Diabetes Flashcards
what are the main health consequences of being overwt or obese in childhood?
HTN T2DM increased cholesterol fatty liver negative psychological outcomes
what are the main health consequences of being overwt or obese in childhood?
HTN T2DM increased cholesterol fatty liver negative psychological outcomes
What is the only hunger hormone?
ghrelin
how do you calculate BMI
body wt (kg)/ ht (m)squared
what is underweight in adults? children?
what is obese in adults? children?
> 30 (morbid is >40)
>95th percentile
what is obese in adults? children?
> 30 (morbid is >40)
>95th percentile
What is the only hunger hormone?
ghrelin
how do you calculate BMI
body wt (kg)/ ht (m)squared
what is underweight in adults? children?
what is overweight in adults? children?
> 25-29
85th-95th percentile
what is obese in adults? children?
> 30 (morbid is >40)
>95th percentile
what are health consequences of being overwt/obese?
inflammation atherosclerosis HTN dyslipidemia T2DM thrombosis -> stroke depression GERD (other GI dz) gout etc
what conditions are used to diagnose metabolic syndrome? how many need to be present?
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)
what are the therapeutic goals for metabolic syndrome?
treat underlying causes- lifestyle changes (exercise, diet)
treat cardiovascular risk factors
Where are the GLUT 2 transporters found? what do they signal?
found in pancreatic beta cells
signal insulin release
what is the MOA for insulin release?
glucose binds GLUT2 -> inc ATP intracellularly -> K channels closing -> Ca going into the cell -> depolarization -> insulin release
Where is GLUT 4 found?
Muscle and adipose
insulin binds and upregulats them on cell surfaces
what are the actions of insulin?
through the IP3 pathway
it stimulates glycogen, fat, and protein synthesis to get rid of glucose in the blood
what is the function of glucagon?
produce in alpha cells
stimulates glycogenolysis, fat catabolism, and gluconeogenesis
when is glucagon secreted?
very low carb and high protein meals
what are the 4 anti insulin hormones?
glucagon
epi/norepi
GH
ACTH
where is the GLUT 3 transporter?
brain
what are the different hormones released from the pancreas?
insulin glucagon somatostatin pancreatic polypeptide ghrelin
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
how does DKA develop?
acute insulin deficiency -> inc lipolysis -> inc ketogenesis
what are the symptoms of DKA?
N/V, stomach pain, fruity breath, polyuria, polydipsia, weakness, fatigue, confusion, heavy deep breathing
What is the function of PPARgamma
inhibits pro inflammatory cytokines activates adiponectin dec insulin resistance leptin levels dec highly expressed in adipose
what do thialzolidinediones do?
activate PPAR gamma
what are the FPG, OGTT, and HbA1C of pre diabetes
FPG- 100-125
OGTT- 140-199
A1C- 5.7-6.4
what is normal A1C?
what are the FPG, OGTT, and HbA1C of diabetes?
FPG- >126
OGTT- >200
A1c- >6.5
how often do you check A1C?
every 3 mo
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
when can you diagnose diabetes with one test?
if they have symptoms and random plasma glucose is >200
everything else needs repeating
which diabetes shows acanthosis nigricans?
Type 2 DM
In which diabetics do HHS and DKA present?
HHS- type 2
DKA- type 1
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
what is the genetic etiology of gestational diabetes
MODY
what endocrinopathies are related to secondary etiologies of T2DM?
cushings acromegaly pheo glucagonoma somatostatinoma hyperthyroid
What are the microvascular complications of diabetes
retinopathy
neuropathy
nephropathy
what is the key feature of proliferative retinopathy?
neovascularization
no reversible
how often do you check for retinopathy?
every year
what does diabetic neuropathy lead to?
foot ulcers
muscle and joint disease
how often do you check for neuropathy?
annual comprehensive exam with monofilament
visual inspection every visit
what happens with diabetic nephropathy?
mesangial expansion
thickening of BM
glomerular HTN
leads to hyperfiltration
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
how do you treat diabetic nephropathy?
ACE or ARB
how do you protect against macrovascular complications?
glycemic, lipid, blood pressure control smoking cessation wt loss diet/exercise possible daily baby aspirin
what BP do we want diabetics to have
what do you do first for a T2 diabetic?
lifestyle modification
metformin
what is the tx course for T1 diabetics?
combined insulin therapy
short acting + long acting (lispro + glargine)
what are the + and - of insulin pump?
convenience
cost, reliance on tech, feeling tethered
what is the treatment of DKA and HHS
insulin, fluid replacement, potassium and other lyte replacement
What is HHS?
hyperosmolar hyperglycemic state
what is DKA?
diabetic ketoacidosis
has dehydration, inc ketoacids, hyperglycemia
HHS labs?
very very high glucose
small amt of ketones
increased serum osmolality
slight acidity
DKA labs?
mildly elevated glucose
very acidic
positive ketones
high ion gap
