Gen Med Endo: Type 2 Diabetes|
latest |COMPREHENSIVE MOST TESTED
(frequently tested) QUESTIONS AND
VERIFIED ANSWERS | GET IT 100%
ACCURATE!!
Which type of diabetes is more common?
Type 2 (∼90%)
In the US, which populations have a higher diabetes rate (are more at risk of
getting diabetes)?
(basically non-white populations) Alaska Natives, non-Hispanic Blacks, Hispanics,
Asian-American
HbA1c level for diabetes
≥6.5%
HbA1c level for prediabetes
5.7-6.4%
FPG and OGTT level for diabetes
- FPG: 126 (mg/dL)
- PPG: 200 (mg/dL)
FPG and OGTT for prediabetes
- FPG: 100-125 (mg/dL)
- PPG: 140-199 (mg/dL)
In the pancreas, which islet cells secrete insulin?
Beta cells
In the pancreas, which islet cells secrete glucagon?
Alpha cells
Biochem: how is C-peptide related to insulin?
- proinsulin is insulin + C-peptide
- when insulin is made, C-peptide gets released
Transporter that insulin uses to get into cells
GLUT-2
Storage form of glucose
glycogen
Glucagon impact on cells
- we need MORE glucose in blood
- liver: breakdown glycogen, ↑ gluconeogenesis
, - adipose: break stuff down into fatty acids
- muscle: break stuff down into amino acids
Insulin impact on cells
- we need LESS glucose in blood
- liver: store up glucose, make glycogen
- adipose: turn fatty acids → TGs (store!)
- muscle: take up glucose, turn amino acids → proteins (store!)
Why does insulin resistance cause dyslipidemia?
A normal adipose cell will take the insulin and go "I should store more lipids!" but a
resistant cell will go "I don't care, I'm releasing lipids anyway" and more lipids end up in
the blood stream → dyslipidemia
Type 1 diabetes: what's the problem?
- Type 1 = autoimmune
- pancreas beta cells destroyed, no insulin can be made
- testing: autoantibodies + no insulin + no C-peptide
gestational diabetes: what's the problem?
- all pregnant patients get glucose intolerance, but when it peaks (24 wks), some people
get new-onset diabetes
- most go back to normal after pregnancy
After a gestational diabetes pregnancy is over, what do we do?
- test at 6 weeks (did they have T2DM before pregnancy and we missed it?)
- screen regularly for T2DM (50% chance of developing it later)
Who gets screened for gestational diabetes and what do we test?
- ALL pregnant patients
- oral glucose tolerance test
maturity-onset diabetes of the young (MODY)
- autosomal dominant
- young adults get it (we think it's type 1) but it acts like type 2
- no autoantibodies, insulin deficient but usually you have C-peptides
latent autoimmune diabetes in adults (LADA)
- we think it's type 2 but it acts like type 1
- trigger → adult starts making autoantibodies against pancreas
- we give oral meds but they don't work → early insulin
prediabetes treatment recommendations
- weight loss
- exercise 150 min/week (moderate, brisk walking/Zumba)
- change diet
- metformin (obese, 35-70, prior GDM)
True or false: family history of diabetes is only important in Type 1 diabetes.
False! Type 2 also has a strong genetic component.
T2DM risk factors
- obesity, sedentary, race/ethnicity
- HTN or HLD
- hx of PCOS or CV dz
- antipsychotics, antiretrovirals (HIV)
Type 2 diabetes: what's the problem?
latest |COMPREHENSIVE MOST TESTED
(frequently tested) QUESTIONS AND
VERIFIED ANSWERS | GET IT 100%
ACCURATE!!
Which type of diabetes is more common?
Type 2 (∼90%)
In the US, which populations have a higher diabetes rate (are more at risk of
getting diabetes)?
(basically non-white populations) Alaska Natives, non-Hispanic Blacks, Hispanics,
Asian-American
HbA1c level for diabetes
≥6.5%
HbA1c level for prediabetes
5.7-6.4%
FPG and OGTT level for diabetes
- FPG: 126 (mg/dL)
- PPG: 200 (mg/dL)
FPG and OGTT for prediabetes
- FPG: 100-125 (mg/dL)
- PPG: 140-199 (mg/dL)
In the pancreas, which islet cells secrete insulin?
Beta cells
In the pancreas, which islet cells secrete glucagon?
Alpha cells
Biochem: how is C-peptide related to insulin?
- proinsulin is insulin + C-peptide
- when insulin is made, C-peptide gets released
Transporter that insulin uses to get into cells
GLUT-2
Storage form of glucose
glycogen
Glucagon impact on cells
- we need MORE glucose in blood
- liver: breakdown glycogen, ↑ gluconeogenesis
, - adipose: break stuff down into fatty acids
- muscle: break stuff down into amino acids
Insulin impact on cells
- we need LESS glucose in blood
- liver: store up glucose, make glycogen
- adipose: turn fatty acids → TGs (store!)
- muscle: take up glucose, turn amino acids → proteins (store!)
Why does insulin resistance cause dyslipidemia?
A normal adipose cell will take the insulin and go "I should store more lipids!" but a
resistant cell will go "I don't care, I'm releasing lipids anyway" and more lipids end up in
the blood stream → dyslipidemia
Type 1 diabetes: what's the problem?
- Type 1 = autoimmune
- pancreas beta cells destroyed, no insulin can be made
- testing: autoantibodies + no insulin + no C-peptide
gestational diabetes: what's the problem?
- all pregnant patients get glucose intolerance, but when it peaks (24 wks), some people
get new-onset diabetes
- most go back to normal after pregnancy
After a gestational diabetes pregnancy is over, what do we do?
- test at 6 weeks (did they have T2DM before pregnancy and we missed it?)
- screen regularly for T2DM (50% chance of developing it later)
Who gets screened for gestational diabetes and what do we test?
- ALL pregnant patients
- oral glucose tolerance test
maturity-onset diabetes of the young (MODY)
- autosomal dominant
- young adults get it (we think it's type 1) but it acts like type 2
- no autoantibodies, insulin deficient but usually you have C-peptides
latent autoimmune diabetes in adults (LADA)
- we think it's type 2 but it acts like type 1
- trigger → adult starts making autoantibodies against pancreas
- we give oral meds but they don't work → early insulin
prediabetes treatment recommendations
- weight loss
- exercise 150 min/week (moderate, brisk walking/Zumba)
- change diet
- metformin (obese, 35-70, prior GDM)
True or false: family history of diabetes is only important in Type 1 diabetes.
False! Type 2 also has a strong genetic component.
T2DM risk factors
- obesity, sedentary, race/ethnicity
- HTN or HLD
- hx of PCOS or CV dz
- antipsychotics, antiretrovirals (HIV)
Type 2 diabetes: what's the problem?
