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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
Q

what is the pathogenesis of T2DM?

A

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
Q

how does DKA develop?

A

acute insulin deficiency -> inc lipolysis -> inc ketogenesis

27
Q

what are the symptoms of DKA?

A

N/V, stomach pain, fruity breath, polyuria, polydipsia, weakness, fatigue, confusion, heavy deep breathing

28
Q

What is the function of PPARgamma

A 
inhibits pro inflammatory cytokines
activates adiponectin
dec insulin resistance
leptin levels dec
highly expressed in adipose
29
Q

what do thialzolidinediones do?

A

activate PPAR gamma

30
Q

what are the FPG, OGTT, and HbA1C of pre diabetes

A

FPG- 100-125
OGTT- 140-199
A1C- 5.7-6.4

31
Q

what is normal A1C?

A
32
Q

what are the FPG, OGTT, and HbA1C of diabetes?

A

FPG- >126
OGTT- >200
A1c- >6.5

33
Q

how often do you check A1C?

A

every 3 mo

34
Q

what would the BG be if A1C is 7? what is the increase in BG for every 1 pt inc in A1C

A

7=150

raises 30 pts for every 1 pt

35
Q

when can you diagnose diabetes with one test?

A

if they have symptoms and random plasma glucose is >200

everything else needs repeating

36
Q

which diabetes shows acanthosis nigricans?

A

Type 2 DM

37
Q

In which diabetics do HHS and DKA present?

A

HHS- type 2

DKA- type 1

38
Q

what is acanthosis nigricans

A

skin condition characterized by dark, thick, velvety skin in body folds and creases
mostly neck and axilla
associated with inc insulin and malignancy

39
Q

what is the genetic etiology of gestational diabetes

A

MODY

40
Q

what endocrinopathies are related to secondary etiologies of T2DM?

A 
cushings
acromegaly
pheo
glucagonoma
somatostatinoma
hyperthyroid
41
Q

What are the microvascular complications of diabetes

A

retinopathy
neuropathy
nephropathy

42
Q

what is the key feature of proliferative retinopathy?

A

neovascularization

no reversible

43
Q

how often do you check for retinopathy?

A

every year

44
Q

what does diabetic neuropathy lead to?

A

foot ulcers

muscle and joint disease

45
Q

how often do you check for neuropathy?

A

annual comprehensive exam with monofilament

visual inspection every visit

46
Q

what happens with diabetic nephropathy?

A

mesangial expansion
thickening of BM
glomerular HTN
leads to hyperfiltration

47
Q

how often do you screen for nephropathy and how do you test for it?

A

annually
albumin to creatinine ratio
increased urinary albumin excretion starting at 30 mg/day

48
Q

how do you treat diabetic nephropathy?

A

ACE or ARB

49
Q

how do you protect against macrovascular complications?

A 
glycemic, lipid, blood pressure control
smoking cessation
wt loss
diet/exercise
possible daily baby aspirin
50
Q

what BP do we want diabetics to have

A
51
Q

what do you do first for a T2 diabetic?

A

lifestyle modification

metformin

52
Q

what is the tx course for T1 diabetics?

A

combined insulin therapy

short acting + long acting (lispro + glargine)

53
Q

what are the + and - of insulin pump?

A

convenience

cost, reliance on tech, feeling tethered

54
Q

what is the treatment of DKA and HHS

A

insulin, fluid replacement, potassium and other lyte replacement

55
Q

What is HHS?

A

hyperosmolar hyperglycemic state

56
Q

what is DKA?

A

diabetic ketoacidosis

has dehydration, inc ketoacids, hyperglycemia

57
Q

HHS labs?

A

very very high glucose
small amt of ketones
increased serum osmolality
slight acidity

58
Q

DKA labs?

A

mildly elevated glucose
very acidic
positive ketones
high ion gap

REM II (11 decks)

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