetic nephropathy?
mesangial expansion thickening of BM glomerular HTN leads to hyperfiltration
47
how often do you screen for nephropathy and how do you test for it?
annually albumin to creatinine ratio increased urinary albumin excretion starting at 30 mg/day
48
how do you treat diabetic nephropathy?
ACE or ARB
49
how do you protect against macrovascular complications?
``` glycemic, lipid, blood pressure control smoking cessation wt loss diet/exercise possible daily baby aspirin ```
50
what BP do we want diabetics to have
51
what do you do first for a T2 diabetic?
lifestyle modification | metformin
52
what is the tx course for T1 diabetics?
combined insulin therapy | short acting + long acting (lispro + glargine)
53
what are the + and - of insulin pump?
convenience | cost, reliance on tech, feeling tethered
54
what is the treatment of DKA and HHS
insulin, fluid replacement, potassium and other lyte replacement
55
What is HHS?
hyperosmolar hyperglycemic state
56
what is DKA?
diabetic ketoacidosis | has dehydration, inc ketoacids, hyperglycemia
57
HHS labs?
very very high glucose small amt of ketones increased serum osmolality slight acidity
58
DKA labs?
mildly elevated glucose very acidic positive ketones high ion gap

REM II (11 decks)

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